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In the Ancient Near East the Copper Age covered about the same period, beginning in the late 5th millennium BC and lasting for about a millennium before it gave rise to the Early Bronze Age.
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Chalcolithic - Wikipedia
vidence of copper smelting at high temperature, from c. 5000 BC (7000 BP).[3] The transition from Copper Age to Bronze Age in Europe occurred between the late 5th and the late 3rd millennia BC. <span>In the Ancient Near East the Copper Age covered about the same period, beginning in the late 5th millennium BC and lasting for about a millennium before it gave rise to the Early Bronze Age. Contents 1 Terminology 2 Near East 3 Europe 4 South Asia 5 Pre-Columbian Americas 6 East Asia 7 Sub-Saharan Africa 8 See also 9 References 10 Sources 11 External links Terminology[edit]




Flashcard 7105819577612

Question
In the Ancient Near East the Copper Age covered about the same period, beginning in the late [...]th millennium BC and lasting for about a millennium before it gave rise to the Early Bronze Age.
Answer
5

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In the Ancient Near East the Copper Age covered about the same period, beginning in the late 5th millennium BC and lasting for about a millennium before it gave rise to the Early Bronze Age.

Original toplevel document

Chalcolithic - Wikipedia
vidence of copper smelting at high temperature, from c. 5000 BC (7000 BP).[3] The transition from Copper Age to Bronze Age in Europe occurred between the late 5th and the late 3rd millennia BC. <span>In the Ancient Near East the Copper Age covered about the same period, beginning in the late 5th millennium BC and lasting for about a millennium before it gave rise to the Early Bronze Age. Contents 1 Terminology 2 Near East 3 Europe 4 South Asia 5 Pre-Columbian Americas 6 East Asia 7 Sub-Saharan Africa 8 See also 9 References 10 Sources 11 External links Terminology[edit]







In the year 1000, the county of Anjou (in west-central France) was ruled by Fulk Nerra (987–1040), a brutal and rapacious warlord.
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The Crusades: The Authoritative History of the War for the Holy Land PDF Book by Thomas Asbridge Read Online Free - Page 3
hy, but more pressing still is the question of how this age of conflict affected history, and why these ancient struggles still seem to cast a shadow over the world to this day. MEDIEVAL EUROPE <span>In the year 1000, the county of Anjou (in west-central France) was ruled by Fulk Nerra (987–1040), a brutal and rapacious warlord. Fulk spent most of his fifty-three years in power locked in near-constant struggle: fighting on every front to retain control of his unruly county; scheming to preserve his independence




Flashcard 7105826393356

Question
In the year [...], the county of Anjou (in west-central France) was ruled by Fulk Nerra (987–1040), a brutal and rapacious warlord.
Answer
1000

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In the year 1000, the county of Anjou (in west-central France) was ruled by Fulk Nerra (987–1040), a brutal and rapacious warlord.

Original toplevel document

The Crusades: The Authoritative History of the War for the Holy Land PDF Book by Thomas Asbridge Read Online Free - Page 3
hy, but more pressing still is the question of how this age of conflict affected history, and why these ancient struggles still seem to cast a shadow over the world to this day. MEDIEVAL EUROPE <span>In the year 1000, the county of Anjou (in west-central France) was ruled by Fulk Nerra (987–1040), a brutal and rapacious warlord. Fulk spent most of his fifty-three years in power locked in near-constant struggle: fighting on every front to retain control of his unruly county; scheming to preserve his independence







Flashcard 7105827966220

Question
In the year 1000, the county of Anjou (in west-central France) was ruled by [...] (987–1040), a brutal and rapacious warlord.
Answer
Fulk Nerra

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In the year 1000, the county of Anjou (in west-central France) was ruled by Fulk Nerra (987–1040), a brutal and rapacious warlord.

Original toplevel document

The Crusades: The Authoritative History of the War for the Holy Land PDF Book by Thomas Asbridge Read Online Free - Page 3
hy, but more pressing still is the question of how this age of conflict affected history, and why these ancient struggles still seem to cast a shadow over the world to this day. MEDIEVAL EUROPE <span>In the year 1000, the county of Anjou (in west-central France) was ruled by Fulk Nerra (987–1040), a brutal and rapacious warlord. Fulk spent most of his fifty-three years in power locked in near-constant struggle: fighting on every front to retain control of his unruly county; scheming to preserve his independence







Roman imperial rule had provided stability and affluence in the West until the late fourth century CE (Common Era). In the East the Roman Empire lived on until 1453, ruled from the great city of Constantinople, founded in 324 by Constantine the Great–the first emperor to convert to Christianity.
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order to the world in accordance with His divine will. This rather hazily imagined ideal was by no means a perfect recollection of Europe’s history, but it did encapsulate some shards of truth. <span>Roman imperial rule had provided stability and affluence in the West until the late fourth century CE (Common Era). In the East the Roman Empire lived on until 1453, ruled from the great city of Constantinople, founded in 324 by Constantine the Great–the first emperor to convert to Christianity. Today, historians refer to this enduring realm as Byzantium. In the West between the fifth and the seventh centuries power devolved on to a bewildering array of ‘barbarian’ tribes, but




Flashcard 7105831111948

Question
Roman imperial rule had provided stability and affluence in the West until the late fourth century CE (Common Era). In the East the Roman Empire lived on until [...], ruled from the great city of [...] , founded in [...] by [...] –the first emperor to convert to Christianity.
Answer

1453

Constantinople

324

Constantine the Great


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Roman imperial rule had provided stability and affluence in the West until the late fourth century CE (Common Era). In the East the Roman Empire lived on until 1453, ruled from the great city of Constantinople, founded in 324 by Constantine the Great–the first emperor to convert to Christianity.

Original toplevel document

The Crusades: The Authoritative History of the War for the Holy Land PDF Book by Thomas Asbridge Read Online Free - Page 3
order to the world in accordance with His divine will. This rather hazily imagined ideal was by no means a perfect recollection of Europe’s history, but it did encapsulate some shards of truth. <span>Roman imperial rule had provided stability and affluence in the West until the late fourth century CE (Common Era). In the East the Roman Empire lived on until 1453, ruled from the great city of Constantinople, founded in 324 by Constantine the Great–the first emperor to convert to Christianity. Today, historians refer to this enduring realm as Byzantium. In the West between the fifth and the seventh centuries power devolved on to a bewildering array of ‘barbarian’ tribes, but







In the West between the fifth and the seventh centuries power devolved on to a bewildering array of ‘barbarian’ tribes, but around the year 500 one of these groups, the Franks, established control over north-eastern Gaul, giving rise to a kingdom known as Francia
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, ruled from the great city of Constantinople, founded in 324 by Constantine the Great–the first emperor to convert to Christianity. Today, historians refer to this enduring realm as Byzantium. <span>In the West between the fifth and the seventh centuries power devolved on to a bewildering array of ‘barbarian’ tribes, but around the year 500 one of these groups, the Franks, established control over north-eastern Gaul, giving rise to a kingdom known as Francia (from which the modern nation of France took its name).* By 800, a descendant of these Franks, Charlemagne (768– 814), had united such a huge swathe of territory–encompassing much of mo




Flashcard 7105834519820

Question
In the West between the fifth and the seventh centuries power devolved on to a bewildering array of ‘barbarian’ tribes, but around the year 500 one of these groups, the [...], established control over north-eastern Gaul, giving rise to a kingdom known as [...]
Answer

Franks

Francia


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In the West between the fifth and the seventh centuries power devolved on to a bewildering array of ‘barbarian’ tribes, but around the year 500 one of these groups, the Franks, established control over north-eastern Gaul, giving rise to a kingdom known as Francia

Original toplevel document

The Crusades: The Authoritative History of the War for the Holy Land PDF Book by Thomas Asbridge Read Online Free - Page 3
, ruled from the great city of Constantinople, founded in 324 by Constantine the Great–the first emperor to convert to Christianity. Today, historians refer to this enduring realm as Byzantium. <span>In the West between the fifth and the seventh centuries power devolved on to a bewildering array of ‘barbarian’ tribes, but around the year 500 one of these groups, the Franks, established control over north-eastern Gaul, giving rise to a kingdom known as Francia (from which the modern nation of France took its name).* By 800, a descendant of these Franks, Charlemagne (768– 814), had united such a huge swathe of territory–encompassing much of mo







By 800, a descendant of these Franks, Charlemagne (768–

814), had united such a huge swathe of territory–encompassing much of modern France, Germany, Italy and the Low Countries–that he could lay claim to the long-dormant title of emperor of the West.

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und the year 500 one of these groups, the Franks, established control over north-eastern Gaul, giving rise to a kingdom known as Francia (from which the modern nation of France took its name).* <span>By 800, a descendant of these Franks, Charlemagne (768– 814), had united such a huge swathe of territory–encompassing much of modern France, Germany, Italy and the Low Countries–that he could lay claim to the long-dormant title of emperor of the West. Charlemagne and his successors, the Carolingians, presided over a short-lived period of renewed security, but their empire crumbled under the weight of succession disputes and repeated




Flashcard 7105837927692

Question

By [...], a descendant of these Franks, Charlemagne (768–

814), had united such a huge swathe of territory–encompassing much of modern France, Germany, Italy and the Low Countries–that he could lay claim to the long-dormant title of emperor of the West.

Answer
800

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By 800, a descendant of these Franks, Charlemagne (768– 814), had united such a huge swathe of territory–encompassing much of modern France, Germany, Italy and the Low Countries–that he could

Original toplevel document

The Crusades: The Authoritative History of the War for the Holy Land PDF Book by Thomas Asbridge Read Online Free - Page 3
und the year 500 one of these groups, the Franks, established control over north-eastern Gaul, giving rise to a kingdom known as Francia (from which the modern nation of France took its name).* <span>By 800, a descendant of these Franks, Charlemagne (768– 814), had united such a huge swathe of territory–encompassing much of modern France, Germany, Italy and the Low Countries–that he could lay claim to the long-dormant title of emperor of the West. Charlemagne and his successors, the Carolingians, presided over a short-lived period of renewed security, but their empire crumbled under the weight of succession disputes and repeated







Charlemagne and his successors, the Carolingians, presided over a short-lived period of renewed security, but their empire crumbled under the weight of succession disputes and repeated invasions by Scandinavian Vikings and eastern European Magyars.
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4), had united such a huge swathe of territory–encompassing much of modern France, Germany, Italy and the Low Countries–that he could lay claim to the long-dormant title of emperor of the West. <span>Charlemagne and his successors, the Carolingians, presided over a short-lived period of renewed security, but their empire crumbled under the weight of succession disputes and repeated invasions by Scandinavian Vikings and eastern European Magyars. From the 850s onwards, Europe was again ripped apart by political fragmentation, warfare and unrest. The embattled kings of Germany still sought to claim the imperial title and a royal




Flashcard 7105841073420

Question
Charlemagne and his successors, the [...], presided over a short-lived period of renewed security, but their empire crumbled under the weight of succession disputes and repeated invasions by Scandinavian Vikings and eastern European Magyars.
Answer
Carolingians

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Charlemagne and his successors, the Carolingians, presided over a short-lived period of renewed security, but their empire crumbled under the weight of succession disputes and repeated invasions by Scandinavian Vikings and eastern Eur

Original toplevel document

The Crusades: The Authoritative History of the War for the Holy Land PDF Book by Thomas Asbridge Read Online Free - Page 3
4), had united such a huge swathe of territory–encompassing much of modern France, Germany, Italy and the Low Countries–that he could lay claim to the long-dormant title of emperor of the West. <span>Charlemagne and his successors, the Carolingians, presided over a short-lived period of renewed security, but their empire crumbled under the weight of succession disputes and repeated invasions by Scandinavian Vikings and eastern European Magyars. From the 850s onwards, Europe was again ripped apart by political fragmentation, warfare and unrest. The embattled kings of Germany still sought to claim the imperial title and a royal







Although Gregory went too far, too fast and ended his pontificate in ignominious exile in southern Italy, his bold strides did much to advance the twinned causes of reform and papal empowerment, establishing a platform from which one of his successors (and former adviser), Pope Urban II (1088–99), could instigate the First Crusade.
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cal affairs. In pursuit of this ambition, he was willing to embrace almost any available means–even the potential use of violence, enacted by papal servants whom he called ‘soldiers of Christ’. <span>Although Gregory went too far, too fast and ended his pontificate in ignominious exile in southern Italy, his bold strides did much to advance the twinned causes of reform and papal empowerment, establishing a platform from which one of his successors (and former adviser), Pope Urban II (1088–99), could instigate the First Crusade.4 Urban’s call for a holy war found a willing audience across Europe, in large part because of the prevailing religious atmosphere in the Latin world. Across the West, Christianity was a




Flashcard 7105846054156

Question
Although Gregory went too far, too fast and ended his pontificate in ignominious exile in southern Italy, his bold strides did much to advance the twinned causes of reform and papal empowerment, establishing a platform from which one of his successors (and former adviser), [...] (1088–99), could instigate the First Crusade.
Answer
Pope Urban II

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exile in southern Italy, his bold strides did much to advance the twinned causes of reform and papal empowerment, establishing a platform from which one of his successors (and former adviser), <span>Pope Urban II (1088–99), could instigate the First Crusade. <span>

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The Crusades: The Authoritative History of the War for the Holy Land PDF Book by Thomas Asbridge Read Online Free - Page 4
cal affairs. In pursuit of this ambition, he was willing to embrace almost any available means–even the potential use of violence, enacted by papal servants whom he called ‘soldiers of Christ’. <span>Although Gregory went too far, too fast and ended his pontificate in ignominious exile in southern Italy, his bold strides did much to advance the twinned causes of reform and papal empowerment, establishing a platform from which one of his successors (and former adviser), Pope Urban II (1088–99), could instigate the First Crusade.4 Urban’s call for a holy war found a willing audience across Europe, in large part because of the prevailing religious atmosphere in the Latin world. Across the West, Christianity was a







The most influential early Christian thinker to wrestle with these issues was the North African bishop St Augustine of Hippo (354–430 CE).
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gressive warfare might be permissible; and in the New Testament, Jesus had said that he came to bring not peace but a sword, and had used a whip of cords to beat moneylenders out of the Temple. <span>The most influential early Christian thinker to wrestle with these issues was the North African bishop St Augustine of Hippo (354–430 CE). His work laid the foundation upon which the papacy eventually built the notion of crusading. St Augustine argued that a war could be both lawful and justifiable if fought under strict c




Flashcard 7105851034892

Question
The most influential early Christian thinker to wrestle with these issues (violence vs pacifism) was the North African bishop [...] (354–430 CE). His work laid the foundation upon which the papacy eventually built the notion of crusading.
Answer
St Augustine of Hippo

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The most influential early Christian thinker to wrestle with these issues was the North African bishop St Augustine of Hippo (354–430 CE).

Original toplevel document

The Crusades: The Authoritative History of the War for the Holy Land PDF Book by Thomas Asbridge Read Online Free - Page 5
gressive warfare might be permissible; and in the New Testament, Jesus had said that he came to bring not peace but a sword, and had used a whip of cords to beat moneylenders out of the Temple. <span>The most influential early Christian thinker to wrestle with these issues was the North African bishop St Augustine of Hippo (354–430 CE). His work laid the foundation upon which the papacy eventually built the notion of crusading. St Augustine argued that a war could be both lawful and justifiable if fought under strict c







His work laid the foundation upon which the papacy eventually built the notion of crusading. St Augustine argued that a war could be both lawful and justifiable if fought under strict conditions. His complex theories were later simplified to produce just three prerequisites of a Just War: proclamation by a ‘legitimate authority’, such as a king or bishop; a ‘just cause’, like defence against enemy attack or the recovery of lost territory; and prosecution with

‘right intention’, that is, with the least possible violence.

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whip of cords to beat moneylenders out of the Temple. The most influential early Christian thinker to wrestle with these issues was the North African bishop St Augustine of Hippo (354–430 CE). <span>His work laid the foundation upon which the papacy eventually built the notion of crusading. St Augustine argued that a war could be both lawful and justifiable if fought under strict conditions. His complex theories were later simplified to produce just three prerequisites of a Just War: proclamation by a ‘legitimate authority’, such as a king or bishop; a ‘just cause’, like defence against enemy attack or the recovery of lost territory; and prosecution with ‘right intention’, that is, with the least possible violence. < Prev Page Jump to .... 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 5




Flashcard 7105855753484

Question

His work laid the foundation upon which the papacy eventually built the notion of crusading. St Augustine argued that a war could be both lawful and justifiable if fought under strict conditions. His complex theories were later simplified to produce just three prerequisites of a Just War:

[...]

Answer

proclamation by a ‘legitimate authority’, such as a king or bishop; a ‘just cause’, like defence against enemy attack or the recovery of lost territory; and prosecution with

‘right intention’, that is, with the least possible violence.


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Augustine argued that a war could be both lawful and justifiable if fought under strict conditions. His complex theories were later simplified to produce just three prerequisites of a Just War: <span>proclamation by a ‘legitimate authority’, such as a king or bishop; a ‘just cause’, like defence against enemy attack or the recovery of lost territory; and prosecution with ‘right intention’, that is, with the least possible violence. <span>

Original toplevel document

The Crusades: The Authoritative History of the War for the Holy Land PDF Book by Thomas Asbridge Read Online Free - Page 5
whip of cords to beat moneylenders out of the Temple. The most influential early Christian thinker to wrestle with these issues was the North African bishop St Augustine of Hippo (354–430 CE). <span>His work laid the foundation upon which the papacy eventually built the notion of crusading. St Augustine argued that a war could be both lawful and justifiable if fought under strict conditions. His complex theories were later simplified to produce just three prerequisites of a Just War: proclamation by a ‘legitimate authority’, such as a king or bishop; a ‘just cause’, like defence against enemy attack or the recovery of lost territory; and prosecution with ‘right intention’, that is, with the least possible violence. < Prev Page Jump to .... 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 5







During the second half of the eleventh century, Latin Christianity began to edge ever closer towards the acceptance of holy war. In the early stages of the Reform movement, the papacy began to perceive the need for a military arm with which to reinforce its agenda and manifest its will. This prompted a succession of popes to experiment with the sponsoring of warfare, calling upon Christian supporters to defend the Church in return for vaguely expressed forms of spiritual reward. It was under the forceful guidance of Pope Gregory VII that the doctrine and application of sacred violence jumped ahead. Intent upon recruiting a papal army that owed its allegiance to Rome, he set about reinterpreting Christian tradition. For centuries theologians had characterised the internal, spiritual battle that devoted Christians waged against sin as the ‘warfare of Christ’, and monks were sometimes described as the ‘soldiers of Christ’. Gregory twisted this idea to suit his purpose, proclaiming that all lay society had one overriding obligation: to defend the Latin Church as ‘soldiers of Christ’ through actual physical warfare.
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tern Europe. And by the turn of the millennium it had become relatively common for Christian clergy to bless weapons and armour, and the lives of various ‘warrior saints’ were being celebrated. <span>During the second half of the eleventh century, Latin Christianity began to edge ever closer towards the acceptance of holy war. In the early stages of the Reform movement, the papacy began to perceive the need for a military arm with which to reinforce its agenda and manifest its will. This prompted a succession of popes to experiment with the sponsoring of warfare, calling upon Christian supporters to defend the Church in return for vaguely expressed forms of spiritual reward. It was under the forceful guidance of Pope Gregory VII that the doctrine and application of sacred violence jumped ahead. Intent upon recruiting a papal army that owed its allegiance to Rome, he set about reinterpreting Christian tradition. For centuries theologians had characterised the internal, spiritual battle that devoted Christians waged against sin as the ‘warfare of Christ’, and monks were sometimes described as the ‘soldiers of Christ’. Gregory twisted this idea to suit his purpose, proclaiming that all lay society had one overriding obligation: to defend the Latin Church as ‘soldiers of Christ’ through actual physical warfare. Early in his pontificate, Gregory laid plans for a grand military enterprise that can be regarded as the first real prototype for a crusade. In 1074 he tried to launch a holy war in the




Flashcard 7105860734220

Question
During the second half of the eleventh century, Latin Christianity began to edge ever closer towards the acceptance of holy war. In the early stages of the Reform movement, the papacy began to perceive the need for a military arm with which to reinforce its agenda and manifest its will. This prompted a succession of popes to experiment with the sponsoring of warfare, calling upon Christian supporters to defend the Church in return for vaguely expressed forms of spiritual reward. It was under the forceful guidance of [...] that the doctrine and application of sacred violence jumped ahead. Intent upon recruiting a papal army that owed its allegiance to Rome, he set about reinterpreting Christian tradition. For centuries theologians had characterised the internal, spiritual battle that devoted Christians waged against sin as the ‘warfare of Christ’, and monks were sometimes described as the ‘soldiers of Christ’. [...] twisted this idea to suit his purpose, proclaiming that all lay society had one overriding obligation: to defend the Latin Church as ‘soldiers of Christ’ through actual physical warfare.
Answer
Pope Gregory VII

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xperiment with the sponsoring of warfare, calling upon Christian supporters to defend the Church in return for vaguely expressed forms of spiritual reward. It was under the forceful guidance of <span>Pope Gregory VII that the doctrine and application of sacred violence jumped ahead. Intent upon recruiting a papal army that owed its allegiance to Rome, he set about reinterpreting Christian tradition.

Original toplevel document

The Crusades: The Authoritative History of the War for the Holy Land PDF Book by Thomas Asbridge Read Online Free - Page 6
tern Europe. And by the turn of the millennium it had become relatively common for Christian clergy to bless weapons and armour, and the lives of various ‘warrior saints’ were being celebrated. <span>During the second half of the eleventh century, Latin Christianity began to edge ever closer towards the acceptance of holy war. In the early stages of the Reform movement, the papacy began to perceive the need for a military arm with which to reinforce its agenda and manifest its will. This prompted a succession of popes to experiment with the sponsoring of warfare, calling upon Christian supporters to defend the Church in return for vaguely expressed forms of spiritual reward. It was under the forceful guidance of Pope Gregory VII that the doctrine and application of sacred violence jumped ahead. Intent upon recruiting a papal army that owed its allegiance to Rome, he set about reinterpreting Christian tradition. For centuries theologians had characterised the internal, spiritual battle that devoted Christians waged against sin as the ‘warfare of Christ’, and monks were sometimes described as the ‘soldiers of Christ’. Gregory twisted this idea to suit his purpose, proclaiming that all lay society had one overriding obligation: to defend the Latin Church as ‘soldiers of Christ’ through actual physical warfare. Early in his pontificate, Gregory laid plans for a grand military enterprise that can be regarded as the first real prototype for a crusade. In 1074 he tried to launch a holy war in the







Early in his pontificate, Gregory laid plans for a grand military enterprise that can be regarded as the first real prototype for a crusade. In 1074 he tried to launch a holy war in the eastern Mediterranean in aid of the Greek Orthodox Christians of Byzantium, who were, he claimed, ‘daily being butchered like cattle’ by the Muslims of Asia Minor.
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regory twisted this idea to suit his purpose, proclaiming that all lay society had one overriding obligation: to defend the Latin Church as ‘soldiers of Christ’ through actual physical warfare. <span>Early in his pontificate, Gregory laid plans for a grand military enterprise that can be regarded as the first real prototype for a crusade. In 1074 he tried to launch a holy war in the eastern Mediterranean in aid of the Greek Orthodox Christians of Byzantium, who were, he claimed, ‘daily being butchered like cattle’ by the Muslims of Asia Minor. Latins fighting in this campaign were promised a ‘heavenly reward’. His grandiose project fell flat, eliciting very limited recruitment, perhaps because Gregory had boldly pronounced hi




Flashcard 7105864666380

Question
Early in his pontificate, Gregory laid plans for a grand military enterprise that can be regarded as the first real prototype for a crusade. In [...] he tried to launch a holy war in the eastern Mediterranean in aid of the Greek Orthodox Christians of Byzantium, who were, he claimed, ‘daily being butchered like cattle’ by the Muslims of Asia Minor.
Answer
1074

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Early in his pontificate, Gregory laid plans for a grand military enterprise that can be regarded as the first real prototype for a crusade. In 1074 he tried to launch a holy war in the eastern Mediterranean in aid of the Greek Orthodox Christians of Byzantium, who were, he claimed, ‘daily being butchered like cattle’ by the Muslims

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regory twisted this idea to suit his purpose, proclaiming that all lay society had one overriding obligation: to defend the Latin Church as ‘soldiers of Christ’ through actual physical warfare. <span>Early in his pontificate, Gregory laid plans for a grand military enterprise that can be regarded as the first real prototype for a crusade. In 1074 he tried to launch a holy war in the eastern Mediterranean in aid of the Greek Orthodox Christians of Byzantium, who were, he claimed, ‘daily being butchered like cattle’ by the Muslims of Asia Minor. Latins fighting in this campaign were promised a ‘heavenly reward’. His grandiose project fell flat, eliciting very limited recruitment, perhaps because Gregory had boldly pronounced hi







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Question
Early in his pontificate, Gregory laid plans for a grand military enterprise that can be regarded as the first real prototype for a crusade. In 1074 he tried to launch a holy war in the eastern Mediterranean in aid of the [...] who were, he claimed, ‘daily being butchered like cattle’ by the Muslims of Asia Minor.
Answer
Greek Orthodox Christians of Byzantium,

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egory laid plans for a grand military enterprise that can be regarded as the first real prototype for a crusade. In 1074 he tried to launch a holy war in the eastern Mediterranean in aid of the <span>Greek Orthodox Christians of Byzantium, who were, he claimed, ‘daily being butchered like cattle’ by the Muslims of Asia Minor. <span>

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regory twisted this idea to suit his purpose, proclaiming that all lay society had one overriding obligation: to defend the Latin Church as ‘soldiers of Christ’ through actual physical warfare. <span>Early in his pontificate, Gregory laid plans for a grand military enterprise that can be regarded as the first real prototype for a crusade. In 1074 he tried to launch a holy war in the eastern Mediterranean in aid of the Greek Orthodox Christians of Byzantium, who were, he claimed, ‘daily being butchered like cattle’ by the Muslims of Asia Minor. Latins fighting in this campaign were promised a ‘heavenly reward’. His grandiose project fell flat, eliciting very limited recruitment, perhaps because Gregory had boldly pronounced hi







But in the early 1080s, with the conflict with the German emperor in full flow, Gregory took a critical step towards clarification. He wrote that his supporters should fight the emperor and face ‘the danger of the coming battle for the remission of all their sins’.
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pronounced his intention to lead the campaign in person. The pope’s 1074 formulation of the link between military service to God and the resultant spiritual recompense still lacked specificity. <span>But in the early 1080s, with the conflict with the German emperor in full flow, Gregory took a critical step towards clarification. He wrote that his supporters should fight the emperor and face ‘the danger of the coming battle for the remission of all their sins’. This seemed to indicate that participation in this holy struggle had the same power to purify the soul as other forms of penance because it promised, just like a pilgrimage, to be both




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Question
But in the early 1080s, with the conflict with the German emperor in full flow, Gregory took a critical step towards clarification. He wrote that his supporters should fight the emperor and face ‘[...]’.
Answer
the danger of the coming battle for the remission of all their sins

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t in the early 1080s, with the conflict with the German emperor in full flow, Gregory took a critical step towards clarification. He wrote that his supporters should fight the emperor and face ‘<span>the danger of the coming battle for the remission of all their sins’. <span>

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pronounced his intention to lead the campaign in person. The pope’s 1074 formulation of the link between military service to God and the resultant spiritual recompense still lacked specificity. <span>But in the early 1080s, with the conflict with the German emperor in full flow, Gregory took a critical step towards clarification. He wrote that his supporters should fight the emperor and face ‘the danger of the coming battle for the remission of all their sins’. This seemed to indicate that participation in this holy struggle had the same power to purify the soul as other forms of penance because it promised, just like a pilgrimage, to be both







Nonetheless, Gregory cannot be regarded as the prime architect of the crusades because he manifestly failed to construct a compelling and convincing notion of holy war that resonated with the Christians of Europe. That would be the work of Pope Urban II.
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d and the Latin Church. He also went some considerable way to grounding the concept of sanctified violence within a penitential framework–an idea that would be part of the essence of crusading. <span>Nonetheless, Gregory cannot be regarded as the prime architect of the crusades because he manifestly failed to construct a compelling and convincing notion of holy war that resonated with the Christians of Europe. That would be the work of Pope Urban II. THE MUSLIM WORLD From the end of the eleventh century onwards, the crusades pitted western European Franks against the Muslims of the eastern Mediterranean. This was not because these h




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Question
Nonetheless, Gregory cannot be regarded as the prime architect of the crusades because he manifestly failed to construct a compelling and convincing notion of holy war that resonated with the Christians of Europe. That would be the work of [...].
Answer
Pope Urban II

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prime architect of the crusades because he manifestly failed to construct a compelling and convincing notion of holy war that resonated with the Christians of Europe. That would be the work of <span>Pope Urban II. <span>

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d and the Latin Church. He also went some considerable way to grounding the concept of sanctified violence within a penitential framework–an idea that would be part of the essence of crusading. <span>Nonetheless, Gregory cannot be regarded as the prime architect of the crusades because he manifestly failed to construct a compelling and convincing notion of holy war that resonated with the Christians of Europe. That would be the work of Pope Urban II. THE MUSLIM WORLD From the end of the eleventh century onwards, the crusades pitted western European Franks against the Muslims of the eastern Mediterranean. This was not because these h







According to Muslim tradition, Islam was born in c. 610 CE when Muhammad–an illiterate, forty-year-old Arab native of Mecca (in modern Saudi Arabia)–began to experience a series of ‘revelations’ from Allah (God), relayed by the Archangel Gabriel.
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dicate Islam, or even to convert Muslims to the Christian faith. Rather, it was a consequence of Islam’s dominion over the Holy Land and the sacred city of Jerusalem. The early history of Islam <span>According to Muslim tradition, Islam was born in c. 610 CE when Muhammad–an illiterate, forty-year-old Arab native of Mecca (in modern Saudi Arabia)–began to experience a series of ‘revelations’ from Allah (God), relayed by the Archangel Gabriel. These ‘revelations’, regarded as the sacred and immutable words of God, were later set down in written form to become the Koran. During his lifetime, Muhammad set out to convert the pag




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Question
According to Muslim tradition, Islam was born in c. [...] CE when Muhammad–an illiterate, forty-year-old Arab native of Mecca (in modern Saudi Arabia)–began to experience a series of ‘revelations’ from Allah (God), relayed by the Archangel Gabriel.
Answer
610

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According to Muslim tradition, Islam was born in c. 610 CE when Muhammad–an illiterate, forty-year-old Arab native of Mecca (in modern Saudi Arabia)–began to experience a series of ‘revelations’ from Allah (God), relayed by the Archangel Gab

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dicate Islam, or even to convert Muslims to the Christian faith. Rather, it was a consequence of Islam’s dominion over the Holy Land and the sacred city of Jerusalem. The early history of Islam <span>According to Muslim tradition, Islam was born in c. 610 CE when Muhammad–an illiterate, forty-year-old Arab native of Mecca (in modern Saudi Arabia)–began to experience a series of ‘revelations’ from Allah (God), relayed by the Archangel Gabriel. These ‘revelations’, regarded as the sacred and immutable words of God, were later set down in written form to become the Koran. During his lifetime, Muhammad set out to convert the pag







In 622 the Prophet was forced to flee to the nearby city of Medina, a journey which served as the starting date for the Muslim calendar, and he then waged a bloody and prolonged war of religion against Mecca, finally conquering the city shortly before his death in 632.
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ut to convert the pagan polytheist Arabs of Mecca and the surrounding Hijaz region (on the Arabian Peninsula’s western coast) to the monotheistic faith of Islam. This proved to be no easy task. <span>In 622 the Prophet was forced to flee to the nearby city of Medina, a journey which served as the starting date for the Muslim calendar, and he then waged a bloody and prolonged war of religion against Mecca, finally conquering the city shortly before his death in 632. The religion founded by Muhammad–Islam, meaning submission to the will of God–had common roots with Judaism and Christianity. During his life, the Prophet came into contact with adheren




Flashcard 7105878822156

Question
In [...] the Prophet was forced to flee to the nearby city of Medina, a journey which served as the starting date for the Muslim calendar, and he then waged a bloody and prolonged war of religion against Mecca, finally conquering the city shortly before his death in [...] .
Answer

622

632


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In 622 the Prophet was forced to flee to the nearby city of Medina, a journey which served as the starting date for the Muslim calendar, and he then waged a bloody and prolonged war of religio

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The Crusades: The Authoritative History of the War for the Holy Land PDF Book by Thomas Asbridge Read Online Free - Page 6
ut to convert the pagan polytheist Arabs of Mecca and the surrounding Hijaz region (on the Arabian Peninsula’s western coast) to the monotheistic faith of Islam. This proved to be no easy task. <span>In 622 the Prophet was forced to flee to the nearby city of Medina, a journey which served as the starting date for the Muslim calendar, and he then waged a bloody and prolonged war of religion against Mecca, finally conquering the city shortly before his death in 632. The religion founded by Muhammad–Islam, meaning submission to the will of God–had common roots with Judaism and Christianity. During his life, the Prophet came into contact with adheren







In the mid-630s ferocious armies of highly mobile, mounted Arab tribesmen began to pour out of the Arabian Peninsula. By 650 they had achieved startling success. With mercurial speed, Palestine, Syria, Iraq, Iran and Egypt were absorbed into the new Arab-Islamic state. Over the next century the pace of expansion slowed from this breakneck pace, but inexorable gains continued, such that in the mid-eighth century the Muslim world stretched from the Indus River and the borders of China in the east, across North Africa to Spain and southern France in the west.
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total submission and immediate conversion to Islam, the Muslims allowed ‘Peoples of the Book’, such as Jews and Christians, to continue in their faiths in return for the payment of a poll tax. <span>In the mid-630s ferocious armies of highly mobile, mounted Arab tribesmen began to pour out of the Arabian Peninsula. By 650 they had achieved startling success. With mercurial speed, Palestine, Syria, Iraq, Iran and Egypt were absorbed into the new Arab-Islamic state. Over the next century the pace of expansion slowed from this breakneck pace, but inexorable gains continued, such that in the mid-eighth century the Muslim world stretched from the Indus River and the borders of China in the east, across North Africa to Spain and southern France in the west. In the context of crusading history, a critical stage in this whole process was the capture of Jerusalem in 638 from the Greek Christians of Byzantium. This ancient city came to be reve




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Question
In the mid-[...]s ferocious armies of highly mobile, mounted Arab tribesmen began to pour out of the Arabian Peninsula. By [...] they had achieved startling success. With mercurial speed, Palestine, Syria, Iraq, Iran and Egypt were absorbed into the new Arab-Islamic state. Over the next century the pace of expansion slowed from this breakneck pace, but inexorable gains continued, such that in the mid-eighth century the Muslim world stretched from the Indus River and the borders of China in the east, across North Africa to Spain and southern France in the west.
Answer

630

650


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In the mid-630s ferocious armies of highly mobile, mounted Arab tribesmen began to pour out of the Arabian Peninsula. By 650 they had achieved startling success. With mercurial speed, Palestine, Syria

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total submission and immediate conversion to Islam, the Muslims allowed ‘Peoples of the Book’, such as Jews and Christians, to continue in their faiths in return for the payment of a poll tax. <span>In the mid-630s ferocious armies of highly mobile, mounted Arab tribesmen began to pour out of the Arabian Peninsula. By 650 they had achieved startling success. With mercurial speed, Palestine, Syria, Iraq, Iran and Egypt were absorbed into the new Arab-Islamic state. Over the next century the pace of expansion slowed from this breakneck pace, but inexorable gains continued, such that in the mid-eighth century the Muslim world stretched from the Indus River and the borders of China in the east, across North Africa to Spain and southern France in the west. In the context of crusading history, a critical stage in this whole process was the capture of Jerusalem in 638 from the Greek Christians of Byzantium. This ancient city came to be reve







In the context of crusading history, a critical stage in this whole process was the capture of Jerusalem in 638 from the Greek Christians of Byzantium. This ancient city came to be revered as Islam’s third-holiest site, after Mecca and Medina.
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ontinued, such that in the mid-eighth century the Muslim world stretched from the Indus River and the borders of China in the east, across North Africa to Spain and southern France in the west. <span>In the context of crusading history, a critical stage in this whole process was the capture of Jerusalem in 638 from the Greek Christians of Byzantium. This ancient city came to be revered as Islam’s third-holiest site, after Mecca and Medina. In part this was due to Islam’s Abrahamic heritage, but it was also dependent upon the belief that Muhammad had ascended to Heaven from Jerusalem during his ‘Night Journey’, and the ass




Flashcard 7105887997196

Question
In the context of crusading history, a critical stage in this whole process was the capture of Jerusalem in [...] from the Greek Christians of Byzantium. This ancient city came to be revered as Islam’s third-holiest site, after Mecca and Medina.
Answer
638

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In the context of crusading history, a critical stage in this whole process was the capture of Jerusalem in 638 from the Greek Christians of Byzantium. This ancient city came to be revered as Islam’s third-holiest site, after Mecca and Medina.

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ontinued, such that in the mid-eighth century the Muslim world stretched from the Indus River and the borders of China in the east, across North Africa to Spain and southern France in the west. <span>In the context of crusading history, a critical stage in this whole process was the capture of Jerusalem in 638 from the Greek Christians of Byzantium. This ancient city came to be revered as Islam’s third-holiest site, after Mecca and Medina. In part this was due to Islam’s Abrahamic heritage, but it was also dependent upon the belief that Muhammad had ascended to Heaven from Jerusalem during his ‘Night Journey’, and the ass







It was once popular to suggest that the Islamic world might have swept across all Europe, had not the Muslims been twice thwarted in their attempts to capture Constantinople (in 673 and 718) and then defeated in 732 at Poitiers by Charlemagne’s Frankish grandfather Charles the Hammer.
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pon the belief that Muhammad had ascended to Heaven from Jerusalem during his ‘Night Journey’, and the associated tradition identifying the Holy City as the focus for the impending End of Days. <span>It was once popular to suggest that the Islamic world might have swept across all Europe, had not the Muslims been twice thwarted in their attempts to capture Constantinople (in 673 and 718) and then defeated in 732 at Poitiers by Charlemagne’s Frankish grandfather Charles the Hammer. In fact, important as these reversals were, a fundamental and profoundly limiting weakness within Islam had already shown its face: intractable and embittered religious and political di




Flashcard 7105891142924

Question
It was once popular to suggest that the Islamic world might have swept across all Europe, had not the Muslims been twice thwarted in their attempts to capture Constantinople (in 673 and 718) and then defeated in 732 at Poitiers by Charlemagne’s Frankish grandfather [...].
Answer
Charles the Hammer

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cross all Europe, had not the Muslims been twice thwarted in their attempts to capture Constantinople (in 673 and 718) and then defeated in 732 at Poitiers by Charlemagne’s Frankish grandfather <span>Charles the Hammer. <span>

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pon the belief that Muhammad had ascended to Heaven from Jerusalem during his ‘Night Journey’, and the associated tradition identifying the Holy City as the focus for the impending End of Days. <span>It was once popular to suggest that the Islamic world might have swept across all Europe, had not the Muslims been twice thwarted in their attempts to capture Constantinople (in 673 and 718) and then defeated in 732 at Poitiers by Charlemagne’s Frankish grandfather Charles the Hammer. In fact, important as these reversals were, a fundamental and profoundly limiting weakness within Islam had already shown its face: intractable and embittered religious and political di







Problems were apparent as early as 661, when the established line of

‘Rightly Guided Caliphs’ ended with the death of ‘Ali (the Prophet’s cousin and son-in-law) and the rise of a rival Arab clan–the Umayyad dynasty.

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d embittered religious and political division. At their core, these issues related to disputes over the legitimacy of Muhammad’s caliphal successors and the interpretation of his ‘revelations’. <span>Problems were apparent as early as 661, when the established line of ‘Rightly Guided Caliphs’ ended with the death of ‘Ali (the Prophet’s cousin and son-in-law) and the rise of a rival Arab clan–the Umayyad dynasty. The Umayyads moved the capital of the Muslim world beyond the confines of Arabia for the first time, settling in the great Syrian metropolis of Damascus, and they held sway over Islam u




Flashcard 7105894288652

Question

Problems were apparent as early as 661, when the established line of

‘Rightly Guided Caliphs’ ended with the death of ‘Ali (the Prophet’s cousin and son-in-law) and the rise of a rival Arab clan–the [...].

Answer
Umayyad dynasty

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ems were apparent as early as 661, when the established line of ‘Rightly Guided Caliphs’ ended with the death of ‘Ali (the Prophet’s cousin and son-in-law) and the rise of a rival Arab clan–the <span>Umayyad dynasty. <span>

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d embittered religious and political division. At their core, these issues related to disputes over the legitimacy of Muhammad’s caliphal successors and the interpretation of his ‘revelations’. <span>Problems were apparent as early as 661, when the established line of ‘Rightly Guided Caliphs’ ended with the death of ‘Ali (the Prophet’s cousin and son-in-law) and the rise of a rival Arab clan–the Umayyad dynasty. The Umayyads moved the capital of the Muslim world beyond the confines of Arabia for the first time, settling in the great Syrian metropolis of Damascus, and they held sway over Islam u







The Umayyads moved the capital of the Muslim world beyond the confines of Arabia for the first time, settling in the great Syrian metropolis of Damascus, and they held sway over Islam until the mid-eighth century.
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as early as 661, when the established line of ‘Rightly Guided Caliphs’ ended with the death of ‘Ali (the Prophet’s cousin and son-in-law) and the rise of a rival Arab clan–the Umayyad dynasty. <span>The Umayyads moved the capital of the Muslim world beyond the confines of Arabia for the first time, settling in the great Syrian metropolis of Damascus, and they held sway over Islam until the mid-eighth century. However, this same period witnessed the emergence of the Shi‘a (literally the ‘party’ or ‘faction’), a Muslim sect who argued that only descendants of ‘Ali and his wife Fatima (Muhammad




Flashcard 7105897434380

Question
The Umayyads moved the capital of the Muslim world beyond the confines of Arabia for the first time, settling in [...], and they held sway over Islam until the mid-eighth century.
Answer
the great Syrian metropolis of Damascus

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The Umayyads moved the capital of the Muslim world beyond the confines of Arabia for the first time, settling in the great Syrian metropolis of Damascus, and they held sway over Islam until the mid-eighth century.

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as early as 661, when the established line of ‘Rightly Guided Caliphs’ ended with the death of ‘Ali (the Prophet’s cousin and son-in-law) and the rise of a rival Arab clan–the Umayyad dynasty. <span>The Umayyads moved the capital of the Muslim world beyond the confines of Arabia for the first time, settling in the great Syrian metropolis of Damascus, and they held sway over Islam until the mid-eighth century. However, this same period witnessed the emergence of the Shi‘a (literally the ‘party’ or ‘faction’), a Muslim sect who argued that only descendants of ‘Ali and his wife Fatima (Muhammad







However, this same period witnessed the emergence of the Shi‘a (literally the ‘party’ or ‘faction’), a Muslim sect who argued that only descendants of

‘Ali and his wife Fatima (Muhammad’s daughter) could lawfully hold the title of caliph.

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he capital of the Muslim world beyond the confines of Arabia for the first time, settling in the great Syrian metropolis of Damascus, and they held sway over Islam until the mid-eighth century. <span>However, this same period witnessed the emergence of the Shi‘a (literally the ‘party’ or ‘faction’), a Muslim sect who argued that only descendants of ‘Ali and his wife Fatima (Muhammad’s daughter) could lawfully hold the title of caliph. Shi‘ite Muslims initially set out to contest the political authority of the mainstream Sunni form of Islam, but over time the schism between these two branches of the faith took on a do




Flashcard 7105900580108

Question

However, this same period witnessed the emergence of the Shi‘a (literally the ‘party’ or ‘faction’), a Muslim sect who argued that only descendants of

[...] could lawfully hold the title of caliph.

Answer
‘Ali and his wife Fatima (Muhammad’s daughter)

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However, this same period witnessed the emergence of the Shi‘a (literally the ‘party’ or ‘faction’), a Muslim sect who argued that only descendants of ‘Ali and his wife Fatima (Muhammad’s daughter) could lawfully hold the title of caliph.

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he capital of the Muslim world beyond the confines of Arabia for the first time, settling in the great Syrian metropolis of Damascus, and they held sway over Islam until the mid-eighth century. <span>However, this same period witnessed the emergence of the Shi‘a (literally the ‘party’ or ‘faction’), a Muslim sect who argued that only descendants of ‘Ali and his wife Fatima (Muhammad’s daughter) could lawfully hold the title of caliph. Shi‘ite Muslims initially set out to contest the political authority of the mainstream Sunni form of Islam, but over time the schism between these two branches of the faith took on a do







In 750 a bloody coup brought Umayyad rule to an end, propelling another Arab dynasty–the Abbasids–to power.
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distinct approaches to theology, religious ritual and law.8 The fragmentation of the Muslim world Over the next four centuries, the divisions within the Muslim world deepened and proliferated. <span>In 750 a bloody coup brought Umayyad rule to an end, propelling another Arab dynasty–the Abbasids–to power. They shifted the centre of Sunni Islam even further from the Arabian homelands, founding a spectacular new capital in Iraq: the purpose-built city of Baghdad. This visionary measure had




Flashcard 7105903725836

Question
In [...] a bloody coup brought Umayyad rule to an end, propelling another Arab dynasty–the [...] –to power.
Answer

750

Abbasids


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In 750 a bloody coup brought Umayyad rule to an end, propelling another Arab dynasty–the Abbasids–to power.

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distinct approaches to theology, religious ritual and law.8 The fragmentation of the Muslim world Over the next four centuries, the divisions within the Muslim world deepened and proliferated. <span>In 750 a bloody coup brought Umayyad rule to an end, propelling another Arab dynasty–the Abbasids–to power. They shifted the centre of Sunni Islam even further from the Arabian homelands, founding a spectacular new capital in Iraq: the purpose-built city of Baghdad. This visionary measure had







Communities of Shi‘ite Muslims continued to live, largely in peace, alongside and among Sunnis across the Near and Middle East. But in 969 a particularly assertive Shi‘ite faction seized control of North Africa.

Championed by a dynasty known as the Fatimids (because they claimed descent from Fatima, Muhammad’s daughter), they set up their own rival Shi‘ite caliph, rejecting Sunni Baghdad’s authority.

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times known as the Moors) broke away to establish an independent realm in the eighth century; and, over the decades, the rift between the Sunni and Shi‘a strands of Islam gradually intensified. <span>Communities of Shi‘ite Muslims continued to live, largely in peace, alongside and among Sunnis across the Near and Middle East. But in 969 a particularly assertive Shi‘ite faction seized control of North Africa. Championed by a dynasty known as the Fatimids (because they claimed descent from Fatima, Muhammad’s daughter), they set up their own rival Shi‘ite caliph, rejecting Sunni Baghdad’s authority. The Fatimids soon proved themselves to be potent adversaries–conquering large swathes of the Near East from the Abbasids, including Jerusalem, Damascus and sections of the eastern Medit




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Communities of Shi‘ite Muslims continued to live, largely in peace, alongside and among Sunnis across the Near and Middle East. But in 969 a particularly assertive Shi‘ite faction seized control of North Africa.

Championed by a dynasty known as the [...], they set up their own rival Shi‘ite caliph, rejecting Sunni Baghdad’s authority.

Answer
Fatimids (because they claimed descent from Fatima, Muhammad’s daughter)

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ly in peace, alongside and among Sunnis across the Near and Middle East. But in 969 a particularly assertive Shi‘ite faction seized control of North Africa. Championed by a dynasty known as the <span>Fatimids (because they claimed descent from Fatima, Muhammad’s daughter), they set up their own rival Shi‘ite caliph, rejecting Sunni Baghdad’s authority. <span>

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The Crusades: The Authoritative History of the War for the Holy Land PDF Book by Thomas Asbridge Read Online Free - Page 7
times known as the Moors) broke away to establish an independent realm in the eighth century; and, over the decades, the rift between the Sunni and Shi‘a strands of Islam gradually intensified. <span>Communities of Shi‘ite Muslims continued to live, largely in peace, alongside and among Sunnis across the Near and Middle East. But in 969 a particularly assertive Shi‘ite faction seized control of North Africa. Championed by a dynasty known as the Fatimids (because they claimed descent from Fatima, Muhammad’s daughter), they set up their own rival Shi‘ite caliph, rejecting Sunni Baghdad’s authority. The Fatimids soon proved themselves to be potent adversaries–conquering large swathes of the Near East from the Abbasids, including Jerusalem, Damascus and sections of the eastern Medit







A further, dramatic change transformed the world of Islam in the eleventh century–the coming of the Turks. From around 1040, these nomadic tribesmen from Central Asia–noted for their warlike character and agile skill as mounted archers–began to seep into the Middle East. One particular clan, the Seljuqs (from the steppes of Russia, beyond the Aral Sea), spearheaded the Turkish migration.
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ry retaining absolute control over religious and political affairs–but in practice executive power came to be wielded by their secular lieutenants: in Baghdad, the sultan; in Cairo, the vizier. <span>A further, dramatic change transformed the world of Islam in the eleventh century–the coming of the Turks. From around 1040, these nomadic tribesmen from Central Asia–noted for their warlike character and agile skill as mounted archers–began to seep into the Middle East. One particular clan, the Seljuqs (from the steppes of Russia, beyond the Aral Sea), spearheaded the Turkish migration. Having adopted the religion of Sunni Islam, these fearsome Seljuqs declared their unswerving allegiance to the Abbasid caliph and readily supplanted the now sedentary Arab and Persian a




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A further, dramatic change transformed the world of Islam in the eleventh century–the coming of the Turks. From around 1040, these nomadic tribesmen from Central Asia–noted for their warlike character and agile skill as mounted archers–began to seep into the Middle East. One particular clan, the [...] (from the steppes of Russia, beyond the Aral Sea), spearheaded the Turkish migration.
Answer
Seljuqs

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ks. From around 1040, these nomadic tribesmen from Central Asia–noted for their warlike character and agile skill as mounted archers–began to seep into the Middle East. One particular clan, the <span>Seljuqs (from the steppes of Russia, beyond the Aral Sea), spearheaded the Turkish migration. <span>

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The Crusades: The Authoritative History of the War for the Holy Land PDF Book by Thomas Asbridge Read Online Free - Page 7
ry retaining absolute control over religious and political affairs–but in practice executive power came to be wielded by their secular lieutenants: in Baghdad, the sultan; in Cairo, the vizier. <span>A further, dramatic change transformed the world of Islam in the eleventh century–the coming of the Turks. From around 1040, these nomadic tribesmen from Central Asia–noted for their warlike character and agile skill as mounted archers–began to seep into the Middle East. One particular clan, the Seljuqs (from the steppes of Russia, beyond the Aral Sea), spearheaded the Turkish migration. Having adopted the religion of Sunni Islam, these fearsome Seljuqs declared their unswerving allegiance to the Abbasid caliph and readily supplanted the now sedentary Arab and Persian a







Having adopted the religion of Sunni Islam, these fearsome Seljuqs declared their unswerving allegiance to the Abbasid caliph and readily supplanted the now sedentary Arab and Persian aristocracy of Iran and Iraq.
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ter and agile skill as mounted archers–began to seep into the Middle East. One particular clan, the Seljuqs (from the steppes of Russia, beyond the Aral Sea), spearheaded the Turkish migration. <span>Having adopted the religion of Sunni Islam, these fearsome Seljuqs declared their unswerving allegiance to the Abbasid caliph and readily supplanted the now sedentary Arab and Persian aristocracy of Iran and Iraq. By 1055, the Seljuq warlord Tughrul Beg had been appointed as sultan of Baghdad and could claim effective overlordship of Sunni Islam; a role which members of his dynasty would hold as




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Having adopted the religion of [...] Islam, these fearsome Seljuqs declared their unswerving allegiance to the Abbasid caliph and readily supplanted the now sedentary Arab and Persian aristocracy of Iran and Iraq.
Answer
Sunni

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Having adopted the religion of Sunni Islam, these fearsome Seljuqs declared their unswerving allegiance to the Abbasid caliph and readily supplanted the now sedentary Arab and Persian aristocracy of Iran and Iraq. <

Original toplevel document

The Crusades: The Authoritative History of the War for the Holy Land PDF Book by Thomas Asbridge Read Online Free - Page 7
ter and agile skill as mounted archers–began to seep into the Middle East. One particular clan, the Seljuqs (from the steppes of Russia, beyond the Aral Sea), spearheaded the Turkish migration. <span>Having adopted the religion of Sunni Islam, these fearsome Seljuqs declared their unswerving allegiance to the Abbasid caliph and readily supplanted the now sedentary Arab and Persian aristocracy of Iran and Iraq. By 1055, the Seljuq warlord Tughrul Beg had been appointed as sultan of Baghdad and could claim effective overlordship of Sunni Islam; a role which members of his dynasty would hold as







By 1055, the Seljuq warlord Tughrul Beg had been appointed as sultan of Baghdad and could claim effective overlordship of Sunni Islam; a role which members of his dynasty would hold as a hereditary right for more than a century. The advent of the Seljuq Turks brought a new, vital lease of life and unity to the Abbasid world.
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eligion of Sunni Islam, these fearsome Seljuqs declared their unswerving allegiance to the Abbasid caliph and readily supplanted the now sedentary Arab and Persian aristocracy of Iran and Iraq. <span>By 1055, the Seljuq warlord Tughrul Beg had been appointed as sultan of Baghdad and could claim effective overlordship of Sunni Islam; a role which members of his dynasty would hold as a hereditary right for more than a century. The advent of the Seljuq Turks brought a new, vital lease of life and unity to the Abbasid world. Their restless energy and martial ferocity soon brought sweeping gains. < Prev Page Jump to .... 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 3




Flashcard 7105917095180

Question
By 1055, the Seljuq warlord [...] had been appointed as sultan of Baghdad and could claim effective overlordship of Sunni Islam; a role which members of his dynasty would hold as a hereditary right for more than a century. The advent of the Seljuq Turks brought a new, vital lease of life and unity to the Abbasid world.
Answer
Tughrul Beg

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By 1055, the Seljuq warlord Tughrul Beg had been appointed as sultan of Baghdad and could claim effective overlordship of Sunni Islam; a role which members of his dynasty would hold as a hereditary right for more than a centu

Original toplevel document

The Crusades: The Authoritative History of the War for the Holy Land PDF Book by Thomas Asbridge Read Online Free - Page 7
eligion of Sunni Islam, these fearsome Seljuqs declared their unswerving allegiance to the Abbasid caliph and readily supplanted the now sedentary Arab and Persian aristocracy of Iran and Iraq. <span>By 1055, the Seljuq warlord Tughrul Beg had been appointed as sultan of Baghdad and could claim effective overlordship of Sunni Islam; a role which members of his dynasty would hold as a hereditary right for more than a century. The advent of the Seljuq Turks brought a new, vital lease of life and unity to the Abbasid world. Their restless energy and martial ferocity soon brought sweeping gains. < Prev Page Jump to .... 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 3







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Reversible posterior leukoencephalopathy syndrome (RPLS) is a clinical radiographic syndrome of heterogeneous etiologies that are grouped together because of similar findings on neuroimaging studies. It is also often referred to as:

● Posterior reversible encephalopathy syndrome (PRES)

● Reversible posterior cerebral edema syndrome

● Posterior leukoencephalopathy syndrome

● Hyperperfusion encephalopathy

● Brain capillary leak syndrome

None of these names are completely satisfactory; the syndrome is not always reversible, and it is often not confined to either the white matter or the posterior regions of the brain.

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d as new evidence becomes available and our peer review process is complete. Literature review current through: Jun 2022. | This topic last updated: Jun 20, 2022. INTRODUCTION AND TERMINOLOGY — <span>Reversible posterior leukoencephalopathy syndrome (RPLS) is a clinical radiographic syndrome of heterogeneous etiologies that are grouped together because of similar findings on neuroimaging studies. It is also often referred to as: ●Posterior reversible encephalopathy syndrome (PRES) ●Reversible posterior cerebral edema syndrome ●Posterior leukoencephalopathy syndrome ●Hyperperfusion encephalopathy ●Brain capillary leak syndrome None of these names are completely satisfactory; the syndrome is not always reversible, and it is often not confined to either the white matter or the posterior regions of the brain. Although described in various specific case reports for some time, it was first codified as a single named syndrome in a 1996 case series, which described a clinical syndrome of headach




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CLINICAL MANIFESTATIONS — The symptoms of RPLS evolve rapidly over hours to days. Hypertension is frequent but not invariable. The hypertensive crisis may precede the neurologic syndrome by 24 hours or longer [2,10].
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r, as discussed above, as well as solid organ, bone marrow, or stem cell transplantation [67,68]. Sickle cell disease [69] and sepsis [38,68] are also settings in which RPLS has been described. <span>CLINICAL MANIFESTATIONS — The symptoms of RPLS evolve rapidly over hours to days. Hypertension is frequent but not invariable. The hypertensive crisis may precede the neurologic syndrome by 24 hours or longer [2,10]. The clinical syndrome of RPLS is characterized by [38]: ●Headaches – The headache is typically constant, nonlocalized, moderate to severe, and unresponsive to analgesia [10]. ●Altered c




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The clinical syndrome of RPLS is characterized by [38]:

Headaches – The headache is typically constant, nonlocalized, moderate to severe, and unresponsive to analgesia [10].

Altered consciousness – Altered consciousness ranges from mild somnolence to confusion and agitation, progressing to stupor or coma in extreme cases [1,10,59,70].

Visual disturbances – Visual perception abnormalities are often detectable. Hemianopia, visual neglect, auras, visual hallucinations, and cortical blindness may occur [1,71]. Cortical blindness may be accompanied by denial of blindness (Anton syndrome).

Seizures – Seizures are often the presenting manifestation [1,7,52,72]. Seizures are usually generalized tonic-clonic; they may begin focally and often recur. Status epilepticus has been reported [60,73]. Preceding visual loss or visual hallucinations suggest occipital lobe origin in some patients. Only a minority of patients, usually those with milder disease, are seizure free [2].

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— The symptoms of RPLS evolve rapidly over hours to days. Hypertension is frequent but not invariable. The hypertensive crisis may precede the neurologic syndrome by 24 hours or longer [2,10]. <span>The clinical syndrome of RPLS is characterized by [38]: ●Headaches – The headache is typically constant, nonlocalized, moderate to severe, and unresponsive to analgesia [10]. ●Altered consciousness – Altered consciousness ranges from mild somnolence to confusion and agitation, progressing to stupor or coma in extreme cases [1,10,59,70]. ●Visual disturbances – Visual perception abnormalities are often detectable. Hemianopia, visual neglect, auras, visual hallucinations, and cortical blindness may occur [1,71]. Cortical blindness may be accompanied by denial of blindness (Anton syndrome). ●Seizures – Seizures are often the presenting manifestation [1,7,52,72]. Seizures are usually generalized tonic-clonic; they may begin focally and often recur. Status epilepticus has been reported [60,73]. Preceding visual loss or visual hallucinations suggest occipital lobe origin in some patients. Only a minority of patients, usually those with milder disease, are seizure free [2]. The funduscopic examination is often normal, particularly in eclamptic and chronically hypertensive patients, but papilledema may be present with accompanying flame-shaped retinal hemor




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The funduscopic examination is often normal, particularly in eclamptic and chronically hypertensive patients, but papilledema may be present with accompanying flame-shaped retinal hemorrhages and exudates.
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ted [60,73]. Preceding visual loss or visual hallucinations suggest occipital lobe origin in some patients. Only a minority of patients, usually those with milder disease, are seizure free [2]. <span>The funduscopic examination is often normal, particularly in eclamptic and chronically hypertensive patients, but papilledema may be present with accompanying flame-shaped retinal hemorrhages and exudates. The deep tendon reflexes may be brisk, and Babinski signs may be present [10]. A few patients may have weakness and incoordination of the limbs [1,8,74]. Other focal neurologic deficits




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The deep tendon reflexes may be brisk, and Babinski signs may be present [ 10]. A few patients may have weakness and incoordination of the limbs [1,8,74]. Other focal neurologic deficits are rare.
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pic examination is often normal, particularly in eclamptic and chronically hypertensive patients, but papilledema may be present with accompanying flame-shaped retinal hemorrhages and exudates. <span>The deep tendon reflexes may be brisk, and Babinski signs may be present [10]. A few patients may have weakness and incoordination of the limbs [1,8,74]. Other focal neurologic deficits are rare. Relatively unusual patients with symptoms referable to the upper cervical spinal cord (limb weakness, bladder dysfunction), along with one or more of the symptoms above have also been d




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Relatively unusual patients with symptoms referable to the upper cervical spinal cord (limb weakness, bladder dysfunction), along with one or more of the symptoms above have also been described [75].
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e deep tendon reflexes may be brisk, and Babinski signs may be present [10]. A few patients may have weakness and incoordination of the limbs [1,8,74]. Other focal neurologic deficits are rare. <span>Relatively unusual patients with symptoms referable to the upper cervical spinal cord (limb weakness, bladder dysfunction), along with one or more of the symptoms above have also been described [75]. EVALUATION Neuroimaging — Neuroimaging is essential to the diagnosis of RPLS. While a noncontrast brain magnetic resonance imaging (MRI) should be performed in all cases, a noncontrast




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Neuroradiographic abnormalities of RPLS are often apparent on CT scans (image 1) [76] but are best depicted by MRI (image 2) [22].
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noncontrast brain magnetic resonance imaging (MRI) should be performed in all cases, a noncontrast head computed tomography (CT) is often the first study performed in the emergency department. <span>Neuroradiographic abnormalities of RPLS are often apparent on CT scans (image 1) [76] but are best depicted by MRI (image 2) [22]. Typical findings are bilateral areas of white matter edema in the posterior cerebral hemispheres, particularly the parieto-occipital regions, but variations do occur [37,38,77]. Extensi




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Typical findings are bilateral areas of white matter edema in the posterior cerebral hemispheres, particularly the parieto-occipital regions, but variations do occur [37,38,77]. Extensive vasogenic edema has been associated with worse clinical outcomes in some series [2,78], but not with the severity of clinical presentation [38,66]
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s often the first study performed in the emergency department. Neuroradiographic abnormalities of RPLS are often apparent on CT scans (image 1) [76] but are best depicted by MRI (image 2) [22]. <span>Typical findings are bilateral areas of white matter edema in the posterior cerebral hemispheres, particularly the parieto-occipital regions, but variations do occur [37,38,77]. Extensive vasogenic edema has been associated with worse clinical outcomes in some series [2,78], but not with the severity of clinical presentation [38,66]. (See 'Prognosis' below.) ●Features common to CT or MRI include: •The white matter edema is typically most prominent in both posterior cerebral hemispheres (image 1); however, the calca




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Other testing — The clinical and radiologic features of RPLS are not specific; other conditions such as toxic-metabolic encephalopathy should be evaluated thoroughly. Thus, laboratory studies should include a blood count, electrolytes, creatinine, blood urea nitrogen (BUN), and liver function tests. Comorbid medical conditions (eg, sepsis, hyponatremia, renal failure, ischemic bowel disease) can exacerbate neurologic deterioration and are important to identify for that reason as well [8]. (See "Acute toxic-metabolic encephalopathy in adults" and "Acute toxic-metabolic encephalopathy in children".)
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mental in other groups [96]. A finding of prominent vasoconstriction suggests co-occurrence of reversible vasoconstriction syndrome. (See 'Reversible cerebral vasoconstriction syndrome' below.) <span>Other testing — The clinical and radiologic features of RPLS are not specific; other conditions such as toxic-metabolic encephalopathy should be evaluated thoroughly. Thus, laboratory studies should include a blood count, electrolytes, creatinine, blood urea nitrogen (BUN), and liver function tests. Comorbid medical conditions (eg, sepsis, hyponatremia, renal failure, ischemic bowel disease) can exacerbate neurologic deterioration and are important to identify for that reason as well [8]. (See "Acute toxic-metabolic encephalopathy in adults" and "Acute toxic-metabolic encephalopathy in children".) A lumbar puncture is not required for the evaluation of most patients with suspected RPLS but may be obtained if there is a specific concern for meningitis, encephalitis, or malignancy.




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A lumbar puncture is not required for the evaluation of most patients with suspected RPLS but may be obtained if there is a specific concern for meningitis, encephalitis, or malignancy. In RPLS, cerebrospinal fluid (CSF) typically shows a modestly elevated protein level (mean 58 mg/dL in one study) but no pleocytosis [103]. An elevated white blood cell count in the CSF should prompt consideration of other diagnoses. (See 'Differential diagnosis' below.)
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eurologic deterioration and are important to identify for that reason as well [8]. (See "Acute toxic-metabolic encephalopathy in adults" and "Acute toxic-metabolic encephalopathy in children".) <span>A lumbar puncture is not required for the evaluation of most patients with suspected RPLS but may be obtained if there is a specific concern for meningitis, encephalitis, or malignancy. In RPLS, cerebrospinal fluid (CSF) typically shows a modestly elevated protein level (mean 58 mg/dL in one study) but no pleocytosis [103]. An elevated white blood cell count in the CSF should prompt consideration of other diagnoses. (See 'Differential diagnosis' below.) Due to the significant prevalence of seizures with RPLS, there should be a low threshold to perform electroencephalographic (EEG) monitoring in a patient with persistent altered level o




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DIAGNOSIS — While there are no specific diagnostic criteria for RPLS, it is becoming an increasingly recognized disorder. In the appropriate clinical setting (in particular hypertension, immunosuppressive or cytotoxic therapy, kidney disease), clinicians should recognize the neurologic syndrome of headache, visual symptoms, confusion, and seizures, and order brain MRI, which typically supports the diagnosis. Diffusion-weighted imaging (DWI), if available, adds considerable diagnostic and prognostic information. (See 'Neuroimaging' above.)
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a patient with persistent altered level of consciousness to exclude nonconvulsive status epilepticus. (See "Nonconvulsive status epilepticus: Classification, clinical features, and diagnosis".) <span>DIAGNOSIS — While there are no specific diagnostic criteria for RPLS, it is becoming an increasingly recognized disorder. In the appropriate clinical setting (in particular hypertension, immunosuppressive or cytotoxic therapy, kidney disease), clinicians should recognize the neurologic syndrome of headache, visual symptoms, confusion, and seizures, and order brain MRI, which typically supports the diagnosis. Diffusion-weighted imaging (DWI), if available, adds considerable diagnostic and prognostic information. (See 'Neuroimaging' above.) Because the neuroradiographic findings are not specific, repeat neuroimaging may be necessary. With treatment, resolution of findings on neuroimaging within days to weeks is expected. A




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Because the neuroradiographic findings are not specific, repeat neuroimaging may be necessary. With treatment, resolution of findings on neuroimaging within days to weeks is expected.
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and order brain MRI, which typically supports the diagnosis. Diffusion-weighted imaging (DWI), if available, adds considerable diagnostic and prognostic information. (See 'Neuroimaging' above.) <span>Because the neuroradiographic findings are not specific, repeat neuroimaging may be necessary. With treatment, resolution of findings on neuroimaging within days to weeks is expected. Atypical MRI findings and clinical treatment failure should prompt consideration of other diagnoses. (See 'Differential diagnosis' below.) DIFFERENTIAL DIAGNOSIS Related conditions — It




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Most case series and case reports suggest that RPLS is usually benign. In many cases, RPLS seems to be fully reversible within a period of days to weeks, after removal of the inciting factor and control of the blood pressure [1,7,46,47,70,133]. Radiologic improvement lags behind clinical recovery.
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, fluid overload, and electrolyte disturbance as well as the fact that high-dose steroid therapy has been associated with the development of RPLS, this is not a recommended therapy. PROGNOSIS — <span>Most case series and case reports suggest that RPLS is usually benign. In many cases, RPLS seems to be fully reversible within a period of days to weeks, after removal of the inciting factor and control of the blood pressure [1,7,46,47,70,133]. Radiologic improvement lags behind clinical recovery. However, death and permanent serious neurologic disability have been reported as consequences of RPLS [12]. Death may result from progressive cerebral edema, from intracerebral hemorrha




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Clinical setting and risk factors – RPLS most often occurs in the setting of hypertensive crisis, preeclampsia, or with cytotoxic immunosuppressive therapy; however, it can also occur in many other clinical settings (table 1).
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r cerebral hemispheres. The differentiation of vasogenic versus cytotoxic edema with diffusion-weighted imaging (DWI) is helpful in distinguishing RPLS from stroke. (See 'Neuroimaging' above.) ●<span>Clinical setting and risk factors – RPLS most often occurs in the setting of hypertensive crisis, preeclampsia, or with cytotoxic immunosuppressive therapy; however, it can also occur in many other clinical settings (table 1). (See 'Risk factors and clinical setting' above.) ●Management •Blood pressure – Treatment of hypertension is the mainstay of treatment in patients with RPLS. In addition, we suggest caut




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Blood pressure – Treatment of hypertension is the mainstay of treatment in patients with RPLS.

In addition, we suggest cautious blood pressure lowering in patients with blood pressure that is only borderline hypertensive (eg, 120 to 140 mmHg systolic), particularly if such measurements exceed the patient's baseline values (Grade 2C).

We target an approximate 10 to 25 percent reduction of blood pressure initially and use an easily titratable parenteral agent such as clevidipine, nicardipine, or labetalol. Overaggressive blood pressure lowering can lead to complications; comorbid medical conditions should be considered in management. (See 'Blood pressure management' above.)

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s, preeclampsia, or with cytotoxic immunosuppressive therapy; however, it can also occur in many other clinical settings (table 1). (See 'Risk factors and clinical setting' above.) ●Management •<span>Blood pressure – Treatment of hypertension is the mainstay of treatment in patients with RPLS. In addition, we suggest cautious blood pressure lowering in patients with blood pressure that is only borderline hypertensive (eg, 120 to 140 mmHg systolic), particularly if such measurements exceed the patient's baseline values (Grade 2C). We target an approximate 10 to 25 percent reduction of blood pressure initially and use an easily titratable parenteral agent such as clevidipine, nicardipine, or labetalol. Overaggressive blood pressure lowering can lead to complications; comorbid medical conditions should be considered in management. (See 'Blood pressure management' above.) •Discontinuation of causative agent – We suggest stopping or lowering the dose of the offending immunosuppressant or cytotoxic agent, permanently if possible (Grade 2C). When another ag




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Discontinuation of causative agent – We suggest stopping or lowering the dose of the offending immunosuppressant or cytotoxic agent, permanently if possible (Grade 2C). When another agent is substituted, or if the original agent is restarted, patients should be followed closely for recurrence of RPLS. (See 'Discontinuation of immunosuppressive therapy' above.)

Treatment of other acute medical conditions (eg, sepsis, renal failure) may also hasten patient's recovery. (See 'Other' above.)

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dipine, or labetalol. Overaggressive blood pressure lowering can lead to complications; comorbid medical conditions should be considered in management. (See 'Blood pressure management' above.) •<span>Discontinuation of causative agent – We suggest stopping or lowering the dose of the offending immunosuppressant or cytotoxic agent, permanently if possible (Grade 2C). When another agent is substituted, or if the original agent is restarted, patients should be followed closely for recurrence of RPLS. (See 'Discontinuation of immunosuppressive therapy' above.) Treatment of other acute medical conditions (eg, sepsis, renal failure) may also hasten patient's recovery. (See 'Other' above.) •Seizure management – Antiseizure medications are administered to patients with seizures. Agent selection should take into consideration renal clearance, potential for sedation, and oth




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We suggest that antiseizure medications be discontinued after symptoms and neuroimaging findings resolve (Grade 2C). The risk of late recurrence or epilepsy after uncomplicated RPLS appears to be low. (See 'Seizure management' above.)
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inistered to patients with seizures. Agent selection should take into consideration renal clearance, potential for sedation, and other side effects of the drug and comorbidities of the patient. <span>We suggest that antiseizure medications be discontinued after symptoms and neuroimaging findings resolve (Grade 2C). The risk of late recurrence or epilepsy after uncomplicated RPLS appears to be low. (See 'Seizure management' above.) •Pregnancy – In the partum or postpartum setting, patients with RPLS should be treated as for preeclampsia or eclampsia. (See "Eclampsia".) ●Clinical course and prognosis – Most patient




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Common conditions associated with intracerebral hemorrhage (ICH) include hypertension, cerebral amyloid angiopathy, and ruptured vascular malformation. Other etiologies include cerebral venous thrombosis, vasculopathies, primary or metastatic tumors, and coagulopathies.
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causes – Injury to brain parenchyma occurs via hematoma expansion and perilesional edema as well as secondary excitotoxic and inflammatory injury from the breakdown of the blood-brain barrier. <span>Common conditions associated with intracerebral hemorrhage (ICH) include hypertension, cerebral amyloid angiopathy, and ruptured vascular malformation. Other etiologies include cerebral venous thrombosis, vasculopathies, primary or metastatic tumors, and coagulopathies. (See 'Pathogenesis and etiologies' above.) ●Risk factors – Major risk factors for spontaneous ICH include older age, hypertension, and the use of antithrombotic (antiplatelet and antico




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Major risk factors for spontaneous ICH include older age, hypertension, and the use of antithrombotic (antiplatelet and anticoagulant) therapy.
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r malformation. Other etiologies include cerebral venous thrombosis, vasculopathies, primary or metastatic tumors, and coagulopathies. (See 'Pathogenesis and etiologies' above.) ●Risk factors – <span>Major risk factors for spontaneous ICH include older age, hypertension, and the use of antithrombotic (antiplatelet and anticoagulant) therapy. (See 'Risk factors' above.) ●Presenting signs and symptoms – The signs and symptoms of ICH vary according to the location and size of the hemorrhage (table 1). Patients typically presen




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Predictors of hemorrhage growth associated with neurologic deterioration include a shorter time from symptom onset to initial imaging, initial ICH volume, antithrombotic medication use, and imaging signs of ICH heterogeneity on noncontrast CT or focal contrast extravasation on CT angiography (image 17 and image 18).
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ergency diagnosis and assessment of ICH. CT angiography may be performed along with a noncontrast head CT to help identify an underlying vascular cause to the ICH. (See 'Brain imaging' above.) •<span>Predictors of hemorrhage growth associated with neurologic deterioration include a shorter time from symptom onset to initial imaging, initial ICH volume, antithrombotic medication use, and imaging signs of ICH heterogeneity on noncontrast CT or focal contrast extravasation on CT angiography (image 17 and image 18). (See 'Predicting hemorrhage expansion' above.) ●Subsequent imaging evaluation – Additional imaging may be warranted after the diagnosis of ICH in the event of clinical deterioration to




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The signs and symptoms of ICH vary according to the location and size of the hemorrhage (table 1).
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ta, including chronic kidney disease [103-105], diabetes [106], use of selective serotonin reuptake inhibitors [107,108], migraine [109], and systemic amyloidosis [110]. CLINICAL PRESENTATION — <span>The signs and symptoms of ICH vary according to the location and size of the hemorrhage (table 1). Onset and progression — In most circumstances, ICH onset occurs during routine activity. However, some hypertensive hemorrhages occur with exertion or intense emotional activity [111].




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In most circumstances, ICH onset occurs during routine activity. However, some hypertensive hemorrhages occur with exertion or intense emotional activity [111].
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igraine [109], and systemic amyloidosis [110]. CLINICAL PRESENTATION — The signs and symptoms of ICH vary according to the location and size of the hemorrhage (table 1). Onset and progression — <span>In most circumstances, ICH onset occurs during routine activity. However, some hypertensive hemorrhages occur with exertion or intense emotional activity [111]. The neurologic symptoms and signs may be progressive over minutes or a few hours (figure 1), in contrast with brain embolism and subarachnoid hemorrhage, where the neurologic symptoms a




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The neurologic symptoms and signs may be progressive over minutes or a few hours (figure 1), in contrast with brain embolism and subarachnoid hemorrhage, where the neurologic symptoms and signs are often maximal at onset. However, some patients with large ICH are obtunded or comatose when first discovered or at first evaluation upon arrival to the emergency department.
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able 1). Onset and progression — In most circumstances, ICH onset occurs during routine activity. However, some hypertensive hemorrhages occur with exertion or intense emotional activity [111]. <span>The neurologic symptoms and signs may be progressive over minutes or a few hours (figure 1), in contrast with brain embolism and subarachnoid hemorrhage, where the neurologic symptoms and signs are often maximal at onset. However, some patients with large ICH are obtunded or comatose when first discovered or at first evaluation upon arrival to the emergency department. Headache, vomiting, and a decreased level of consciousness may develop if the hemorrhage is large. This symptom complex is typically absent with small hemorrhages. However, headache and




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Headache, vomiting, and a decreased level of consciousness may develop if the hemorrhage is large. This symptom complex is typically absent with small hemorrhages. However, headache and vomiting occur in approximately one-half of patients with ICH (figure 2). Headache may be due to traction on meningeal pain fibers, increased intracranial pressure (ICP), or blood in the cerebrospinal fluid; it is most common with cerebellar and lobar hemorrhages. Patients may complain of a stiff neck and have meningismus on physical examination if there is intraventricular blood.
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ptoms and signs are often maximal at onset. However, some patients with large ICH are obtunded or comatose when first discovered or at first evaluation upon arrival to the emergency department. <span>Headache, vomiting, and a decreased level of consciousness may develop if the hemorrhage is large. This symptom complex is typically absent with small hemorrhages. However, headache and vomiting occur in approximately one-half of patients with ICH (figure 2). Headache may be due to traction on meningeal pain fibers, increased intracranial pressure (ICP), or blood in the cerebrospinal fluid; it is most common with cerebellar and lobar hemorrhages. Patients may complain of a stiff neck and have meningismus on physical examination if there is intraventricular blood. Stupor or coma attributed to the ICH is often an ominous sign. Exceptions include patients with thalamic hemorrhage with involvement of the reticular activating system who may recover a




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Stupor or coma attributed to the ICH is often an ominous sign. Exceptions include patients with thalamic hemorrhage with involvement of the reticular activating system who may recover after acute blood is resorbed and those with acute hydrocephalus who might improve if treated with an external ventricular drain. Patients may also present with stupor or coma due to reversible causes such as acute metabolic derangements or seizure.
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ebrospinal fluid; it is most common with cerebellar and lobar hemorrhages. Patients may complain of a stiff neck and have meningismus on physical examination if there is intraventricular blood. <span>Stupor or coma attributed to the ICH is often an ominous sign. Exceptions include patients with thalamic hemorrhage with involvement of the reticular activating system who may recover after acute blood is resorbed and those with acute hydrocephalus who might improve if treated with an external ventricular drain. Patients may also present with stupor or coma due to reversible causes such as acute metabolic derangements or seizure. Neurologic signs and ICH location — Neurologic signs vary depending upon the location of the hemorrhage (image 1). In one study, bleeding involved the putamen in approximately 35 percen




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Neurologic signs and ICH location — Neurologic signs vary depending upon the location of the hemorrhage (image 1). In one study, bleeding involved the putamen in approximately 35 percent of cases, cerebral lobes in 30 percent, cerebellum in 16 percent, thalamus in 15 percent, and pons in 5 to 12 percent [112].
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cephalus who might improve if treated with an external ventricular drain. Patients may also present with stupor or coma due to reversible causes such as acute metabolic derangements or seizure. <span>Neurologic signs and ICH location — Neurologic signs vary depending upon the location of the hemorrhage (image 1). In one study, bleeding involved the putamen in approximately 35 percent of cases, cerebral lobes in 30 percent, cerebellum in 16 percent, thalamus in 15 percent, and pons in 5 to 12 percent [112]. In the subsequent Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial (INTERACT2) of over 2000 subjects with imaging-confirmed ICH and hypertension, the frequency of a




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In the subsequent Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial (INTERACT2) of over 2000 subjects with imaging-confirmed ICH and hypertension, the frequency of affected brain structures was as follows [ 113]:

● Putamen/globus pallidus – 56 percent

● Posterior limb of internal capsule – 46 percent

● Anterior limb of internal capsule – 5 percent

● Thalamus – 31 percent

● External capsule – 27 percent

● Lobar – 14 percent

● Cerebellum or brainstem – 7 percent

● Caudate head – 2 percent

Intraventricular extension of the ICH was identified in 29 percent in this study.

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one study, bleeding involved the putamen in approximately 35 percent of cases, cerebral lobes in 30 percent, cerebellum in 16 percent, thalamus in 15 percent, and pons in 5 to 12 percent [112]. <span>In the subsequent Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial (INTERACT2) of over 2000 subjects with imaging-confirmed ICH and hypertension, the frequency of affected brain structures was as follows [113]: ●Putamen/globus pallidus – 56 percent ●Posterior limb of internal capsule – 46 percent ●Anterior limb of internal capsule – 5 percent ●Thalamus – 31 percent ●External capsule – 27 percent ●Lobar – 14 percent ●Cerebellum or brainstem – 7 percent ●Caudate head – 2 percent Intraventricular extension of the ICH was identified in 29 percent in this study. Neurologic exam deficits typically correspond to the location of the hemorrhage and associated edema. Patients with deficits not attributable to the hemorrhage should be evaluated for o




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Neurologic exam deficits typically correspond to the location of the hemorrhage and associated edema. Patients with deficits not attributable to the hemorrhage should be evaluated for other causes, such as expansion of the hemorrhage, post-ictal symptoms after a seizure, or increased intracranial pressure.
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xternal capsule – 27 percent ●Lobar – 14 percent ●Cerebellum or brainstem – 7 percent ●Caudate head – 2 percent Intraventricular extension of the ICH was identified in 29 percent in this study. <span>Neurologic exam deficits typically correspond to the location of the hemorrhage and associated edema. Patients with deficits not attributable to the hemorrhage should be evaluated for other causes, such as expansion of the hemorrhage, post-ictal symptoms after a seizure, or increased intracranial pressure. The localization of ICH may be associated with typical neurologic exam findings: ●Putaminal hemorrhage – Spread of hemorrhage into the putamen most commonly occurs along white matter fi




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Putaminal hemorrhage – Spread of hemorrhage into the putamen most commonly occurs along white matter fiber tracts, causing hemiplegia, hemisensory loss, homonymous hemianopsia, and gaze palsy. Stupor and coma may develop if the hemorrhage is large.
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, such as expansion of the hemorrhage, post-ictal symptoms after a seizure, or increased intracranial pressure. The localization of ICH may be associated with typical neurologic exam findings: ●<span>Putaminal hemorrhage – Spread of hemorrhage into the putamen most commonly occurs along white matter fiber tracts, causing hemiplegia, hemisensory loss, homonymous hemianopsia, and gaze palsy. Stupor and coma may develop if the hemorrhage is large. ●Caudate hemorrhage – Hemorrhage typically originating within the head of the caudate nucleus may cause acute-onset confusion, personality changes, or memory impairment as well as trans




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Caudate hemorrhage – Hemorrhage typically originating within the head of the caudate nucleus may cause acute-onset confusion, personality changes, or memory impairment as well as transient contralateral weakness or numbness [114]. Headache and drowsiness may also occur, especially if bleeding extends into the adjacent intraventricular space
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amen most commonly occurs along white matter fiber tracts, causing hemiplegia, hemisensory loss, homonymous hemianopsia, and gaze palsy. Stupor and coma may develop if the hemorrhage is large. ●<span>Caudate hemorrhage – Hemorrhage typically originating within the head of the caudate nucleus may cause acute-onset confusion, personality changes, or memory impairment as well as transient contralateral weakness or numbness [114]. Headache and drowsiness may also occur, especially if bleeding extends into the adjacent intraventricular space. ●Internal capsule hemorrhage – Small hemorrhages restricted to the internal capsule may cause mild dysarthria, contralateral hemiparesis, and sensory deficit [115]. ●Cerebellar hemorrh




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Internal capsule hemorrhage – Small hemorrhages restricted to the internal capsule may cause mild dysarthria, contralateral hemiparesis, and sensory deficit [115].
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emory impairment as well as transient contralateral weakness or numbness [114]. Headache and drowsiness may also occur, especially if bleeding extends into the adjacent intraventricular space. ●<span>Internal capsule hemorrhage – Small hemorrhages restricted to the internal capsule may cause mild dysarthria, contralateral hemiparesis, and sensory deficit [115]. ●Cerebellar hemorrhage – Cerebellar hemorrhage usually originates in the dentate nucleus and may extend into the hemisphere and fourth ventricle and possibly into the pontine tegmentum.




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Cerebellar hemorrhage – Cerebellar hemorrhage usually originates in the dentate nucleus and may extend into the hemisphere and fourth ventricle and possibly into the pontine tegmentum. These bleeds typically cause an inability to walk due to imbalance, vomiting, and occipital headache. Some patients have referred pain to the neck or shoulder, neck stiffness, gaze palsy, and/or facial weakness. Notably, there is often no hemiparesis. The patient may become stuporous due to obstructive hydrocephalus or brainstem compression.

Patients with acute cerebellar hemorrhage may frequently deteriorate and require surgery.

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ent intraventricular space. ●Internal capsule hemorrhage – Small hemorrhages restricted to the internal capsule may cause mild dysarthria, contralateral hemiparesis, and sensory deficit [115]. ●<span>Cerebellar hemorrhage – Cerebellar hemorrhage usually originates in the dentate nucleus and may extend into the hemisphere and fourth ventricle and possibly into the pontine tegmentum. These bleeds typically cause an inability to walk due to imbalance, vomiting, and occipital headache. Some patients have referred pain to the neck or shoulder, neck stiffness, gaze palsy, and/or facial weakness. Notably, there is often no hemiparesis. The patient may become stuporous due to obstructive hydrocephalus or brainstem compression. Patients with acute cerebellar hemorrhage may frequently deteriorate and require surgery. (See "Spontaneous intracerebral hemorrhage: Acute treatment and prognosis", section on 'Surgical approaches for selected patients' and "Spontaneous intracerebral hemorrhage: Acute treat




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Thalamic hemorrhage – Thalamic hemorrhages may extend in a transverse direction to the posterior limb of the internal capsule, downward to put pressure on the tectum of the midbrain, or medially to rupture into the third ventricle. Symptoms include hemiparesis, hemisensory loss, and occasionally transient homonymous hemianopsia. Pupils may be miotic and unreactive along with a gaze palsy (eg, peering at the tip of the nose, skewed, or "wrong-way eyes" toward the weak side [in contrast with hemispheric cortical injury in which the eyes are deviated away from the hemiparesis]). Aphasia may occur if the bleed affects the dominant hemisphere, while neglect may develop if the bleed affects the nondominant hemisphere. Patients with small anterior thalamic hemorrhages may present with drowsiness, acute confusion, or neuropsychiatric symptoms.
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treatment and prognosis", section on 'Surgical approaches for selected patients' and "Spontaneous intracerebral hemorrhage: Acute treatment and prognosis", section on 'Cerebellar hemorrhage'.) ●<span>Thalamic hemorrhage – Thalamic hemorrhages may extend in a transverse direction to the posterior limb of the internal capsule, downward to put pressure on the tectum of the midbrain, or medially to rupture into the third ventricle. Symptoms include hemiparesis, hemisensory loss, and occasionally transient homonymous hemianopsia. Pupils may be miotic and unreactive along with a gaze palsy (eg, peering at the tip of the nose, skewed, or "wrong-way eyes" toward the weak side [in contrast with hemispheric cortical injury in which the eyes are deviated away from the hemiparesis]). Aphasia may occur if the bleed affects the dominant hemisphere, while neglect may develop if the bleed affects the nondominant hemisphere. Patients with small anterior thalamic hemorrhages may present with drowsiness, acute confusion, or neuropsychiatric symptoms. ●Lobar hemorrhage – Lobar hemorrhages vary in their neurologic signs depending upon location. They most often affect the parietal and occipital lobes. These bleeds are associated with a




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Lobar hemorrhage – Lobar hemorrhages vary in their neurologic signs depending upon location. They most often affect the parietal and occipital lobes. These bleeds are associated with a higher incidence of seizures. Occipital hemorrhages frequently present with a very dense contralateral homonymous hemianopsia. Hemorrhages in the frontoparietal region will produce a contralateral plegia or paresis of the leg with relative sparing of the arm
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glect may develop if the bleed affects the nondominant hemisphere. Patients with small anterior thalamic hemorrhages may present with drowsiness, acute confusion, or neuropsychiatric symptoms. ●<span>Lobar hemorrhage – Lobar hemorrhages vary in their neurologic signs depending upon location. They most often affect the parietal and occipital lobes. These bleeds are associated with a higher incidence of seizures. Occipital hemorrhages frequently present with a very dense contralateral homonymous hemianopsia. Hemorrhages in the frontoparietal region will produce a contralateral plegia or paresis of the leg with relative sparing of the arm. ●Pontine hemorrhage – Pontine hemorrhages typically originate in brainstem nuclei and may extend into the base of the pons. These often lead to deep coma over the first few minutes fol




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Pontine hemorrhage – Pontine hemorrhages typically originate in brainstem nuclei and may extend into the base of the pons. These often lead to deep coma over the first few minutes following the hemorrhage, probably due to disruption of the reticular activating system. The motor examination may be marked by bilateral paralysis. The pupils are pinpoint and react to a strong light source. Horizontal eye movements are often absent, and there may be ocular bobbing, facial palsy, deafness, and dysarthria if the patient is awake
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ent with a very dense contralateral homonymous hemianopsia. Hemorrhages in the frontoparietal region will produce a contralateral plegia or paresis of the leg with relative sparing of the arm. ●<span>Pontine hemorrhage – Pontine hemorrhages typically originate in brainstem nuclei and may extend into the base of the pons. These often lead to deep coma over the first few minutes following the hemorrhage, probably due to disruption of the reticular activating system. The motor examination may be marked by bilateral paralysis. The pupils are pinpoint and react to a strong light source. Horizontal eye movements are often absent, and there may be ocular bobbing, facial palsy, deafness, and dysarthria if the patient is awake. Seizures — Seizures may accompany acute ICH. Seizures in the first days after ICH occur approximately 15 percent of patients [116,117]; they are more common in lobar hemorrhages (affec




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Seizures — Seizures may accompany acute ICH. Seizures in the first days after ICH occur approximately 15 percent of patients [116,117]; they are more common in lobar hemorrhages (affecting cortical tissue) than in deep or cerebellar ICH [118-121].
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pils are pinpoint and react to a strong light source. Horizontal eye movements are often absent, and there may be ocular bobbing, facial palsy, deafness, and dysarthria if the patient is awake. <span>Seizures — Seizures may accompany acute ICH. Seizures in the first days after ICH occur approximately 15 percent of patients [116,117]; they are more common in lobar hemorrhages (affecting cortical tissue) than in deep or cerebellar ICH [118-121]. (See "Overview of the management of epilepsy in adults", section on 'Poststroke seizures'.) Cardiac abnormalities — Cardiac abnormalities are commonly associated with spontaneous ICH [1




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Cardiac abnormalities — Cardiac abnormalities are commonly associated with spontaneous ICH [122]. The most frequently associated electrocardiographic (ECG) changes are prolonged QT interval and ST-T wave changes. These changes may reflect catecholamine-induced cardiac injury, which is most likely due to a centrally mediated release of excess catecholamines caused by increased intracranial pressure or autonomic disturbance [123].
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ore common in lobar hemorrhages (affecting cortical tissue) than in deep or cerebellar ICH [118-121]. (See "Overview of the management of epilepsy in adults", section on 'Poststroke seizures'.) <span>Cardiac abnormalities — Cardiac abnormalities are commonly associated with spontaneous ICH [122]. The most frequently associated electrocardiographic (ECG) changes are prolonged QT interval and ST-T wave changes. These changes may reflect catecholamine-induced cardiac injury, which is most likely due to a centrally mediated release of excess catecholamines caused by increased intracranial pressure or autonomic disturbance [123]. (See "Clinical manifestations and diagnosis of stress (takotsubo) cardiomyopathy" and "Complications of stroke: An overview", section on 'Neurogenic cardiac damage'.) Mild elevations in




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Mild elevations in serum myocardial enzymes often accompany the ECG changes, including cardiac troponin and beta natriuretic peptide [122]. Echocardiographic abnormalities may involve global or regional wall motion abnormalities and reduced ejection fraction. Ventricular arrhythmias may occur with brainstem compression [124].
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tonomic disturbance [123]. (See "Clinical manifestations and diagnosis of stress (takotsubo) cardiomyopathy" and "Complications of stroke: An overview", section on 'Neurogenic cardiac damage'.) <span>Mild elevations in serum myocardial enzymes often accompany the ECG changes, including cardiac troponin and beta natriuretic peptide [122]. Echocardiographic abnormalities may involve global or regional wall motion abnormalities and reduced ejection fraction. Ventricular arrhythmias may occur with brainstem compression [124]. BRAIN IMAGING — Both computed tomography (CT) or magnetic resonance imaging (MRI) are considered first-choice imaging options for the emergency diagnosis and assessment of ICH (image 14




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Head CT — Noncontrast head computed tomography (CT) accurately identifies the presence of acute ICH, distinguishing it from ischemic stroke. Hyperacute blood will appear hyperdense except in rare cases of severe anemia when it might appear isodense.
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brain contents (herniation), impending expansion, and underlying etiology. ICH severity can be assessed by calculating the volume of the hemorrhage. (See 'Estimating hemorrhage volume' below.) <span>Head CT — Noncontrast head computed tomography (CT) accurately identifies the presence of acute ICH, distinguishing it from ischemic stroke. Hyperacute blood will appear hyperdense except in rare cases of severe anemia when it might appear isodense. Over weeks, the blood from an acute hemorrhage will typically become isodense and may have a ring-enhancement appearance. Chronically, the blood is hypodense (image 15). CT angiography




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Clinical suspicion for ICH is based upon features such as acute onset of gradually worsening symptoms and increasing neurologic deficit, particularly if accompanied by severe headache, vomiting, severe hypertension, and decreased level of consciousness or coma. However, the distinction between brain hemorrhage and ischemia cannot be made on the basis of clinical characteristics alone [158]. Importantly, headache may be absent in some cases of ICH.
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omy or surgical hematoma evacuation (table 1). These issues are discussed in detail separately. (See "Spontaneous intracerebral hemorrhage: Acute treatment and prognosis".) Initial evaluation — <span>Clinical suspicion for ICH is based upon features such as acute onset of gradually worsening symptoms and increasing neurologic deficit, particularly if accompanied by severe headache, vomiting, severe hypertension, and decreased level of consciousness or coma. However, the distinction between brain hemorrhage and ischemia cannot be made on the basis of clinical characteristics alone [158]. Importantly, headache may be absent in some cases of ICH. (See 'Clinical presentation' above.) Neuroimaging with brain computed tomography (CT) or magnetic resonance imaging (MRI) is mandatory to confirm the diagnosis of ICH and to exclude isc




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Neuroimaging with brain computed tomography (CT) or magnetic resonance imaging (MRI) is mandatory to confirm the diagnosis of ICH and to exclude ischemic stroke and stroke mimics as possible causes [158].
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brain hemorrhage and ischemia cannot be made on the basis of clinical characteristics alone [158]. Importantly, headache may be absent in some cases of ICH. (See 'Clinical presentation' above.) <span>Neuroimaging with brain computed tomography (CT) or magnetic resonance imaging (MRI) is mandatory to confirm the diagnosis of ICH and to exclude ischemic stroke and stroke mimics as possible causes [158]. Laboratory and other dignostic testing — Routine laboratory evaluation to evaluate for underlying causes or associated risks in patients with ICH includes [158]: ●Complete blood count,




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We obtain follow-up imaging when an underlying cause is suspected by clinical features or initial imaging findings (table 3) [158]. Initial imaging findings that may suggest a specific underlying cause include:

• Early perihematomal edema out of proportion to the underlying ICH (image 9) [161]

• ICH within arterial vascular territory suggesting primary ischemic infarction (image 7)

• Multifocal hemorrhage (image 19)

• Isolated intraventricular hemorrhage (image 20)

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ve vasculopathy who has a history of longstanding hypertension. For other patients, initial imaging studies do not sufficiently exclude other causes of ICH and follow-up evaluation is required. <span>We obtain follow-up imaging when an underlying cause is suspected by clinical features or initial imaging findings (table 3) [158]. Initial imaging findings that may suggest a specific underlying cause include: •Early perihematomal edema out of proportion to the underlying ICH (image 9) [161] •ICH within arterial vascular territory suggesting primary ischemic infarction (image 7) •Multifocal hemorrhage (image 19) •Isolated intraventricular hemorrhage (image 20) The assessment of the possible underlying structural pathology may be shrouded and distorted by the hematoma or surrounding edema. In these cases, delayed imaging performed after bleedi




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Clinical presentation – The overwhelming majority of patients with aneurysmal subarachnoid hemorrhage (SAH) present with a sudden-onset severe headache, which may be associated with brief loss of consciousness, seizures, nausea or vomiting, or meningismus.
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Basics topics (see "Patient education: Stroke symptoms and diagnosis (Beyond the Basics)" and "Patient education: Hemorrhagic stroke treatment (Beyond the Basics)") SUMMARY AND RECOMMENDATIONS ●<span>Clinical presentation – The overwhelming majority of patients with aneurysmal subarachnoid hemorrhage (SAH) present with a sudden-onset severe headache, which may be associated with brief loss of consciousness, seizures, nausea or vomiting, or meningismus. (See 'Clinical presentation' above.) ●Evaluation and diagnosis – Sudden onset of headache, regardless of severity or prior headache history, should raise the clinical suspicion for SAH




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Imaging – Noncontrast head computed tomography (CT) reveals the diagnosis in more than 90 percent of cases if performed within 24 hours of bleeding onset
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den onset of headache, regardless of severity or prior headache history, should raise the clinical suspicion for SAH and compel a diagnostic evaluation. (See 'Evaluation and diagnosis' above.) •<span>Imaging – Noncontrast head computed tomography (CT) reveals the diagnosis in more than 90 percent of cases if performed within 24 hours of bleeding onset. (See 'Head CT scan' above.) •Lumbar puncture – Lumbar puncture is mandatory if there is a strong suspicion of SAH despite a normal head CT, with the disputed exception of select patien




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Lumbar puncture – Lumbar puncture is mandatory if there is a strong suspicion of SAH despite a normal head CT, with the disputed exception of select patients with isolated headache and normal examination presenting early and scanned within six hours of headache onset.
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above.) •Imaging – Noncontrast head computed tomography (CT) reveals the diagnosis in more than 90 percent of cases if performed within 24 hours of bleeding onset. (See 'Head CT scan' above.) •<span>Lumbar puncture – Lumbar puncture is mandatory if there is a strong suspicion of SAH despite a normal head CT, with the disputed exception of select patients with isolated headache and normal examination presenting early and scanned within six hours of headache onset. (See 'Lumbar puncture' above.) The classic findings are an elevated opening pressure, an elevated red blood cell count that does not diminish from cerebrospinal fluid (CSF) tube 1 to tu




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The classic findings are an elevated opening pressure, an elevated red blood cell count that does not diminish from cerebrospinal fluid (CSF) tube 1 to tube 4, and xanthochromia. Immediate centrifugation of the CSF can help differentiate bleeding in SAH from that due to a traumatic spinal tap
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CT, with the disputed exception of select patients with isolated headache and normal examination presenting early and scanned within six hours of headache onset. (See 'Lumbar puncture' above.) <span>The classic findings are an elevated opening pressure, an elevated red blood cell count that does not diminish from cerebrospinal fluid (CSF) tube 1 to tube 4, and xanthochromia. Immediate centrifugation of the CSF can help differentiate bleeding in SAH from that due to a traumatic spinal tap. ●Identifying the source of bleeding – Once a diagnosis of SAH has been made, the etiology of the hemorrhage must be determined with vascular imaging. Of the available tests, digital su




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Identifying the source of bleeding – Once a diagnosis of SAH has been made, the etiology of the hemorrhage must be determined with vascular imaging. Of the available tests, digital subtraction angiography (DSA) has the highest resolution to detect intracranial aneurysms and define their anatomic features and remains the gold standard test for this, but CT angiography is being increasingly used as a first-line vascular test.
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diminish from cerebrospinal fluid (CSF) tube 1 to tube 4, and xanthochromia. Immediate centrifugation of the CSF can help differentiate bleeding in SAH from that due to a traumatic spinal tap. ●<span>Identifying the source of bleeding – Once a diagnosis of SAH has been made, the etiology of the hemorrhage must be determined with vascular imaging. Of the available tests, digital subtraction angiography (DSA) has the highest resolution to detect intracranial aneurysms and define their anatomic features and remains the gold standard test for this, but CT angiography is being increasingly used as a first-line vascular test. (See 'Identifying the source of bleeding' above.) Repeat angiography is necessary if the initial study is negative, unless the pattern of hemorrhage is perimesencephalic, in which a rep




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Repeat angiography is necessary if the initial study is negative, unless the pattern of hemorrhage is perimesencephalic, in which a repeat angiography may be considered optional. Additional testing is required for SAH that is nonaneurysmal.
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eir anatomic features and remains the gold standard test for this, but CT angiography is being increasingly used as a first-line vascular test. (See 'Identifying the source of bleeding' above.) <span>Repeat angiography is necessary if the initial study is negative, unless the pattern of hemorrhage is perimesencephalic, in which a repeat angiography may be considered optional. Additional testing is required for SAH that is nonaneurysmal. (See 'Patients with negative angiography' above.) Use of UpToDate is subject to the Terms of Use. REFERENCES Edlow JA, Caplan LR. Avoiding pitfalls in the diagnosis of subarachnoid hemo




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Headache characteristics – The classic presentation of patients with aneurysmal SAH is a sudden-onset, severe headache typically described as the "worst headache of my life" [1]. Every patient with this kind of headache, often referred to as a "thunderclap headache" (see "Overview of thunderclap headache"), should be evaluated for SAH. Headache is often an isolated finding. In neurologically intact patients with a severe-onset headache peaking within one hour, three large sequential studies with a total of 5283 patients found that 329 patients (6 percent) had SAH [2-5].
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urysms" and "Overview of infected (mycotic) arterial aneurysm" and "Nonaneurysmal subarachnoid hemorrhage" and "Perimesencephalic nonaneurysmal subarachnoid hemorrhage".) CLINICAL PRESENTATION ●<span>Headache characteristics – The classic presentation of patients with aneurysmal SAH is a sudden-onset, severe headache typically described as the "worst headache of my life" [1]. Every patient with this kind of headache, often referred to as a "thunderclap headache" (see "Overview of thunderclap headache"), should be evaluated for SAH. Headache is often an isolated finding. In neurologically intact patients with a severe-onset headache peaking within one hour, three large sequential studies with a total of 5283 patients found that 329 patients (6 percent) had SAH [2-5]. Importantly, the headache onset in SAH is not always noted as instantaneous, either because the patient does not perceive it that way or because the physician does not elicit that infor




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Importantly, the headache onset in SAH is not always noted as instantaneous, either because the patient does not perceive it that way or because the physician does not elicit that information. In a study that included 132 patients with SAH, the time to peak intensity was one hour in six (5 percent), and the physician interobserver agreement for sudden onset was only moderate (kappa = 0.49) [2].

Location is not useful since the headache can be localized or generalized.

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rologically intact patients with a severe-onset headache peaking within one hour, three large sequential studies with a total of 5283 patients found that 329 patients (6 percent) had SAH [2-5]. <span>Importantly, the headache onset in SAH is not always noted as instantaneous, either because the patient does not perceive it that way or because the physician does not elicit that information. In a study that included 132 patients with SAH, the time to peak intensity was one hour in six (5 percent), and the physician interobserver agreement for sudden onset was only moderate (kappa = 0.49) [2]. Location is not useful since the headache can be localized or generalized. ●Associated symptoms – In addition to headache, common associated symptoms of SAH include a brief loss of consciousness, vomiting, and neck pain or stiffness. In one series, these occur




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In addition to headache, common associated symptoms of SAH include a brief loss of consciousness, vomiting, and neck pain or stiffness. In one series, these occurred in 9, 61, and 75 percent of patients, respectively, and each of these symptoms was more common in patients with SAH compared with patients without SAH [3].
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nd the physician interobserver agreement for sudden onset was only moderate (kappa = 0.49) [2]. Location is not useful since the headache can be localized or generalized. ●Associated symptoms – <span>In addition to headache, common associated symptoms of SAH include a brief loss of consciousness, vomiting, and neck pain or stiffness. In one series, these occurred in 9, 61, and 75 percent of patients, respectively, and each of these symptoms was more common in patients with SAH compared with patients without SAH [3]. Meningismus, often accompanied by lower back pain, may develop several hours after the bleed, since they are caused by the breakdown of blood products within the cerebrospinal fluid (CS




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Meningismus, often accompanied by lower back pain, may develop several hours after the bleed, since they are caused by the breakdown of blood products within the cerebrospinal fluid (CSF), which lead to an aseptic meningitis [ 6].
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ffness. In one series, these occurred in 9, 61, and 75 percent of patients, respectively, and each of these symptoms was more common in patients with SAH compared with patients without SAH [3]. <span>Meningismus, often accompanied by lower back pain, may develop several hours after the bleed, since they are caused by the breakdown of blood products within the cerebrospinal fluid (CSF), which lead to an aseptic meningitis [6]. While many patients have an altered level of consciousness, coma is unusual. Seizures occur during the first 24 hours in less than 10 percent of patients but are a predictor of poor out




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While many patients have an altered level of consciousness, coma is unusual. Seizures occur during the first 24 hours in less than 10 percent of patients but are a predictor of poor outcome [ 7]. SAH may also present as sudden death; as many as 22 percent of patients die before reaching the hospital [8]
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wer back pain, may develop several hours after the bleed, since they are caused by the breakdown of blood products within the cerebrospinal fluid (CSF), which lead to an aseptic meningitis [6]. <span>While many patients have an altered level of consciousness, coma is unusual. Seizures occur during the first 24 hours in less than 10 percent of patients but are a predictor of poor outcome [7]. SAH may also present as sudden death; as many as 22 percent of patients die before reaching the hospital [8]. ●Prodromal symptoms – Some patients report a history of a sudden and severe headache (the sentinel headache) that precedes a major SAH, occurring days to weeks prior to aneurysm ruptur




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Clinical settings – While the onset of symptoms in the setting of physical exertion, activities associated with a Valsalva maneuver, or emotional stress suggest SAH, aneurysmal SAH occurs most often during nonstrenuous activity, rest, or sleep [10,11].
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umber of reports question the existence of "warning leaks" as the cause of sentinel headaches, as reviewed separately. (See "Overview of thunderclap headache", section on 'Sentinel headache'.) ●<span>Clinical settings – While the onset of symptoms in the setting of physical exertion, activities associated with a Valsalva maneuver, or emotional stress suggest SAH, aneurysmal SAH occurs most often during nonstrenuous activity, rest, or sleep [10,11]. (See "Aneurysmal subarachnoid hemorrhage: Epidemiology, risk factors, and pathogenesis", section on 'Pathogenesis'.) ●Examination findings – Physical examination often shows hypertensio




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Examination findings – Physical examination often shows hypertension and may show meningismus.
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SAH occurs most often during nonstrenuous activity, rest, or sleep [10,11]. (See "Aneurysmal subarachnoid hemorrhage: Epidemiology, risk factors, and pathogenesis", section on 'Pathogenesis'.) ●<span>Examination findings – Physical examination often shows hypertension and may show meningismus. Terson syndrome (preretinal hemorrhages) may be seen and implies a poorer prognosis. In a systematic review, patients with Terson syndrome had higher Hunt and Hess grades (table 1) and




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Terson syndrome (preretinal hemorrhages) may be seen and implies a poorer prognosis. In a systematic review, patients with Terson syndrome had higher Hunt and Hess grades ( table 1) and significantly higher mortality than those without [12]. The preretinal hemorrhages of Terson syndrome may indicate a more abrupt increase in intracranial pressure and must be distinguished from the more benign retinal hemorrhages sometimes associated with SAH [13].
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barachnoid hemorrhage: Epidemiology, risk factors, and pathogenesis", section on 'Pathogenesis'.) ●Examination findings – Physical examination often shows hypertension and may show meningismus. <span>Terson syndrome (preretinal hemorrhages) may be seen and implies a poorer prognosis. In a systematic review, patients with Terson syndrome had higher Hunt and Hess grades (table 1) and significantly higher mortality than those without [12]. The preretinal hemorrhages of Terson syndrome may indicate a more abrupt increase in intracranial pressure and must be distinguished from the more benign retinal hemorrhages sometimes associated with SAH [13]. Nearly any neurologic sign may be present (table 2) and will depend on the location of the hemorrhage, presence or absence of hydrocephalus, elevated intracranial pressure, ischemia, in




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Nearly any neurologic sign may be present (table 2) and will depend on the location of the hemorrhage, presence or absence of hydrocephalus, elevated intracranial pressure, ischemia, infarction, or hematoma [14].
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emorrhages of Terson syndrome may indicate a more abrupt increase in intracranial pressure and must be distinguished from the more benign retinal hemorrhages sometimes associated with SAH [13]. <span>Nearly any neurologic sign may be present (table 2) and will depend on the location of the hemorrhage, presence or absence of hydrocephalus, elevated intracranial pressure, ischemia, infarction, or hematoma [14]. Although a pupil-involving third nerve palsy is often cited as a finding of SAH, it is more common with an expanding but unruptured aneurysm of the posterior communicating artery or sup




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Although a pupil-involving third nerve palsy is often cited as a finding of SAH, it is more common with an expanding but unruptured aneurysm of the posterior communicating artery or superior cerebellar artery, which is located close to where the third nerve exits the brainstem [15,16]. If present, this finding mandates a work-up for an aneurysm including some form of cerebral angiography, but its absence does not decrease the likelihood of SAH in patients with acute headache.
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ic sign may be present (table 2) and will depend on the location of the hemorrhage, presence or absence of hydrocephalus, elevated intracranial pressure, ischemia, infarction, or hematoma [14]. <span>Although a pupil-involving third nerve palsy is often cited as a finding of SAH, it is more common with an expanding but unruptured aneurysm of the posterior communicating artery or superior cerebellar artery, which is located close to where the third nerve exits the brainstem [15,16]. If present, this finding mandates a work-up for an aneurysm including some form of cerebral angiography, but its absence does not decrease the likelihood of SAH in patients with acute headache. ●Grading severity – A number of grading systems are used in practice to standardize the clinical classification of patients with SAH at the time of initial presentation. However, clinic




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However, clinical grade assessment at the time of nadir, or after neurologic resuscitation, appears to be more predictive of outcome [17,18]. The grading system proposed by Hunt and Hess (table 1) and that of the World Federation of Neurological Surgeons (WFNS) (table 3) are among the most widely used. The WFNS system incorporates the Glasgow Coma Scale (table 4) combined with the presence of motor deficit.
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ts with acute headache. ●Grading severity – A number of grading systems are used in practice to standardize the clinical classification of patients with SAH at the time of initial presentation. <span>However, clinical grade assessment at the time of nadir, or after neurologic resuscitation, appears to be more predictive of outcome [17,18]. The grading system proposed by Hunt and Hess (table 1) and that of the World Federation of Neurological Surgeons (WFNS) (table 3) are among the most widely used. The WFNS system incorporates the Glasgow Coma Scale (table 4) combined with the presence of motor deficit. The Fisher scale is an index of vasospasm risk based upon a computed tomography (CT)-defined hemorrhage pattern (table 5), and the modified Fisher scale (also known as the Claassen scal




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The Fisher scale is an index of vasospasm risk based upon a computed tomography (CT)-defined hemorrhage pattern (table 5), and the modified Fisher scale (also known as the Claassen scale) is a similar index of the risk of delayed cerebral ischemia due to vasospasm (table 6).
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d Federation of Neurological Surgeons (WFNS) (table 3) are among the most widely used. The WFNS system incorporates the Glasgow Coma Scale (table 4) combined with the presence of motor deficit. <span>The Fisher scale is an index of vasospasm risk based upon a computed tomography (CT)-defined hemorrhage pattern (table 5), and the modified Fisher scale (also known as the Claassen scale) is a similar index of the risk of delayed cerebral ischemia due to vasospasm (table 6). A system proposed by Ogilvy and Carter stratifies patients based upon age, Hunt and Hess grade, Fisher grade, and aneurysm size (table 7). In addition to predicting outcome, this scale




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The complaint of the sudden or rapid onset of severe headache is sufficiently characteristic that SAH should always be considered in the evaluation. All patients with this complaint should undergo immediate evaluation for SAH beginning with head computed tomography (CT), even those who are alert and neurologically intact at the time of initial presentation [2,19].
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tratifies patients for therapy. Grading scales for SAH are discussed in greater detail separately. (See "Subarachnoid hemorrhage grading scales".) EVALUATION AND DIAGNOSIS When to suspect SAH — <span>The complaint of the sudden or rapid onset of severe headache is sufficiently characteristic that SAH should always be considered in the evaluation. All patients with this complaint should undergo immediate evaluation for SAH beginning with head computed tomography (CT), even those who are alert and neurologically intact at the time of initial presentation [2,19]. Additional clues to the diagnosis of SAH, such as preretinal hemorrhages, neck pain, or meningismus, may or may not be present. In a systematic review and meta-analysis that included 22




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Additional clues to the diagnosis of SAH, such as preretinal hemorrhages, neck pain, or meningismus, may or may not be present. In a systematic review and meta-analysis that included 22 diagnostic studies of emergency department patients evaluated for spontaneous SAH, the presence of meningismus on physical examination had a positive likelihood ratio of 6.6 [ 20]
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omplaint should undergo immediate evaluation for SAH beginning with head computed tomography (CT), even those who are alert and neurologically intact at the time of initial presentation [2,19]. <span>Additional clues to the diagnosis of SAH, such as preretinal hemorrhages, neck pain, or meningismus, may or may not be present. In a systematic review and meta-analysis that included 22 diagnostic studies of emergency department patients evaluated for spontaneous SAH, the presence of meningismus on physical examination had a positive likelihood ratio of 6.6 [20]. ●Ottawa Subarachnoid Hemorrhage Rule – In neurologically intact patients presenting with acute nontraumatic headache that reached maximal intensity within one hour, a clinical decision




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Ottawa Subarachnoid Hemorrhage Rule – In neurologically intact patients presenting with acute nontraumatic headache that reached maximal intensity within one hour, a clinical decision rule (the Ottawa Subarachnoid Hemorrhage Rule) that included any of the following features had a sensitivity of 100 percent and a specificity of 15 percent for the diagnosis of SAH [2]:

• Age ≥40 years

• Neck pain or stiffness

• Limited neck flexion on examination

• Witnessed loss of consciousness

• Onset during exertion

• Thunderclap headache (instantly peaking pain)

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included 22 diagnostic studies of emergency department patients evaluated for spontaneous SAH, the presence of meningismus on physical examination had a positive likelihood ratio of 6.6 [20]. ●<span>Ottawa Subarachnoid Hemorrhage Rule – In neurologically intact patients presenting with acute nontraumatic headache that reached maximal intensity within one hour, a clinical decision rule (the Ottawa Subarachnoid Hemorrhage Rule) that included any of the following features had a sensitivity of 100 percent and a specificity of 15 percent for the diagnosis of SAH [2]: •Age ≥40 years •Neck pain or stiffness •Limited neck flexion on examination •Witnessed loss of consciousness •Onset during exertion •Thunderclap headache (instantly peaking pain) Subsequent validation studies, most from the same investigators, reported similar findings [3,21,22]. Moreover, application of this rule would have eliminated the need for evaluation in




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Misdiagnosis and delayed diagnosis – Misdiagnosis and delayed diagnosis of SAH are common and can lead to delays in treatment and worse outcomes [24,25]. Missed or delayed diagnosis of SAH usually results from three errors (table 8) [16]:

• Failure to appreciate the spectrum of clinical presentation associated with SAH

• Failure to obtain a head CT scan or to understand its limitations in diagnosing SAH

• Failure to perform a lumbar puncture or correctly interpret the results

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es, most from the same investigators, reported similar findings [3,21,22]. Moreover, application of this rule would have eliminated the need for evaluation in only 14 percent of patients [23]. ●<span>Misdiagnosis and delayed diagnosis – Misdiagnosis and delayed diagnosis of SAH are common and can lead to delays in treatment and worse outcomes [24,25]. Missed or delayed diagnosis of SAH usually results from three errors (table 8) [16]: •Failure to appreciate the spectrum of clinical presentation associated with SAH •Failure to obtain a head CT scan or to understand its limitations in diagnosing SAH •Failure to perform a lumbar puncture or correctly interpret the results Perhaps the most important source of misdiagnosis results from the misconception that patients with aneurysmal SAH always appear "sick" or have neurologic findings or altered mental sta




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Perhaps the most important source of misdiagnosis results from the misconception that patients with aneurysmal SAH always appear "sick" or have neurologic findings or altered mental status when in fact nearly 40 percent of patients are awake, alert, and neurologically intact [16].
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al presentation associated with SAH •Failure to obtain a head CT scan or to understand its limitations in diagnosing SAH •Failure to perform a lumbar puncture or correctly interpret the results <span>Perhaps the most important source of misdiagnosis results from the misconception that patients with aneurysmal SAH always appear "sick" or have neurologic findings or altered mental status when in fact nearly 40 percent of patients are awake, alert, and neurologically intact [16]. Practitioners with the misconception may not perform CT scans in such patients. From a practice perspective, the vast majority of patients will be correctly diagnosed if all patients wi




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From a practice perspective, the vast majority of patients will be correctly diagnosed if all patients with thunderclap headache undergo head CT (and lumbar puncture if the CT is done after six hours from headache onset).
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ltered mental status when in fact nearly 40 percent of patients are awake, alert, and neurologically intact [16]. Practitioners with the misconception may not perform CT scans in such patients. <span>From a practice perspective, the vast majority of patients will be correctly diagnosed if all patients with thunderclap headache undergo head CT (and lumbar puncture if the CT is done after six hours from headache onset). Only an extremely small minority whose thunderclap headache is from a symptomatic but unruptured aneurysm would be missed by this approach [26-28]. The frequency of SAH misdiagnosis may




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In contrast, a 2017 systematic review identified three studies published from 1996 to 2007 in emergency department populations with a pooled misdiagnosis rate of 7 percent [29].
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misdiagnosis may be decreasing but remains a problem. In four studies of patients hospitalized with SAH published from 1980 to 1997, initial misdiagnosis rates ranged from 23 to 51 percent [1]. <span>In contrast, a 2017 systematic review identified three studies published from 1996 to 2007 in emergency department populations with a pooled misdiagnosis rate of 7 percent [29]. Included the systematic review was a report of 482 patients admitted with SAH; initial misdiagnosis was independently associated with small SAH volume, normal mental status at presentat




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Failure to obtain a head CT scan at initial contact was the most common error, occurring in 73 percent of misdiagnosed patients. Among patients with SAH and normal mental status at first contact (45 percent), the misdiagnosis rate rose to 20 percent and was associated with a nearly fourfold increase in mortality at 12 months as well as increased morbidity among survivors.
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report of 482 patients admitted with SAH; initial misdiagnosis was independently associated with small SAH volume, normal mental status at presentation, and right-sided aneurysm location [24]. <span>Failure to obtain a head CT scan at initial contact was the most common error, occurring in 73 percent of misdiagnosed patients. Among patients with SAH and normal mental status at first contact (45 percent), the misdiagnosis rate rose to 20 percent and was associated with a nearly fourfold increase in mortality at 12 months as well as increased morbidity among survivors. Standard diagnostic approach — The first step in the diagnosis of SAH is noncontrast head CT [19]. A lumbar puncture should be done if the head CT is negative [19]. If both tests are ne




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Standard diagnostic approach — The first step in the diagnosis of SAH is noncontrast head CT [19]. A lumbar puncture should be done if the head CT is negative [19]. If both tests are negative, they effectively eliminate the diagnosis of SAH as long as both tests are performed within two weeks of the event [26,30].
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first contact (45 percent), the misdiagnosis rate rose to 20 percent and was associated with a nearly fourfold increase in mortality at 12 months as well as increased morbidity among survivors. <span>Standard diagnostic approach — The first step in the diagnosis of SAH is noncontrast head CT [19]. A lumbar puncture should be done if the head CT is negative [19]. If both tests are negative, they effectively eliminate the diagnosis of SAH as long as both tests are performed within two weeks of the event [26,30]. In cases presenting more than two weeks after headache onset (at such time when even xanthochromia may have disappeared), additional testing with noninvasive CT angiography (CTA) or mag




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The sensitivity of all diagnostic tests for SAH is time-dependent, measuring time from onset of the bleed. This is due to the physiologic brisk flow of cerebrospinal fluid (CSF). Normally, there is approximately 150 mL of CSF in a person's subarachnoid space at any point in time, but 450 to 500 mL are manufactured per 24 hours. This is why CT scans and red blood cell (RBC) counts are very sensitive early after bleeding onset but lose sensitivity with the passage of time.
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f acute-onset severe headache, magnetic resonance imaging (MRI), catheter cerebral angiography, or cerebral venography may be necessary (table 9) [19]. (See "Overview of thunderclap headache".) <span>The sensitivity of all diagnostic tests for SAH is time-dependent, measuring time from onset of the bleed. This is due to the physiologic brisk flow of cerebrospinal fluid (CSF). Normally, there is approximately 150 mL of CSF in a person's subarachnoid space at any point in time, but 450 to 500 mL are manufactured per 24 hours. This is why CT scans and red blood cell (RBC) counts are very sensitive early after bleeding onset but lose sensitivity with the passage of time. RBCs present in the CSF undergo lysis, resulting in breakdown products such as bilirubin and oxyhemoglobin, a process that takes time, accounting for the fact that xanthochromia is not




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RBCs present in the CSF undergo lysis, resulting in breakdown products such as bilirubin and oxyhemoglobin, a process that takes time, accounting for the fact that xanthochromia is not sensitive early but becomes increasingly sensitive after a few hours.

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ut 450 to 500 mL are manufactured per 24 hours. This is why CT scans and red blood cell (RBC) counts are very sensitive early after bleeding onset but lose sensitivity with the passage of time. <span>RBCs present in the CSF undergo lysis, resulting in breakdown products such as bilirubin and oxyhemoglobin, a process that takes time, accounting for the fact that xanthochromia is not sensitive early but becomes increasingly sensitive after a few hours. Head CT scan — The cornerstone of SAH diagnosis is the noncontrast head CT scan [31,32]. The head CT scan should be performed with thin cuts through the base of the brain to increase th




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Anemia with hematocrits of 30 percent or less and poor scan quality due to patient movement are other causes of ambiguous or false-negative CT results. However, the most important factor that affects CT sensitivity is time from onset.
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dy, for example, a minor SAH was not diagnosed by CT scan in 55 percent of patients; lumbar puncture was positive in all cases [38] However, the time from SAH onset to head CT was not reported. <span>Anemia with hematocrits of 30 percent or less and poor scan quality due to patient movement are other causes of ambiguous or false-negative CT results. However, the most important factor that affects CT sensitivity is time from onset. ●Location of blood – Blood in SAH is generally found in the basal cisterns. Additional locations may include the sylvian fissures, interhemispheric fissure, interpeduncular fossa, and s




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The distribution of blood on CT (performed within 72 hours after the bleed) is a poor predictor of the site of an aneurysm except in patients with ruptured anterior cerebral artery or anterior communicating artery aneurysms and in patients with a parenchymal hematoma [39]. However, the distribution of blood does have implications about whether or not the cause of the SAH is aneurysmal (image 1).
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quadrigeminal cisterns [14]. Intracerebral extension is present in 20 to 40 percent of patients and intraventricular and subdural blood may be seen in 15 to 35 and 2 to 5 percent, respectively. <span>The distribution of blood on CT (performed within 72 hours after the bleed) is a poor predictor of the site of an aneurysm except in patients with ruptured anterior cerebral artery or anterior communicating artery aneurysms and in patients with a parenchymal hematoma [39]. However, the distribution of blood does have implications about whether or not the cause of the SAH is aneurysmal (image 1). Blood restricted to the subarachnoid space in front of the brainstem suggests a nonaneurysmal perimesencephalic (also called pretruncal) SAH. Convexal SAH suggests reversible cerebral v




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Blood restricted to the subarachnoid space in front of the brainstem suggests a nonaneurysmal perimesencephalic (also called pretruncal) SAH. Convexal SAH suggests reversible cerebral vasoconstriction syndrome (RCVS) in younger patients or cerebral amyloid angiopathy in older patients, whereas blood adjacent to bone in the anterior or middle cranial fossae suggests traumatic SAH.
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g artery aneurysms and in patients with a parenchymal hematoma [39]. However, the distribution of blood does have implications about whether or not the cause of the SAH is aneurysmal (image 1). <span>Blood restricted to the subarachnoid space in front of the brainstem suggests a nonaneurysmal perimesencephalic (also called pretruncal) SAH. Convexal SAH suggests reversible cerebral vasoconstriction syndrome (RCVS) in younger patients or cerebral amyloid angiopathy in older patients, whereas blood adjacent to bone in the anterior or middle cranial fossae suggests traumatic SAH. (See "Perimesencephalic nonaneurysmal subarachnoid hemorrhage".) Lumbar puncture — Lumbar puncture is mandatory if there is a strong suspicion of SAH despite a normal head CT [31,40]. A




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Lumbar puncture is mandatory if there is a strong suspicion of SAH despite a normal head CT [31,40]. Although controversial, one possible exception involves select patients with isolated headache, a normal examination, and a negative CT scan performed within six hours from onset of headache and interpreted by an expert reviewer, as discussed below. (
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lder patients, whereas blood adjacent to bone in the anterior or middle cranial fossae suggests traumatic SAH. (See "Perimesencephalic nonaneurysmal subarachnoid hemorrhage".) Lumbar puncture — <span>Lumbar puncture is mandatory if there is a strong suspicion of SAH despite a normal head CT [31,40]. Although controversial, one possible exception involves select patients with isolated headache, a normal examination, and a negative CT scan performed within six hours from onset of headache and interpreted by an expert reviewer, as discussed below. (See 'Need for LP when early CT is negative' below.) Lumbar puncture should include measurement of opening pressure, routine CSF analyses including RBC and white blood cell (WBC) counts,




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Lumbar puncture should include measurement of opening pressure, routine CSF analyses including RBC and white blood cell (WBC) counts, and visual inspection for xanthochromia. The classic lumbar puncture findings of SAH are an elevated opening pressure, an elevated RBC count that does not diminish from CSF tube 1 to tube 4, and xanthochromia. Accidental trauma to a capillary or venule may occur during performance of a lumbar puncture, increasing the number of both RBCs and WBCs in the CSF.
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ination, and a negative CT scan performed within six hours from onset of headache and interpreted by an expert reviewer, as discussed below. (See 'Need for LP when early CT is negative' below.) <span>Lumbar puncture should include measurement of opening pressure, routine CSF analyses including RBC and white blood cell (WBC) counts, and visual inspection for xanthochromia. The classic lumbar puncture findings of SAH are an elevated opening pressure, an elevated RBC count that does not diminish from CSF tube 1 to tube 4, and xanthochromia. Accidental trauma to a capillary or venule may occur during performance of a lumbar puncture, increasing the number of both RBCs and WBCs in the CSF. The differential of RBC counts between tubes 1 and 4, and immediate centrifugation of the CSF, can help differentiate bleeding in SAH from that due to a traumatic spinal tap: ●Clearing




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Clearing of blood (a declining RBC count with successive collection tubes) is purported to be a useful way of distinguishing a traumatic lumbar puncture from SAH. However, this is an unreliable sign of a traumatic tap, since a decrease in the number of RBCs in later tubes can also occur in SAH [41]. This method can reliably exclude SAH only if there is substantial RBC count in the first tube, and the late or final collection tube is normal.
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e differential of RBC counts between tubes 1 and 4, and immediate centrifugation of the CSF, can help differentiate bleeding in SAH from that due to a traumatic spinal tap: ●Clearing of blood – <span>Clearing of blood (a declining RBC count with successive collection tubes) is purported to be a useful way of distinguishing a traumatic lumbar puncture from SAH. However, this is an unreliable sign of a traumatic tap, since a decrease in the number of RBCs in later tubes can also occur in SAH [41]. This method can reliably exclude SAH only if there is substantial RBC count in the first tube, and the late or final collection tube is normal. One study found that the percent change in RBC count between the first and last tubes was more useful than the absolute difference as a test for distinguishing traumatic tap from SAH; t




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Given the brisk flow of CSF (approximately 20 to 25 mL is produced every hour), even discarding 10 mL will take only 30 minutes for the body to replace [43].
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one practical method to increase the likelihood that the last tube of CSF will contain close to zero RBCs is to discard CSF between the first and last tubes with a goal of visual clearing [19]. <span>Given the brisk flow of CSF (approximately 20 to 25 mL is produced every hour), even discarding 10 mL will take only 30 minutes for the body to replace [43]. ●RBC count – The greater the RBC count in the last tube, the more likely SAH is the cause. In one study examining CSF results in 1739 patients with acute nontraumatic headache, fewer th




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The greater the RBC count in the last tube, the more likely SAH is the cause. In one study examining CSF results in 1739 patients with acute nontraumatic headache, fewer than 2000 RBCs/microL in addition to no xanthochromia excluded aneurysmal SAH with a sensitivity of 100 percent [44].
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visual clearing [19]. Given the brisk flow of CSF (approximately 20 to 25 mL is produced every hour), even discarding 10 mL will take only 30 minutes for the body to replace [43]. ●RBC count – <span>The greater the RBC count in the last tube, the more likely SAH is the cause. In one study examining CSF results in 1739 patients with acute nontraumatic headache, fewer than 2000 RBCs/microL in addition to no xanthochromia excluded aneurysmal SAH with a sensitivity of 100 percent [44]. In a retrospective report of over 4400 adults who had lumbar puncture in the emergency department, finding fewer than 100 RBCs/microL in the CSF greatly decreased the likelihood of a SA




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Xanthochromia may be visually detected by comparing a vial of CSF with a vial of plain water held side by side against a white background in bright light [45].
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yellow tint) represents hemoglobin degradation products. An otherwise unexplained xanthochromic supernatant in CSF is highly suggestive of SAH. •Xanthochromia determined by visual inspection – <span>Xanthochromia may be visually detected by comparing a vial of CSF with a vial of plain water held side by side against a white background in bright light [45]. The presence of xanthochromia indicates that blood has been in the CSF for at least two hours. Therefore, if the CSF is analyzed quickly after a traumatic lumbar puncture or SAH, there




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The presence of xanthochromia indicates that blood has been in the CSF for at least two hours. Therefore, if the CSF is analyzed quickly after a traumatic lumbar puncture or SAH, there will not be xanthochromia; the absence of xanthochromia cannot be used as evidence of a traumatic tap if a lumbar puncture is performed in a SAH of less than two hours duration. Over the course of the ensuing hours, more patients will have xanthochromia, and by 12 hours post SAH, 100 percent of patients will have xanthochromia, even when measured visually [ 46]. Xanthochromia lasts for two weeks or more [47,48].
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determined by visual inspection – Xanthochromia may be visually detected by comparing a vial of CSF with a vial of plain water held side by side against a white background in bright light [45]. <span>The presence of xanthochromia indicates that blood has been in the CSF for at least two hours. Therefore, if the CSF is analyzed quickly after a traumatic lumbar puncture or SAH, there will not be xanthochromia; the absence of xanthochromia cannot be used as evidence of a traumatic tap if a lumbar puncture is performed in a SAH of less than two hours duration. Over the course of the ensuing hours, more patients will have xanthochromia, and by 12 hours post SAH, 100 percent of patients will have xanthochromia, even when measured visually [46]. Xanthochromia lasts for two weeks or more [47,48]. One retrospective study identified 117 adults with no known history of aneurysm or previous SAH who presented to the emergency room with thunderclap headache [49]. All had a negative no




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In this series, xanthochromia for the detection of cerebral aneurysms had a sensitivity and specificity of 93 and 95 percent.
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erebral aneurysm in 13 (72 percent). One patient with no xanthochromia had an elevated RBC count (≥20,000 RBC/microL) in four successive collection tubes and a ruptured aneurysm by angiography. <span>In this series, xanthochromia for the detection of cerebral aneurysms had a sensitivity and specificity of 93 and 95 percent. Other conditions that can produce xanthochromia include increased CSF concentrations of protein (150 mg/dL), systemic hyperbilirubinemia (serum bilirubin >10 to 15 mg/dL), and trauma




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Other conditions that can produce xanthochromia include increased CSF concentrations of protein (150 mg/dL), systemic hyperbilirubinemia (serum bilirubin >10 to 15 mg/dL), and traumatic lumbar puncture with more than 100,000 RBCs/microL.
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successive collection tubes and a ruptured aneurysm by angiography. In this series, xanthochromia for the detection of cerebral aneurysms had a sensitivity and specificity of 93 and 95 percent. <span>Other conditions that can produce xanthochromia include increased CSF concentrations of protein (150 mg/dL), systemic hyperbilirubinemia (serum bilirubin >10 to 15 mg/dL), and traumatic lumbar puncture with more than 100,000 RBCs/microL. (See "Cerebrospinal fluid: Physiology and utility of an examination in disease states", section on 'Xanthochromia'.) •Xanthochromia determined by spectrophotometry — Spectrophotometry d




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Spectrophotometry detects blood breakdown products as they progress from oxyhemoglobin to methemoglobin and finally to bilirubin [47,50,51]. Bilirubin concentration peaks about 48 hours after SAH onset, and may last as long as four weeks after extensive, large-volume SAH [52]. While CSF spectrophotometry is more sensitive than visual inspection for xanthochromia, it is not universally recommended. As a practical matter, spectrophotometry of CSF is rarely available in North American hospitals [53].
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e than 100,000 RBCs/microL. (See "Cerebrospinal fluid: Physiology and utility of an examination in disease states", section on 'Xanthochromia'.) •Xanthochromia determined by spectrophotometry — <span>Spectrophotometry detects blood breakdown products as they progress from oxyhemoglobin to methemoglobin and finally to bilirubin [47,50,51]. Bilirubin concentration peaks about 48 hours after SAH onset, and may last as long as four weeks after extensive, large-volume SAH [52]. While CSF spectrophotometry is more sensitive than visual inspection for xanthochromia, it is not universally recommended. As a practical matter, spectrophotometry of CSF is rarely available in North American hospitals [53]. The sample of CSF to be tested by spectrophotometry should be the one that contains the least amount of bloodstain. It should be protected from light and sent immediately to the laborat




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The sample of CSF to be tested by spectrophotometry should be the one that contains the least amount of bloodstain. It should be protected from light and sent immediately to the laboratory for analysis [47,52].
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more sensitive than visual inspection for xanthochromia, it is not universally recommended. As a practical matter, spectrophotometry of CSF is rarely available in North American hospitals [53]. <span>The sample of CSF to be tested by spectrophotometry should be the one that contains the least amount of bloodstain. It should be protected from light and sent immediately to the laboratory for analysis [47,52]. Spectrophotometry for detection of bilirubin is highly sensitive (>95 percent) when lumbar puncture is done at least 12 hours after SAH [48]. Although xanthochromia is generally iden




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Despite a higher sensitivity than visual inspection for the detection of xanthochromia, CSF spectrophotometry has only a low to moderate specificity for the diagnosis of SAH [58].
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els of bilirubin. However, in a study comparing visual inspection with spectrophotometry, CSF that was considered colorless by visual inspection was not compatible with a diagnosis of SAH [57]. <span>Despite a higher sensitivity than visual inspection for the detection of xanthochromia, CSF spectrophotometry has only a low to moderate specificity for the diagnosis of SAH [58]. Alternative approaches — One alternative approach to the diagnosis of aneurysmal SAH is to follow a negative head CT with CTA rather than lumbar puncture (LP). Another involves omitting




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Two cost-effectiveness studies concluded that the standard approach with CT followed by LP approach is equivalent or better than a CT/CTA approach [63,64]. Therefore, we recommend the standard approach using CT, followed by LP if CT is negative, reserving CTA for patients with a positive noncontrast CT or CSF analysis.
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osis of aneurysmal SAH [59,60]. Chief among the various potential downstream implications is finding an asymptomatic aneurysm, which occurs in approximately 3 percent of the population [61,62]. <span>Two cost-effectiveness studies concluded that the standard approach with CT followed by LP approach is equivalent or better than a CT/CTA approach [63,64]. Therefore, we recommend the standard approach using CT, followed by LP if CT is negative, reserving CTA for patients with a positive noncontrast CT or CSF analysis. Need for LP when early CT is negative — Because the consequences of missing SAH are potentially dire, we recommend a LP when the CT scan is negative for blood, as do most guidelines [40




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Because the consequences of missing SAH are potentially dire, we recommend a LP when the CT scan is negative for blood, as do most guidelines [40,60]. In contrast, some experts have argued that the sensitivity of CT when performed within six hours of the onset of symptoms is sufficiently sensitive (95.5 to 100 percent) to make a follow-up LP unnecessary [21,37,65,66].
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we recommend the standard approach using CT, followed by LP if CT is negative, reserving CTA for patients with a positive noncontrast CT or CSF analysis. Need for LP when early CT is negative — <span>Because the consequences of missing SAH are potentially dire, we recommend a LP when the CT scan is negative for blood, as do most guidelines [40,60]. In contrast, some experts have argued that the sensitivity of CT when performed within six hours of the onset of symptoms is sufficiently sensitive (95.5 to 100 percent) to make a follow-up LP unnecessary [21,37,65,66]. In a prospective study that reported 95.5 percent sensitivity, there were five missed SAH cases, which included two false positives (attributed to a traumatic LP), one CT scan misinterp




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There are important caveats (table 10) that suggest that this approach must be applied carefully and cautiously [19]. One is that such studies are performed in centers where CT scans are generally interpreted by expert reviewers (eg, at least the level of an attending radiologist). A second is that the sensitivity of CT may be reduced when symptoms are atypical, such as isolated neck pain. A third is that detection of blood on CT is unreliable when there is significant anemia (ie, hemoglobin <10g/dL [<100 g/l] or hematocrit <30 percent [<0.30]) [21,67].
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rs of headache onset (with a clear time of onset); CT interpretation by an experienced radiologist; a normal neurologic examination; and presentation with an isolated thunderclap headache [27]. <span>There are important caveats (table 10) that suggest that this approach must be applied carefully and cautiously [19]. One is that such studies are performed in centers where CT scans are generally interpreted by expert reviewers (eg, at least the level of an attending radiologist). A second is that the sensitivity of CT may be reduced when symptoms are atypical, such as isolated neck pain. A third is that detection of blood on CT is unreliable when there is significant anemia (ie, hemoglobin <10g/dL [<100 g/l] or hematocrit <30 percent [<0.30]) [21,67]. Other experts have questioned whether LP is ever needed after a negative head CT in the diagnosis of SAH, based upon both Bayesian analysis (the post-test likelihood after a negative CT




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Approximately 15 to 20 percent of patients presenting with SAH do not have a vascular lesion on initial four-vessel cerebral angiography [1,2]. The causes of these nonaneurysmal SAH (NASAH) are potentially diverse, and the mechanism of bleeding in these cases is often not identified.
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rachnoid space, which lies between the arachnoid and pia mater and is normally filled with cerebrospinal fluid. Most nontraumatic cases of SAH are caused by rupture of an intracranial aneurysm. <span>Approximately 15 to 20 percent of patients presenting with SAH do not have a vascular lesion on initial four-vessel cerebral angiography [1,2]. The causes of these nonaneurysmal SAH (NASAH) are potentially diverse, and the mechanism of bleeding in these cases is often not identified. This topic discusses NASAH. Aneurysmal SAH and perimesencephalic SAH are discussed separately. (See "Aneurysmal subarachnoid hemorrhage: Clinical manifestations and diagnosis" and "Aneu




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A subtype of NASAH, so-called perimesencephalic NASAH is characterized by a specific pattern of localized blood on CT, normal cerebral angiography, and a benign course that distinguishes these patients not only from aneurysmal SAH, but also from other patients with NASAH [2-5].
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Aneurysmal subarachnoid hemorrhage: Treatment and prognosis" and "Perimesencephalic nonaneurysmal subarachnoid hemorrhage".) ETIOLOGIES Perimesencephalic nonaneurysmal subarachnoid hemorrhage — <span>A subtype of NASAH, so-called perimesencephalic NASAH is characterized by a specific pattern of localized blood on CT, normal cerebral angiography, and a benign course that distinguishes these patients not only from aneurysmal SAH, but also from other patients with NASAH [2-5]. In some case series, perimesencephalic NASAH makes up the majority, up to two-thirds, of patients with NASAH [1]. The CT findings that define perimesencephalic NASAH include blood isola




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Vascular malformations — Less than 10 percent of SAH are caused by vascular malformations [6,8]. These can be intracranial or spinal in location.
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l false-negative angiogram include technical or reading errors, small aneurysm size, and obscuration of the aneurysm because of vasospasm, hematoma, or thrombosis within the aneurysm [1,2,6,7]. <span>Vascular malformations — Less than 10 percent of SAH are caused by vascular malformations [6,8]. These can be intracranial or spinal in location. Intracranial — Intracranial vascular malformations include both acquired and congenital lesions; the latter are more common. These typically exist within the brain parenchyma and produc




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Occult aneurysm — Some cases of perimesencephalic NASAH are caused by an occult aneurysm that is not observed on initial angiography but may be found on repeat angiography (see 'Repeat angiography' below). Reasons for an initial false-negative angiogram include technical or reading errors, small aneurysm size, and obscuration of the aneurysm because of vasospasm, hematoma, or thrombosis within the aneurysm [1,2,6,7].
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sure, anterior interhemispheric fissure, or lateral ventricles (image 1) [1,5]. Perimesencephalic NASAH is discussed separately. (See "Perimesencephalic nonaneurysmal subarachnoid hemorrhage".) <span>Occult aneurysm — Some cases of perimesencephalic NASAH are caused by an occult aneurysm that is not observed on initial angiography but may be found on repeat angiography (see 'Repeat angiography' below). Reasons for an initial false-negative angiogram include technical or reading errors, small aneurysm size, and obscuration of the aneurysm because of vasospasm, hematoma, or thrombosis within the aneurysm [1,2,6,7]. Vascular malformations — Less than 10 percent of SAH are caused by vascular malformations [6,8]. These can be intracranial or spinal in location. Intracranial — Intracranial vascular ma




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Intracranial arterial dissection — Dissection of an intracranial artery can produce SAH; in one case series, this accounted for 4.5 percent of SAH cases, but this high proportion likely reflects referral or case-ascertainment bias [24].
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nts with recurrent SAH. These lesions are generally managed by neurosurgical and/or endovascular interventions. (See "Disorders affecting the spinal cord", section on 'Vascular malformations'.) <span>Intracranial arterial dissection — Dissection of an intracranial artery can produce SAH; in one case series, this accounted for 4.5 percent of SAH cases, but this high proportion likely reflects referral or case-ascertainment bias [24]. Dissection of an intracranial artery is usually initiated by a tear in the media producing an intramural hemorrhage that dissects longitudinally between the adventitia and media [25]. W




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Cerebral venous thrombosis can rarely present with SAH as its primary manifestation [6,28-32].
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rtebral artery, trapping or wrapping of the pseudoaneurysm, bypass, and stenting. These are complicated procedures that can incur additional morbidity in these very sick patients. Other causes ●<span>Cerebral venous thrombosis can rarely present with SAH as its primary manifestation [6,28-32]. Usually the presentation is somewhat less abrupt than with aneurysmal rupture and the bleeding is localized and superficial. The thrombosis may be visualized on venous phase of digital




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Sickle cell disease can be complicated by subarachnoid as well as intracerebral hemorrhage [1,9,33].
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superficial. The thrombosis may be visualized on venous phase of digital subtraction angiography and/or on MRI. (See "Cerebral venous thrombosis: Etiology, clinical features, and diagnosis".) ●<span>Sickle cell disease can be complicated by subarachnoid as well as intracerebral hemorrhage [1,9,33]. Most reported cases occur in children with an established diagnosis. These children are often found to have one or more aneurysms; in some cases SAH is believed to result from fragile c




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Bleeding disorders and anticoagulant therapy can be complicated by SAH, but this is a somewhat rare complication; intracerebral and subdural hemorrhages are more common [4,9,34-36]
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ort [33]. Survivors appear to have a low rate of recurrence. (See "Acute ischemic and hemorrhagic stroke in sickle cell disease", section on 'Intracranial hemorrhage - additional management'.) ●<span>Bleeding disorders and anticoagulant therapy can be complicated by SAH, but this is a somewhat rare complication; intracerebral and subdural hemorrhages are more common [4,9,34-36]. Systemic bleeding usually accompanies the SAH if this is the primary cause; if it does not, the patient should be assumed to have an underlying aneurysm or other vascular lesion until




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Pituitary apoplexy often presents with sudden onset of headache and vomiting, and there can be prominent subarachnoid blood on CT scan, which may distract from or obscure the pituitary adenoma [38-41]. Pituitary apoplexy is usually heralded by vision change and is accompanied by extraocular nerve palsy.
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xtensive hemorrhage, in the setting of reduced platelet activity [37]. However, this would be a diagnosis of exclusion as well. (See "Perimesencephalic nonaneurysmal subarachnoid hemorrhage".) ●<span>Pituitary apoplexy often presents with sudden onset of headache and vomiting, and there can be prominent subarachnoid blood on CT scan, which may distract from or obscure the pituitary adenoma [38-41]. Pituitary apoplexy is usually heralded by vision change and is accompanied by extraocular nerve palsy. If not visualized on the initial CT scan, MRI will demonstrate the tumor [42,43]. Neurosurgical decompression is indicated for visual loss. Patients also require endocrine evaluation fo




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Traumatic SAH is usually identified by the clinical setting. However, if a clinical history is unavailable, radiologic clues of a traumatic origin include localized bleeding in superficial sulci, adjacent skull fracture, and cerebral contusion, as well as external evidence of traumatic injury [9,36]. Isolated SAH in the setting of mild traumatic brain injury (TBI; Glasgow Coma Scale [GCS] score ≥13) is typically associated with a benign neurologic outcome [44,45].
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dicated for visual loss. Patients also require endocrine evaluation for potentially life-threatening, acute hypopituitarism. (See "Causes of hypopituitarism", section on 'Pituitary apoplexy'.) ●<span>Traumatic SAH is usually identified by the clinical setting. However, if a clinical history is unavailable, radiologic clues of a traumatic origin include localized bleeding in superficial sulci, adjacent skull fracture, and cerebral contusion, as well as external evidence of traumatic injury [9,36]. Isolated SAH in the setting of mild traumatic brain injury (TBI; Glasgow Coma Scale [GCS] score ≥13) is typically associated with a benign neurologic outcome [44,45]. More severe TBI is typically associated with additional forms of brain injury (eg, intracerebral hemorrhage, diffuse axonal injury, etc). (See "Acute mild traumatic brain injury (concus




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Cocaine abuse has been associated with both aneurysmal and nonaneurysmal SAH [6,9,46,47]. The mechanism of bleeding in the latter is not known, but may be related to acute blood pressure surges and/or an underlying hypertensive or toxic vasculopathy [9,48]. Patients with SAH and cocaine abuse should be assumed to have an underlying aneurysm or other vascular lesion until proven otherwise.
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g, intracerebral hemorrhage, diffuse axonal injury, etc). (See "Acute mild traumatic brain injury (concussion) in adults" and "Management of acute moderate and severe traumatic brain injury".) ●<span>Cocaine abuse has been associated with both aneurysmal and nonaneurysmal SAH [6,9,46,47]. The mechanism of bleeding in the latter is not known, but may be related to acute blood pressure surges and/or an underlying hypertensive or toxic vasculopathy [9,48]. Patients with SAH and cocaine abuse should be assumed to have an underlying aneurysm or other vascular lesion until proven otherwise. ●Cerebral amyloid angiopathy can cause SAH in older adults. Bleeding is usually quite restricted, often to a single sulcus; microbleeds and/or superficial siderosis are often present on




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Cerebral amyloid angiopathy can cause SAH in older adults.
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r an underlying hypertensive or toxic vasculopathy [9,48]. Patients with SAH and cocaine abuse should be assumed to have an underlying aneurysm or other vascular lesion until proven otherwise. ●<span>Cerebral amyloid angiopathy can cause SAH in older adults. Bleeding is usually quite restricted, often to a single sulcus; microbleeds and/or superficial siderosis are often present on MRI [49-52]. (See "Cerebral amyloid angiopathy".) ●Rare cau




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Rare causes of SAH include spinal aneurysms that can produce SAH, usually with prominent neck or back pain and myeloradicular symptoms [53,54].
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in older adults. Bleeding is usually quite restricted, often to a single sulcus; microbleeds and/or superficial siderosis are often present on MRI [49-52]. (See "Cerebral amyloid angiopathy".) ●<span>Rare causes of SAH include spinal aneurysms that can produce SAH, usually with prominent neck or back pain and myeloradicular symptoms [53,54]. Brain or cervical tumors have been reported to produce SAH as the presenting manifestation [6,55,56]. Moyamoya disease is associated with cerebral aneurysms that can rupture and produce




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Moyamoya disease is associated with cerebral aneurysms that can rupture and produce SAH; rarely, SAH occurs due to rupture of the fragile transdural anastomotic vessels [57,58].
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produce SAH, usually with prominent neck or back pain and myeloradicular symptoms [53,54]. Brain or cervical tumors have been reported to produce SAH as the presenting manifestation [6,55,56]. <span>Moyamoya disease is associated with cerebral aneurysms that can rupture and produce SAH; rarely, SAH occurs due to rupture of the fragile transdural anastomotic vessels [57,58]. (See "Moyamoya disease and moyamoya syndrome: Etiology, clinical features, and diagnosis".) SAH has also been reported with cerebral vasculitis, reversible cerebral vasoconstriction syn




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SAH has also been reported with cerebral vasculitis, reversible cerebral vasoconstriction syndrome (RCVS), cerebral hyperperfusion syndrome after carotid endarterectomy, and also reversible posterior leukoencephalopathy syndrome [49,52,59-62].
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produce SAH; rarely, SAH occurs due to rupture of the fragile transdural anastomotic vessels [57,58]. (See "Moyamoya disease and moyamoya syndrome: Etiology, clinical features, and diagnosis".) <span>SAH has also been reported with cerebral vasculitis, reversible cerebral vasoconstriction syndrome (RCVS), cerebral hyperperfusion syndrome after carotid endarterectomy, and also reversible posterior leukoencephalopathy syndrome [49,52,59-62]. (See "Overview of thunderclap headache", section on 'Reversible cerebral vasoconstriction syndromes' and "Reversible posterior leukoencephalopathy syndrome" and "Complications of caroti




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Brain or cervical tumors have been reported to produce SAH as the presenting manifestation [6,55,56].
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RI [49-52]. (See "Cerebral amyloid angiopathy".) ●Rare causes of SAH include spinal aneurysms that can produce SAH, usually with prominent neck or back pain and myeloradicular symptoms [53,54]. <span>Brain or cervical tumors have been reported to produce SAH as the presenting manifestation [6,55,56]. Moyamoya disease is associated with cerebral aneurysms that can rupture and produce SAH; rarely, SAH occurs due to rupture of the fragile transdural anastomotic vessels [57,58]. (See "M




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The clinical presentation of NASAH often mimics that of aneurysmal SAH. (See "Aneurysmal subarachnoid hemorrhage: Clinical manifestations and diagnosis", section on 'Clinical presentation'.)

However, the manifestations may differ, often depending on the underlying etiology (see 'Etiologies' above). In particular, restricted SAH over the convexity may manifest with transient motor or sensory symptoms that suggest epileptic phenomena and/or frank seizures [52].

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vasoconstriction syndromes' and "Reversible posterior leukoencephalopathy syndrome" and "Complications of carotid endarterectomy", section on 'Hyperperfusion syndrome'.) CLINICAL PRESENTATION — <span>The clinical presentation of NASAH often mimics that of aneurysmal SAH. (See "Aneurysmal subarachnoid hemorrhage: Clinical manifestations and diagnosis", section on 'Clinical presentation'.) However, the manifestations may differ, often depending on the underlying etiology (see 'Etiologies' above). In particular, restricted SAH over the convexity may manifest with transient motor or sensory symptoms that suggest epileptic phenomena and/or frank seizures [52]. DIAGNOSTIC EVALUATION — SAH should be considered in any patient complaining of a severe headache of sudden onset. Emergent CT of the head should immediately follow consideration of the




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Reversible cerebral vasoconstriction syndrome (RCVS) represents a group of conditions that show reversible multifocal narrowing of the cerebral arteries with clinical manifestations that typically include thunderclap headache and sometimes include neurologic deficits related to brain edema, stroke, or seizure. The clinical outcome is usually benign, although major strokes can result in severe disability or death in a minority
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opics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Jun 2022. | This topic last updated: Mar 01, 2022. INTRODUCTION — <span>Reversible cerebral vasoconstriction syndrome (RCVS) represents a group of conditions that show reversible multifocal narrowing of the cerebral arteries with clinical manifestations that typically include thunderclap headache and sometimes include neurologic deficits related to brain edema, stroke, or seizure. The clinical outcome is usually benign, although major strokes can result in severe disability or death in a minority. This topic will review RCVS. Other conditions associated with thunderclap headache are discussed separately. (See "Overview of thunderclap headache" and "Primary cough headache" and "E




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RCVS has been reported using variable terminology, including the following:

● Migrainous vasospasm or migraine angiitis [1,2]

● Call-Fleming syndrome (or Call syndrome) [3,4]

● Thunderclap headache-associated vasospasm [5-7]

● Drug-induced cerebral arteritis [8]

● Postpartum cerebral angiopathy [9]

● Benign angiopathy of the central nervous system [10]

● Central nervous system pseudovasculitis [11]

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ssed separately. (See "Overview of thunderclap headache" and "Primary cough headache" and "Exercise (exertional) headache" and "Primary headache associated with sexual activity".) TERMINOLOGY — <span>RCVS has been reported using variable terminology, including the following: ●Migrainous vasospasm or migraine angiitis [1,2] ●Call-Fleming syndrome (or Call syndrome) [3,4] ●Thunderclap headache-associated vasospasm [5-7] ●Drug-induced cerebral arteritis [8] ●Postpartum cerebral angiopathy [9] ●Benign angiopathy of the central nervous system [10] ●Central nervous system pseudovasculitis [11] These conditions are characterized by clinical manifestations that typically include thunderclap headache and, less commonly, focal neurologic deficits related to brain edema, stroke, o




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It is now apparent that patients with reversible cerebral arterial narrowing have nearly identical clinical, laboratory, imaging, and prognostic features regardless of the associated condition [12-14]
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include thunderclap headache and, less commonly, focal neurologic deficits related to brain edema, stroke, or seizure and angiographic reversible multifocal narrowing of the cerebral arteries. <span>It is now apparent that patients with reversible cerebral arterial narrowing have nearly identical clinical, laboratory, imaging, and prognostic features regardless of the associated condition [12-14]. The descriptive term "reversible cerebral vasoconstriction syndrome" has been proposed to facilitate the recognition and management of this group of disorders [15]. The adoption of the




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The anatomic basis to explain both the vasoconstriction and headaches is the innervation of cerebral blood vessels with sensory afferents from the trigeminal nerve (V1) and dorsal root of C2.
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f cerebrovascular tone [24]. It remains unclear whether the angiographic abnormalities trigger the headaches or result from severe headache, but there certainly is a close relationship [25,26]. <span>The anatomic basis to explain both the vasoconstriction and headaches is the innervation of cerebral blood vessels with sensory afferents from the trigeminal nerve (V1) and dorsal root of C2. Cerebral vasoconstriction, when severe or progressive, may result in ischemic stroke and in some cases brain hemorrhages that probably reflect postischemic reperfusion injury due to the




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erebral vasoconstriction, when severe or progressive, may result in ischemic stroke and in some cases brain hemorrhages that probably reflect postischemic reperfusion injury due to the dynamic and reversible nature of the arterial narrowing
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The anatomic basis to explain both the vasoconstriction and headaches is the innervation of cerebral blood vessels with sensory afferents from the trigeminal nerve (V1) and dorsal root of C2. C<span>erebral vasoconstriction, when severe or progressive, may result in ischemic stroke and in some cases brain hemorrhages that probably reflect postischemic reperfusion injury due to the dynamic and reversible nature of the arterial narrowing. Some patients develop convexal subarachnoid hemorrhages, presumably from the rupture of small surface arteries undergoing dynamic vasoconstriction-vasodilation. The pathophysiologies o




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The mean age of onset of RCVS is approximately 42 years. In adults, RCVS affects females more often than males.
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ions (including Call-Fleming syndrome, benign angiopathy of the central nervous system, and postpartum angiopathy) characterized by reversible narrowing and dilatation of the cerebral arteries. <span>The mean age of onset of RCVS is approximately 42 years. In adults, RCVS affects females more often than males. (See 'Terminology' above and 'Epidemiology' above.) ●Clinical presentation and risk factors – The clinical presentation of RCVS is usually dramatic with sudden, severe thunderclap heada




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Cerebral angiographic abnormalities of RCVS are dynamic and progress proximally, resulting in a "sausage on a string" appearance of the circle of Willis arteries and their branches. These abnormalities resolve spontaneously over a few weeks.
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ding exposure to vasoconstrictive drugs and medications, other headache disorders, and recent pregnancy (table 1). (See 'Risk factors and associated conditions' above.) ●Neuroimaging features – <span>Cerebral angiographic abnormalities of RCVS are dynamic and progress proximally, resulting in a "sausage on a string" appearance of the circle of Willis arteries and their branches. These abnormalities resolve spontaneously over a few weeks. (See 'Neurovascular imaging' above.) Magnetic resonance imaging (MRI) of the brain is normal in over 50 percent of patients with RCVS. In the ensuing days, many patients may develop com




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Magnetic resonance imaging (MRI) of the brain is normal in over 50 percent of patients with RCVS. In the ensuing days, many patients may develop complications such as ischemic stroke, convexity (nonaneurysmal) subarachnoid hemorrhage, lobar hemorrhage, and reversible brain edema, alone or in combination.
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lting in a "sausage on a string" appearance of the circle of Willis arteries and their branches. These abnormalities resolve spontaneously over a few weeks. (See 'Neurovascular imaging' above.) <span>Magnetic resonance imaging (MRI) of the brain is normal in over 50 percent of patients with RCVS. In the ensuing days, many patients may develop complications such as ischemic stroke, convexity (nonaneurysmal) subarachnoid hemorrhage, lobar hemorrhage, and reversible brain edema, alone or in combination. (See 'Brain imaging' above.) ●Diagnostic evaluation – Patients who present with thunderclap headache must be evaluated as a medical emergency, beginning with cranial computed tomography




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Patients who present with thunderclap headache must be evaluated as a medical emergency, beginning with cranial computed tomography (CT) or brain MRI and head and neck CT angiography (CTA) or magnetic resonance angiography (MRA). If imaging is normal, lumbar puncture and cerebrospinal fluid analysis is appropriate to exclude other causes such as subarachnoid hemorrhage.
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ischemic stroke, convexity (nonaneurysmal) subarachnoid hemorrhage, lobar hemorrhage, and reversible brain edema, alone or in combination. (See 'Brain imaging' above.) ●Diagnostic evaluation – <span>Patients who present with thunderclap headache must be evaluated as a medical emergency, beginning with cranial computed tomography (CT) or brain MRI and head and neck CT angiography (CTA) or magnetic resonance angiography (MRA). If imaging is normal, lumbar puncture and cerebrospinal fluid analysis is appropriate to exclude other causes such as subarachnoid hemorrhage. (See 'Urgent evaluation' above.) The diagnosis of RCVS is based upon the characteristic clinical, brain imaging, and angiographic features, as summarized in the tables (table 3 and tabl




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The diagnosis of RCVS is based upon the characteristic clinical, brain imaging, and angiographic features, as summarized in the tables (table 3 and table 6 and table 4 and table 5).
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ngiography (MRA). If imaging is normal, lumbar puncture and cerebrospinal fluid analysis is appropriate to exclude other causes such as subarachnoid hemorrhage. (See 'Urgent evaluation' above.) <span>The diagnosis of RCVS is based upon the characteristic clinical, brain imaging, and angiographic features, as summarized in the tables (table 3 and table 6 and table 4 and table 5). (See 'Diagnosis' above.) ●Differential diagnosis – The individual clinical and imaging features if RCVS carry a wide range of differential diagnoses, particularly aneurysmal subarachnoi




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Differential diagnosis – The individual clinical and imaging features if RCVS carry a wide range of differential diagnoses, particularly aneurysmal subarachnoid hemorrhage, other conditions associated with thunderclap headache, and intracranial arteriopathies including intracranial atherosclerosis, primary angiitis of the central nervous system, moyamoya disease, and fibromuscular dysplasia.
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of RCVS is based upon the characteristic clinical, brain imaging, and angiographic features, as summarized in the tables (table 3 and table 6 and table 4 and table 5). (See 'Diagnosis' above.) ●<span>Differential diagnosis – The individual clinical and imaging features if RCVS carry a wide range of differential diagnoses, particularly aneurysmal subarachnoid hemorrhage, other conditions associated with thunderclap headache, and intracranial arteriopathies including intracranial atherosclerosis, primary angiitis of the central nervous system, moyamoya disease, and fibromuscular dysplasia. (See 'Differential diagnosis' above.) ●Management – There is no proven therapy for RCVS. Supportive care is directed toward managing blood pressure, severe headaches, and other complica




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Management – There is no proven therapy for RCVS. Supportive care is directed toward managing blood pressure, severe headaches, and other complications such as seizures. We generally do not use calcium channel blockers or other agents to treat vasoconstriction, as evidence for this strategy is lacking. Intra-arterial vasodilator therapy has been attempted in fulminant cases with variable success.
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nial arteriopathies including intracranial atherosclerosis, primary angiitis of the central nervous system, moyamoya disease, and fibromuscular dysplasia. (See 'Differential diagnosis' above.) ●<span>Management – There is no proven therapy for RCVS. Supportive care is directed toward managing blood pressure, severe headaches, and other complications such as seizures. We generally do not use calcium channel blockers or other agents to treat vasoconstriction, as evidence for this strategy is lacking. Intra-arterial vasodilator therapy has been attempted in fulminant cases with variable success. (See 'Management' above.) ●Prognosis – The clinical outcome is benign in 90 to 95 percent of patients. Rare patients develop severe irreversible deficits or death from progressive strok




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Prognosis – The clinical outcome is benign in 90 to 95 percent of patients. Rare patients develop severe irreversible deficits or death from progressive strokes or cerebral edema. Recurrence of an episode of RCVS is rare.
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s to treat vasoconstriction, as evidence for this strategy is lacking. Intra-arterial vasodilator therapy has been attempted in fulminant cases with variable success. (See 'Management' above.) ●<span>Prognosis – The clinical outcome is benign in 90 to 95 percent of patients. Rare patients develop severe irreversible deficits or death from progressive strokes or cerebral edema. Recurrence of an episode of RCVS is rare. (See 'Clinical course and prognosis' above.) Use of UpToDate is subject to the Terms of Use. REFERENCES Serdaru M, Chiras J, Cujas M, Lhermitte F. Isolated benign cerebral vasculitis or




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RCVS has been associated with a variety of conditions including pregnancy [8,43], migraine [1,2,44], use of vasoconstrictive drugs [8,36,45,46] and other medications [29,47], neurosurgical procedures [48], hypercalcemia [49], unruptured saccular aneurysms [5,50], cervical artery dissection [50,51], cerebral venous thrombosis [52,53], and others [41,54-57].
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ross published studies is 42 to 48 years, with an age range of 4 months to 65 years [16,22,36,39-42]. RCVS occurs worldwide in individuals of all races. RISK FACTORS AND ASSOCIATED CONDITIONS — <span>RCVS has been associated with a variety of conditions including pregnancy [8,43], migraine [1,2,44], use of vasoconstrictive drugs [8,36,45,46] and other medications [29,47], neurosurgical procedures [48], hypercalcemia [49], unruptured saccular aneurysms [5,50], cervical artery dissection [50,51], cerebral venous thrombosis [52,53], and others [41,54-57]. The individual risk factors, triggers, and conditions associated with RCVS (table 1) appear unrelated (ie, without a common pathophysiological theme) and may simply reflect the biases o




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The individual risk factors, triggers, and conditions associated with RCVS (table 1) appear unrelated (ie, without a common pathophysiological theme) and may simply reflect the biases of investigators in attributing risk
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[29,47], neurosurgical procedures [48], hypercalcemia [49], unruptured saccular aneurysms [5,50], cervical artery dissection [50,51], cerebral venous thrombosis [52,53], and others [41,54-57]. <span>The individual risk factors, triggers, and conditions associated with RCVS (table 1) appear unrelated (ie, without a common pathophysiological theme) and may simply reflect the biases of investigators in attributing risk. Indeed, the variable nosology previously used by different physician groups (eg, stroke neurologists, headache specialists, obstetricians, internists, and rheumatologists) to report th




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The clinical presentation of RCVS is usually dramatic, with sudden, excruciating headaches that reach peak intensity within seconds, meeting the definition for "thunderclap headache" [59,60]. The thunderclap headaches tend to recur over a span of days to weeks.
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and extensive serological tests are normal, and pathological studies of the brain and temporal arteries have shown no abnormality [58]. CLINICAL PRESENTATION AND COURSE ●Thunderclap headaches – <span>The clinical presentation of RCVS is usually dramatic, with sudden, excruciating headaches that reach peak intensity within seconds, meeting the definition for "thunderclap headache" [59,60]. The thunderclap headaches tend to recur over a span of days to weeks. The onset headaches are usually diffuse or located in the occipital region or vertex. They are often accompanied with nausea and photosensitivity. The character of these headaches is us




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The onset headaches are usually diffuse or located in the occipital region or vertex. They are often accompanied with nausea and photosensitivity. The character of these headaches is usually different from the patient's prior migraine headaches, if any. Most patients experience moderate pain relief within a few minutes to hours, only to be followed by sudden, severe exacerbations that can recur for days. In one study, patients reported an average of four recurrences [16]
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excruciating headaches that reach peak intensity within seconds, meeting the definition for "thunderclap headache" [59,60]. The thunderclap headaches tend to recur over a span of days to weeks. <span>The onset headaches are usually diffuse or located in the occipital region or vertex. They are often accompanied with nausea and photosensitivity. The character of these headaches is usually different from the patient's prior migraine headaches, if any. Most patients experience moderate pain relief within a few minutes to hours, only to be followed by sudden, severe exacerbations that can recur for days. In one study, patients reported an average of four recurrences [16]. Less than 10 percent of patients with RCVS present with subacute or less severe headaches; the absence of headache at onset is exceptional [16,22,61,62]. ●Triggering factors – Many pat




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Less than 10 percent of patients with RCVS present with subacute or less severe headaches; the absence of headache at onset is exceptional [16,22,61,62].
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rate pain relief within a few minutes to hours, only to be followed by sudden, severe exacerbations that can recur for days. In one study, patients reported an average of four recurrences [16]. <span>Less than 10 percent of patients with RCVS present with subacute or less severe headaches; the absence of headache at onset is exceptional [16,22,61,62]. ●Triggering factors – Many patients have triggering factors, such as orgasm, physical exertion, acute stressful or emotional situations, Valsalva maneuvers (eg, straining, coughing, sne




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Many patients have triggering factors, such as orgasm, physical exertion, acute stressful or emotional situations, Valsalva maneuvers (eg, straining, coughing, sneezing), bathing, and swimming [22,63].
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recurrences [16]. Less than 10 percent of patients with RCVS present with subacute or less severe headaches; the absence of headache at onset is exceptional [16,22,61,62]. ●Triggering factors – <span>Many patients have triggering factors, such as orgasm, physical exertion, acute stressful or emotional situations, Valsalva maneuvers (eg, straining, coughing, sneezing), bathing, and swimming [22,63]. ●Blood pressure – The initial blood pressure can be elevated with RCVS due to severe headache pain, the disease itself, or the associated condition (eg, eclampsia, cocaine exposure). ●N




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The initial blood pressure can be elevated with RCVS due to severe headache pain, the disease itself, or the associated condition (eg, eclampsia, cocaine exposure).
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ing factors, such as orgasm, physical exertion, acute stressful or emotional situations, Valsalva maneuvers (eg, straining, coughing, sneezing), bathing, and swimming [22,63]. ●Blood pressure – <span>The initial blood pressure can be elevated with RCVS due to severe headache pain, the disease itself, or the associated condition (eg, eclampsia, cocaine exposure). ●Neurologic involvement – Headache remains the only symptom in many patients with RCVS; others develop focal deficits from underlying ischemic stroke, intracerebral hemorrhage, or rever




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Headache remains the only symptom in many patients with RCVS; others develop focal deficits from underlying ischemic stroke, intracerebral hemorrhage, or reversible cerebral edema [15,16,22]. In published series, the frequency of focal neurologic deficits ranged from 9 to 63 percent, being higher in inpatient case series.
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– The initial blood pressure can be elevated with RCVS due to severe headache pain, the disease itself, or the associated condition (eg, eclampsia, cocaine exposure). ●Neurologic involvement – <span>Headache remains the only symptom in many patients with RCVS; others develop focal deficits from underlying ischemic stroke, intracerebral hemorrhage, or reversible cerebral edema [15,16,22]. In published series, the frequency of focal neurologic deficits ranged from 9 to 63 percent, being higher in inpatient case series. In one report of 139 patients with RCVS, a majority (81 percent) eventually developed brain lesions including ischemic infarction (39 percent), brain edema (38 percent), convexity subar




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Hemiplegia, tremor, hyperreflexia, ataxia, and aphasia can develop. Visual deficits, including scotomas, blurring, hemianopia, and cortical blindness, are common, and these patients typically have concomitant reversible posterior leukoencephalopathy syndrome [62].
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ercent), and lobar hemorrhage (20 percent) [22]. Generalized tonic-clonic seizures are reported in 0 to 21 percent of patients at the time of presentation; however, recurrent seizures are rare. <span>Hemiplegia, tremor, hyperreflexia, ataxia, and aphasia can develop. Visual deficits, including scotomas, blurring, hemianopia, and cortical blindness, are common, and these patients typically have concomitant reversible posterior leukoencephalopathy syndrome [62]. Many patients show features of Balint syndrome, which is made up of the triad of simultanagnosia (the inability to integrate a visual scene despite adequate acuity to resolve individual




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Many patients show features of Balint syndrome, which is made up of the triad of simultanagnosia (the inability to integrate a visual scene despite adequate acuity to resolve individual elements), optic ataxia (the inability to reach accurately under visual guidance), and ocular apraxia (the inability to direct gaze accurately to a new target, frequently leading to difficulty reading) [ 22,64]
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ual deficits, including scotomas, blurring, hemianopia, and cortical blindness, are common, and these patients typically have concomitant reversible posterior leukoencephalopathy syndrome [62]. <span>Many patients show features of Balint syndrome, which is made up of the triad of simultanagnosia (the inability to integrate a visual scene despite adequate acuity to resolve individual elements), optic ataxia (the inability to reach accurately under visual guidance), and ocular apraxia (the inability to direct gaze accurately to a new target, frequently leading to difficulty reading) [22,64]. ●Neuroimaging – Brain imaging is often normal early in the course of RCVS. Typical abnormalities include vasogenic edema and/or fluid-attenuated inversion recovery (FLAIR) sulcal hyper




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Nearly all patients with RCVS present with one or more thunderclap headaches.
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icits, and angiographic narrowing, usually occurs over days to weeks but does not always follow the same time course. (See 'Clinical course and prognosis' below.) EVALUATION Urgent evaluation — <span>Nearly all patients with RCVS present with one or more thunderclap headaches. Thunderclap headache must be evaluated and treated as a medical emergency, beginning with an evaluation for potentially serious secondary causes such as a ruptured brain aneurysm, brain




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Between 30 and 70 percent of patients with RCVS have no abnormality on initial neuroimaging studies with cranial CT or MRI, despite having (eventually) widespread cerebral vasoconstriction [16,22,26,36,65,66].
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ealing, although the initial blood pressure can be elevated due to either severe headache pain, the disease itself, or an associated condition (eg, eclampsia, cocaine exposure). Brain imaging — <span>Between 30 and 70 percent of patients with RCVS have no abnormality on initial neuroimaging studies with cranial CT or MRI, despite having (eventually) widespread cerebral vasoconstriction [16,22,26,36,65,66]. However, approximately 75 percent of admitted patients eventually develop parenchymal lesions (image 1 and image 2). The most frequent lesions are ischemic stroke and cortical surface (




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However, approximately 75 percent of admitted patients eventually develop parenchymal lesions ( image 1 and image 2). The most frequent lesions are ischemic stroke and cortical surface (convexity) nonaneurysmal subarachnoid hemorrhage, followed by reversible vasogenic brain edema and parenchymal hemorrhage [16,22,36]
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0 percent of patients with RCVS have no abnormality on initial neuroimaging studies with cranial CT or MRI, despite having (eventually) widespread cerebral vasoconstriction [16,22,26,36,65,66]. <span>However, approximately 75 percent of admitted patients eventually develop parenchymal lesions (image 1 and image 2). The most frequent lesions are ischemic stroke and cortical surface (convexity) nonaneurysmal subarachnoid hemorrhage, followed by reversible vasogenic brain edema and parenchymal hemorrhage [16,22,36]. Any combination of lesions can be present. CT and MRI remain normal in approximately 25 percent of cases reported from in-hospital settings; this number is much higher in emergency dep




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Several studies have shown that RCVS is the most frequent cause of cortical surface (convexity) subarachnoid hemorrhage (image 3 and image 1) in individuals below age 60 years [69-71].
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usion-weighted MRI may show areas of hypoperfusion in border-zone regions. Cortical surface (convexity) subarachnoid hemorrhage is typically minor, restricted to a few sulcal spaces [27,67,68]. <span>Several studies have shown that RCVS is the most frequent cause of cortical surface (convexity) subarachnoid hemorrhage (image 3 and image 1) in individuals below age 60 years [69-71]. Single as well as multiple lobar hemorrhages can occur, and brain hemorrhages can develop a few days after onset, which again suggests a mechanistic role for reperfusion injury. Subdura




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Timing of imaging – Initial CTA or MRA can be normal because the condition starts distally in small vessels that are not well visualized; one study found that 21 percent had normal findings on initial MRA and 9 percent had normal findings on both MRA and transcranial Doppler ultrasonography [16]. Vasoconstriction may not become evident for more than one week after clinical onset, peaks at two to three weeks, and is typically reversible within three months (image 4). For patients with a high degree of clinical suspicion for RCVS, a follow-up CTA or MRA should be done after three to five days
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asound has been used for diagnosis; however, normal results do not exclude this diagnosis [9]. This noninvasive bedside tool has utility in monitoring the progression of vasoconstriction [17]. ●<span>Timing of imaging – Initial CTA or MRA can be normal because the condition starts distally in small vessels that are not well visualized; one study found that 21 percent had normal findings on initial MRA and 9 percent had normal findings on both MRA and transcranial Doppler ultrasonography [16]. Vasoconstriction may not become evident for more than one week after clinical onset, peaks at two to three weeks, and is typically reversible within three months (image 4). For patients with a high degree of clinical suspicion for RCVS, a follow-up CTA or MRA should be done after three to five days. Vascular imaging may reveal concomitant cervicocephalic arterial dissection or unruptured aneurysms [5,51,74,75]. In some patients, the extracranial internal carotid or vertebral arter




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Other tests — Serum and urine toxicology screens should be routinely performed to investigate for exposure to vasoconstrictive drugs such as cannabinoids and cocaine. Laboratory evaluation should also include urine vanillylmandelic acid and 5-hydroxyindoleacetic levels to evaluate for vasoactive tumors (eg, pheochromocytoma, carcinoid) that are associated with RCVS, and a serum calcium level to exclude hypercalcemia as a cause of RCVS, if there is clinical suspicion for these conditions based on symptoms or signs.
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dissection or unruptured aneurysms [5,51,74,75]. In some patients, the extracranial internal carotid or vertebral artery can be affected by RCVS. Systemic arteries are rarely involved [76,77]. <span>Other tests — Serum and urine toxicology screens should be routinely performed to investigate for exposure to vasoconstrictive drugs such as cannabinoids and cocaine. Laboratory evaluation should also include urine vanillylmandelic acid and 5-hydroxyindoleacetic levels to evaluate for vasoactive tumors (eg, pheochromocytoma, carcinoid) that are associated with RCVS, and a serum calcium level to exclude hypercalcemia as a cause of RCVS, if there is clinical suspicion for these conditions based on symptoms or signs. Serum magnesium should be obtained if there is local preference to treat vasoconstriction with intravenous magnesium. When there is uncertainty about the cause of cerebral arteriopathy,




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Although lumbar puncture is required in patients presenting with thunderclap headache to exclude secondary causes such as a ruptured cerebral aneurysm or meningitis, it could be avoided in patients with multiple thunderclap headaches, since three or more recurrent thunderclap headaches are diagnostic for RCVS [36,62]
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ely, based upon the presence of recurrent thunderclap headaches (table 3) or RCVS2 score (table 4 and table 5). (See 'Diagnosis' below and 'Angiographic differential' below.) ●Lumbar puncture – <span>Although lumbar puncture is required in patients presenting with thunderclap headache to exclude secondary causes such as a ruptured cerebral aneurysm or meningitis, it could be avoided in patients with multiple thunderclap headaches, since three or more recurrent thunderclap headaches are diagnostic for RCVS [36,62]. In patients with a single thunderclap headache, lumbar puncture may be needed to exclude secondary causes unless there is clear evidence for RCVS on CTA or MRA with multifocal segmenta




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The sensitivity and specificity of variables useful to diagnose RCVS and to distinguish it from primary angiitis of the central nervous system (a historic mimic of RCVS) is shown in the table (table 6).
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week of symptom onset [15,36,62]. The presence of multiple thunderclap headaches recurring over a few days has nearly 100 percent sensitivity and specificity for the diagnosis of RCVS [36,62]. <span>The sensitivity and specificity of variables useful to diagnose RCVS and to distinguish it from primary angiitis of the central nervous system (a historic mimic of RCVS) is shown in the table (table 6). In patients with a newly detected cerebral arteriopathy, the RCVS2 score (table 4 and table 5) has excellent sensitivity and specificity for diagnosing RCVS and distinguishing it from a




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Patients with PACNS usually have an insidious progressive clinical course with chronic headaches and rarely have thunderclap headache that is typical of RCVS.
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ions. (See "Primary angiitis of the central nervous system in adults".) While there is overlap, the nature of the headaches and imaging abnormalities are quite different [15,16,22,36,61,79,80]. <span>Patients with PACNS usually have an insidious progressive clinical course with chronic headaches and rarely have thunderclap headache that is typical of RCVS. The characteristic vasoconstriction of RCVS usually manifests as smooth, tapered narrowing followed by abnormal dilated segments of second- and third-order branches of the cerebral arte




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The characteristic vasoconstriction of RCVS usually manifests as smooth, tapered narrowing followed by abnormal dilated segments of second- and third-order branches of the cerebral arteries. This angiographic appearance distinguishes RCVS from PACNS, where the arterial narrowing is much more irregular. Brain imaging in RCVS can be normal or show watershed infarcts or lobar hemorrhages, whereas PACNS is usually associated with accumulating T2-hyperintense brain lesions, leptomeningeal enhancement, and scattered deep infarcts [ 36].
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different [15,16,22,36,61,79,80]. Patients with PACNS usually have an insidious progressive clinical course with chronic headaches and rarely have thunderclap headache that is typical of RCVS. <span>The characteristic vasoconstriction of RCVS usually manifests as smooth, tapered narrowing followed by abnormal dilated segments of second- and third-order branches of the cerebral arteries. This angiographic appearance distinguishes RCVS from PACNS, where the arterial narrowing is much more irregular. Brain imaging in RCVS can be normal or show watershed infarcts or lobar hemorrhages, whereas PACNS is usually associated with accumulating T2-hyperintense brain lesions, leptomeningeal enhancement, and scattered deep infarcts [36]. In a retrospective report that compared 159 patients with RCVS and 47 patients with PACNS, several features had 98 to 100 percent specificity for the diagnosis of RCVS and a similarly h




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Spontaneous intracranial hypotension arises from CSF leakage located in the spine due to three main sources: spontaneous dural tear, rupture of meningeal diverticula, and CSF-venous fistula (figure 1)
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f the brain within the skull. The resultant traction on connected nerves and other structures can cause a clinical syndrome often described by postural headaches. (See 'Pathophysiology' above.) <span>Spontaneous intracranial hypotension arises from CSF leakage located in the spine due to three main sources: spontaneous dural tear, rupture of meningeal diverticula, and CSF-venous fistula (figure 1). ●Epidemiology – The estimated annual incidence of spontaneous intracranial hypotension is 4 to 5 per 100,000. The mean age of patients is 43 years with a range from 2 to 88 years of ag




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Epidemiology – The estimated annual incidence of spontaneous intracranial hypotension is 4 to 5 per 100,000. The mean age of patients is 43 years with a range from 2 to 88 years of age, and the proportion of female individuals is 63 percent.
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us intracranial hypotension arises from CSF leakage located in the spine due to three main sources: spontaneous dural tear, rupture of meningeal diverticula, and CSF-venous fistula (figure 1). ●<span>Epidemiology – The estimated annual incidence of spontaneous intracranial hypotension is 4 to 5 per 100,000. The mean age of patients is 43 years with a range from 2 to 88 years of age, and the proportion of female individuals is 63 percent. (See 'Epidemiology' above.) ●Clinical features •Orthostatic headache – Postural headache is usually the major manifestation of spontaneous intracranial hypotension. The headache ordinar




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Spontaneous intracranial hypotension may mimic several headache syndromes and other neurologic conditions such as migraine, cervicogenic headache, symptomatic Chiari I malformation, and postural tachycardia and other orthostatic intolerance syndromes.
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roimaging is nondiagnostic or as a part of imaging studies that require dural puncture, such as radioisotope cisternography. (See 'The role of lumbar puncture' above.) ●Differential diagnosis – <span>Spontaneous intracranial hypotension may mimic several headache syndromes and other neurologic conditions such as migraine, cervicogenic headache, symptomatic Chiari I malformation, and postural tachycardia and other orthostatic intolerance syndromes. (See 'Differential diagnosis' above.) Patients with post-dural puncture headaches and CSF shunt overdrainage presenting with the same clinical syndrome as patients with spontaneous intr




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Postural headache is usually, but not always, the major manifestation of spontaneous intracranial hypotension [6,23]. Infrequently, patients report no headache, typically when other symptoms of low cerebrospinal fluid (CSF) pressure are evident [39,41]. (See 'Associated symptoms' below.)

The neurologic examination is often normal in patients with spontaneous intracranial hypotension [44]. However, various neurologic symptoms and signs may be present.

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actors for spontaneous intracranial hypotension include connective tissue abnormalities, spinal pathologies, and bariatric surgery [41-43]. (See 'Causes of CSF leak' above.) CLINICAL FEATURES — <span>Postural headache is usually, but not always, the major manifestation of spontaneous intracranial hypotension [6,23]. Infrequently, patients report no headache, typically when other symptoms of low cerebrospinal fluid (CSF) pressure are evident [39,41]. (See 'Associated symptoms' below.) The neurologic examination is often normal in patients with spontaneous intracranial hypotension [44]. However, various neurologic symptoms and signs may be present. (See 'Associated symptoms' below.) Headache — Headache attributed to spontaneous intracranial hypotension may be of sudden or gradual onset. The headache ordinarily develops within two




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Headache — Headache attributed to spontaneous intracranial hypotension may be of sudden or gradual onset. The headache ordinarily develops within two hours, and in most cases within 15 minutes, of sitting or standing [45]. Rarely, it starts as a thunderclap headache [29].
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rologic examination is often normal in patients with spontaneous intracranial hypotension [44]. However, various neurologic symptoms and signs may be present. (See 'Associated symptoms' below.) <span>Headache — Headache attributed to spontaneous intracranial hypotension may be of sudden or gradual onset. The headache ordinarily develops within two hours, and in most cases within 15 minutes, of sitting or standing [45]. Rarely, it starts as a thunderclap headache [29]. (See "Overview of thunderclap headache".) The typical headache with this syndrome is often described as throbbing or a dull pain that may be generalized or focal. The headache severity




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The typical headache with this syndrome is often described as throbbing or a dull pain that may be generalized or focal. The headache severity is widely variable and ranges from mild to incapacitating [39]. Frontal head pain is reported by patients as often as occipital and diffuse pain [33,41].
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dinarily develops within two hours, and in most cases within 15 minutes, of sitting or standing [45]. Rarely, it starts as a thunderclap headache [29]. (See "Overview of thunderclap headache".) <span>The typical headache with this syndrome is often described as throbbing or a dull pain that may be generalized or focal. The headache severity is widely variable and ranges from mild to incapacitating [39]. Frontal head pain is reported by patients as often as occipital and diffuse pain [33,41]. ●Classic orthostatic features – At symptom onset, headache typically occurs upon sitting or standing upright and relief is obtained with recumbency, usually within minutes. In rare case




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Classic orthostatic features – At symptom onset, headache typically occurs upon sitting or standing upright and relief is obtained with recumbency, usually within minutes. In rare cases associated with an asymmetric cervical CSF leak, headache relief occurs only with lying on one side of the body [46]. The headache is seldom relieved with analgesics. Exacerbating factors include erect posture, head movement, coughing, straining, sneezing, jugular venous compression, and high altitude [47]. Orthostatic character of the headache may wane as symptoms become chronic.
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alized or focal. The headache severity is widely variable and ranges from mild to incapacitating [39]. Frontal head pain is reported by patients as often as occipital and diffuse pain [33,41]. ●<span>Classic orthostatic features – At symptom onset, headache typically occurs upon sitting or standing upright and relief is obtained with recumbency, usually within minutes. In rare cases associated with an asymmetric cervical CSF leak, headache relief occurs only with lying on one side of the body [46]. The headache is seldom relieved with analgesics. Exacerbating factors include erect posture, head movement, coughing, straining, sneezing, jugular venous compression, and high altitude [47]. Orthostatic character of the headache may wane as symptoms become chronic. ●Alternative headache patterns – While headache attributed to spontaneous intracranial hypotension is characteristically orthostatic, other patterns can occur [18,48]: •Chronic daily he




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Chronic daily headache may replace an orthostatic pattern as symptoms become chronic [20,29]. On occasion, the postural component may not be present at all.
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symptoms become chronic. ●Alternative headache patterns – While headache attributed to spontaneous intracranial hypotension is characteristically orthostatic, other patterns can occur [18,48]: •<span>Chronic daily headache may replace an orthostatic pattern as symptoms become chronic [20,29]. On occasion, the postural component may not be present at all. •Paradoxical headache, worse with recumbency and better with the upright position, has been reported in rare patients with spontaneous low CSF pressure [49,50]. •A diurnal headache char




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Paradoxical headache, worse with recumbency and better with the upright position, has been reported in rare patients with spontaneous low CSF pressure [49,50].
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other patterns can occur [18,48]: •Chronic daily headache may replace an orthostatic pattern as symptoms become chronic [20,29]. On occasion, the postural component may not be present at all. •<span>Paradoxical headache, worse with recumbency and better with the upright position, has been reported in rare patients with spontaneous low CSF pressure [49,50]. •A diurnal headache characterized by onset late in the day may be reported by patients with a low-volume ("slow-flow") CSF leak or leaks that have slowed due to chronicity or treatment.




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A diurnal headache characterized by onset late in the day may be reported by patients with a low-volume ("slow-flow") CSF leak or leaks that have slowed due to chronicity or treatment. A clear orthostatic character may be inapparent as headaches are usually absent despite upright posture through the early morning. Symptoms begin in late morning or early afternoon but do typically increase in severity as more time is spent upright [51].
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nent may not be present at all. •Paradoxical headache, worse with recumbency and better with the upright position, has been reported in rare patients with spontaneous low CSF pressure [49,50]. •<span>A diurnal headache characterized by onset late in the day may be reported by patients with a low-volume ("slow-flow") CSF leak or leaks that have slowed due to chronicity or treatment. A clear orthostatic character may be inapparent as headaches are usually absent despite upright posture through the early morning. Symptoms begin in late morning or early afternoon but do typically increase in severity as more time is spent upright [51]. •Intermittent headaches with headache-free intervals of varying duration may occur in patients with intermittent CSF leaks. •In other cases, the headache can mimic a primary headache sy




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Intermittent headaches with headache-free intervals of varying duration may occur in patients with intermittent CSF leaks.
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re usually absent despite upright posture through the early morning. Symptoms begin in late morning or early afternoon but do typically increase in severity as more time is spent upright [51]. •<span>Intermittent headaches with headache-free intervals of varying duration may occur in patients with intermittent CSF leaks. •In other cases, the headache can mimic a primary headache syndrome, such as primary cough headache [52] or primary exertional headache [53]. These primary headache syndromes are discus




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In other cases, the headache can mimic a primary headache syndrome, such as primary cough headache [52] or primary exertional headache [53]. These primary headache syndromes are discussed separately.
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o typically increase in severity as more time is spent upright [51]. •Intermittent headaches with headache-free intervals of varying duration may occur in patients with intermittent CSF leaks. •<span>In other cases, the headache can mimic a primary headache syndrome, such as primary cough headache [52] or primary exertional headache [53]. These primary headache syndromes are discussed separately. (See "Primary cough headache" and "Exercise (exertional) headache".) Headache attributed to spontaneous intracranial hypotension may resolve spontaneously within two weeks or with succe




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Headache attributed to spontaneous intracranial hypotension may resolve spontaneously within two weeks or with successful treatment [44]. In some cases, it lasts months or years.
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primary cough headache [52] or primary exertional headache [53]. These primary headache syndromes are discussed separately. (See "Primary cough headache" and "Exercise (exertional) headache".) <span>Headache attributed to spontaneous intracranial hypotension may resolve spontaneously within two weeks or with successful treatment [44]. In some cases, it lasts months or years. Associated symptoms — In 1825, Magendie described vertigo and unsteadiness in a patient following the removal of CSF [54]. Today, the list of reported associated symptoms is varied and




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In a systematic review including 32 articles and 1531 patients, the most common associated symptoms of spontaneous intracranial hypotension were [41]:

● Nausea or vomiting – 51 percent

● Neck pain or stiffness – 33 percent

● Tinnitus – 19 percent

● Dizziness – 14 percent

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ymptoms — In 1825, Magendie described vertigo and unsteadiness in a patient following the removal of CSF [54]. Today, the list of reported associated symptoms is varied and extensive [6,39,41]. <span>In a systematic review including 32 articles and 1531 patients, the most common associated symptoms of spontaneous intracranial hypotension were [41]: ●Nausea or vomiting – 51 percent ●Neck pain or stiffness – 33 percent ●Tinnitus – 19 percent ●Dizziness – 14 percent Other associated symptoms include the following [2,14,33,39,41,55,56]: ●Change in hearing (eg, hyperacusis, echoing, or tinnitus) ●Photophobia ●Other visual disturbances (eg, blurred vi




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Other associated symptoms include the following [2,14,33,39,41,55,56]:

● Change in hearing (eg, hyperacusis, echoing, or tinnitus)

● Photophobia

● Other visual disturbances (eg, blurred vision, diplopia, visual obscurations)

● Vertigo

● Diaphoresis

● Anorexia

● Unsteadiness or staggering gait

● Back pain

● Hiccups

● Dysgeusia

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ommon associated symptoms of spontaneous intracranial hypotension were [41]: ●Nausea or vomiting – 51 percent ●Neck pain or stiffness – 33 percent ●Tinnitus – 19 percent ●Dizziness – 14 percent <span>Other associated symptoms include the following [2,14,33,39,41,55,56]: ●Change in hearing (eg, hyperacusis, echoing, or tinnitus) ●Photophobia ●Other visual disturbances (eg, blurred vision, diplopia, visual obscurations) ●Vertigo ●Diaphoresis ●Anorexia ●Unsteadiness or staggering gait ●Back pain ●Hiccups ●Dysgeusia Cognitive deficits have also been associated with spontaneous intracranial hypotension including cases of reversible frontotemporal dementia attributed to low CSF pressure [39,57,58]. A




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Uncommon severe manifestations — Some patients with spontaneous intracranial hypotension may present infrequently with more severe symptoms or findings on imaging associated with caudal descent and compression of brainstem structures.

Signs and symptoms

• Ataxia (posterior fossa) [60]

• Quadriparesis (brainstem and upper cervical spinal cord) [50]

• Movement disorders including parkinsonism, tremor, chorea, and dystonia (deep midline structures) [60-62]

• Hypoactive-hypoalert behavior, including apathy and akinetic mutism (pons and midbrain) [63]

• Decreased level of consciousness, stupor, and coma (diencephalon) [64-66]

• Galactorrhea and hyperprolactinemia (pituitary stalk) [67]

• Abducens nerve palsy (pontomedullary junction) [68]

Imaging findings

• Acute subdural hematoma (image 3) [69-72]

• Cerebellar hemorrhage (cerebellar bridging veins) [50]

• Posterior circulation infarction (deformation of cerebral arteries) [73-75]

• Cerebral venous sinus thrombosis [76]

• Reversible posterior leukoencephalopathy syndrome (also known as posterior reversible encephalopathy syndrome or PRES) [

...
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nts directed at intracranial hypotension led to improvement in a few patients. Frontotemporal dementia is discussed separately. (See "Frontotemporal dementia: Clinical features and diagnosis".) <span>Uncommon severe manifestations — Some patients with spontaneous intracranial hypotension may present infrequently with more severe symptoms or findings on imaging associated with caudal descent and compression of brainstem structures. ●Signs and symptoms •Ataxia (posterior fossa) [60] •Quadriparesis (brainstem and upper cervical spinal cord) [50] •Movement disorders including parkinsonism, tremor, chorea, and dystonia (deep midline structures) [60-62] •Hypoactive-hypoalert behavior, including apathy and akinetic mutism (pons and midbrain) [63] •Decreased level of consciousness, stupor, and coma (diencephalon) [64-66] •Galactorrhea and hyperprolactinemia (pituitary stalk) [67] •Abducens nerve palsy (pontomedullary junction) [68] ●Imaging findings •Acute subdural hematoma (image 3) [69-72] •Cerebellar hemorrhage (cerebellar bridging veins) [50] •Posterior circulation infarction (deformation of cerebral arteries) [73-75] •Cerebral venous sinus thrombosis [76] •Reversible posterior leukoencephalopathy syndrome (also known as posterior reversible encephalopathy syndrome or PRES) [77,78] •Reversible cerebral vasoconstriction syndrome [79] •Superficial siderosis [77,80-83] Except for hemorrhage and infarction, these manifestations are typically reversible with successful treatment of the CSF leak. The role of anticoagulation in cerebral venous sinus throm




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The diagnosis of spontaneous intracranial hypotension should be considered in patients who present with positional orthostatic headache not caused by dural puncture, with or without other neurologic symptoms [39]. Headache caused by low cerebrospinal fluid (CSF) pressure following a dural puncture rarely creates a diagnostic dilemma.

In addition, the diagnosis of spontaneous intracranial hypotension should also be considered in patients undergoing magnetic resonance imaging (MRI) of the brain to evaluate for headache or other neurologic symptoms when imaging findings are suggestive of spontaneous orthostatic hypotension. (See 'Brain MRI' below.)

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particularly for patients with subdural fluid collections. (See "Cerebral venous thrombosis: Treatment and prognosis", section on 'Acute antithrombotic management'.) EVALUATION AND DIAGNOSIS — <span>The diagnosis of spontaneous intracranial hypotension should be considered in patients who present with positional orthostatic headache not caused by dural puncture, with or without other neurologic symptoms [39]. Headache caused by low cerebrospinal fluid (CSF) pressure following a dural puncture rarely creates a diagnostic dilemma. In addition, the diagnosis of spontaneous intracranial hypotension should also be considered in patients undergoing magnetic resonance imaging (MRI) of the brain to evaluate for headache or other neurologic symptoms when imaging findings are suggestive of spontaneous orthostatic hypotension. (See 'Brain MRI' below.) Diagnosis — The diagnosis of spontaneous intracranial hypotension is made in patients with headache, typically orthostatic in quality, with or without associated symptoms, and with evid




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The acronym SEEPS (for Subdural fluid collections, Enhancement of the pachymeninges, Engorgement of the venous structures, Pituitary enlargement, and Sagging of the brain) recalls major features of spontaneous intracranial hypotension on brain MRI [39].
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aths and dilated superior ophthalmic veins (image 5) ●Reduced diameter of suprasellar and prepontine cisterns (image 7 and image 8) ●Increased anteroposterior diameter of the midbrain (image 5) <span>The acronym SEEPS (for Subdural fluid collections, Enhancement of the pachymeninges, Engorgement of the venous structures, Pituitary enlargement, and Sagging of the brain) recalls major features of spontaneous intracranial hypotension on brain MRI [39]. The most common abnormality on brain MRI is diffuse pachymeningeal enhancement, found in nearly 75 percent of patients with intracranial hypotension (image 4) [15,41]. Pachymeningeal en




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Cervicogenic headache – Patients with cervicogenic headaches may report onset or worsening symptoms with upright positioning due to cervical muscle strain [18]. Other clinical features of spontaneous intracranial hypotension and imaging abnormalities are not typically found in patients with cervicogenic headache.
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rovement of symptoms with recumbency is uncommon with migraine headaches. (See "Pathophysiology, clinical manifestations, and diagnosis of migraine in adults", section on 'Clinical features'.) ●<span>Cervicogenic headache – Patients with cervicogenic headaches may report onset or worsening symptoms with upright positioning due to cervical muscle strain [18]. Other clinical features of spontaneous intracranial hypotension and imaging abnormalities are not typically found in patients with cervicogenic headache. (See "Cervicogenic headache".) ●Chiari I malformation – Some patients with low-lying cerebellar tonsils consistent with a Chiari I malformation may present with occipital headaches or d




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Chiari I malformation – Some patients with low-lying cerebellar tonsils consistent with a Chiari I malformation may present with occipital headaches or dizziness. However, the headaches in patients with a symptomatic Chiari I malformation are typically associated with physical activity or Valsalva maneuvers rather than upright positioning, and brain magnetic resonance imaging does not show evidence of low cerebrospinal fluid (CSF) pressure, unlike those with spontaneous intracranial hypotension [18].
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n [18]. Other clinical features of spontaneous intracranial hypotension and imaging abnormalities are not typically found in patients with cervicogenic headache. (See "Cervicogenic headache".) ●<span>Chiari I malformation – Some patients with low-lying cerebellar tonsils consistent with a Chiari I malformation may present with occipital headaches or dizziness. However, the headaches in patients with a symptomatic Chiari I malformation are typically associated with physical activity or Valsalva maneuvers rather than upright positioning, and brain magnetic resonance imaging does not show evidence of low cerebrospinal fluid (CSF) pressure, unlike those with spontaneous intracranial hypotension [18]. (See "Chiari malformations", section on 'Chiari I clinical features'.) ●Postural tachycardia syndrome – Orthostatic headache in the absence of CSF leak may also be a manifestation of th




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Postural tachycardia syndrome – Orthostatic headache in the absence of CSF leak may also be a manifestation of the postural tachycardia syndrome (POTS) or orthostatic intolerance [115]. The presence of tachycardia with upright positioning identifies patients with POTS.
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not show evidence of low cerebrospinal fluid (CSF) pressure, unlike those with spontaneous intracranial hypotension [18]. (See "Chiari malformations", section on 'Chiari I clinical features'.) ●<span>Postural tachycardia syndrome – Orthostatic headache in the absence of CSF leak may also be a manifestation of the postural tachycardia syndrome (POTS) or orthostatic intolerance [115]. The presence of tachycardia with upright positioning identifies patients with POTS. (See "Postural tachycardia syndrome".) ●Post-dural puncture headache – Patients with symptoms of post-dural puncture headache following a lumbar puncture or inadvertent dural puncture f




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Chiari I anatomy — CM-I is characterized by cerebellar tonsils that are abnormally shaped and downwardly displaced below the level of the foramen magnum (image 1).
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normally placed cerebellar tonsils [5], and the Chiari 1.5 malformation, which is a CM-II like malformation without spina bifida [6]. Both of these subtypes show crowding at the foramen magnum. <span>Chiari I anatomy — CM-I is characterized by cerebellar tonsils that are abnormally shaped and downwardly displaced below the level of the foramen magnum (image 1). The normal cerebellar tonsils may lie up to 3 mm below the foramen magnum in adults. In general, tonsils lying 5 mm or more below the foramen magnum on neuroimaging are considered to be




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Chiari I clinical features — The true natural history of Chiari type I malformation (CM-I) has not been established [38]. In most cases, CM-I does not become symptomatic until adolescence or adulthood [1,19,39]. In addition, symptom onset is often insidious. In one study of 43 patients with CM-I, the mean age at presentation was approximately 18 years [40].
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o had surgery for CM-I, neurofibromatosis type 1 was diagnosed in 5 percent [35]. (See "Neurofibromatosis type 1 (NF1): Pathogenesis, clinical features, and diagnosis".) CLINICAL MANIFESTATIONS <span>Chiari I clinical features — The true natural history of Chiari type I malformation (CM-I) has not been established [38]. In most cases, CM-I does not become symptomatic until adolescence or adulthood [1,19,39]. In addition, symptom onset is often insidious. In one study of 43 patients with CM-I, the mean age at presentation was approximately 18 years [40]. Although CM-I is typically asymptomatic in young children, one retrospective series identified 39 patients younger than six years who had early surgical treatment [41]. Children up to a




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Pain or headache is the most common presentation in older children and adults with CM-I [42].
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rgical treatment [41]. Children up to age two most often presented with oropharyngeal dysfunction, while those ages three to five typically presented with syringomyelia, scoliosis, or headache. <span>Pain or headache is the most common presentation in older children and adults with CM-I [42]. The manifestations of CM-I include the following categories [1,4,43-45]: ●Asymptomatic – Asymptomatic cases are those where CM-I is discovered on magnetic resonance imaging (MRI), often




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Asymptomatic – Asymptomatic cases are those where CM-I is discovered on magnetic resonance imaging (MRI), often incidentally, in patients without findings referrable to Chiari malformation by history and examination [30,31,42,45-47]. In one report of 218 children with incidentally discovered CM-I, the initial MRI was obtained for various indications including seizures (15 percent), nonspecific headache (15 percent), trauma (10 percent), or developmental delay (8 percent) [46].
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, scoliosis, or headache. Pain or headache is the most common presentation in older children and adults with CM-I [42]. The manifestations of CM-I include the following categories [1,4,43-45]: ●<span>Asymptomatic – Asymptomatic cases are those where CM-I is discovered on magnetic resonance imaging (MRI), often incidentally, in patients without findings referrable to Chiari malformation by history and examination [30,31,42,45-47]. In one report of 218 children with incidentally discovered CM-I, the initial MRI was obtained for various indications including seizures (15 percent), nonspecific headache (15 percent), trauma (10 percent), or developmental delay (8 percent) [46]. ●Cerebellar dysfunction – Cerebellar symptoms include nystagmus, scanning speech and ataxia, with truncal ataxia being more common than appendicular ataxia [32,43]. ●Cranial neuropathie




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Cerebellar dysfunction – Cerebellar symptoms include nystagmus, scanning speech and ataxia, with truncal ataxia being more common than appendicular ataxia [32,43].
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red CM-I, the initial MRI was obtained for various indications including seizures (15 percent), nonspecific headache (15 percent), trauma (10 percent), or developmental delay (8 percent) [46]. ●<span>Cerebellar dysfunction – Cerebellar symptoms include nystagmus, scanning speech and ataxia, with truncal ataxia being more common than appendicular ataxia [32,43]. ●Cranial neuropathies/brainstem compression – Cranial neuropathies or brainstem compression can present with hoarseness, vocal cord paralysis, dysarthria, palatal weakness, pharyngeal a




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Cranial neuropathies/brainstem compression – Cranial neuropathies or brainstem compression can present with hoarseness, vocal cord paralysis, dysarthria, palatal weakness, pharyngeal achalasia, tongue atrophy, recurrent aspiration, nystagmus (especially down-beating), or sleep-related breathing disorders such as central and obstructive sleep apnea [1,4,43,44,48,49]. Less common symptoms and signs include oscillopsia, sensorineural hearing loss, sinus bradycardia, syncope, and hiccups. Other manifestations of brainstem compression include long-tract signs such as weakness, spasticity, hyperreflexia, and Babinski responses. The latter can result from either brainstem or spinal cord compression.
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tal delay (8 percent) [46]. ●Cerebellar dysfunction – Cerebellar symptoms include nystagmus, scanning speech and ataxia, with truncal ataxia being more common than appendicular ataxia [32,43]. ●<span>Cranial neuropathies/brainstem compression – Cranial neuropathies or brainstem compression can present with hoarseness, vocal cord paralysis, dysarthria, palatal weakness, pharyngeal achalasia, tongue atrophy, recurrent aspiration, nystagmus (especially down-beating), or sleep-related breathing disorders such as central and obstructive sleep apnea [1,4,43,44,48,49]. Less common symptoms and signs include oscillopsia, sensorineural hearing loss, sinus bradycardia, syncope, and hiccups. Other manifestations of brainstem compression include long-tract signs such as weakness, spasticity, hyperreflexia, and Babinski responses. The latter can result from either brainstem or spinal cord compression. ●Headache – Headache or pain due to meningeal irritation is the most common presentation in older children and adults with CM-I [42]. The pain is usually either occipital or nuchal in l




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Headache – Headache or pain due to meningeal irritation is the most common presentation in older children and adults with CM-I [42]. The pain is usually either occipital or nuchal in location. The pain is typically paroxysmal, but it may be dull and persistent [32]. Both the pain and a feeling of dizziness are exacerbated by physical activity or by Valsalva maneuvers such as coughing, laughing, or sneezing [4,32,50].
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s of brainstem compression include long-tract signs such as weakness, spasticity, hyperreflexia, and Babinski responses. The latter can result from either brainstem or spinal cord compression. ●<span>Headache – Headache or pain due to meningeal irritation is the most common presentation in older children and adults with CM-I [42]. The pain is usually either occipital or nuchal in location. The pain is typically paroxysmal, but it may be dull and persistent [32]. Both the pain and a feeling of dizziness are exacerbated by physical activity or by Valsalva maneuvers such as coughing, laughing, or sneezing [4,32,50]. Thus, patients with CM-I may present with cough headache, and CM-I should be considered as a potential etiology in secondary cough headache. It is postulated that Valsalva maneuvers lea




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As defined by the International Classification of Headache Disorders, 3rd edition (ICHD-3), headache attributed to CM-I is precipitated by cough or other Valsalva maneuver, is occipital or suboccipital in location, and lasts less than five minutes [51].
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ntial etiology in secondary cough headache. It is postulated that Valsalva maneuvers leads to exacerbation of the pain by causing impaction of the cerebellar tonsils at the foramen magnum [32]. <span>As defined by the International Classification of Headache Disorders, 3rd edition (ICHD-3), headache attributed to CM-I is precipitated by cough or other Valsalva maneuver, is occipital or suboccipital in location, and lasts less than five minutes [51]. ●Hydrocephalus – Obstructive hydrocephalus is sometimes associated with CM-I; the prevalence of hydrocephalus associated with CM-I in one small study was approximately 10 percent [40].




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Hydrocephalus – Obstructive hydrocephalus is sometimes associated with CM-I; the prevalence of hydrocephalus associated with CM-I in one small study was approximately 10 percent [40].
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sorders, 3rd edition (ICHD-3), headache attributed to CM-I is precipitated by cough or other Valsalva maneuver, is occipital or suboccipital in location, and lasts less than five minutes [51]. ●<span>Hydrocephalus – Obstructive hydrocephalus is sometimes associated with CM-I; the prevalence of hydrocephalus associated with CM-I in one small study was approximately 10 percent [40]. Common signs and symptoms of hydrocephalus in children include headache, irritability, behavior changes, developmental delays, vomiting, and lethargy. ●Myelopathy – Myelopathy, manifest




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Myelopathy – Myelopathy, manifesting as motor weakness, sensory disturbances, or autonomic dysfunction, can result from compression of the cervical spinal cord by herniated cerebellar tonsils, or from the effects of a syrinx [42]
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study was approximately 10 percent [40]. Common signs and symptoms of hydrocephalus in children include headache, irritability, behavior changes, developmental delays, vomiting, and lethargy. ●<span>Myelopathy – Myelopathy, manifesting as motor weakness, sensory disturbances, or autonomic dysfunction, can result from compression of the cervical spinal cord by herniated cerebellar tonsils, or from the effects of a syrinx [42]. ●Oropharyngeal dysfunction – Oropharyngeal dysfunction associated with CM-I is most prevalent in children younger than three years of age and manifests with sleep apnea or feeding prob




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Oropharyngeal dysfunction – Oropharyngeal dysfunction associated with CM-I is most prevalent in children younger than three years of age and manifests with sleep apnea or feeding problems [41,42].
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s motor weakness, sensory disturbances, or autonomic dysfunction, can result from compression of the cervical spinal cord by herniated cerebellar tonsils, or from the effects of a syrinx [42]. ●<span>Oropharyngeal dysfunction – Oropharyngeal dysfunction associated with CM-I is most prevalent in children younger than three years of age and manifests with sleep apnea or feeding problems [41,42]. ●Scoliosis – Scoliosis is usually due to an asymmetric spinal syringomyelia leading to differential growth of the hemicords and the vertebral column [8]. Since the advent of MRI, syring




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Scoliosis – Scoliosis is usually due to an asymmetric spinal syringomyelia leading to differential growth of the hemicords and the vertebral column [8]. Since the advent of MRI, syringomyelia is often diagnosed prior to reaching the stage of the classic cape-like suspended sensory loss. Thus, scoliosis has become the most common presenting symptom of a spinal syrinx.
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haryngeal dysfunction – Oropharyngeal dysfunction associated with CM-I is most prevalent in children younger than three years of age and manifests with sleep apnea or feeding problems [41,42]. ●<span>Scoliosis – Scoliosis is usually due to an asymmetric spinal syringomyelia leading to differential growth of the hemicords and the vertebral column [8]. Since the advent of MRI, syringomyelia is often diagnosed prior to reaching the stage of the classic cape-like suspended sensory loss. Thus, scoliosis has become the most common presenting symptom of a spinal syrinx. ●Sleep-related breathing disorders – Emerging data have linked both central and obstructive sleep apnea as manifestations of CM-I in both children and adults [52]. ●Syringomyelia (syrin




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Sleep-related breathing disorders – Emerging data have linked both central and obstructive sleep apnea as manifestations of CM-I in both children and adults [52].
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syringomyelia is often diagnosed prior to reaching the stage of the classic cape-like suspended sensory loss. Thus, scoliosis has become the most common presenting symptom of a spinal syrinx. ●<span>Sleep-related breathing disorders – Emerging data have linked both central and obstructive sleep apnea as manifestations of CM-I in both children and adults [52]. ●Syringomyelia (syrinx) – Syringomyelia (image 5), often accompanied by scoliosis, occurs in approximately 35 percent of patients with symptomatic CM-I [7]. Among patients with neurolog




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Syringomyelia (syrinx) – Syringomyelia (image 5), often accompanied by scoliosis, occurs in approximately 35 percent of patients with symptomatic CM-I [7]. Among patients with neurologic deficits due to a syrinx, the earliest sign is loss of the superficial abdominal reflexes. Other signs and symptoms include gait disturbance, radicular pain, dysesthesia, upper motor neuron signs in the legs, and lower motor neuron signs maximally in the arms in those with a cervical syrinx, the most common location associated with CM-I. Of note, patients may also have signs and symptoms of brainstem dysfunction if the syrinx extends into the medulla (syringobulbia).
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symptom of a spinal syrinx. ●Sleep-related breathing disorders – Emerging data have linked both central and obstructive sleep apnea as manifestations of CM-I in both children and adults [52]. ●<span>Syringomyelia (syrinx) – Syringomyelia (image 5), often accompanied by scoliosis, occurs in approximately 35 percent of patients with symptomatic CM-I [7]. Among patients with neurologic deficits due to a syrinx, the earliest sign is loss of the superficial abdominal reflexes. Other signs and symptoms include gait disturbance, radicular pain, dysesthesia, upper motor neuron signs in the legs, and lower motor neuron signs maximally in the arms in those with a cervical syrinx, the most common location associated with CM-I. Of note, patients may also have signs and symptoms of brainstem dysfunction if the syrinx extends into the medulla (syringobulbia). Presyrinx is a potentially reversible condition characterized by spinal cord edema due to obstruction of cerebrospinal fluid flow [44,53]. It occurs most often in the cervical region an




Tughrul Beg’s able and ambitious grandson Malik Shah held the office of sultan and, together with his brother Tutush, enjoyed relatively secure rule of Mesopotamia and most of the Levant. This new Turkish empire–

sometimes referred to as the Great Seljuq Sultanate of Baghdad–was forged through ruthless despotism and the presentation of the Shi‘ites as dangerous, heretical enemies against whom Sunnis must unite.

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nst the Byzantines in Asia Minor; and a Seljuq splinter group eventually founded their own independent sultanate in Anatolia. By the early 1090s the Seljuqs had reshaped the Sunni Muslim world. <span>Tughrul Beg’s able and ambitious grandson Malik Shah held the office of sultan and, together with his brother Tutush, enjoyed relatively secure rule of Mesopotamia and most of the Levant. This new Turkish empire– sometimes referred to as the Great Seljuq Sultanate of Baghdad–was forged through ruthless despotism and the presentation of the Shi‘ites as dangerous, heretical enemies against whom Sunnis must unite. But when Malik Shah died in 1092, his mighty realm quickly collapsed amid succession crises and chaotic civil war. His two young sons fought to be named sultan, contesting control of Ir




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Question

Tughrul Beg’s able and ambitious grandson [...] held the office of sultan and, together with his brother Tutush, enjoyed relatively secure rule of Mesopotamia and most of the Levant. This new Turkish empire–

sometimes referred to as the Great Seljuq Sultanate of Baghdad–was forged through ruthless despotism and the presentation of the Shi‘ites as dangerous, heretical enemies against whom Sunnis must unite.

Answer
Malik Shah

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Tughrul Beg’s able and ambitious grandson Malik Shah held the office of sultan and, together with his brother Tutush, enjoyed relatively secure rule of Mesopotamia and most of the Levant. This new Turkish empire– sometimes referred to as

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The Crusades: The Authoritative History of the War for the Holy Land PDF Book by Thomas Asbridge Read Online Free - Page 8
nst the Byzantines in Asia Minor; and a Seljuq splinter group eventually founded their own independent sultanate in Anatolia. By the early 1090s the Seljuqs had reshaped the Sunni Muslim world. <span>Tughrul Beg’s able and ambitious grandson Malik Shah held the office of sultan and, together with his brother Tutush, enjoyed relatively secure rule of Mesopotamia and most of the Levant. This new Turkish empire– sometimes referred to as the Great Seljuq Sultanate of Baghdad–was forged through ruthless despotism and the presentation of the Shi‘ites as dangerous, heretical enemies against whom Sunnis must unite. But when Malik Shah died in 1092, his mighty realm quickly collapsed amid succession crises and chaotic civil war. His two young sons fought to be named sultan, contesting control of Ir







But when Malik Shah died in 1092, his mighty realm quickly collapsed amid succession crises and chaotic civil war. His two young sons fought to be named sultan, contesting control of Iraq and Iran; while in Syria, Tutush sought to seize power for himself. When he died in 1095, his sons Ridwan and Duqaq likewise squabbled over their inheritance, snatching Aleppo and Damascus respectively.
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The Crusades: The Authoritative History of the War for the Holy Land PDF Book by Thomas Asbridge Read Online Free - Page 8
s referred to as the Great Seljuq Sultanate of Baghdad–was forged through ruthless despotism and the presentation of the Shi‘ites as dangerous, heretical enemies against whom Sunnis must unite. <span>But when Malik Shah died in 1092, his mighty realm quickly collapsed amid succession crises and chaotic civil war. His two young sons fought to be named sultan, contesting control of Iraq and Iran; while in Syria, Tutush sought to seize power for himself. When he died in 1095, his sons Ridwan and Duqaq likewise squabbled over their inheritance, snatching Aleppo and Damascus respectively. At this same time, conditions in Shi‘ite Egypt were little better. Here, too, the precipitous deaths of the Fatimid caliph and his vizier in 1094 and 1095 brought sudden change, culmina




Flashcard 7106209910028

Question
But when Malik Shah died in [...], his mighty realm quickly collapsed amid succession crises and chaotic civil war. His two young sons fought to be named sultan, contesting control of Iraq and Iran; while in Syria, Tutush sought to seize power for himself. When he died in 1095, his sons Ridwan and Duqaq likewise squabbled over their inheritance, snatching Aleppo and Damascus respectively.
Answer
1092

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But when Malik Shah died in 1092, his mighty realm quickly collapsed amid succession crises and chaotic civil war. His two young sons fought to be named sultan, contesting control of Iraq and Iran; while in Syria, Tutu

Original toplevel document

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s referred to as the Great Seljuq Sultanate of Baghdad–was forged through ruthless despotism and the presentation of the Shi‘ites as dangerous, heretical enemies against whom Sunnis must unite. <span>But when Malik Shah died in 1092, his mighty realm quickly collapsed amid succession crises and chaotic civil war. His two young sons fought to be named sultan, contesting control of Iraq and Iran; while in Syria, Tutush sought to seize power for himself. When he died in 1095, his sons Ridwan and Duqaq likewise squabbled over their inheritance, snatching Aleppo and Damascus respectively. At this same time, conditions in Shi‘ite Egypt were little better. Here, too, the precipitous deaths of the Fatimid caliph and his vizier in 1094 and 1095 brought sudden change, culmina







#Chest #Douleur #Emergency #Pain #SAU #Thoracique #U2D
Chest pain accounts for approximately 7.6 million annual visits to emergency departments (ED) in the United States, making chest pain the second most common complaint [1]
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opics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Jun 2022. | This topic last updated: Mar 03, 2022. INTRODUCTION — <span>Chest pain accounts for approximately 7.6 million annual visits to emergency departments (ED) in the United States, making chest pain the second most common complaint [1]. Patients present with a spectrum of signs and symptoms reflecting the many potential etiologies of chest pain. Diseases of the heart, aorta, lungs, esophagus, stomach, mediastinum, ple




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Patients with life-threatening etiologies for chest pain may appear deceptively well, manifesting neither vital sign nor physical examination abnormalities.
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omach, mediastinum, pleura, and abdominal viscera may all cause chest discomfort. Clinicians in the ED focus on the immediate recognition and exclusion of life-threatening causes of chest pain. <span>Patients with life-threatening etiologies for chest pain may appear deceptively well, manifesting neither vital sign nor physical examination abnormalities. This topic review will discuss life-threatening and common causes of chest pain and provide an approach to the evaluation of chest pain patients in the ED. Detailed discussions of speci




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Life-threatening conditions — Causes of chest pain that pose an immediate threat to life include are listed and described briefly below.

• Acute coronary syndrome

• Acute aortic dissection

• Pulmonary embolism

• Tension pneumothorax

• Pericardial tamponade

• Mediastinitis (eg, esophageal rupture)

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emiology and etiology" and "Treatment of secondary spontaneous pneumothorax in adults" and "Cardiac tamponade" and "Boerhaave syndrome: Effort rupture of the esophagus".) DIFFERENTIAL DIAGNOSIS <span>Life-threatening conditions — Causes of chest pain that pose an immediate threat to life include are listed and described briefly below. •Acute coronary syndrome •Acute aortic dissection •Pulmonary embolism •Tension pneumothorax •Pericardial tamponade •Mediastinitis (eg, esophageal rupture) ●Acute coronary syndrome – Coronary vascular disease remains the leading killer of adults in developed countries. The 28 day case mortality rate for an acute coronary syndrome (ACS) amo




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Less than 15 to 30 percent of patients who present to the emergency department (ED) with nontraumatic chest pain have ACS, which includes myocardial infarction and unstable angina [2,3]
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day case mortality rate for an acute coronary syndrome (ACS) among patients in developed nations is approximately 10 percent, but varies with the severity of disease and the treatment provided. <span>Less than 15 to 30 percent of patients who present to the emergency department (ED) with nontraumatic chest pain have ACS, which includes myocardial infarction and unstable angina [2,3]. (See "Initial evaluation and management of suspected acute coronary syndrome (myocardial infarction, unstable angina) in the emergency department" and "Evaluation of emergency departme




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The incidence of aortic dissection is estimated at 3 per 100,000 patients per year. This number may be a gross underestimation of the true incidence as many patients die prior to diagnosis.
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cardial ischemia without injury (unstable angina) or myocardial ischemia with injury (myocardial infarction). (See "The role of platelets in coronary heart disease".) ●Acute aortic dissection – <span>The incidence of aortic dissection is estimated at 3 per 100,000 patients per year. This number may be a gross underestimation of the true incidence as many patients die prior to diagnosis. Aortic dissection most commonly affects patients with systemic hypertension in their seventh decade of life, but it can affect younger individuals, particularly those with known aortic




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Aortic dissection most commonly affects patients with systemic hypertension in their seventh decade of life, but it can affect younger individuals, particularly those with known aortic valve or connective tissue abnormalities.
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n – The incidence of aortic dissection is estimated at 3 per 100,000 patients per year. This number may be a gross underestimation of the true incidence as many patients die prior to diagnosis. <span>Aortic dissection most commonly affects patients with systemic hypertension in their seventh decade of life, but it can affect younger individuals, particularly those with known aortic valve or connective tissue abnormalities. Dissection typically begins with a tear in the inner layer of the aortic wall allowing blood to track between the intima (inner layer) and media (middle layer). Pulsatile blood flow cau




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The clinical picture of aortic intramural hematoma and other acute aortic syndrome (eg, penetrating aortic ulcer, aortic rupture) is similar to classic acute aortic dissection.
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cases, no intimal tear is identified. Such patients have an acute intramural hematoma likely caused by bleeding of the vasa vasorum with intramural hematoma formation in the wall of the aorta. <span>The clinical picture of aortic intramural hematoma and other acute aortic syndrome (eg, penetrating aortic ulcer, aortic rupture) is similar to classic acute aortic dissection. (See "Clinical features and diagnosis of acute aortic dissection" and "Overview of acute aortic dissection and other acute aortic syndromes".) ●Pulmonary embolism – The incidence of pul




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The incidence of pulmonary embolism (PE) is estimated at over 1 in 1000 patients, but the diagnosis is often missed and the incidence may be higher. Mortality rates vary widely based upon comorbid conditions and the size of the embolus.
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sic acute aortic dissection. (See "Clinical features and diagnosis of acute aortic dissection" and "Overview of acute aortic dissection and other acute aortic syndromes".) ●Pulmonary embolism – <span>The incidence of pulmonary embolism (PE) is estimated at over 1 in 1000 patients, but the diagnosis is often missed and the incidence may be higher. Mortality rates vary widely based upon comorbid conditions and the size of the embolus. Early diagnosis and treatment reduce mortality for large hemodynamically unstable pulmonary emboli. Pulmonary embolism occurs when a dislodged venous clot migrates through the right sid




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Pneumothorax can occur following trauma or pulmonary procedures. It also occurs spontaneously in patients with underlying lung disease (secondary pneumothorax) and without (primary pneumothorax).
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sults in pulmonary hypertension, right ventricular dysfunction, poor gas exchange, and ultimately parenchymal infarction. (See "Overview of acute pulmonary embolism in adults".) ●Pneumothorax – <span>Pneumothorax can occur following trauma or pulmonary procedures. It also occurs spontaneously in patients with underlying lung disease (secondary pneumothorax) and without (primary pneumothorax). Patients with primary spontaneous pneumothorax tend to be younger males who are tall and thin. Secondary spontaneous pneumothorax occurs with greatest frequency in patients with chronic




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Patients with primary spontaneous pneumothorax tend to be younger males who are tall and thin.
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eumothorax can occur following trauma or pulmonary procedures. It also occurs spontaneously in patients with underlying lung disease (secondary pneumothorax) and without (primary pneumothorax). <span>Patients with primary spontaneous pneumothorax tend to be younger males who are tall and thin. Secondary spontaneous pneumothorax occurs with greatest frequency in patients with chronic obstructive pulmonary disease, cystic fibrosis, and asthma. Regardless of etiology, the accumu




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Secondary spontaneous pneumothorax occurs with greatest frequency in patients with chronic obstructive pulmonary disease, cystic fibrosis, and asthma.
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patients with underlying lung disease (secondary pneumothorax) and without (primary pneumothorax). Patients with primary spontaneous pneumothorax tend to be younger males who are tall and thin. <span>Secondary spontaneous pneumothorax occurs with greatest frequency in patients with chronic obstructive pulmonary disease, cystic fibrosis, and asthma. Regardless of etiology, the accumulation of air in the pleural space can lead to tension pneumothorax with compression of the mediastinum, causing rapid clinical deterioration and death




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Common causes of mediastinitis include odontogenic infections, esophageal perforation, and iatrogenic complications of cardiac surgery or upper gastrointestinal and airway procedures. Mortality for patients with mediastinitis remains high (14 to 42 percent), even when treated with operative debridement and antibiotics [4-7]. Delays in diagnosis further increase mortality.
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ion pneumothorax with compression of the mediastinum, causing rapid clinical deterioration and death if unrecognized. (See "Pneumothorax in adults: Epidemiology and etiology".) ●Mediastinitis – <span>Common causes of mediastinitis include odontogenic infections, esophageal perforation, and iatrogenic complications of cardiac surgery or upper gastrointestinal and airway procedures. Mortality for patients with mediastinitis remains high (14 to 42 percent), even when treated with operative debridement and antibiotics [4-7]. Delays in diagnosis further increase mortality. (See "Boerhaave syndrome: Effort rupture of the esophagus" and "Postoperative mediastinitis after cardiac surgery".) ●Pericardial tamponade – Pericardial tamponade occurs when there is




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Tamponade covers a spectrum of clinical severity. Some patients have mild compromise, while others develop a severe compromise in cardiac filling, producing a picture resembling cardiogenic shock that requires immediate reduction in pericardial pressure by pericardiocentesis. Tamponade may occur with aortic dissection, after thoracic trauma, or as a consequence of acute pericarditis from infection, malignancy, uremia, or some other cause.
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mediastinitis after cardiac surgery".) ●Pericardial tamponade – Pericardial tamponade occurs when there is accumulation of pericardial fluid under pressure, leading to impaired cardiac filling. <span>Tamponade covers a spectrum of clinical severity. Some patients have mild compromise, while others develop a severe compromise in cardiac filling, producing a picture resembling cardiogenic shock that requires immediate reduction in pericardial pressure by pericardiocentesis. Tamponade may occur with aortic dissection, after thoracic trauma, or as a consequence of acute pericarditis from infection, malignancy, uremia, or some other cause. (See "Cardiac tamponade".) Common conditions — Below is a brief description of diseases that commonly occur among emergency department (ED) patients complaining of chest pain. Gastroint




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Common conditions — Below is a brief description of diseases that commonly occur among emergency department (ED) patients complaining of chest pain. Gastrointestinal problems, such as gastroesophageal reflux disease, comprise a significant number of such patients [2].
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Tamponade may occur with aortic dissection, after thoracic trauma, or as a consequence of acute pericarditis from infection, malignancy, uremia, or some other cause. (See "Cardiac tamponade".) <span>Common conditions — Below is a brief description of diseases that commonly occur among emergency department (ED) patients complaining of chest pain. Gastrointestinal problems, such as gastroesophageal reflux disease, comprise a significant number of such patients [2]. Common causes of chest pain that are not life-threatening are discussed in greater detail separately. ●Cardiac causes – Acute heart failure is frequently associated with chest discomfor




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Cardiac causes – Acute heart failure is frequently associated with chest discomfort. Patients with stable angina can usually identify their anginal chest pain and relay a history of exertional triggers. Valvular heart disease, such as mitral valve prolapse and aortic stenosis, may cause chest discomfort, which may signify worsening valvular function. Infectious or inflammatory causes of chest discomfort include pericarditis, myocarditis, and endocarditis. Accumulation of pericardial fluid can result in chest discomfort as can cardiac arrhythmias, especially if coronary blood flow is impaired.
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ch as gastroesophageal reflux disease, comprise a significant number of such patients [2]. Common causes of chest pain that are not life-threatening are discussed in greater detail separately. ●<span>Cardiac causes – Acute heart failure is frequently associated with chest discomfort. Patients with stable angina can usually identify their anginal chest pain and relay a history of exertional triggers. Valvular heart disease, such as mitral valve prolapse and aortic stenosis, may cause chest discomfort, which may signify worsening valvular function. Infectious or inflammatory causes of chest discomfort include pericarditis, myocarditis, and endocarditis. Accumulation of pericardial fluid can result in chest discomfort as can cardiac arrhythmias, especially if coronary blood flow is impaired. (See "Approach to diagnosis and evaluation of acute decompensated heart failure in adults" and "Chronic coronary syndrome: Overview of care" and "Clinical manifestations and diagnosis o




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Pulmonary/pleural causes – Respiratory infections, such as pneumonia, tracheitis, and bronchitis, are frequently accompanied by chest discomfort and cough. Chest tightness is a common complaint with asthma exacerbations. A number of disease processes can result in increased pulmonary arterial pressures and resultant right sided heart dysfunction (cor pulmonale). Pulmonary malignancy can cause chest pain particularly if there is pleural involvement. Chest heaviness or discomfort may be noted with pleural effusions.
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adults with suspected left-sided native valve endocarditis" and "Acute pericarditis: Clinical presentation and diagnosis" and "Clinical manifestations and diagnosis of myocarditis in adults".) ●<span>Pulmonary/pleural causes – Respiratory infections, such as pneumonia, tracheitis, and bronchitis, are frequently accompanied by chest discomfort and cough. Chest tightness is a common complaint with asthma exacerbations. A number of disease processes can result in increased pulmonary arterial pressures and resultant right sided heart dysfunction (cor pulmonale). Pulmonary malignancy can cause chest pain particularly if there is pleural involvement. Chest heaviness or discomfort may be noted with pleural effusions. (See "Clinical evaluation and diagnostic testing for community-acquired pneumonia in adults" and "Acute exacerbations of asthma in adults: Home and office management" and "Pulmonary hyp




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Gastrointestinal causes – Gastroesophageal reflux and esophageal spasm, rupture (Boerhaave's syndrome), or inflammation can all present as chest discomfort. A sliding hiatal hernia may result in chest pain. Pain from pancreatitis can be referred to the chest. Gastrointestinal causes account for the symptoms of a sizable number of patients who complain of chest pain and do not have an acute coronary syndrome.
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d/or hypoxemia (group 3 pulmonary hypertension): Epidemiology, pathogenesis, and diagnostic evaluation in adults" and "Diagnostic evaluation of a pleural effusion in adults: Initial testing".) ●<span>Gastrointestinal causes – Gastroesophageal reflux and esophageal spasm, rupture (Boerhaave's syndrome), or inflammation can all present as chest discomfort. A sliding hiatal hernia may result in chest pain. Pain from pancreatitis can be referred to the chest. Gastrointestinal causes account for the symptoms of a sizable number of patients who complain of chest pain and do not have an acute coronary syndrome. (See "Clinical manifestations and diagnosis of gastroesophageal reflux in adults" and "Evaluation of the adult with chest pain of esophageal origin" and "Boerhaave syndrome: Effort rupt




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Musculoskeletal causes – Musculoskeletal causes of chest pain include rib contusions and fractures, intercostal muscle strains, and costochondritis.
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and "Evaluation of the adult with chest pain of esophageal origin" and "Boerhaave syndrome: Effort rupture of the esophagus" and "Clinical manifestations and diagnosis of acute pancreatitis".) ●<span>Musculoskeletal causes – Musculoskeletal causes of chest pain include rib contusions and fractures, intercostal muscle strains, and costochondritis. (See "Major causes of musculoskeletal chest pain in adults".) ●Psychiatric causes – Patients with panic attack often complain of chest tightness and a sense of impending doom. This rema




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Psychiatric causes – Patients with panic attack often complain of chest tightness and a sense of impending doom. This remains a diagnosis of exclusion in the ED.
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uses – Musculoskeletal causes of chest pain include rib contusions and fractures, intercostal muscle strains, and costochondritis. (See "Major causes of musculoskeletal chest pain in adults".) ●<span>Psychiatric causes – Patients with panic attack often complain of chest tightness and a sense of impending doom. This remains a diagnosis of exclusion in the ED. (See "Pharmacotherapy for panic disorder with or without agoraphobia in adults".) ●Other conditions – Less commonly encountered conditions that may manifest as chest pain include: herpe




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Other conditions – Less commonly encountered conditions that may manifest as chest pain include: herpes zoster, referred pain, and pain associated with various inflammatory conditions and collagen vascular diseases, including lupus, sarcoid, scleroderma, Kawasaki's disease, polyarteritis nodosa, and Takayasu's arteritis.
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en complain of chest tightness and a sense of impending doom. This remains a diagnosis of exclusion in the ED. (See "Pharmacotherapy for panic disorder with or without agoraphobia in adults".) ●<span>Other conditions – Less commonly encountered conditions that may manifest as chest pain include: herpes zoster, referred pain, and pain associated with various inflammatory conditions and collagen vascular diseases, including lupus, sarcoid, scleroderma, Kawasaki's disease, polyarteritis nodosa, and Takayasu's arteritis. (See "Postherpetic neuralgia".) HISTORY — Thoracic organs share afferent nervous system pathways. This creates significant overlap in the symptoms patients experience when thoracic orga




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Thoracic organs share afferent nervous system pathways. This creates significant overlap in the symptoms patients experience when thoracic organs develop disease, and makes it difficult to distinguish which organ system is involved purely on the basis of history.
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y conditions and collagen vascular diseases, including lupus, sarcoid, scleroderma, Kawasaki's disease, polyarteritis nodosa, and Takayasu's arteritis. (See "Postherpetic neuralgia".) HISTORY — <span>Thoracic organs share afferent nervous system pathways. This creates significant overlap in the symptoms patients experience when thoracic organs develop disease, and makes it difficult to distinguish which organ system is involved purely on the basis of history. Patient descriptions of their symptoms can be helpful in some instances, but emergency clinicians must guard against premature diagnostic closure based upon history. Several studies dem




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Patient descriptions of their symptoms can be helpful in some instances, but emergency clinicians must guard against premature diagnostic closure based upon history. Several studies demonstrate that so-called "atypical" presentations occur more often than was previously thought and misinterpretation of such presentations increases the risk for misdiagnosis and adverse outcomes [ 8,9].
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ignificant overlap in the symptoms patients experience when thoracic organs develop disease, and makes it difficult to distinguish which organ system is involved purely on the basis of history. <span>Patient descriptions of their symptoms can be helpful in some instances, but emergency clinicians must guard against premature diagnostic closure based upon history. Several studies demonstrate that so-called "atypical" presentations occur more often than was previously thought and misinterpretation of such presentations increases the risk for misdiagnosis and adverse outcomes [8,9]. General approach — Obtain a detailed history of the patient's chest pain, including: ●Onset of pain (eg, abrupt or gradual) ●Provocation/Palliation (which activities provoke pain; which




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Pain that starts suddenly and is severe at onset is associated with acute aortic dissection, pneumothorax, and pulmonary embolism.
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obilization (eg, long plane ride) ●Other factors: cocaine use, cigarette use, family history Onset of pain — The timing of the onset of chest pain can help to narrow the differential diagnosis. <span>Pain that starts suddenly and is severe at onset is associated with acute aortic dissection, pneumothorax, and pulmonary embolism. Abrupt onset of pain was reported in 85 percent of patients in one registry of patients with acute aortic dissection [10]. Chest pain associated with pulmonary embolism can begin sudden




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Abrupt onset of pain was reported in 85 percent of patients in one registry of patients with acute aortic dissection [ 10]
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t of chest pain can help to narrow the differential diagnosis. Pain that starts suddenly and is severe at onset is associated with acute aortic dissection, pneumothorax, and pulmonary embolism. <span>Abrupt onset of pain was reported in 85 percent of patients in one registry of patients with acute aortic dissection [10]. Chest pain associated with pulmonary embolism can begin suddenly, but may worsen over time. Nontraumatic pneumothorax most often occurs suddenly at rest, without any precipitating even




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Chest pain associated with pulmonary embolism can begin suddenly, but may worsen over time.
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ed with acute aortic dissection, pneumothorax, and pulmonary embolism. Abrupt onset of pain was reported in 85 percent of patients in one registry of patients with acute aortic dissection [10]. <span>Chest pain associated with pulmonary embolism can begin suddenly, but may worsen over time. Nontraumatic pneumothorax most often occurs suddenly at rest, without any precipitating event. A history of forceful vomiting preceding symptoms in a toxic appearing patient raises conc




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Nontraumatic pneumothorax most often occurs suddenly at rest, without any precipitating event.
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was reported in 85 percent of patients in one registry of patients with acute aortic dissection [10]. Chest pain associated with pulmonary embolism can begin suddenly, but may worsen over time. <span>Nontraumatic pneumothorax most often occurs suddenly at rest, without any precipitating event. A history of forceful vomiting preceding symptoms in a toxic appearing patient raises concern for a ruptured esophagus and mediastinitis. However, a significant portion of patients who




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A history of forceful vomiting preceding symptoms in a toxic appearing patient raises concern for a ruptured esophagus and mediastinitis. However, a significant portion of patients who rupture their esophagus give no history of vomiting and presentations vary [ 11-13].
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[10]. Chest pain associated with pulmonary embolism can begin suddenly, but may worsen over time. Nontraumatic pneumothorax most often occurs suddenly at rest, without any precipitating event. <span>A history of forceful vomiting preceding symptoms in a toxic appearing patient raises concern for a ruptured esophagus and mediastinitis. However, a significant portion of patients who rupture their esophagus give no history of vomiting and presentations vary [11-13]. Conversely, discomfort from an acute coronary syndrome typically starts gradually and may worsen with exertion. With stable angina, discomfort occurs only when activity creates an oxyge




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Conversely, discomfort from an acute coronary syndrome typically starts gradually and may worsen with exertion
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ent raises concern for a ruptured esophagus and mediastinitis. However, a significant portion of patients who rupture their esophagus give no history of vomiting and presentations vary [11-13]. <span>Conversely, discomfort from an acute coronary syndrome typically starts gradually and may worsen with exertion. With stable angina, discomfort occurs only when activity creates an oxygen demand that outstrips supply limitations imposed by a fixed atherosclerotic lesion. This occurs at relatively




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With stable angina, discomfort occurs only when activity creates an oxygen demand that outstrips supply limitations imposed by a fixed atherosclerotic lesion. This occurs at relatively predictable points and changes slowly over time.
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pture their esophagus give no history of vomiting and presentations vary [11-13]. Conversely, discomfort from an acute coronary syndrome typically starts gradually and may worsen with exertion. <span>With stable angina, discomfort occurs only when activity creates an oxygen demand that outstrips supply limitations imposed by a fixed atherosclerotic lesion. This occurs at relatively predictable points and changes slowly over time. Unstable angina represents an abrupt change from baseline functioning, which may manifest as discomfort that begins at lower levels of exercise or at rest. Pain quality and location — P




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Unstable angina represents an abrupt change from baseline functioning, which may manifest as discomfort that begins at lower levels of exercise or at rest.
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ly when activity creates an oxygen demand that outstrips supply limitations imposed by a fixed atherosclerotic lesion. This occurs at relatively predictable points and changes slowly over time. <span>Unstable angina represents an abrupt change from baseline functioning, which may manifest as discomfort that begins at lower levels of exercise or at rest. Pain quality and location — Patients often describe the symptoms of an acute coronary syndrome (ACS) as discomfort rather than pain. The discomfort may be a pressure, heaviness, tightne




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Patients often describe the symptoms of an acute coronary syndrome (ACS) as discomfort rather than pain. The discomfort may be a pressure, heaviness, tightness, fullness, or squeezing. Ischemia is less likely if the discomfort is knifelike, sharp, pleuritic, or positional. The classic location is substernal or in the left chest, and radiation to the arm, neck, jaw, back, abdomen, or shoulders may occur. Pain that radiates to the shoulders or occurs with exertion significantly increases the relative risk for ACS.
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ver time. Unstable angina represents an abrupt change from baseline functioning, which may manifest as discomfort that begins at lower levels of exercise or at rest. Pain quality and location — <span>Patients often describe the symptoms of an acute coronary syndrome (ACS) as discomfort rather than pain. The discomfort may be a pressure, heaviness, tightness, fullness, or squeezing. Ischemia is less likely if the discomfort is knifelike, sharp, pleuritic, or positional. The classic location is substernal or in the left chest, and radiation to the arm, neck, jaw, back, abdomen, or shoulders may occur. Pain that radiates to the shoulders or occurs with exertion significantly increases the relative risk for ACS. Relief of pain following the administration of sublingual nitroglycerin does not reliably distinguish between cardiac ischemia and noncardiac causes of chest pain [14,15]. Beware of "at




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Relief of pain following the administration of sublingual nitroglycerin does not reliably distinguish between cardiac ischemia and noncardiac causes of chest pain [14,15]
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chest, and radiation to the arm, neck, jaw, back, abdomen, or shoulders may occur. Pain that radiates to the shoulders or occurs with exertion significantly increases the relative risk for ACS. <span>Relief of pain following the administration of sublingual nitroglycerin does not reliably distinguish between cardiac ischemia and noncardiac causes of chest pain [14,15]. Beware of "atypical" presentations of ACS, which are common and occur more often in the elderly, diabetics, and women. Patients with "atypical" symptoms (eg, dyspnea, weakness) associa




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An acute aortic dissection most often presents with the sudden onset of sharp, severe pain [10,16]. Patients may describe the pain as tearing, or ripping. However, according to the International Registry of Acute Aortic Dissection (IRAD), presentations can be diverse and classic findings absent. The pain most often occurs in the chest, but can begin in the back, and may migrate or radiate into other areas of the chest, back, or abdomen, depending upon the portion of the aorta involved and the extent of the dissection.
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ntation' and "Initial evaluation and management of suspected acute coronary syndrome (myocardial infarction, unstable angina) in the emergency department", section on 'Atypical presentations'.) <span>An acute aortic dissection most often presents with the sudden onset of sharp, severe pain [10,16]. Patients may describe the pain as tearing, or ripping. However, according to the International Registry of Acute Aortic Dissection (IRAD), presentations can be diverse and classic findings absent. The pain most often occurs in the chest, but can begin in the back, and may migrate or radiate into other areas of the chest, back, or abdomen, depending upon the portion of the aorta involved and the extent of the dissection. Sharp pain may also accompany pulmonary embolism, pneumothorax, or pericarditis. A pulmonary embolism (PE) can create different kinds of pain, or painless dyspnea. Pain associated with




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Sharp pain may also accompany pulmonary embolism, pneumothorax, or pericarditis.
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chest, but can begin in the back, and may migrate or radiate into other areas of the chest, back, or abdomen, depending upon the portion of the aorta involved and the extent of the dissection. <span>Sharp pain may also accompany pulmonary embolism, pneumothorax, or pericarditis. A pulmonary embolism (PE) can create different kinds of pain, or painless dyspnea. Pain associated with PE may worsen with deep inspiration, and may localize to the chest wall. Patients




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A pulmonary embolism (PE) can create different kinds of pain, or painless dyspnea. Pain associated with PE may worsen with deep inspiration, and may localize to the chest wall.
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the chest, back, or abdomen, depending upon the portion of the aorta involved and the extent of the dissection. Sharp pain may also accompany pulmonary embolism, pneumothorax, or pericarditis. <span>A pulmonary embolism (PE) can create different kinds of pain, or painless dyspnea. Pain associated with PE may worsen with deep inspiration, and may localize to the chest wall. Patients with pneumothorax report ipsilateral chest pain which may initially be sharp and pleuritic but may become dull or achy over time. The discomfort of pericarditis is classically




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Patients with pneumothorax report ipsilateral chest pain which may initially be sharp and pleuritic but may become dull or achy over time.
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or pericarditis. A pulmonary embolism (PE) can create different kinds of pain, or painless dyspnea. Pain associated with PE may worsen with deep inspiration, and may localize to the chest wall. <span>Patients with pneumothorax report ipsilateral chest pain which may initially be sharp and pleuritic but may become dull or achy over time. The discomfort of pericarditis is classically positional: worse when lying supine and relieved somewhat when leaning forward. It may also worsen with deep inspiration. Sharp, well-local




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The discomfort of pericarditis is classically positional: worse when lying supine and relieved somewhat when leaning forward. It may also worsen with deep inspiration.
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deep inspiration, and may localize to the chest wall. Patients with pneumothorax report ipsilateral chest pain which may initially be sharp and pleuritic but may become dull or achy over time. <span>The discomfort of pericarditis is classically positional: worse when lying supine and relieved somewhat when leaning forward. It may also worsen with deep inspiration. Sharp, well-localized pain reproduced with movement or palpation of the chest wall is characteristic of musculoskeletal causes. Often the patient relates a history of trauma or strenuou




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Sharp, well-localized pain reproduced with movement or palpation of the chest wall is characteristic of musculoskeletal causes. Often the patient relates a history of trauma or strenuous activity prior to developing pain.
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e dull or achy over time. The discomfort of pericarditis is classically positional: worse when lying supine and relieved somewhat when leaning forward. It may also worsen with deep inspiration. <span>Sharp, well-localized pain reproduced with movement or palpation of the chest wall is characteristic of musculoskeletal causes. Often the patient relates a history of trauma or strenuous activity prior to developing pain. Burning pain in the chest and epigastrium is commonly associated with gastrointestinal causes. Esophageal rupture can cause chest and/or abdominal pain. Cardiac disease can cause identi




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Burning pain in the chest and epigastrium is commonly associated with gastrointestinal causes. Esophageal rupture can cause chest and/or abdominal pain. Cardiac disease can cause identical symptoms, however, and emergency clinicians must avoid prematurely attributing such symptoms to gastrointestinal disease.
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eproduced with movement or palpation of the chest wall is characteristic of musculoskeletal causes. Often the patient relates a history of trauma or strenuous activity prior to developing pain. <span>Burning pain in the chest and epigastrium is commonly associated with gastrointestinal causes. Esophageal rupture can cause chest and/or abdominal pain. Cardiac disease can cause identical symptoms, however, and emergency clinicians must avoid prematurely attributing such symptoms to gastrointestinal disease. Associated symptoms — Diaphoresis, nausea, and vomiting frequently accompany chest discomfort associated with acute coronary syndrome (ACS), but are not predictive of ACS [17]. Elderly




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Diaphoresis, nausea, and vomiting frequently accompany chest discomfort associated with acute coronary syndrome (ACS), but are not predictive of ACS [17].
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dominal pain. Cardiac disease can cause identical symptoms, however, and emergency clinicians must avoid prematurely attributing such symptoms to gastrointestinal disease. Associated symptoms — <span>Diaphoresis, nausea, and vomiting frequently accompany chest discomfort associated with acute coronary syndrome (ACS), but are not predictive of ACS [17]. Elderly patients with ACS may only complain of symptoms other than chest pain, such as dyspnea, weakness, altered mental status, or syncope. Symptoms, such as diaphoresis and nausea, ma




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Elderly patients with ACS may only complain of symptoms other than chest pain, such as dyspnea, weakness, altered mental status, or syncope.
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estinal disease. Associated symptoms — Diaphoresis, nausea, and vomiting frequently accompany chest discomfort associated with acute coronary syndrome (ACS), but are not predictive of ACS [17]. <span>Elderly patients with ACS may only complain of symptoms other than chest pain, such as dyspnea, weakness, altered mental status, or syncope. Symptoms, such as diaphoresis and nausea, may also occur with nonischemic chest pain, including aortic dissection, pulmonary embolus, acute heart failure, and esophageal spasm. Acute ao




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Symptoms, such as diaphoresis and nausea, may also occur with nonischemic chest pain, including aortic dissection, pulmonary embolus, acute heart failure, and esophageal spasm.
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syndrome (ACS), but are not predictive of ACS [17]. Elderly patients with ACS may only complain of symptoms other than chest pain, such as dyspnea, weakness, altered mental status, or syncope. <span>Symptoms, such as diaphoresis and nausea, may also occur with nonischemic chest pain, including aortic dissection, pulmonary embolus, acute heart failure, and esophageal spasm. Acute aortic dissection has a wide range of potential associated symptoms, depending on the arterial branches involved, which may confound the diagnosis (table 1). According to one revi




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Acute aortic dissection has a wide range of potential associated symptoms, depending on the arterial branches involved, which may confound the diagnosis (table 1). According to one review, syncope accompanies 13 percent of dissections involving the ascending aorta [18]. Neurological symptoms, ranging from hoarseness to paraplegia and altered mental status, occur in 18 to 30 percent of patients with aortic dissection [18]. ACS can occur when the dissection involves the coronary arteries.
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tus, or syncope. Symptoms, such as diaphoresis and nausea, may also occur with nonischemic chest pain, including aortic dissection, pulmonary embolus, acute heart failure, and esophageal spasm. <span>Acute aortic dissection has a wide range of potential associated symptoms, depending on the arterial branches involved, which may confound the diagnosis (table 1). According to one review, syncope accompanies 13 percent of dissections involving the ascending aorta [18]. Neurological symptoms, ranging from hoarseness to paraplegia and altered mental status, occur in 18 to 30 percent of patients with aortic dissection [18]. ACS can occur when the dissection involves the coronary arteries. Shortness of breath frequently accompanies pulmonary causes of chest pain and may be the predominant symptom in pulmonary embolus, pneumothorax, and pneumonia. Tachypnea is common with




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Shortness of breath frequently accompanies pulmonary causes of chest pain and may be the predominant symptom in pulmonary embolus, pneumothorax, and pneumonia.
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ing from hoarseness to paraplegia and altered mental status, occur in 18 to 30 percent of patients with aortic dissection [18]. ACS can occur when the dissection involves the coronary arteries. <span>Shortness of breath frequently accompanies pulmonary causes of chest pain and may be the predominant symptom in pulmonary embolus, pneumothorax, and pneumonia. Tachypnea is common with PE and may be accompanied by wheezing and fever. Young healthy patients may manifest only a relative tachypnea or tachycardia despite the presence of pneumonia




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Tachypnea is common with PE and may be accompanied by wheezing and fever.
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n involves the coronary arteries. Shortness of breath frequently accompanies pulmonary causes of chest pain and may be the predominant symptom in pulmonary embolus, pneumothorax, and pneumonia. <span>Tachypnea is common with PE and may be accompanied by wheezing and fever. Young healthy patients may manifest only a relative tachypnea or tachycardia despite the presence of pneumonia or pulmonary embolism. Dyspnea is often the only complaint among elderly p




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Young healthy patients may manifest only a relative tachypnea or tachycardia despite the presence of pneumonia or pulmonary embolism.
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es pulmonary causes of chest pain and may be the predominant symptom in pulmonary embolus, pneumothorax, and pneumonia. Tachypnea is common with PE and may be accompanied by wheezing and fever. <span>Young healthy patients may manifest only a relative tachypnea or tachycardia despite the presence of pneumonia or pulmonary embolism. Dyspnea is often the only complaint among elderly patients with ACS. Cough, syncope, and hemoptysis may occur with pulmonary embolism or valvular heart disease (particularly mitral sten




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Dyspnea is often the only complaint among elderly patients with ACS.
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ommon with PE and may be accompanied by wheezing and fever. Young healthy patients may manifest only a relative tachypnea or tachycardia despite the presence of pneumonia or pulmonary embolism. <span>Dyspnea is often the only complaint among elderly patients with ACS. Cough, syncope, and hemoptysis may occur with pulmonary embolism or valvular heart disease (particularly mitral stenosis), although cough and hemoptysis are more common with bronchitis,




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Cough, syncope, and hemoptysis may occur with pulmonary embolism or valvular heart disease (particularly mitral stenosis), although cough and hemoptysis are more common with bronchitis, pharyngitis, or exacerbations of COPD.
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lthy patients may manifest only a relative tachypnea or tachycardia despite the presence of pneumonia or pulmonary embolism. Dyspnea is often the only complaint among elderly patients with ACS. <span>Cough, syncope, and hemoptysis may occur with pulmonary embolism or valvular heart disease (particularly mitral stenosis), although cough and hemoptysis are more common with bronchitis, pharyngitis, or exacerbations of COPD. Dyspnea and cough may accompany pericardial and pleural effusions regardless of etiology. Preceding or concomitant pain and swelling in an extremity suggests deep venous thrombosis (DVT




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Dyspnea and cough may accompany pericardial and pleural effusions regardless of etiology
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may occur with pulmonary embolism or valvular heart disease (particularly mitral stenosis), although cough and hemoptysis are more common with bronchitis, pharyngitis, or exacerbations of COPD. <span>Dyspnea and cough may accompany pericardial and pleural effusions regardless of etiology. Preceding or concomitant pain and swelling in an extremity suggests deep venous thrombosis (DVT) complicated by pulmonary embolism. DVT occurs most often in the lower extremities but c




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Preceding or concomitant pain and swelling in an extremity suggests deep venous thrombosis (DVT) complicated by pulmonary embolism. DVT occurs most often in the lower extremities but clots may also originate in the upper extremities and the large veins of the pelvis, where they may produce bilateral lower extremity swelling if the inferior vena cava becomes occluded
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, although cough and hemoptysis are more common with bronchitis, pharyngitis, or exacerbations of COPD. Dyspnea and cough may accompany pericardial and pleural effusions regardless of etiology. <span>Preceding or concomitant pain and swelling in an extremity suggests deep venous thrombosis (DVT) complicated by pulmonary embolism. DVT occurs most often in the lower extremities but clots may also originate in the upper extremities and the large veins of the pelvis, where they may produce bilateral lower extremity swelling if the inferior vena cava becomes occluded. Nausea and belching frequently accompany gastrointestinal causes of chest pain, but can also occur in patients with inferior myocardial infarction. Fever raises concern for infectious




#Chest #Douleur #Emergency #Pain #SAU #Thoracique #U2D
Nausea and belching frequently accompany gastrointestinal causes of chest pain, but can also occur in patients with inferior myocardial infarction.
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es but clots may also originate in the upper extremities and the large veins of the pelvis, where they may produce bilateral lower extremity swelling if the inferior vena cava becomes occluded. <span>Nausea and belching frequently accompany gastrointestinal causes of chest pain, but can also occur in patients with inferior myocardial infarction. Fever raises concern for infectious causes, but is also associated with pericarditis, myocarditis, and rarely acute myocardial infarction. A low-grade fever may accompany pulmonary embo




#Chest #Douleur #Emergency #Pain #SAU #Thoracique #U2D
Fever raises concern for infectious causes, but is also associated with pericarditis, myocarditis, and rarely acute myocardial infarction.
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