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As the world warmed up, a new culture based on agriculture and sedentary dwelling emerged, which archaeologists have termed "Pre-Pottery Neolithic A" (abbreviated as PPNA). Its cultures lacked pottery, but featured the following:[ citation needed ]

  • small circular dwellings
  • burial of the dead under the floor of buildings
  • reliance on hunting of wild game
  • cultivation of wild or domestic cereals
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Jericho - Wikipedia
arch 2022) (Learn how and when to remove this template message) The first permanent settlement on the site of Jericho developed near the Ein es-Sultan spring between 9,500 and 9000 BCE.[24][25] <span>As the world warmed up, a new culture based on agriculture and sedentary dwelling emerged, which archaeologists have termed "Pre-Pottery Neolithic A" (abbreviated as PPNA). Its cultures lacked pottery, but featured the following:[citation needed] small circular dwellings burial of the dead under the floor of buildings reliance on hunting of wild game cultivation of wild or domestic cereals Head of an ancestor statue, Jericho, from c. 9000 years ago, among the oldest representations of a human face ever found. Rockefeller Archeological Museum, Jerusalem.[26] At Jericho, ci




Flashcard 7104391941388

Question

As the world warmed up, a new culture based on agriculture and sedentary dwelling emerged, which archaeologists have termed [...] Its cultures lacked pottery, but featured the following:[ citation needed ]

  • small circular dwellings
  • burial of the dead under the floor of buildings
  • reliance on hunting of wild game
  • cultivation of wild or domestic cereals
Answer
"Pre-Pottery Neolithic A" (abbreviated as PPNA).

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As the world warmed up, a new culture based on agriculture and sedentary dwelling emerged, which archaeologists have termed "Pre-Pottery Neolithic A" (abbreviated as PPNA). Its cultures lacked pottery, but featured the following:[ citation needed ] small circular dwellings burial of the dead under the floor of buildings reliance on hunting of wild game cul

Original toplevel document

Jericho - Wikipedia
arch 2022) (Learn how and when to remove this template message) The first permanent settlement on the site of Jericho developed near the Ein es-Sultan spring between 9,500 and 9000 BCE.[24][25] <span>As the world warmed up, a new culture based on agriculture and sedentary dwelling emerged, which archaeologists have termed "Pre-Pottery Neolithic A" (abbreviated as PPNA). Its cultures lacked pottery, but featured the following:[citation needed] small circular dwellings burial of the dead under the floor of buildings reliance on hunting of wild game cultivation of wild or domestic cereals Head of an ancestor statue, Jericho, from c. 9000 years ago, among the oldest representations of a human face ever found. Rockefeller Archeological Museum, Jerusalem.[26] At Jericho, ci







At Jericho, circular dwellings were built of clay and straw bricks left to dry in the sun, which were plastered together with a mud mortar. Each house measured about 5 metres (16 ft) across, and was roofed with mud-smeared brush. Hearths were located within and outside the homes.
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Jericho - Wikipedia
ld or domestic cereals Head of an ancestor statue, Jericho, from c. 9000 years ago, among the oldest representations of a human face ever found. Rockefeller Archeological Museum, Jerusalem.[26] <span>At Jericho, circular dwellings were built of clay and straw bricks left to dry in the sun, which were plastered together with a mud mortar. Each house measured about 5 metres (16 ft) across, and was roofed with mud-smeared brush. Hearths were located within and outside the homes.[27] The 8000 BCE Tower of Jericho at Tell es-Sultan The Pre-Sultan (c. 8350 – 7370 BCE)[dubious – discuss] is sometimes called Sultanian. The site is a 40,000 square metres (430,000 sq




Flashcard 7104395087116

Question
At Jericho, circular dwellings were built of [...] which were plastered together with a mud mortar. Each house measured about 5 metres (16 ft) across, and was roofed with mud-smeared brush. Hearths were located within and outside the homes.
Answer
clay and straw bricks left to dry in the sun,

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At Jericho, circular dwellings were built of clay and straw bricks left to dry in the sun, which were plastered together with a mud mortar. Each house measured about 5 metres (16 ft) across, and was roofed with mud-smeared brush. Hearths were located within and outside the ho

Original toplevel document

Jericho - Wikipedia
ld or domestic cereals Head of an ancestor statue, Jericho, from c. 9000 years ago, among the oldest representations of a human face ever found. Rockefeller Archeological Museum, Jerusalem.[26] <span>At Jericho, circular dwellings were built of clay and straw bricks left to dry in the sun, which were plastered together with a mud mortar. Each house measured about 5 metres (16 ft) across, and was roofed with mud-smeared brush. Hearths were located within and outside the homes.[27] The 8000 BCE Tower of Jericho at Tell es-Sultan The Pre-Sultan (c. 8350 – 7370 BCE)[dubious – discuss] is sometimes called Sultanian. The site is a 40,000 square metres (430,000 sq







The Pre-Pottery Neolithic B (PPNB) was a period of about 1.4 millennia, from 7220 to 5850 BCE[ clarification needed ] (though carbon-14-dates are few and early). The following are PPNB cultural features:[ citation needed ]

  • Expanded range of domesticated plants
  • Possible domestication of sheep
  • Apparent cult involving the preservation of human skulls, with facial features reconstructed using plaster, and eyes set with shells in some cases
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Jericho - Wikipedia
on. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (March 2022) (Learn how and when to remove this template message) <span>The Pre-Pottery Neolithic B (PPNB) was a period of about 1.4 millennia, from 7220 to 5850 BCE[clarification needed] (though carbon-14-dates are few and early). The following are PPNB cultural features:[citation needed] Expanded range of domesticated plants Possible domestication of sheep Apparent cult involving the preservation of human skulls, with facial features reconstructed using plaster, and eyes set with shells in some cases Area of the fertile crescent, c. 7500 BC, with main sites. Jericho was a foremost site of the Pre-Pottery Neolithic period. The area of Mesopotamia proper was not yet settled by humans.




Flashcard 7104398232844

Question

[...] was a period of about 1.4 millennia, from 7220 to 5850 BCE[ clarification needed ] (though carbon-14-dates are few and early). The following are PPNB cultural features:[ citation needed ]

  • Expanded range of domesticated plants
  • Possible domestication of sheep
  • Apparent cult involving the preservation of human skulls, with facial features reconstructed using plaster, and eyes set with shells in some cases
Answer
The Pre-Pottery Neolithic B (PPNB)

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The Pre-Pottery Neolithic B (PPNB) was a period of about 1.4 millennia, from 7220 to 5850 BCE[ clarification needed ] (though carbon-14-dates are few and early). The following are PPNB cultural features:[ citation needed

Original toplevel document

Jericho - Wikipedia
on. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (March 2022) (Learn how and when to remove this template message) <span>The Pre-Pottery Neolithic B (PPNB) was a period of about 1.4 millennia, from 7220 to 5850 BCE[clarification needed] (though carbon-14-dates are few and early). The following are PPNB cultural features:[citation needed] Expanded range of domesticated plants Possible domestication of sheep Apparent cult involving the preservation of human skulls, with facial features reconstructed using plaster, and eyes set with shells in some cases Area of the fertile crescent, c. 7500 BC, with main sites. Jericho was a foremost site of the Pre-Pottery Neolithic period. The area of Mesopotamia proper was not yet settled by humans.







After a few centuries, the first settlement was abandoned. After the PPNA settlement phase, there was a settlement hiatus of several centuries, then the PPNB settlement was founded on the eroded surface of the tell. This second settlement, established in 6800 BCE, perhaps represents the work of an invading people who absorbed the original inhabitants into their dominant culture.
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Jericho - Wikipedia
e cases Area of the fertile crescent, c. 7500 BC, with main sites. Jericho was a foremost site of the Pre-Pottery Neolithic period. The area of Mesopotamia proper was not yet settled by humans. <span>After a few centuries, the first settlement was abandoned. After the PPNA settlement phase, there was a settlement hiatus of several centuries, then the PPNB settlement was founded on the eroded surface of the tell. This second settlement, established in 6800 BCE, perhaps represents the work of an invading people who absorbed the original inhabitants into their dominant culture. Artifacts dating from this period include ten plastered human skulls, painted so as to reconstitute the individuals' features.[18] These represent either teraphim or the first example o




Flashcard 7104401378572

Question
After a few centuries, the first settlement was abandoned. After the PPNA settlement phase, there was a settlement hiatus of several centuries, then the PPNB settlement was founded on the eroded surface of the tell. This second settlement, established in [...] BCE, perhaps represents the work of an invading people who absorbed the original inhabitants into their dominant culture.
Answer
6800

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ter the PPNA settlement phase, there was a settlement hiatus of several centuries, then the PPNB settlement was founded on the eroded surface of the tell. This second settlement, established in <span>6800 BCE, perhaps represents the work of an invading people who absorbed the original inhabitants into their dominant culture. <span>

Original toplevel document

Jericho - Wikipedia
e cases Area of the fertile crescent, c. 7500 BC, with main sites. Jericho was a foremost site of the Pre-Pottery Neolithic period. The area of Mesopotamia proper was not yet settled by humans. <span>After a few centuries, the first settlement was abandoned. After the PPNA settlement phase, there was a settlement hiatus of several centuries, then the PPNB settlement was founded on the eroded surface of the tell. This second settlement, established in 6800 BCE, perhaps represents the work of an invading people who absorbed the original inhabitants into their dominant culture. Artifacts dating from this period include ten plastered human skulls, painted so as to reconstitute the individuals' features.[18] These represent either teraphim or the first example o







During the Middle Bronze Age, Jericho was a small prominent city of the Canaan region, reaching its greatest Bronze Age extent in the period from 1700 to 1550 BCE.
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rs, and possessed an extensive cemetery with vertical shaft-tombs and underground burial chambers; the elaborate funeral offerings in some of these may reflect the emergence of local kings.[37] <span>During the Middle Bronze Age, Jericho was a small prominent city of the Canaan region, reaching its greatest Bronze Age extent in the period from 1700 to 1550 BCE. It seems to have reflected the greater urbanization in the area at that time, and has been linked to the rise of the Maryannu, a class of chariot-using aristocrats linked to the rise of




Flashcard 7104404524300

Question
During the Middle Bronze Age, Jericho was a small prominent city of the [...], reaching its greatest Bronze Age extent in the period from 1700 to 1550 BCE.
Answer
Canaan region

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During the Middle Bronze Age, Jericho was a small prominent city of the Canaan region, reaching its greatest Bronze Age extent in the period from 1700 to 1550 BCE.

Original toplevel document

Jericho - Wikipedia
rs, and possessed an extensive cemetery with vertical shaft-tombs and underground burial chambers; the elaborate funeral offerings in some of these may reflect the emergence of local kings.[37] <span>During the Middle Bronze Age, Jericho was a small prominent city of the Canaan region, reaching its greatest Bronze Age extent in the period from 1700 to 1550 BCE. It seems to have reflected the greater urbanization in the area at that time, and has been linked to the rise of the Maryannu, a class of chariot-using aristocrats linked to the rise of







It seems to have reflected the greater urbanization in the area at that time, and has been linked to the rise of the Maryannu, a class of chariot-using aristocrats linked to the rise of the Mitannite state to the north.
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emergence of local kings.[37] During the Middle Bronze Age, Jericho was a small prominent city of the Canaan region, reaching its greatest Bronze Age extent in the period from 1700 to 1550 BCE. <span>It seems to have reflected the greater urbanization in the area at that time, and has been linked to the rise of the Maryannu, a class of chariot-using aristocrats linked to the rise of the Mitannite state to the north. Kathleen Kenyon reported "the Middle Bronze Age is perhaps the most prosperous in the whole history of Kna'an. ... The defenses ... belong to a fairly advanced date in that period" and




Flashcard 7104407145740

Question
It seems to have reflected the greater urbanization in the area at that time, and has been linked to the rise of the [...] a class of chariot-using aristocrats linked to the rise of the Mitannite state to the north.
Answer

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It seems to have reflected the greater urbanization in the area at that time, and has been linked to the rise of the Maryannu, a class of chariot-using aristocrats linked to the rise of the Mitannite state to the north.

Original toplevel document

Jericho - Wikipedia
emergence of local kings.[37] During the Middle Bronze Age, Jericho was a small prominent city of the Canaan region, reaching its greatest Bronze Age extent in the period from 1700 to 1550 BCE. <span>It seems to have reflected the greater urbanization in the area at that time, and has been linked to the rise of the Maryannu, a class of chariot-using aristocrats linked to the rise of the Mitannite state to the north. Kathleen Kenyon reported "the Middle Bronze Age is perhaps the most prosperous in the whole history of Kna'an. ... The defenses ... belong to a fairly advanced date in that period" and







Flashcard 7104408194316

Question
It seems to have reflected the greater urbanization in the area at that time, and has been linked to the rise of the [...], a class of chariot-using aristocrats linked to the rise of the Mitannite state to the north.
Answer
Maryannu

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It seems to have reflected the greater urbanization in the area at that time, and has been linked to the rise of the Maryannu, a class of chariot-using aristocrats linked to the rise of the Mitannite state to the north.

Original toplevel document

Jericho - Wikipedia
emergence of local kings.[37] During the Middle Bronze Age, Jericho was a small prominent city of the Canaan region, reaching its greatest Bronze Age extent in the period from 1700 to 1550 BCE. <span>It seems to have reflected the greater urbanization in the area at that time, and has been linked to the rise of the Maryannu, a class of chariot-using aristocrats linked to the rise of the Mitannite state to the north. Kathleen Kenyon reported "the Middle Bronze Age is perhaps the most prosperous in the whole history of Kna'an. ... The defenses ... belong to a fairly advanced date in that period" and







Flashcard 7104409767180

Question
It seems to have reflected the greater urbanization in the area at that time, and has been linked to the rise of the Maryannu, a class of chariot-using aristocrats linked to the rise of the [...] state to the north.
Answer
Mitannite

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an> It seems to have reflected the greater urbanization in the area at that time, and has been linked to the rise of the Maryannu, a class of chariot-using aristocrats linked to the rise of the <span>Mitannite state to the north. <span>

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Jericho - Wikipedia
emergence of local kings.[37] During the Middle Bronze Age, Jericho was a small prominent city of the Canaan region, reaching its greatest Bronze Age extent in the period from 1700 to 1550 BCE. <span>It seems to have reflected the greater urbanization in the area at that time, and has been linked to the rise of the Maryannu, a class of chariot-using aristocrats linked to the rise of the Mitannite state to the north. Kathleen Kenyon reported "the Middle Bronze Age is perhaps the most prosperous in the whole history of Kna'an. ... The defenses ... belong to a fairly advanced date in that period" and







Tell es-Sultan remained unoccupied from the end of the 15th to the 10th–9th centuries BCE, when the city was rebuilt.[41][40][42] Of this new city not much more remains than a four-room house on the eastern slope.[43] By the 7th century, Jericho had become an extensive town, but this settlement was destroyed in the Babylonian conquest of Judah in the late 6th century.[41]
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ence of a small settlement in the Late Bronze Age (c. 1400s BCE) on the site, but erosion and destruction from previous excavations have erased significant parts of this layer.[39][40] Iron Age <span>Tell es-Sultan remained unoccupied from the end of the 15th to the 10th–9th centuries BCE, when the city was rebuilt.[41][40][42] Of this new city not much more remains than a four-room house on the eastern slope.[43] By the 7th century, Jericho had become an extensive town, but this settlement was destroyed in the Babylonian conquest of Judah in the late 6th century.[41] Persian and Early Hellenistic periods After the destruction of the Judahite city by the Babylonians in the late 6th century,[41] whatever was rebuilt in the Persian period as part of th




Flashcard 7104412912908

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Tell es-Sultan remained unoccupied from the end of the 15th to the 10th–9th centuries BCE, when the city was rebuilt.[41][40][42] Of this new city not much more remains than a four-room house on the eastern slope.[43] By the 7th century, Jericho had become an extensive town, but this settlement was destroyed in the [...] in the late 6th century.[41]
Answer
Babylonian conquest of Judah

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0][42] Of this new city not much more remains than a four-room house on the eastern slope.[43] By the 7th century, Jericho had become an extensive town, but this settlement was destroyed in the <span>Babylonian conquest of Judah in the late 6th century.[41] <span>

Original toplevel document

Jericho - Wikipedia
ence of a small settlement in the Late Bronze Age (c. 1400s BCE) on the site, but erosion and destruction from previous excavations have erased significant parts of this layer.[39][40] Iron Age <span>Tell es-Sultan remained unoccupied from the end of the 15th to the 10th–9th centuries BCE, when the city was rebuilt.[41][40][42] Of this new city not much more remains than a four-room house on the eastern slope.[43] By the 7th century, Jericho had become an extensive town, but this settlement was destroyed in the Babylonian conquest of Judah in the late 6th century.[41] Persian and Early Hellenistic periods After the destruction of the Judahite city by the Babylonians in the late 6th century,[41] whatever was rebuilt in the Persian period as part of th







After the destruction of the Judahite city by the Babylonians in the late 6th century,[41] whatever was rebuilt in the Persian period as part of the Restoration after the Babylonian captivity, left only very few remains.[43] The tell was abandoned as a place of settlement not long after this period.
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y the 7th century, Jericho had become an extensive town, but this settlement was destroyed in the Babylonian conquest of Judah in the late 6th century.[41] Persian and Early Hellenistic periods <span>After the destruction of the Judahite city by the Babylonians in the late 6th century,[41] whatever was rebuilt in the Persian period as part of the Restoration after the Babylonian captivity, left only very few remains.[43] The tell was abandoned as a place of settlement not long after this period.[43] During the Persian through Hellenistic periods, there is little in terms of occupation attested throughout the region.[41] Jericho went from being an administrative centre of Yehud




Jericho went from being an administrative centre of Yehud Medinata ("the Province of Judah") under Persian rule to
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was abandoned as a place of settlement not long after this period.[43] During the Persian through Hellenistic periods, there is little in terms of occupation attested throughout the region.[41] <span>Jericho went from being an administrative centre of Yehud Medinata ("the Province of Judah") under Persian rule to serving as the private estate of Alexander the Great between 336 and 323 BCE after his conquest of the region.[citation needed] In the middle of the 2nd century BCE Jericho was under He




Flashcard 7104419204364

Question
Jericho went from being an administrative centre of [...] under Persian rule to
Answer
Yehud Medinata ("the Province of Judah")

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Jericho went from being an administrative centre of Yehud Medinata ("the Province of Judah") under Persian rule to

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Jericho - Wikipedia
was abandoned as a place of settlement not long after this period.[43] During the Persian through Hellenistic periods, there is little in terms of occupation attested throughout the region.[41] <span>Jericho went from being an administrative centre of Yehud Medinata ("the Province of Judah") under Persian rule to serving as the private estate of Alexander the Great between 336 and 323 BCE after his conquest of the region.[citation needed] In the middle of the 2nd century BCE Jericho was under He







Jericho went from being an administrative centre of Yehud Medinata ("the Province of Judah") under Persian rule to serving as the private estate of Alexander the Great between 336 and 323 BCE after his conquest of the region.
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Jericho - Wikipedia
was abandoned as a place of settlement not long after this period.[43] During the Persian through Hellenistic periods, there is little in terms of occupation attested throughout the region.[41] <span>Jericho went from being an administrative centre of Yehud Medinata ("the Province of Judah") under Persian rule to serving as the private estate of Alexander the Great between 336 and 323 BCE after his conquest of the region.[citation needed] In the middle of the 2nd century BCE Jericho was under Hellenistic rule of the Seleucid Empire, when the Syrian General Bacchides built a number of forts to strengthen




Flashcard 7104422350092

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Jericho went from being an administrative centre of Yehud Medinata ("the Province of Judah") under Persian rule to serving as the private estate of [...] between 336 and 323 BCE after his conquest of the region.

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Jericho went from being an administrative centre of Yehud Medinata ("the Province of Judah") under Persian rule to serving as the private estate of Alexander the Great between 336 and 323 BCE after his conquest of the region.

Original toplevel document

Jericho - Wikipedia
was abandoned as a place of settlement not long after this period.[43] During the Persian through Hellenistic periods, there is little in terms of occupation attested throughout the region.[41] <span>Jericho went from being an administrative centre of Yehud Medinata ("the Province of Judah") under Persian rule to serving as the private estate of Alexander the Great between 336 and 323 BCE after his conquest of the region.[citation needed] In the middle of the 2nd century BCE Jericho was under Hellenistic rule of the Seleucid Empire, when the Syrian General Bacchides built a number of forts to strengthen







In the middle of the 2nd century BCE Jericho was under Hellenistic rule of the Seleucid Empire
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of Yehud Medinata ("the Province of Judah") under Persian rule to serving as the private estate of Alexander the Great between 336 and 323 BCE after his conquest of the region.[citation needed] <span>In the middle of the 2nd century BCE Jericho was under Hellenistic rule of the Seleucid Empire, when the Syrian General Bacchides built a number of forts to strengthen the defences of the area around Jericho against the revolt by the Macabees.[44] One of these forts, built at the




Flashcard 7104425495820

Question
In the middle of the 2nd century BCE Jericho was under Hellenistic rule of the [...]

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In the middle of the 2nd century BCE Jericho was under Hellenistic rule of the Seleucid Empire

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Jericho - Wikipedia
of Yehud Medinata ("the Province of Judah") under Persian rule to serving as the private estate of Alexander the Great between 336 and 323 BCE after his conquest of the region.[citation needed] <span>In the middle of the 2nd century BCE Jericho was under Hellenistic rule of the Seleucid Empire, when the Syrian General Bacchides built a number of forts to strengthen the defences of the area around Jericho against the revolt by the Macabees.[44] One of these forts, built at the







when the Syrian General Bacchides built a number of forts to strengthen the defences of the area around Jericho against the revolt by the Macabees.[44] One of these forts, built at the entrance to Wadi Qelt, was later refortified by Herod the Great, who named it Kypros after his mother.[45]
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of Alexander the Great between 336 and 323 BCE after his conquest of the region.[citation needed] In the middle of the 2nd century BCE Jericho was under Hellenistic rule of the Seleucid Empire, <span>when the Syrian General Bacchides built a number of forts to strengthen the defences of the area around Jericho against the revolt by the Macabees.[44] One of these forts, built at the entrance to Wadi Qelt, was later refortified by Herod the Great, who named it Kypros after his mother.[45] Hasmonean and Herodian periods After the abandonment of the Tell es-Sultan location, the new Jericho of the Late Hellenistic or Hasmonean and Early Roman or Herodian periods was establi




Flashcard 7104428641548

Question
when the Syrian General Bacchides built a number of forts to strengthen the defences of the area around Jericho against the revolt by the [...].[44] One of these forts, built at the entrance to Wadi Qelt, was later refortified by Herod the Great, who named it Kypros after his mother.[45]
Answer

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when the Syrian General Bacchides built a number of forts to strengthen the defences of the area around Jericho against the revolt by the Macabees.[44] One of these forts, built at the entrance to Wadi Qelt, was later refortified by Herod the Great, who named it Kypros after his mother.[45]

Original toplevel document

Jericho - Wikipedia
of Alexander the Great between 336 and 323 BCE after his conquest of the region.[citation needed] In the middle of the 2nd century BCE Jericho was under Hellenistic rule of the Seleucid Empire, <span>when the Syrian General Bacchides built a number of forts to strengthen the defences of the area around Jericho against the revolt by the Macabees.[44] One of these forts, built at the entrance to Wadi Qelt, was later refortified by Herod the Great, who named it Kypros after his mother.[45] Hasmonean and Herodian periods After the abandonment of the Tell es-Sultan location, the new Jericho of the Late Hellenistic or Hasmonean and Early Roman or Herodian periods was establi







After the abandonment of the Tell es-Sultan location, the new Jericho of the Late Hellenistic or Hasmonean and Early Roman or Herodian periods was established as a garden city in the vicinity of the royal estate at Tulul Abu el-'Alayiq and expanded greatly thanks to the intensive exploitation of the springs of the area.
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Jericho - Wikipedia
t by the Macabees.[44] One of these forts, built at the entrance to Wadi Qelt, was later refortified by Herod the Great, who named it Kypros after his mother.[45] Hasmonean and Herodian periods <span>After the abandonment of the Tell es-Sultan location, the new Jericho of the Late Hellenistic or Hasmonean and Early Roman or Herodian periods was established as a garden city in the vicinity of the royal estate at Tulul Abu el-'Alayiq and expanded greatly thanks to the intensive exploitation of the springs of the area.[43] The new site consists of a group of low mounds on both banks of Wadi Qelt.[41] The Hasmoneans were a dynasty descending from a priestly group (kohanim) from the tribe of Levi, who r




Flashcard 7104431787276

Question
After the abandonment of the Tell es-Sultan location, the new Jericho of the Late Hellenistic or Hasmonean and Early Roman or Herodian periods was established as a [...] city in the vicinity of the royal estate at Tulul Abu el-'Alayiq and expanded greatly thanks to the intensive exploitation of the springs of the area.
Answer
garden

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After the abandonment of the Tell es-Sultan location, the new Jericho of the Late Hellenistic or Hasmonean and Early Roman or Herodian periods was established as a garden city in the vicinity of the royal estate at Tulul Abu el-'Alayiq and expanded greatly thanks to the intensive exploitation of the springs of the area.

Original toplevel document

Jericho - Wikipedia
t by the Macabees.[44] One of these forts, built at the entrance to Wadi Qelt, was later refortified by Herod the Great, who named it Kypros after his mother.[45] Hasmonean and Herodian periods <span>After the abandonment of the Tell es-Sultan location, the new Jericho of the Late Hellenistic or Hasmonean and Early Roman or Herodian periods was established as a garden city in the vicinity of the royal estate at Tulul Abu el-'Alayiq and expanded greatly thanks to the intensive exploitation of the springs of the area.[43] The new site consists of a group of low mounds on both banks of Wadi Qelt.[41] The Hasmoneans were a dynasty descending from a priestly group (kohanim) from the tribe of Levi, who r







The Hasmoneans were a dynasty descending from a priestly group (kohanim) from the tribe of Levi,
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at Tulul Abu el-'Alayiq and expanded greatly thanks to the intensive exploitation of the springs of the area.[43] The new site consists of a group of low mounds on both banks of Wadi Qelt.[41] <span>The Hasmoneans were a dynasty descending from a priestly group (kohanim) from the tribe of Levi, who ruled over Judea following the success of the Maccabean Revolt until Roman influence over the region brought Herod to claim the Hasmonean throne.[46] The rock-cut tombs of a Herodia




Flashcard 7104434933004

Question
The [...] were a dynasty descending from a priestly group (kohanim) from the tribe of Levi,
Answer
Hasmoneans

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The Hasmoneans were a dynasty descending from a priestly group (kohanim) from the tribe of Levi,

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Jericho - Wikipedia
at Tulul Abu el-'Alayiq and expanded greatly thanks to the intensive exploitation of the springs of the area.[43] The new site consists of a group of low mounds on both banks of Wadi Qelt.[41] <span>The Hasmoneans were a dynasty descending from a priestly group (kohanim) from the tribe of Levi, who ruled over Judea following the success of the Maccabean Revolt until Roman influence over the region brought Herod to claim the Hasmonean throne.[46] The rock-cut tombs of a Herodia







The Hasmoneans were a dynasty descending from a priestly group ( kohanim ) from the tribe of Levi , who ruled over Judea following the success of the Maccabean Revolt until Roman influence over the region brought Herod to claim the Hasmonean throne.
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at Tulul Abu el-'Alayiq and expanded greatly thanks to the intensive exploitation of the springs of the area.[43] The new site consists of a group of low mounds on both banks of Wadi Qelt.[41] <span>The Hasmoneans were a dynasty descending from a priestly group (kohanim) from the tribe of Levi, who ruled over Judea following the success of the Maccabean Revolt until Roman influence over the region brought Herod to claim the Hasmonean throne.[46] The rock-cut tombs of a Herodian- and Hasmonean-era cemetery lie in the lowest part of the cliffs between Nuseib al-Aweishireh and Mount of Temptation. They date between 100 BCE and




Flashcard 7104438078732

Question
The Hasmoneans were a dynasty descending from a priestly group ( kohanim ) from the [...] , who ruled over Judea following the success of the Maccabean Revolt until Roman influence over the region brought Herod to claim the Hasmonean throne.

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The Hasmoneans were a dynasty descending from a priestly group ( kohanim ) from the tribe of Levi , who ruled over Judea following the success of the Maccabean Revolt until Roman influence over the region brought Herod to claim the Hasmonean throne.

Original toplevel document

Jericho - Wikipedia
at Tulul Abu el-'Alayiq and expanded greatly thanks to the intensive exploitation of the springs of the area.[43] The new site consists of a group of low mounds on both banks of Wadi Qelt.[41] <span>The Hasmoneans were a dynasty descending from a priestly group (kohanim) from the tribe of Levi, who ruled over Judea following the success of the Maccabean Revolt until Roman influence over the region brought Herod to claim the Hasmonean throne.[46] The rock-cut tombs of a Herodian- and Hasmonean-era cemetery lie in the lowest part of the cliffs between Nuseib al-Aweishireh and Mount of Temptation. They date between 100 BCE and







Flashcard 7104439651596

Question
The Hasmoneans were a dynasty descending from a priestly group ( kohanim ) from the tribe of Levi , who ruled over Judea following the success of the [...] until Roman influence over the region brought Herod to claim the Hasmonean throne.
Answer
Maccabean Revolt

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The Hasmoneans were a dynasty descending from a priestly group ( kohanim ) from the tribe of Levi , who ruled over Judea following the success of the Maccabean Revolt until Roman influence over the region brought Herod to claim the Hasmonean throne.

Original toplevel document

Jericho - Wikipedia
at Tulul Abu el-'Alayiq and expanded greatly thanks to the intensive exploitation of the springs of the area.[43] The new site consists of a group of low mounds on both banks of Wadi Qelt.[41] <span>The Hasmoneans were a dynasty descending from a priestly group (kohanim) from the tribe of Levi, who ruled over Judea following the success of the Maccabean Revolt until Roman influence over the region brought Herod to claim the Hasmonean throne.[46] The rock-cut tombs of a Herodian- and Hasmonean-era cemetery lie in the lowest part of the cliffs between Nuseib al-Aweishireh and Mount of Temptation. They date between 100 BCE and







Herod had to lease back the royal estate at Jericho from Cleopatra, after Mark Antony had given it to her as a gift.
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nean-era cemetery lie in the lowest part of the cliffs between Nuseib al-Aweishireh and Mount of Temptation. They date between 100 BCE and 68 CE.[45] Herodian period Remains from Herod's palace <span>Herod had to lease back the royal estate at Jericho from Cleopatra, after Mark Antony had given it to her as a gift. After their joint suicide in 30 BCE, Octavian assumed control of the Roman Empire and granted Herod absolute rule over Jericho, as part of the new Herodian domain. Herod's rule oversaw




Flashcard 7104442797324

Question
Herod had to lease back the royal estate at Jericho from [...], after Mark Antony had given it to her as a gift.
Answer

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Herod had to lease back the royal estate at Jericho from Cleopatra, after Mark Antony had given it to her as a gift.

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Jericho - Wikipedia
nean-era cemetery lie in the lowest part of the cliffs between Nuseib al-Aweishireh and Mount of Temptation. They date between 100 BCE and 68 CE.[45] Herodian period Remains from Herod's palace <span>Herod had to lease back the royal estate at Jericho from Cleopatra, after Mark Antony had given it to her as a gift. After their joint suicide in 30 BCE, Octavian assumed control of the Roman Empire and granted Herod absolute rule over Jericho, as part of the new Herodian domain. Herod's rule oversaw







After their joint suicide in 30 BCE, Octavian assumed control of the Roman Empire and granted Herod absolute rule over Jericho, as part of the new Herodian domain.
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e between 100 BCE and 68 CE.[45] Herodian period Remains from Herod's palace Herod had to lease back the royal estate at Jericho from Cleopatra, after Mark Antony had given it to her as a gift. <span>After their joint suicide in 30 BCE, Octavian assumed control of the Roman Empire and granted Herod absolute rule over Jericho, as part of the new Herodian domain. Herod's rule oversaw the construction of a hippodrome-theatre (Tell es-Samrat) to entertain his guests and new aqueducts to irrigate the area below the cliffs and reach his winter palac




Flashcard 7104445943052

Question
After their joint suicide in [...] BCE, Octavian assumed control of the Roman Empire and granted Herod absolute rule over Jericho, as part of the new Herodian domain.
Answer
30

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After their joint suicide in 30 BCE, Octavian assumed control of the Roman Empire and granted Herod absolute rule over Jericho, as part of the new Herodian domain.

Original toplevel document

Jericho - Wikipedia
e between 100 BCE and 68 CE.[45] Herodian period Remains from Herod's palace Herod had to lease back the royal estate at Jericho from Cleopatra, after Mark Antony had given it to her as a gift. <span>After their joint suicide in 30 BCE, Octavian assumed control of the Roman Empire and granted Herod absolute rule over Jericho, as part of the new Herodian domain. Herod's rule oversaw the construction of a hippodrome-theatre (Tell es-Samrat) to entertain his guests and new aqueducts to irrigate the area below the cliffs and reach his winter palac







Herod was succeeded in Judea by his son, Herod Archelaus, who built a village in his name not far to the north, Archelaïs (modern Khirbet al-Beiyudat), to house workers for his date plantation.
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mother-in-law. After the construction of the palaces, the city had functioned not only as an agricultural center and as a crossroad, but also as a winter resort for Jerusalem's aristocracy.[48] <span>Herod was succeeded in Judea by his son, Herod Archelaus, who built a village in his name not far to the north, Archelaïs (modern Khirbet al-Beiyudat), to house workers for his date plantation.[citation needed] First-century Jericho is described in Strabo's Geography as follows: Jericho is a plain surrounded by a kind of mountainous country, which in a way, slopes toward it li




After the fall of Jerusalem to Vespasian's armies in the Great Revolt of Judea in 70 CE
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Jericho - Wikipedia
e descendant of Rahab did not disdain the hospitality of Zaccaeus the publican. Finally, between Jerusalem and Jericho was laid the scene of his story of the good Samaritan."[51] Roman province <span>After the fall of Jerusalem to Vespasian's armies in the Great Revolt of Judea in 70 CE, Jericho declined rapidly, and by 100 CE it was but a small Roman garrison town.[52] A fort was built there in 130 and played a role in putting down the Bar Kochba revolt in 133.[citati




Flashcard 7104452234508

Question
After the fall of Jerusalem to [...] in 70 CE
Answer
Vespasian's armies in the Great Revolt of Judea

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After the fall of Jerusalem to Vespasian's armies in the Great Revolt of Judea in 70 CE

Original toplevel document

Jericho - Wikipedia
e descendant of Rahab did not disdain the hospitality of Zaccaeus the publican. Finally, between Jerusalem and Jericho was laid the scene of his story of the good Samaritan."[51] Roman province <span>After the fall of Jerusalem to Vespasian's armies in the Great Revolt of Judea in 70 CE, Jericho declined rapidly, and by 100 CE it was but a small Roman garrison town.[52] A fort was built there in 130 and played a role in putting down the Bar Kochba revolt in 133.[citati







Flashcard 7104453807372

Question
After the fall of Jerusalem to Vespasian's armies in the Great Revolt of Judea in [...]
Answer
70 CE

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After the fall of Jerusalem to Vespasian's armies in the Great Revolt of Judea in 70 CE

Original toplevel document

Jericho - Wikipedia
e descendant of Rahab did not disdain the hospitality of Zaccaeus the publican. Finally, between Jerusalem and Jericho was laid the scene of his story of the good Samaritan."[51] Roman province <span>After the fall of Jerusalem to Vespasian's armies in the Great Revolt of Judea in 70 CE, Jericho declined rapidly, and by 100 CE it was but a small Roman garrison town.[52] A fort was built there in 130 and played a role in putting down the Bar Kochba revolt in 133.[citati







Jericho declined rapidly, and by 100 CE it was but a small Roman garrison town.
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between Jerusalem and Jericho was laid the scene of his story of the good Samaritan."[51] Roman province After the fall of Jerusalem to Vespasian's armies in the Great Revolt of Judea in 70 CE, <span>Jericho declined rapidly, and by 100 CE it was but a small Roman garrison town.[52] A fort was built there in 130 and played a role in putting down the Bar Kochba revolt in 133.[citation needed] Byzantine period Copy of Mosaic of the Shalom Al Yisrael Synagogue, 6t




Flashcard 7104456953100

Question
Jericho declined rapidly, and by [...] it was but a small Roman garrison town.
Answer
100 CE

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Jericho declined rapidly, and by 100 CE it was but a small Roman garrison town.

Original toplevel document

Jericho - Wikipedia
between Jerusalem and Jericho was laid the scene of his story of the good Samaritan."[51] Roman province After the fall of Jerusalem to Vespasian's armies in the Great Revolt of Judea in 70 CE, <span>Jericho declined rapidly, and by 100 CE it was but a small Roman garrison town.[52] A fort was built there in 130 and played a role in putting down the Bar Kochba revolt in 133.[citation needed] Byzantine period Copy of Mosaic of the Shalom Al Yisrael Synagogue, 6t







A fort was built there in 130 and played a role in putting down the Bar Kochba revolt in 133.
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"[51] Roman province After the fall of Jerusalem to Vespasian's armies in the Great Revolt of Judea in 70 CE, Jericho declined rapidly, and by 100 CE it was but a small Roman garrison town.[52] <span>A fort was built there in 130 and played a role in putting down the Bar Kochba revolt in 133.[citation needed] Byzantine period Copy of Mosaic of the Shalom Al Yisrael Synagogue, 6th–7th century CE Accounts of Jericho by a Christian pilgrim are given in 333. Shortly thereafter t




Flashcard 7104460098828

Question
A fort was built there in 130 and played a role in putting down the [...] in 133.

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A fort was built there in 130 and played a role in putting down the Bar Kochba revolt in 133.

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Jericho - Wikipedia
"[51] Roman province After the fall of Jerusalem to Vespasian's armies in the Great Revolt of Judea in 70 CE, Jericho declined rapidly, and by 100 CE it was but a small Roman garrison town.[52] <span>A fort was built there in 130 and played a role in putting down the Bar Kochba revolt in 133.[citation needed] Byzantine period Copy of Mosaic of the Shalom Al Yisrael Synagogue, 6th–7th century CE Accounts of Jericho by a Christian pilgrim are given in 333. Shortly thereafter t







Accounts of Jericho by a Christian pilgrim are given in 333. Shortly thereafter the built-up area of the town was abandoned and a Byzantine Jericho, Ericha, was built 1600 metres (1 mi) to the east, on which the modern town is centered.[52] Christianity took hold in the city during the Byzantine era and the area was heavily populated. A number of monasteries and churches were built, including St George of Koziba in 340 CE and a domed church dedicated to Saint Eliseus.[48] At least two synagogues were also built in the 6th century CE.[45] The monasteries were abandoned after the Persian invasion of 614.
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rt was built there in 130 and played a role in putting down the Bar Kochba revolt in 133.[citation needed] Byzantine period Copy of Mosaic of the Shalom Al Yisrael Synagogue, 6th–7th century CE <span>Accounts of Jericho by a Christian pilgrim are given in 333. Shortly thereafter the built-up area of the town was abandoned and a Byzantine Jericho, Ericha, was built 1600 metres (1 mi) to the east, on which the modern town is centered.[52] Christianity took hold in the city during the Byzantine era and the area was heavily populated. A number of monasteries and churches were built, including St George of Koziba in 340 CE and a domed church dedicated to Saint Eliseus.[48] At least two synagogues were also built in the 6th century CE.[45] The monasteries were abandoned after the Persian invasion of 614.[18] The Jericho synagogue in the Royal Maccabean winter palace at Jericho dates from 70 to 50 BCE. A synagogue dating to the late 6th or early 7th century CE was discovered in Jericho i




Flashcard 7104463244556

Question
Accounts of Jericho by a Christian pilgrim are given in 333. Shortly thereafter the built-up area of the town was abandoned and a Byzantine Jericho, Ericha, was built 1600 metres (1 mi) to the east, on which the modern town is centered.[52] Christianity took hold in the city during the Byzantine era and the area was heavily populated. A number of monasteries and churches were built, including St George of Koziba in 340 CE and a domed church dedicated to Saint Eliseus.[48] At least two synagogues were also built in the 6th century CE.[45] The monasteries were abandoned after the [...]

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ding St George of Koziba in 340 CE and a domed church dedicated to Saint Eliseus.[48] At least two synagogues were also built in the 6th century CE.[45] The monasteries were abandoned after the <span>Persian invasion of 614. <span>

Original toplevel document

Jericho - Wikipedia
rt was built there in 130 and played a role in putting down the Bar Kochba revolt in 133.[citation needed] Byzantine period Copy of Mosaic of the Shalom Al Yisrael Synagogue, 6th–7th century CE <span>Accounts of Jericho by a Christian pilgrim are given in 333. Shortly thereafter the built-up area of the town was abandoned and a Byzantine Jericho, Ericha, was built 1600 metres (1 mi) to the east, on which the modern town is centered.[52] Christianity took hold in the city during the Byzantine era and the area was heavily populated. A number of monasteries and churches were built, including St George of Koziba in 340 CE and a domed church dedicated to Saint Eliseus.[48] At least two synagogues were also built in the 6th century CE.[45] The monasteries were abandoned after the Persian invasion of 614.[18] The Jericho synagogue in the Royal Maccabean winter palace at Jericho dates from 70 to 50 BCE. A synagogue dating to the late 6th or early 7th century CE was discovered in Jericho i







Accounts of Jericho by a Christian pilgrim are given in 333. Shortly thereafter the built-up area of the town was abandoned and a Byzantine Jericho, Ericha, was built 1600 metres (1 mi) to the east, on which the modern town is centered.[52] Christianity took hold in the city during the Byzantine era and the area was heavily populated. A number of monasteries and churches were built, including St George of Koziba in 340 CE and a domed church dedicated to Saint Eliseus.[48] At least two synagogues were also built in the 6th century CE.[45] The monasteries were abandoned after the Persian invasion of 614.
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Jericho - Wikipedia
rt was built there in 130 and played a role in putting down the Bar Kochba revolt in 133.[citation needed] Byzantine period Copy of Mosaic of the Shalom Al Yisrael Synagogue, 6th–7th century CE <span>Accounts of Jericho by a Christian pilgrim are given in 333. Shortly thereafter the built-up area of the town was abandoned and a Byzantine Jericho, Ericha, was built 1600 metres (1 mi) to the east, on which the modern town is centered.[52] Christianity took hold in the city during the Byzantine era and the area was heavily populated. A number of monasteries and churches were built, including St George of Koziba in 340 CE and a domed church dedicated to Saint Eliseus.[48] At least two synagogues were also built in the 6th century CE.[45] The monasteries were abandoned after the Persian invasion of 614.[18] The Jericho synagogue in the Royal Maccabean winter palace at Jericho dates from 70 to 50 BCE. A synagogue dating to the late 6th or early 7th century CE was discovered in Jericho i




Flashcard 7104466390284

Question
Accounts of Jericho by a Christian pilgrim are given in 333. Shortly thereafter the built-up area of the town was abandoned and a Byzantine Jericho, Ericha, was built 1600 metres (1 mi) to the east, on which the modern town is centered.[52] Christianity took hold in the city during the Byzantine era and the area was heavily populated. A number of monasteries and churches were built, including St George of Koziba in 340 CE and a domed church dedicated to Saint Eliseus.[48] At least two synagogues were also built in the 6th century CE.[45] The monasteries were abandoned after the [...]

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ding St George of Koziba in 340 CE and a domed church dedicated to Saint Eliseus.[48] At least two synagogues were also built in the 6th century CE.[45] The monasteries were abandoned after the <span>Persian invasion of 614. <span>

Original toplevel document

Jericho - Wikipedia
rt was built there in 130 and played a role in putting down the Bar Kochba revolt in 133.[citation needed] Byzantine period Copy of Mosaic of the Shalom Al Yisrael Synagogue, 6th–7th century CE <span>Accounts of Jericho by a Christian pilgrim are given in 333. Shortly thereafter the built-up area of the town was abandoned and a Byzantine Jericho, Ericha, was built 1600 metres (1 mi) to the east, on which the modern town is centered.[52] Christianity took hold in the city during the Byzantine era and the area was heavily populated. A number of monasteries and churches were built, including St George of Koziba in 340 CE and a domed church dedicated to Saint Eliseus.[48] At least two synagogues were also built in the 6th century CE.[45] The monasteries were abandoned after the Persian invasion of 614.[18] The Jericho synagogue in the Royal Maccabean winter palace at Jericho dates from 70 to 50 BCE. A synagogue dating to the late 6th or early 7th century CE was discovered in Jericho i







Jericho, by then named "Ariha" in Arabic variation, became part of Jund Filastin ("Military District of Palestine"), part of the larger province of Bilad al-Sham. The Arab Muslim historian Musa b. 'Uqba (died 758) recorded that caliph Umar ibn al-Khattab exiled the Jews and Christians of Khaybar to Jericho (and Tayma).
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icho in 1918. While less is known of it than Shalom Al Yisrael, it has a larger mosaic and is in similar condition.[54] Early Muslim period Arabic Umayyad mosaic from Hisham's Palace in Jericho <span>Jericho, by then named "Ariha" in Arabic variation, became part of Jund Filastin ("Military District of Palestine"), part of the larger province of Bilad al-Sham. The Arab Muslim historian Musa b. 'Uqba (died 758) recorded that caliph Umar ibn al-Khattab exiled the Jews and Christians of Khaybar to Jericho (and Tayma).[55] By 659, that district had come under the control of Mu'awiya, founder of the Umayyad dynasty. That year, an earthquake destroyed Jericho.[56] A decade later, the pilgrim Arculf visi




Flashcard 7104469536012

Question
Jericho, by then named "Ariha" in Arabic variation, became part of [...] ("Military District of Palestine"), part of the larger province of Bilad al-Sham. The Arab Muslim historian Musa b. 'Uqba (died 758) recorded that caliph Umar ibn al-Khattab exiled the Jews and Christians of Khaybar to Jericho (and Tayma).
Answer

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Jericho, by then named "Ariha" in Arabic variation, became part of Jund Filastin ("Military District of Palestine"), part of the larger province of Bilad al-Sham. The Arab Muslim historian Musa b. 'Uqba (died 758) recorded that caliph Umar ibn al-Khattab exiled the

Original toplevel document

Jericho - Wikipedia
icho in 1918. While less is known of it than Shalom Al Yisrael, it has a larger mosaic and is in similar condition.[54] Early Muslim period Arabic Umayyad mosaic from Hisham's Palace in Jericho <span>Jericho, by then named "Ariha" in Arabic variation, became part of Jund Filastin ("Military District of Palestine"), part of the larger province of Bilad al-Sham. The Arab Muslim historian Musa b. 'Uqba (died 758) recorded that caliph Umar ibn al-Khattab exiled the Jews and Christians of Khaybar to Jericho (and Tayma).[55] By 659, that district had come under the control of Mu'awiya, founder of the Umayyad dynasty. That year, an earthquake destroyed Jericho.[56] A decade later, the pilgrim Arculf visi







Flashcard 7104471108876

Question
Jericho, by then named "Ariha" in Arabic variation, became part of Jund Filastin ("Military District of Palestine"), part of the larger province of [...]. The Arab Muslim historian Musa b. 'Uqba (died 758) recorded that caliph Umar ibn al-Khattab exiled the Jews and Christians of Khaybar to Jericho (and Tayma).
Answer
Bilad al-Sham

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Jericho, by then named "Ariha" in Arabic variation, became part of Jund Filastin ("Military District of Palestine"), part of the larger province of Bilad al-Sham. The Arab Muslim historian Musa b. 'Uqba (died 758) recorded that caliph Umar ibn al-Khattab exiled the Jews and Christians of Khaybar to Jericho (and Tayma).

Original toplevel document

Jericho - Wikipedia
icho in 1918. While less is known of it than Shalom Al Yisrael, it has a larger mosaic and is in similar condition.[54] Early Muslim period Arabic Umayyad mosaic from Hisham's Palace in Jericho <span>Jericho, by then named "Ariha" in Arabic variation, became part of Jund Filastin ("Military District of Palestine"), part of the larger province of Bilad al-Sham. The Arab Muslim historian Musa b. 'Uqba (died 758) recorded that caliph Umar ibn al-Khattab exiled the Jews and Christians of Khaybar to Jericho (and Tayma).[55] By 659, that district had come under the control of Mu'awiya, founder of the Umayyad dynasty. That year, an earthquake destroyed Jericho.[56] A decade later, the pilgrim Arculf visi







Muhammad ibn Abdullah[n 1] (Arabic: مُحَمَّد ٱبن عَبْد ٱللَّٰه , romanized: Muḥammad ibn ʿAbd Allāh , Classical Arabic pronunciation: [muˈħammad] ; c. 570 – 8 June 632 CE)[
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of Muhammad Hadith of the pen and paper Ahl al-Bayt show Praise Salawat Naat Mawlid show Related Al-Masjid an-Nabawi Possessions Relics Seal History of Islam Islam portal Biography portal v t e <span>Muhammad ibn Abdullah[n 1] (Arabic: مُحَمَّد ٱبن عَبْد ٱللَّٰه, romanized: Muḥammad ibn ʿAbd Allāh, Classical Arabic pronunciation: [muˈħammad]; c. 570 – 8 June 632 CE)[1][2] was an Arab religious, social, and political leader and the founder of the world religion of Islam.[3] According to Islamic doctrine, he was a prophet divinely inspired to preach a




Flashcard 7104476089612

Question
Muhammad ibn Abdullah[n 1] (Arabic: مُحَمَّد ٱبن عَبْد ٱللَّٰه , romanized: Muḥammad ibn ʿAbd Allāh , Classical Arabic pronunciation: [muˈħammad] ; c. [...] CE)[
Answer
570 – 8 June 632

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Muhammad ibn Abdullah[n 1] (Arabic: مُحَمَّد ٱبن عَبْد ٱللَّٰه , romanized: Muḥammad ibn ʿAbd Allāh , Classical Arabic pronunciation: [muˈħammad] ; c. 570 – 8 June 632 CE)[

Original toplevel document

Muhammad - Wikipedia
of Muhammad Hadith of the pen and paper Ahl al-Bayt show Praise Salawat Naat Mawlid show Related Al-Masjid an-Nabawi Possessions Relics Seal History of Islam Islam portal Biography portal v t e <span>Muhammad ibn Abdullah[n 1] (Arabic: مُحَمَّد ٱبن عَبْد ٱللَّٰه, romanized: Muḥammad ibn ʿAbd Allāh, Classical Arabic pronunciation: [muˈħammad]; c. 570 – 8 June 632 CE)[1][2] was an Arab religious, social, and political leader and the founder of the world religion of Islam.[3] According to Islamic doctrine, he was a prophet divinely inspired to preach a







By 659, that district had come under the control of Mu'awiya, founder of the Umayyad dynasty.
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rger province of Bilad al-Sham. The Arab Muslim historian Musa b. 'Uqba (died 758) recorded that caliph Umar ibn al-Khattab exiled the Jews and Christians of Khaybar to Jericho (and Tayma).[55] <span>By 659, that district had come under the control of Mu'awiya, founder of the Umayyad dynasty. That year, an earthquake destroyed Jericho.[56] A decade later, the pilgrim Arculf visited Jericho and found it in ruins, all its "miserable Canaanite" inhabitants now dispersed in shan




Flashcard 7104479235340

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By 659, that district had come under the control of Mu'awiya, founder of the [...]
Answer

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By 659, that district had come under the control of Mu'awiya, founder of the Umayyad dynasty.

Original toplevel document

Jericho - Wikipedia
rger province of Bilad al-Sham. The Arab Muslim historian Musa b. 'Uqba (died 758) recorded that caliph Umar ibn al-Khattab exiled the Jews and Christians of Khaybar to Jericho (and Tayma).[55] <span>By 659, that district had come under the control of Mu'awiya, founder of the Umayyad dynasty. That year, an earthquake destroyed Jericho.[56] A decade later, the pilgrim Arculf visited Jericho and found it in ruins, all its "miserable Canaanite" inhabitants now dispersed in shan







By 659, that district had come under the control of Mu'awiya , founder of the Umayyad dynasty . That year, an earthquake destroyed Jericho. [56] A decade later, the pilgrim Arculf visited Jericho and found it in ruins, all its "miserable Canaanite" inhabitants now dispersed in shanty towns around the Dead Sea shore.[57]
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rger province of Bilad al-Sham. The Arab Muslim historian Musa b. 'Uqba (died 758) recorded that caliph Umar ibn al-Khattab exiled the Jews and Christians of Khaybar to Jericho (and Tayma).[55] <span>By 659, that district had come under the control of Mu'awiya, founder of the Umayyad dynasty. That year, an earthquake destroyed Jericho.[56] A decade later, the pilgrim Arculf visited Jericho and found it in ruins, all its "miserable Canaanite" inhabitants now dispersed in shanty towns around the Dead Sea shore.[57] A palatial complex long attributed to the tenth Umayyad caliph, Hisham ibn Abd al-Malik (r. 724–743) and thus known as Hisham's Palace, is located at Khirbet al-Mafjar, about 1.5 kilome




Flashcard 7104482381068

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By 659, that district had come under the control of Mu'awiya , founder of the Umayyad dynasty . That year, an [...] destroyed Jericho. [56] A decade later, the pilgrim Arculf visited Jericho and found it in ruins, all its "miserable Canaanite" inhabitants now dispersed in shanty towns around the Dead Sea shore.[57]
Answer
earthquake

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By 659, that district had come under the control of Mu'awiya , founder of the Umayyad dynasty . That year, an earthquake destroyed Jericho. [56] A decade later, the pilgrim Arculf visited Jericho and found it in ruins, all its "miserable Canaanite" inhabitants now dispersed in shanty towns around the Dead

Original toplevel document

Jericho - Wikipedia
rger province of Bilad al-Sham. The Arab Muslim historian Musa b. 'Uqba (died 758) recorded that caliph Umar ibn al-Khattab exiled the Jews and Christians of Khaybar to Jericho (and Tayma).[55] <span>By 659, that district had come under the control of Mu'awiya, founder of the Umayyad dynasty. That year, an earthquake destroyed Jericho.[56] A decade later, the pilgrim Arculf visited Jericho and found it in ruins, all its "miserable Canaanite" inhabitants now dispersed in shanty towns around the Dead Sea shore.[57] A palatial complex long attributed to the tenth Umayyad caliph, Hisham ibn Abd al-Malik (r. 724–743) and thus known as Hisham's Palace, is located at Khirbet al-Mafjar, about 1.5 kilome







Umayyad rule ended in 750 and was followed by the Arab caliphates of the Abbasid and Fatimid dynasties.
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.[58] The remains of two mosques, a courtyard, mosaics, and other items can still be seen in situ today. The unfinished structure was largely destroyed in an earthquake in 747.[citation needed] <span>Umayyad rule ended in 750 and was followed by the Arab caliphates of the Abbasid and Fatimid dynasties. Irrigated agriculture was developed under Islamic rule, reaffirming Jericho's reputation as a fertile "City of the Palms".[59] Al-Maqdisi, the Arab geographer, wrote in 985 that "the wa




Flashcard 7104485526796

Question
Umayyad rule ended in [...] and was followed by the Arab caliphates of the Abbasid and Fatimid dynasties.
Answer
750

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Umayyad rule ended in 750 and was followed by the Arab caliphates of the Abbasid and Fatimid dynasties.

Original toplevel document

Jericho - Wikipedia
.[58] The remains of two mosques, a courtyard, mosaics, and other items can still be seen in situ today. The unfinished structure was largely destroyed in an earthquake in 747.[citation needed] <span>Umayyad rule ended in 750 and was followed by the Arab caliphates of the Abbasid and Fatimid dynasties. Irrigated agriculture was developed under Islamic rule, reaffirming Jericho's reputation as a fertile "City of the Palms".[59] Al-Maqdisi, the Arab geographer, wrote in 985 that "the wa







Umayyad rule ended in 750 and was followed by the Arab caliphates of the Abbasid and Fatimid dynasties.
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.[58] The remains of two mosques, a courtyard, mosaics, and other items can still be seen in situ today. The unfinished structure was largely destroyed in an earthquake in 747.[citation needed] <span>Umayyad rule ended in 750 and was followed by the Arab caliphates of the Abbasid and Fatimid dynasties. Irrigated agriculture was developed under Islamic rule, reaffirming Jericho's reputation as a fertile "City of the Palms".[59] Al-Maqdisi, the Arab geographer, wrote in 985 that "the wa




Flashcard 7104488672524

Question
Umayyad rule ended in 750 and was followed by the [...]
Answer
Arab caliphates of the Abbasid and Fatimid dynasties.

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Umayyad rule ended in 750 and was followed by the Arab caliphates of the Abbasid and Fatimid dynasties.

Original toplevel document

Jericho - Wikipedia
.[58] The remains of two mosques, a courtyard, mosaics, and other items can still be seen in situ today. The unfinished structure was largely destroyed in an earthquake in 747.[citation needed] <span>Umayyad rule ended in 750 and was followed by the Arab caliphates of the Abbasid and Fatimid dynasties. Irrigated agriculture was developed under Islamic rule, reaffirming Jericho's reputation as a fertile "City of the Palms".[59] Al-Maqdisi, the Arab geographer, wrote in 985 that "the wa







Umayyad rule ended in 750 and was followed by the Arab caliphates of the Abbasid and Fatimid dynasties. Irrigated agriculture was developed under Islamic rule, reaffirming Jericho's reputation as a fertile "City of the Palms". [59] Al-Maqdisi, the Arab geographer, wrote in 985 that "the water of Jericho is held to be the highest and best in all Islam. Bananas are plentiful, also dates and flowers of fragrant odor".[60] Jericho is also referred to by him as one of the principal cities of Jund Filastin.[61]

The city flourished until 1071 with the invasion of the Seljuk Turks, followed by the upheavals of the Crusades.

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.[58] The remains of two mosques, a courtyard, mosaics, and other items can still be seen in situ today. The unfinished structure was largely destroyed in an earthquake in 747.[citation needed] <span>Umayyad rule ended in 750 and was followed by the Arab caliphates of the Abbasid and Fatimid dynasties. Irrigated agriculture was developed under Islamic rule, reaffirming Jericho's reputation as a fertile "City of the Palms".[59] Al-Maqdisi, the Arab geographer, wrote in 985 that "the water of Jericho is held to be the highest and best in all Islam. Bananas are plentiful, also dates and flowers of fragrant odor".[60] Jericho is also referred to by him as one of the principal cities of Jund Filastin.[61] The city flourished until 1071 with the invasion of the Seljuk Turks, followed by the upheavals of the Crusades.[citation needed] Crusader period In 1179, the Crusaders rebuilt the Monastery of St. George of Koziba, at its original site 10 kilometres (6 mi) from the center of town. They also built




Flashcard 7104491818252

Question

Umayyad rule ended in 750 and was followed by the Arab caliphates of the Abbasid and Fatimid dynasties. Irrigated agriculture was developed under Islamic rule, reaffirming Jericho's reputation as a fertile "City of the Palms". [59] Al-Maqdisi, the Arab geographer, wrote in 985 that "the water of Jericho is held to be the highest and best in all Islam. Bananas are plentiful, also dates and flowers of fragrant odor".[60] Jericho is also referred to by him as one of the principal cities of Jund Filastin.[61]

The city flourished until 1071 with the invasion of the [...], followed by the upheavals of the Crusades.

Answer
Seljuk Turks

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ul, also dates and flowers of fragrant odor".[60] Jericho is also referred to by him as one of the principal cities of Jund Filastin.[61] The city flourished until 1071 with the invasion of the <span>Seljuk Turks, followed by the upheavals of the Crusades. <span>

Original toplevel document

Jericho - Wikipedia
.[58] The remains of two mosques, a courtyard, mosaics, and other items can still be seen in situ today. The unfinished structure was largely destroyed in an earthquake in 747.[citation needed] <span>Umayyad rule ended in 750 and was followed by the Arab caliphates of the Abbasid and Fatimid dynasties. Irrigated agriculture was developed under Islamic rule, reaffirming Jericho's reputation as a fertile "City of the Palms".[59] Al-Maqdisi, the Arab geographer, wrote in 985 that "the water of Jericho is held to be the highest and best in all Islam. Bananas are plentiful, also dates and flowers of fragrant odor".[60] Jericho is also referred to by him as one of the principal cities of Jund Filastin.[61] The city flourished until 1071 with the invasion of the Seljuk Turks, followed by the upheavals of the Crusades.[citation needed] Crusader period In 1179, the Crusaders rebuilt the Monastery of St. George of Koziba, at its original site 10 kilometres (6 mi) from the center of town. They also built







The Crusades were a series of religious wars initiated, supported, and sometimes directed by the Latin Church in the medieval period. The best known of these Crusades are those to the Holy Land in the period between 1095 and 1291 that were intended to recover Jerusalem and its surrounding area from Islamic rule.
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ndish Swedish 1150 1249 1293 Livonian Prussian Lithuanian Crusades against Christians Albigensian Drenther Stedinger Bosnian Bohemian Despenser's Hussite Popular crusades Reconquista (718–1492) <span>The Crusades were a series of religious wars initiated, supported, and sometimes directed by the Latin Church in the medieval period. The best known of these Crusades are those to the Holy Land in the period between 1095 and 1291 that were intended to recover Jerusalem and its surrounding area from Islamic rule. Concurrent military activities in the Iberian Peninsula against the Moors (the Reconquista) and in northern Europe against pagan West Slavic, Baltic, and Finnic peoples (the Northern Cr




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The Crusades were a series of religious wars initiated, supported, and sometimes directed by the Latin Church in the medieval period. The best known of these Crusades are those to the Holy Land in the period between [...] that were intended to recover Jerusalem and its surrounding area from Islamic rule.
Answer
1095 and 1291

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ries of religious wars initiated, supported, and sometimes directed by the Latin Church in the medieval period. The best known of these Crusades are those to the Holy Land in the period between <span>1095 and 1291 that were intended to recover Jerusalem and its surrounding area from Islamic rule. <span>

Original toplevel document

Crusades - Wikipedia
ndish Swedish 1150 1249 1293 Livonian Prussian Lithuanian Crusades against Christians Albigensian Drenther Stedinger Bosnian Bohemian Despenser's Hussite Popular crusades Reconquista (718–1492) <span>The Crusades were a series of religious wars initiated, supported, and sometimes directed by the Latin Church in the medieval period. The best known of these Crusades are those to the Holy Land in the period between 1095 and 1291 that were intended to recover Jerusalem and its surrounding area from Islamic rule. Concurrent military activities in the Iberian Peninsula against the Moors (the Reconquista) and in northern Europe against pagan West Slavic, Baltic, and Finnic peoples (the Northern Cr







In 1179, the Crusaders rebuilt the Monastery of St. George of Koziba, at its original site 10 kilometres (6 mi) from the center of town. They also built another two churches and a monastery dedicated to John the Baptist, and are credited with introducing sugarcane production to the city.
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e of the principal cities of Jund Filastin.[61] The city flourished until 1071 with the invasion of the Seljuk Turks, followed by the upheavals of the Crusades.[citation needed] Crusader period <span>In 1179, the Crusaders rebuilt the Monastery of St. George of Koziba, at its original site 10 kilometres (6 mi) from the center of town. They also built another two churches and a monastery dedicated to John the Baptist, and are credited with introducing sugarcane production to the city.[62] The site of Tawahin es-Sukkar (lit. "sugar mills") holds remains of a Crusader sugar production facility. In 1187, the Crusaders were evicted by the Ayyubid forces of Saladin after




Flashcard 7104499944716

Question
In 1179, the Crusaders rebuilt the Monastery of St. George of Koziba, at its original site 10 kilometres (6 mi) from the center of town. They also built another two churches and a monastery dedicated to John the Baptist, and are credited with introducing [...] production to the city.
Answer

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Koziba, at its original site 10 kilometres (6 mi) from the center of town. They also built another two churches and a monastery dedicated to John the Baptist, and are credited with introducing <span>sugarcane production to the city. <span>

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Jericho - Wikipedia
e of the principal cities of Jund Filastin.[61] The city flourished until 1071 with the invasion of the Seljuk Turks, followed by the upheavals of the Crusades.[citation needed] Crusader period <span>In 1179, the Crusaders rebuilt the Monastery of St. George of Koziba, at its original site 10 kilometres (6 mi) from the center of town. They also built another two churches and a monastery dedicated to John the Baptist, and are credited with introducing sugarcane production to the city.[62] The site of Tawahin es-Sukkar (lit. "sugar mills") holds remains of a Crusader sugar production facility. In 1187, the Crusaders were evicted by the Ayyubid forces of Saladin after







In 1187, the Crusaders were evicted by the Ayyubid forces of Saladin after their victory in the Battle of Hattin, and the town slowly went into decline.[18]
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hn the Baptist, and are credited with introducing sugarcane production to the city.[62] The site of Tawahin es-Sukkar (lit. "sugar mills") holds remains of a Crusader sugar production facility. <span>In 1187, the Crusaders were evicted by the Ayyubid forces of Saladin after their victory in the Battle of Hattin, and the town slowly went into decline.[18] Ayyubid and Mamluk periods 14th-century map of Jericho in Farhi Bible In 1226, Arab geographer Yaqut al-Hamawi said of Jericho, "it has many palm trees, also sugarcane in quantities, an




Flashcard 7104503090444

Question
In 1187, the Crusaders were evicted by the [...] after their victory in the Battle of Hattin, and the town slowly went into decline.[18]
Answer
Ayyubid forces of Saladin

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In 1187, the Crusaders were evicted by the Ayyubid forces of Saladin after their victory in the Battle of Hattin, and the town slowly went into decline.[18]

Original toplevel document

Jericho - Wikipedia
hn the Baptist, and are credited with introducing sugarcane production to the city.[62] The site of Tawahin es-Sukkar (lit. "sugar mills") holds remains of a Crusader sugar production facility. <span>In 1187, the Crusaders were evicted by the Ayyubid forces of Saladin after their victory in the Battle of Hattin, and the town slowly went into decline.[18] Ayyubid and Mamluk periods 14th-century map of Jericho in Farhi Bible In 1226, Arab geographer Yaqut al-Hamawi said of Jericho, "it has many palm trees, also sugarcane in quantities, an







Flashcard 7104504663308

Question
In 1187, the Crusaders were evicted by the Ayyubid forces of Saladin after their victory in the [...], and the town slowly went into decline.[18]

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In 1187, the Crusaders were evicted by the Ayyubid forces of Saladin after their victory in the Battle of Hattin, and the town slowly went into decline.[18]

Original toplevel document

Jericho - Wikipedia
hn the Baptist, and are credited with introducing sugarcane production to the city.[62] The site of Tawahin es-Sukkar (lit. "sugar mills") holds remains of a Crusader sugar production facility. <span>In 1187, the Crusaders were evicted by the Ayyubid forces of Saladin after their victory in the Battle of Hattin, and the town slowly went into decline.[18] Ayyubid and Mamluk periods 14th-century map of Jericho in Farhi Bible In 1226, Arab geographer Yaqut al-Hamawi said of Jericho, "it has many palm trees, also sugarcane in quantities, an







Jericho was incorporated into the Ottoman Empire in 1517 with all of Palestine,
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tury, Abu al-Fida writes there are sulfur mines in Jericho, "the only ones in Palestine".[63] Ottoman period Postcard image depicting Jericho in the late 19th or early 20th century 16th century <span>Jericho was incorporated into the Ottoman Empire in 1517 with all of Palestine, and in 1545 a revenue of 19,000 Akçe was recorded, destined for the new Waqf for the Haseki Sultan Imaret of Jerusalem.[64] The villagers processed indigo as one source of revenue, usin




Flashcard 7104507809036

Question
Jericho was incorporated into the [...] in 1517 with all of Palestine,

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Jericho was incorporated into the Ottoman Empire in 1517 with all of Palestine,

Original toplevel document

Jericho - Wikipedia
tury, Abu al-Fida writes there are sulfur mines in Jericho, "the only ones in Palestine".[63] Ottoman period Postcard image depicting Jericho in the late 19th or early 20th century 16th century <span>Jericho was incorporated into the Ottoman Empire in 1517 with all of Palestine, and in 1545 a revenue of 19,000 Akçe was recorded, destined for the new Waqf for the Haseki Sultan Imaret of Jerusalem.[64] The villagers processed indigo as one source of revenue, usin







Flashcard 7104509381900

Question
Jericho was incorporated into the Ottoman Empire in [...] with all of Palestine,
Answer
1517

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Jericho was incorporated into the Ottoman Empire in 1517 with all of Palestine,

Original toplevel document

Jericho - Wikipedia
tury, Abu al-Fida writes there are sulfur mines in Jericho, "the only ones in Palestine".[63] Ottoman period Postcard image depicting Jericho in the late 19th or early 20th century 16th century <span>Jericho was incorporated into the Ottoman Empire in 1517 with all of Palestine, and in 1545 a revenue of 19,000 Akçe was recorded, destined for the new Waqf for the Haseki Sultan Imaret of Jerusalem.[64] The villagers processed indigo as one source of revenue, usin







After the collapse of the Ottoman Empire at the end of World War I, Jericho came under British rule, as part of Mandatory Palestine.
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the air in 1931 The Greek Orthodox monasteries of St. George of Choziba and John the Baptist were refounded and completed in 1901 and 1904, respectively.[18] British Mandate period Jericho 1938 <span>After the collapse of the Ottoman Empire at the end of World War I, Jericho came under British rule, as part of Mandatory Palestine. According to the 1922 census of Palestine, Jericho had 1,029 inhabitants, consisting of 931 Muslims, 6 Jews and 92 Christians;[77] where the Christians were 45 Orthodox, 12 Roman Cathol




Flashcard 7104512527628

Question
After the collapse of the Ottoman Empire at the end of World War I, Jericho came under [...] rule, as part of Mandatory Palestine.
Answer
British

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After the collapse of the Ottoman Empire at the end of World War I, Jericho came under British rule, as part of Mandatory Palestine.

Original toplevel document

Jericho - Wikipedia
the air in 1931 The Greek Orthodox monasteries of St. George of Choziba and John the Baptist were refounded and completed in 1901 and 1904, respectively.[18] British Mandate period Jericho 1938 <span>After the collapse of the Ottoman Empire at the end of World War I, Jericho came under British rule, as part of Mandatory Palestine. According to the 1922 census of Palestine, Jericho had 1,029 inhabitants, consisting of 931 Muslims, 6 Jews and 92 Christians;[77] where the Christians were 45 Orthodox, 12 Roman Cathol







Jericho came under Jordanian control after the 1948 Arab–Israeli War.
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rtresses in Jericho with the help of the Jewish company Solel Boneh, and bridges were rigged with explosives in preparation for a possible invasion by German allied forces.[85] Jordanian period <span>Jericho came under Jordanian control after the 1948 Arab–Israeli War. The Jericho Conference, organized by King Abdullah and attended by over 2,000 Palestinian delegates in 1948 proclaimed "His Majesty Abdullah as King of all Palestine" and called for "th




Flashcard 7104515673356

Question
Jericho came under [...] control after the 1948 Arab–Israeli War.
Answer
Jordanian

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Jericho came under Jordanian control after the 1948 Arab–Israeli War.

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Jericho - Wikipedia
rtresses in Jericho with the help of the Jewish company Solel Boneh, and bridges were rigged with explosives in preparation for a possible invasion by German allied forces.[85] Jordanian period <span>Jericho came under Jordanian control after the 1948 Arab–Israeli War. The Jericho Conference, organized by King Abdullah and attended by over 2,000 Palestinian delegates in 1948 proclaimed "His Majesty Abdullah as King of all Palestine" and called for "th







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Jericho came under Jordanian control after the [...]

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Jericho came under Jordanian control after the 1948 Arab–Israeli War.

Original toplevel document

Jericho - Wikipedia
rtresses in Jericho with the help of the Jewish company Solel Boneh, and bridges were rigged with explosives in preparation for a possible invasion by German allied forces.[85] Jordanian period <span>Jericho came under Jordanian control after the 1948 Arab–Israeli War. The Jericho Conference, organized by King Abdullah and attended by over 2,000 Palestinian delegates in 1948 proclaimed "His Majesty Abdullah as King of all Palestine" and called for "th







World War II or the Second World War, often abbreviated as WWII or WW2, was a global war that lasted from 1939 to 1945.
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World War II - Wikipedia
II Alphabetical indices A B C D E F G H I J K L M N O P Q R S T U V W X Y Z 0–9 Navigation Campaigns Countries Equipment Timeline Outline Lists Historiography Portal Category Bibliography v t e <span>World War II or the Second World War, often abbreviated as WWII or WW2, was a global war that lasted from 1939 to 1945. It involved the vast majority of the world's countries—including all of the great powers—forming two opposing military alliances: the Allies and the Axis powers. In a total war directly




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World War II or the Second World War, often abbreviated as WWII or WW2, was a global war that lasted from [...].
Answer
1939 to 1945

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World War II or the Second World War, often abbreviated as WWII or WW2, was a global war that lasted from 1939 to 1945.

Original toplevel document

World War II - Wikipedia
II Alphabetical indices A B C D E F G H I J K L M N O P Q R S T U V W X Y Z 0–9 Navigation Campaigns Countries Equipment Timeline Outline Lists Historiography Portal Category Bibliography v t e <span>World War II or the Second World War, often abbreviated as WWII or WW2, was a global war that lasted from 1939 to 1945. It involved the vast majority of the world's countries—including all of the great powers—forming two opposing military alliances: the Allies and the Axis powers. In a total war directly







In mid-1950, Jordan formally annexed the West Bank and Jericho residents, like other residents of West Bank localities became Jordanian citizens.
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Jericho - Wikipedia
er 2,000 Palestinian delegates in 1948 proclaimed "His Majesty Abdullah as King of all Palestine" and called for "the unification of Palestine and Transjordan as a step toward full Arab unity". <span>In mid-1950, Jordan formally annexed the West Bank and Jericho residents, like other residents of West Bank localities became Jordanian citizens.[86] In 1961, the population of Jericho was 10,166,[87] of whom 935 were Christian, and the rest were Muslim.[88] 1967, aftermath 2018 United Nations map of the area, showing the Israeli




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In mid-[...], Jordan formally annexed the West Bank and Jericho residents, like other residents of West Bank localities became Jordanian citizens.
Answer
1950

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In mid-1950, Jordan formally annexed the West Bank and Jericho residents, like other residents of West Bank localities became Jordanian citizens.

Original toplevel document

Jericho - Wikipedia
er 2,000 Palestinian delegates in 1948 proclaimed "His Majesty Abdullah as King of all Palestine" and called for "the unification of Palestine and Transjordan as a step toward full Arab unity". <span>In mid-1950, Jordan formally annexed the West Bank and Jericho residents, like other residents of West Bank localities became Jordanian citizens.[86] In 1961, the population of Jericho was 10,166,[87] of whom 935 were Christian, and the rest were Muslim.[88] 1967, aftermath 2018 United Nations map of the area, showing the Israeli







Jericho has been occupied by Israel since the Six-Day War of 1967 along with the rest of the West Bank.
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Jericho - Wikipedia
population of Jericho was 10,166,[87] of whom 935 were Christian, and the rest were Muslim.[88] 1967, aftermath 2018 United Nations map of the area, showing the Israeli occupation arrangements <span>Jericho has been occupied by Israel since the Six-Day War of 1967 along with the rest of the West Bank. It was the first city handed over to Palestinian Authority control in accordance with the Oslo Accords.[89] The limited Palestinian self-rule of Jericho was agreed on in the Gaza–Jerich




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Question
Jericho has been occupied by Israel since the [...] along with the rest of the West Bank.
Answer
Six-Day War of 1967

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Jericho has been occupied by Israel since the Six-Day War of 1967 along with the rest of the West Bank.

Original toplevel document

Jericho - Wikipedia
population of Jericho was 10,166,[87] of whom 935 were Christian, and the rest were Muslim.[88] 1967, aftermath 2018 United Nations map of the area, showing the Israeli occupation arrangements <span>Jericho has been occupied by Israel since the Six-Day War of 1967 along with the rest of the West Bank. It was the first city handed over to Palestinian Authority control in accordance with the Oslo Accords.[89] The limited Palestinian self-rule of Jericho was agreed on in the Gaza–Jerich







Infection Caused by Other Enteric Campylobacter Species
#Campylobacter #Maladies-infectieuses-et-tropicales
The clinical manifestations of infection caused by other enteric Cam- pylobacter spp. overlap substantially with those of C. jejuni infec- tion. 149,204,205 On average, C. coli may produce milder disease. 62
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#Campylobacter #Maladies-infectieuses-et-tropicales
The gold standard for diagnosis of Campylobacter infection remains isolation by culture; however, multiple new non–culture-based techniques are now in use.
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#Campylobacter #Maladies-infectieuses-et-tropicales
Campylobacter spp. cannot be isolated from fecal specimens unless microaerobic incubation conditions and selective techniques that reduce the growth of competing microorganisms are used. 4,43
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#Campylobacter #Maladies-infectieuses-et-tropicales
C. fetus is usually isolated from blood cultures 4 to 14 days after the specimen has been obtained. 142
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#Campylobacter #Maladies-infectieuses-et-tropicales
NAATs for Campylobacter diagnosis are usually part of a multiple enteric pathogen panel, including Salmonella, Shigella, and others. 237 However, when antibiotic resistance is a concern, the bacterial isolate is still needed and culture should be concurrently performed, especially in outbreak settings
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#Campylobacter #Maladies-infectieuses-et-tropicales
In addition, NAATs detect bacterial DNA, not viable organisms, and should be interpreted with caution
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#Campylobacter #Maladies-infectieuses-et-tropicales
Examination of diarrheal fecal specimens by darkfield or phase-contrast microscopy within 2 hours of passage can permit a rapid presumptive diagnosis of Campylobacter enteritis if the characteristic darting motility of the Campylobacter organism is seen. 145,238
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#Campylobacter #Maladies-infectieuses-et-tropicales
People infected with C. jejuni who are ill enough to seek medical attention and from whom a fecal culture is obtained represent only a subset of all those infected. Nevertheless, even among these patients, fewer than half are candidates for specific antimicrobial therapy. 143 In a meta-analysis of 11 small randomized trials, antimicrobial agents reduced the duration of intestinal symptoms by approximately 1.3 days. 240 Because the greatest therapeutic benefit occurs when antimicrobial therapy is started early, the rapid presumptive diagnosis of Campylobacter infection by means of direct visualization of the organisms in stool is clinically relevant
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#Campylobacter #Maladies-infectieuses-et-tropicales
Treatment with antibiotics seems prudent in those patients with high fever, bloody diarrhea, or more than eight stools per day; in patients whose symptoms have not lessened or are worsening at the time the diagnosis is made; or in those in whom symptoms have persisted for more than 1 week. 241
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#Campylobacter #Maladies-infectieuses-et-tropicales
In vitro, C. jejuni is susceptible to a wide variety of antimicrobial agents, including erythromycin, macrolides, the tetracyclines, the aminoglycosides, chloramphenicol, the quinolones, the nitrofurans, and clindamycin. 242,243
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#Campylobacter #Maladies-infectieuses-et-tropicales
Erythromycin was once considered the agent of choice; however, because erythromycin, is primarily metabolized by cytochrome P-450 isoenzyme 3A4, there is a slight risk for sudden cardiac death. Therefore this agent is no longer recommended.
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#Campylobacter #Maladies-infectieuses-et-tropicales
We agree with the recommendation made in the 2017 Infectious Diseases Society of America guidelines that first-line therapy is either a macrolide or a fluoroquinolone. 244 Therapy with extended-spectrum macrolides such as clarithromycin or azithromycin should be equally effective. 245
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#Campylobacter #Maladies-infectieuses-et-tropicales
The recommended dosage of azithromycin is 500 mg orally daily for 3 days; a single dose of 1000 mg may be equally effective, although this dosage is associated with more nausea. In children, the recommended dosage of azithromycin is 10 mg/kg per day for 3 days.
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#Campylobacter #Maladies-infectieuses-et-tropicales
The dosage of ciprofloxacin is 500 mg orally twice daily for 5 to 7 days, 246 although as with azithromycin, a single dose (750 mg) may be just as effective. 247
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#Campylobacter #Maladies-infectieuses-et-tropicales
Fluoroquinolones have the advantage of possessing activity across a broad spectrum of bacteria causing diarrheal illness, including Campylobacter spp. However, fluoroquinolones should be used with caution because rising rates of resistance to these agents have limited their usefulness in treating Campylobacter infections (see later section on “Resistance to Fluoroquinolones”).
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#Campylobacter #Maladies-infectieuses-et-tropicales
Most C. jejuni and C. coli isolates are not susceptible to most cephalosporins or penicillin, and these agents should not be used. However, amoxicillin or ticarcillin plus clavulanic acid appears to be universally effective. 248
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#Campylobacter #Maladies-infectieuses-et-tropicales
Some macrolide- and fluoroquinolone-resistant C. coli strains may be susceptible to fosfo- mycin. 249 Susceptibility to sulfonamides and metronidazole is variable
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#Campylobacter #Maladies-infectieuses-et-tropicales
Unlike in Salmonella infections, treatment with antimicrobial agents does not prolong carriage of C. jejuni; on the contrary, erythromycin eliminates carriage within 72 hours in most patients. 242
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#Campylobacter #Maladies-infectieuses-et-tropicales
Use of an antimotility agent appears to prolong duration of symptoms and has been associated with fatalities. 251
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#Campylobacter #Maladies-infectieuses-et-tropicales
H. cinaedi and those Campylobacter strains acquired in developing countries, especially C. coli, are more likely to be resistant to macrolides and tetracycline. 250 In such cases, when treatment is indicated, alterna- tive agents should be used until susceptibility is known.
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#Campylobacter #Maladies-infectieuses-et-tropicales
Systemic C. fetus infections should be treated parenterally, but erythromycin should not be used. 253,254
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#Campylobacter #Maladies-infectieuses-et-tropicales
Patients with endovascular infections caused by C. fetus require at least 4 weeks of therapy, and gentamicin or ampicillin is probably the agent of choice. 254 Treatment with imipenem or meropenem constitutes another alternative.
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#Campylobacter #Maladies-infectieuses-et-tropicales
Campylobacter species are often naturally transformable organisms, allowing for the acquisition of resistance genes from other Campylobacter spp. as well as other gram-positive and gram-negative organisms. 255,256
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[unknown IMAGE 7104569412876] #Campylobacter #Maladies-infectieuses-et-tropicales #has-images
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#Campylobacter #Maladies-infectieuses-et-tropicales
In 2013, the Centers for Disease Control and Prevention designated Campylobacter as a microorganism with a serious antibiotic resistance threat. 277 This was driven principally by the increase in fluoroquinolone resistance observed in C. jejuni from 15% in 1998 to 25% in 2015. 278
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#Campylobacter #Maladies-infectieuses-et-tropicales
Resistance rates in certain parts of the world are much higher than in the United States—as high as 75% in travelers to Asia 279 —highlighting the need for an accurate travel history when assessing the traveler with diarrhea.
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#Campylobacter #Maladies-infectieuses-et-tropicales
In 2004, the US Food and Drug Administra- tion reversed its prior approval for the therapeutic use of the veterinary fluoroquinolone enrofloxacin because of the concern that the observed increase in fluoroquinolone resistance in human isolates was due to an increase in fluoroquinolone-resistant poultry isolates. 276,280
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#Campylobacter #Maladies-infectieuses-et-tropicales
Only approximately 2% to 3% of US isolates are resistant to azithromycin, and so macrolides are the first-line therapies. 244 Unfortunately, macrolide resistance rates are much higher in parts of Asia and Africa; for example, in studies in South Africa and Nigeria, 80% or more of isolates were resistant to macrolides. 281,282
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#Campylobacter #Maladies-infectieuses-et-tropicales
Resistance in Campylobacter occurs most commonly via a Thr-86-Ile substitution in the quinolone resistance-determining region (QRDR) of gyrA. Unlike fluoroquinolone resistance in Salmonella and E. coli, this single mutation confers high-level resistance to nalidixic acid and fluoroquinolones. 258 Because only the single Thr-86-Ile mutation is needed to mediate high-level resistance and does so without an appar- ent (or large) fitness cost, fluoroquinolone resistance appears quickly in animals and humans. 285–288
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#Campylobacter #Maladies-infectieuses-et-tropicales
The low spontaneous mutation rate of the 23S rRNA genes (approximately 10 −10 per cell per generation) contributes to the apparent higher barrier to the emergence of resistance compared with fluoroquinolones. 295 In another contrast to fluoroquinolone resistance, competition experiments suggest that macrolide resistance imparts a fitness cost. 301–305
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#Campylobacter #Maladies-infectieuses-et-tropicales
The “reactive arthritis,” formerly called Reiter syndrome, occurring in human leukocyte antigen HLA-B27–positive people closely resembles that seen after Yersinia, Salmonella, or Shigella infections and is not specific to C. jejuni infection. However, rheumatologic symptoms may persist for several months or possibly for years in a few affected people.
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#Campylobacter #Maladies-infectieuses-et-tropicales
GBS is an uncommon sequela of Campylobacter enteritis, but because of their high prevalence, Campylobacter infections are the most important recognized antecedent of this clinically devastating disorder.
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#Campylobacter #Maladies-infectieuses-et-tropicales
C. fetus infection may be lethal to patients with chronic compensated diseases such as cirrhosis or diabetes mellitus or may hasten the demise of seriously immunocompromised patients. For immunocompromised hosts with systemic C. fetus infections, prognosis is most dependent on the rapidity with which appropriate antimicrobial therapy is begun
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#Campylobacter #Maladies-infectieuses-et-tropicales
Previously healthy people infected with C. fetus usually survive the illness without permanent sequelae.
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#Campylobacter #Maladies-infectieuses-et-tropicales
Because most human Campylobacter infections are acquired from consumption or handling of poultry, thorough cooking of chicken and other poultry products is an important step in preventing transmission of infection to people. Furthermore, meticulous attention to avoiding cross-contamination of utensils and cutting boards during food prepara- tion also may reduce the risk of infection. Elimination or reduction of use of antibiotics in animals used for food production may reduce the rate of antibiotic resistance among Campylobacter species
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#Campylobacter #Maladies-infectieuses-et-tropicales
Finally, because C. jejuni infections are “accidentally” acquired by humans, and because there is evidence for the natural development of immunity among people in developing countries, the goal of producing a vaccine is probably achievable
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[unknown IMAGE 7104592481548] #Campylobacter #Maladies-infectieuses-et-tropicales #has-images
Campylobacter en "vol de mouette"
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#Campylobacter #Maladies-infectieuses-et-tropicales
The name Campylobacter is derived from the Greek campylos, meaning “curved”, and baktron, meaning “rod”.
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#Campylobacter #Maladies-infectieuses-et-tropicales
After the recognition of Campylobacter jejuni as a major human pathogen, numerous related Campylobacter, Arcobacter, and Helicobacter species have been identified.
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#Campylobacter #Maladies-infectieuses-et-tropicales
Campylobacter organisms are motile, non–spore-forming, comma-shaped, gram-negative rods. 3
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#Campylobacter #Maladies-infectieuses-et-tropicales
Originally isolated from aborted sheep fetuses in 1909, these and similar organisms were considered subspecies of Vibrio fetus. However, because these organisms did not ferment carbohydrates and differed in their guanine plus cytosine (G + C) DNA content from true members of the genus Vibrio, a new genus, Campylobacter, was created.
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#Campylobacter #Maladies-infectieuses-et-tropicales
The prototype for enteric infection is C. jejuni; for extraintestinal infection it is Campylobacter fetus (Tabl e 216 .2 ). Because the organisms causing enteric and extraintestinal illnesses are generally the same, they are considered together in the following discussion.
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#Campylobacter #Maladies-infectieuses-et-tropicales
Campylobacters and related organisms grow best in an atmosphere containing 5% to 10% oxygen and are thus considered microaerophilic. 3,4
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#Campylobacter #Maladies-infectieuses-et-tropicales
All cam- pylobacters grow at 37°C; however, C. jejuni grows best at 42°C. Because C. jejuni is the most common enteric pathogen of humans, many labo- ratories have used incubation at 42°C for optimal isolation; however, use of this temperature will not permit detection of infections by many of the related species. In particular, Campylobacter upsaliensis may be missed.
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#Campylobacter #Maladies-infectieuses-et-tropicales
Campylobacter spp. multiply more slowly than do the usual bacteria of the enteric flora and therefore cannot be isolated from fecal specimens unless selective techniques are used.
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#Campylobacter #Maladies-infectieuses-et-tropicales
Filtration methods permit isolation without use of antibiotic-containing media. It is now clear that use of filtration tech- niques and nonselective rich media such as chocolate agar, with incuba- tion of plates at 37°C, improves stool culture yields of both C. jejuni and the “atypical” enteric Campylobacter spp. 11,12
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#Campylobacter #Maladies-infectieuses-et-tropicales
Visible colonies usually appear on the plating media within 24 to 48 hours, and usually longer for the “atypical” species.
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#Campylobacter #Maladies-infectieuses-et-tropicales
Isolation of organisms from sites without a normal microbiota, such as the bloodstream, is not difficult, although when Campylobacter is the suspected pathogen, incubation of cultures should be extended to 2 weeks.
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#Campylobacter #Maladies-infectieuses-et-tropicales
As with other bacteria whose ecologic niche is the gastrointestinal tract of mammals and avian species, the serotypical diversity of C. jejuni is enormous.
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#Campylobacter #Maladies-infectieuses-et-tropicales
C. jejuni cannot long withstand drying or freezing temperatures, which are characteristics that limit its transmission. 21 However, C. jejuni survives in milk or other foods or in water kept at 4°C for several weeks. Pasteurization effectively destroys the organism, as does chlorine at concentrations in standard use for water disinfection
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#Campylobacter #Maladies-infectieuses-et-tropicales
Campylobacteriosis is a worldwide zoonosis. Campylobacter spp. are commonly found as commensals of the gastrointestinal tract in wild or domesticated cattle, sheep, swine, goats, dogs, cats, rodents, and all varieties of fowl. 3,21
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#Campylobacter #Maladies-infectieuses-et-tropicales
Meats originating from infected animals frequently become contaminated with intestinal contents during the slaughtering process. 21
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#Campylobacter #Maladies-infectieuses-et-tropicales
In particular, commercially raised poultry is nearly always colonized with C. jejuni, slaughterhouse procedures amplify contamina- tion, and chicken and turkey in supermarkets, ready for consumers to take home, frequently are contaminated. 21,24
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#Campylobacter #Maladies-infectieuses-et-tropicales
Undercooked meats, especially poultry, have been associated with infection. 29–33
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#Campylobacter #Maladies-infectieuses-et-tropicales
In one US study, children riding in grocery store shopping carts next to raw meat or poultry had higher rates of Campylobacter infec- tions. 34,35
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#Campylobacter #Maladies-infectieuses-et-tropicales
Nevertheless, consumption of undercooked poultry is estimated to be responsible for 50% to 70% of sporadic Campylobacter infections in developed countries.
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#Campylobacter #Maladies-infectieuses-et-tropicales
Because healthy dogs, cats, rodents, and birds may excrete Campylobacter and related organisms, it is not surprising that human infections associated with these animals also have been reported.
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#Campylobacter #Maladies-infectieuses-et-tropicales
As with other enteric pathogens, fecal-oral person-to-person transmis- sion of C. jejuni has been reported. People in contact with the excreta of infected individuals who are not feces continent (e.g., infants) are at risk for infection.
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#Campylobacter #Maladies-infectieuses-et-tropicales
Because of a variety of sexual practices, homosexual men appear to be at increased risk for infection caused by H. cinaedi, H. fennelliae, and other “atypical” Campylobacter spp. 41
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#Campylobacter #Maladies-infectieuses-et-tropicales
C. jejuni infections occur year-round in the United States and other developed countries but with a sharp peak in summer and early fall. C. fetus infections show the same seasonal variation, but the peak is less marked.
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#Campylobacter #Maladies-infectieuses-et-tropicales
For many years, the incidence of C. jejuni infections continued to rise in the United States and Europe and exceeded rates of Salmonella and Shigella infections combined. 48,49
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#Campylobacter #Maladies-infectieuses-et-tropicales
Beginning in 2014, the incidence began to increase again. 50,51 Indeed, in 2017, the most recent year reported by the Centers for Disease Control and Prevention’s Foodborne Diseases Active Surveillance Network (FoodNet), the incidence of Campylobacter rose by 10%, climbing to 19.1 per 100,000 population. 52
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#Campylobacter #Maladies-infectieuses-et-tropicales
Based on current estimates, there are probably more than 2 million Campylobacter infections annually in the United States, although there is great geographic variability in incidence rates, even within the United States. 57 Population-based studies show peak incidence in children younger than age 1 year and in people 15 to 29 years old 58 ; however, cases have been reported in patients of all ages. The incidence in males may be higher. The prevalence of infection in healthy people is very low (<%)
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#Campylobacter #Maladies-infectieuses-et-tropicales
The epidemiology of infection in developing countries is markedly different. C. jejuni is often isolated from healthy people, and the infec- tion is especially common during the first 5 years of life. 59–61
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#Campylobacter #Maladies-infectieuses-et-tropicales
Interestingly, even in developed nations, the incidence of infection in rural areas is higher, similar to patterns observed in developing nations, and possibly associated with more direct contact with animal vectors of the infection. 65
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C. jejuni and other Campylobacter spp. are important causes for the acute diarrheal illnesses suffered by travelers. 66
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#Campylobacter #Maladies-infectieuses-et-tropicales
However, it is clear from outbreak investigations and from volunteer studies that not all Campylobacter infections produce illness. Although all factors responsible for this phenomenon are not known, three of the most important appear to be the dose of organisms reaching the small intestine, the virulence of the infecting strain, and the specific immunity of the host to the pathogen ingested
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#Campylobacter #Maladies-infectieuses-et-tropicales
Among exposed people who become ill, the incubation period varies from 1 to 7 days, a characteristic that is probably inversely related to the dose ingested.
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#Campylobacter #Maladies-infectieuses-et-tropicales
Although there are reports of illness occurring within 24 hours of exposure, 67,68 most infections occur 2 to 4 days after exposure
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#Campylobacter #Maladies-infectieuses-et-tropicales
In one study, volunteers became ill after ingesting as few as 500 organisms, but with a dose of less than 10 4 organisms, illness was infrequent. 69,70
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#Campylobacter #Maladies-infectieuses-et-tropicales
C. jejuni, like Salmonella typhimurium, is susceptible to hydrochloric acid. 70 Taken together, these data suggest that the infectious dose for C. jejuni is similar to that for Salmonella. The acidic milieu of the stomach provides an effective barrier against Campylobacter infection. However, vehicles such as milk, fatty foods, and water that favor passage through the gastric acid barrier may permit some infections to occur at relatively low doses. Similarly, patients who use proton pump inhibitors or his- tamine type 2 blockers are more susceptible to infection. 71,72
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#Campylobacter #Maladies-infectieuses-et-tropicales
C. jejuni multiplies in human bile 70 a characteristic that aids coloniza- tion of the bile-rich upper small intestine early in infection.
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#Campylobacter #Maladies-infectieuses-et-tropicales
Rectal biopsy samples with these nonspecific features have been interpreted as showing acute ulcerative colitis or Crohn disease. In other cases, the appearance of the rectal biopsy sample has been similar to that of specimens obtained in Salmonella or Shigella infections.
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#Campylobacter #Maladies-infectieuses-et-tropicales
Unspecified host factors are also clearly important; in volunteers, a single strain produced a wide spectrum of clinical manifestations. 69
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#Campylobacter #Maladies-infectieuses-et-tropicales
The presence of bacteremia in some patients, the finding of cellular infiltration in biopsy specimens, and the presence of blood in stools from patients with Campylobacter colitis also suggest that tissue invasion occurs. The process of C. jejuni invasion is multifactorial.
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#Campylobacter #Maladies-infectieuses-et-tropicales
Unlike other enteric pathogens such as Salmonella, Campylobacter flagellins are not recognized by the host pattern recognition receptor Toll-like receptor (TLR) 5 due to differences in specific regions of flagellin genes, and do not elicit production of the proinflammatory cytokine interleukin-8, suggesting that flagellins are involved in evasion of innate immune responses in their reservoir hosts. 90,91
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#Campylobacter #Maladies-infectieuses-et-tropicales
Campylobacter outer membranes contain lipopolysaccharides (LPSs) with typical endotoxic activity. 108–110 The structure of the LPS O antigen is highly variable. 109,110 Many C. jejuni O antigens possess sialic acid– containing structures that are recognized by host immune cells bearing sialoadhesins. 111–113 The close resemblance of these sialylated structures to those seen in human gangliosides such as GM1, GD1a, GD3, and GT1a and their presence in strains isolated from patients who developed the Guillain-Barré syndrome (GBS) support a role in the pathogenesis of this disorder, via molecular mimicry. 111,112,114
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#Campylobacter #Maladies-infectieuses-et-tropicales
Most bacteremias reported to the Centers for Disease Control and Prevention have been due to C. fetus subsp. fetus, whereas C. jejuni is by far the more common pathogen overall.
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#Campylobacter #Maladies-infectieuses-et-tropicales
One explanation for the apparently greater tendency of C. fetus to cause bacteremia is that it is usually resistant to the bactericidal activity present in normal human serum. 118
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#Campylobacter #Maladies-infectieuses-et-tropicales
Important risk factors for C. fetus bacteremia and meningitis include immunosuppression and occupational exposure to infant animals that are the reservoir hosts for C. fetus. 119,120
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#Campylobacter #Maladies-infectieuses-et-tropicales
Protection from recurrent disease may not develop following a single infection, as has been shown in human experimental infection and reinfection models of C.jejuni 127 ; early antibiotic treatment might thwart the development of a full immune response to the infection
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#Campylobacter #Maladies-infectieuses-et-tropicales
Patients infected with Campylobacter spp. develop specific immuno- globulin (Ig) G, IgM, and IgA antibodies in serum 128,129 and IgA antibodies in intestinal secretions. 129,130
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#Campylobacter #Maladies-infectieuses-et-tropicales
Further supporting the importance of humoral immunity are multiple reports of severe and recurrent C. jejuni infection in patients with congenital or acquired hypogammaglobu- linemia. 131,132
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#Campylobacter #Maladies-infectieuses-et-tropicales
As discussed earlier, one important virulence factor in C. fetus that is not found in C. jejuni is a proteinaceous paracrystalline array attached to the O antigen of LPS known as an S layer. This renders C. fetus serum resistant, owing to the inability of the complement component C3b to opsonize its surface. 140
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#Campylobacter #Maladies-infectieuses-et-tropicales
Patients with C. fetus infections much more frequently have evidence of impaired immunity, including conditions such as chronic alcoholism, liver disease, old age, diabetes mellitus, and malignancies, 141,142 permitting an organism that a priori can resist innate immunity to take hold.
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#Antibiotics #Antibiotiques #Macrolides #Maladies-infectieuses-et-tropicales
Macrolides are bacteriostatic in that they suppress or inhibit bacterial growth rather than killing bacteria completely.
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Macrolide - Wikipedia
are usually 14-, 15-, or 16-membered. Macrolides belong to the polyketide class of natural products. Some macrolides have antibiotic or antifungal activity and are used as pharmaceutical drugs. <span>Macrolides are bacteriostatic in that they suppress or inhibit bacterial growth rather than killing bacteria completely. Contents 1 Definition 2 History 3 Uses 4 Mechanism of action 4.1 Antibacterial 4.2 Immunomodulation 4.2.1 Diffuse panbronchiolitis 5 Examples 5.1 Antibiotic macrolides 5.2 Ketolides 5.3




#Antibiotics #Antibiotiques #Macrolides #Maladies-infectieuses-et-tropicales
The first macrolide discovered was erythromycin, which was first used in 1952
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Macrolide - Wikipedia
om tannins. Also lactams instead of lactones (as in the ansamycin family) are excluded. Included are not only 12-16 membered macrocycles but also larger rings as in tacrolimus.[1] History[edit] <span>The first macrolide discovered was erythromycin, which was first used in 1952. Erythromycin was widely used as a substitute to penicillin in cases where patients were allergic to penicillin or had penicillin-resistant illnesses. Later macrolides developed, includ




#Antibiotics #Antibiotiques #Macrolides #Maladies-infectieuses-et-tropicales
Later macrolides developed, including azithromycin and clarithromycin, stemmed from chemically modifying erythromycin; these compounds were designed to be more easily absorbed and have fewer side-effects (erythromycin caused gastrointestinal side-effects in a significant proportion of users). [2]
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Macrolide - Wikipedia
erythromycin, which was first used in 1952. Erythromycin was widely used as a substitute to penicillin in cases where patients were allergic to penicillin or had penicillin-resistant illnesses. <span>Later macrolides developed, including azithromycin and clarithromycin, stemmed from chemically modifying erythromycin; these compounds were designed to be more easily absorbed and have fewer side-effects (erythromycin caused gastrointestinal side-effects in a significant proportion of users). [2] Uses[edit] Antibiotic macrolides are used to treat infections caused by Gram-positive bacteria (e.g., Streptococcus pneumoniae) and limited Gram-negative bacteria (e.g., Bordetella pert




#Antibiotics #Antibiotiques #Macrolides #Maladies-infectieuses-et-tropicales
The antimicrobial spectrum of macrolides is slightly wider than that of penicillin, and, therefore, macrolides are a common substitute for patients with a penicillin allergy.
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Macrolide - Wikipedia
tive bacteria (e.g., Streptococcus pneumoniae) and limited Gram-negative bacteria (e.g., Bordetella pertussis, Haemophilus influenzae), and some respiratory tract and soft-tissue infections.[3] <span>The antimicrobial spectrum of macrolides is slightly wider than that of penicillin, and, therefore, macrolides are a common substitute for patients with a penicillin allergy. Beta-hemolytic streptococci, pneumococci, staphylococci, and enterococci are usually susceptible to macrolides. Unlike penicillin, macrolides have been shown to be effective against Leg




#Antibiotics #Antibiotiques #Macrolides #Maladies-infectieuses-et-tropicales
Beta-hemolytic streptococci, pneumococci, staphylococci, and enterococci are usually susceptible to macrolides.
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Macrolide - Wikipedia
sue infections.[3] The antimicrobial spectrum of macrolides is slightly wider than that of penicillin, and, therefore, macrolides are a common substitute for patients with a penicillin allergy. <span>Beta-hemolytic streptococci, pneumococci, staphylococci, and enterococci are usually susceptible to macrolides. Unlike penicillin, macrolides have been shown to be effective against Legionella pneumophila, mycoplasma, mycobacteria, some rickettsia, and chlamydia. Macrolides are not to be used on




#Antibiotics #Antibiotiques #Macrolides #Maladies-infectieuses-et-tropicales
Unlike penicillin, macrolides have been shown to be effective against Legionella pneumophila, mycoplasma, mycobacteria, some rickettsia, and chlamydia.
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Macrolide - Wikipedia
efore, macrolides are a common substitute for patients with a penicillin allergy. Beta-hemolytic streptococci, pneumococci, staphylococci, and enterococci are usually susceptible to macrolides. <span>Unlike penicillin, macrolides have been shown to be effective against Legionella pneumophila, mycoplasma, mycobacteria, some rickettsia, and chlamydia. Macrolides are not to be used on nonruminant herbivores, such as horses and rabbits. They rapidly produce a reaction causing fatal digestive disturbance.[4] It can be used in horses les




#Antibiotics #Antibiotiques #Macrolides #Maladies-infectieuses-et-tropicales
Macrolide antibiotics do so by binding reversibly to the P site on the 50S subunit of the bacterial ribosome. This action is considered to be bacteriostatic. Macrolides are actively concentrated within leukocytes, and thus are transported into the site of infection.[9]
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Macrolide - Wikipedia
d[6] (similarly to chloramphenicol[7]) as well as inhibiting bacterial ribosomal translation.[6] Another potential mechanism is premature dissociation of the peptidyl-tRNA from the ribosome.[8] <span>Macrolide antibiotics do so by binding reversibly to the P site on the 50S subunit of the bacterial ribosome. This action is considered to be bacteriostatic. Macrolides are actively concentrated within leukocytes, and thus are transported into the site of infection.[9] Immunomodulation[edit] Diffuse panbronchiolitis[edit] The macrolide antibiotics erythromycin, clarithromycin, and roxithromycin have proven to be an effective long-term treatment for th




#Antibiotics #Antibiotiques #Macrolides #Maladies-infectieuses-et-tropicales
With macrolide therapy in DPB, great reduction in bronchiolar inflammation and damage is achieved through suppression of not only neutrophil granulocyte proliferation but also lymphocyte activity and obstructive secretions in airways.[10] The antimicrobial and antibiotic effects of macrolides, however, are not believed to be involved in their beneficial effects toward treating DPB.[12]
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Macrolide - Wikipedia
1] The successful results of macrolides in DPB stems from controlling symptoms through immunomodulation (adjusting the immune response),[11] with the added benefit of low-dose requirements.[10] <span>With macrolide therapy in DPB, great reduction in bronchiolar inflammation and damage is achieved through suppression of not only neutrophil granulocyte proliferation but also lymphocyte activity and obstructive secretions in airways.[10] The antimicrobial and antibiotic effects of macrolides, however, are not believed to be involved in their beneficial effects toward treating DPB.[12] This is evident, as the treatment dosage is much too low to fight infection, and in DPB cases with the occurrence of the macrolide-resistant bacterium Pseudomonas aeruginosa, macrolide




#Antibiotics #Antibiotiques #Macrolides #Maladies-infectieuses-et-tropicales

Ketolides are a class of antibiotics that are structurally related to the macrolides. They are used to treat respiratory tract infections caused by macrolide-resistant bacteria. Ketolides are especially effective, as they have two ribosomal binding sites.

Ketolides include:

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ate Oleandomycin Solithromycin Spiramycin - approved in the EU, and in other countries Troleandomycin - used in Italy and Turkey Tylosin/tylocine - used in animals Roxithromycin Ketolides[edit] <span>Ketolides are a class of antibiotics that are structurally related to the macrolides. They are used to treat respiratory tract infections caused by macrolide-resistant bacteria. Ketolides are especially effective, as they have two ribosomal binding sites. Ketolides include: Telithromycin - the first and only approved ketolide[13] Cethromycin Solithromycin Fluoroketolides[edit] Fluoroketolides are a class of antibiotics that are structurally related to the ketolides. The fluoroketolides have three ribosomal interaction sites. Fluoroketoli




#Antibiotics #Antibiotiques #Macrolides #Maladies-infectieuses-et-tropicales

Fluoroketolides are a class of antibiotics that are structurally related to the ketolides. The fluoroketolides have three ribosomal interaction sites.

Fluoroketolides include:

  • Solithromycin - the first and currently the only fluoroketolide (not yet approved)
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Macrolide - Wikipedia
s are especially effective, as they have two ribosomal binding sites. Ketolides include: Telithromycin - the first and only approved ketolide[13] Cethromycin Solithromycin Fluoroketolides[edit] <span>Fluoroketolides are a class of antibiotics that are structurally related to the ketolides. The fluoroketolides have three ribosomal interaction sites. Fluoroketolides include: Solithromycin - the first and currently the only fluoroketolide (not yet approved) Non-antibiotic macrolides[edit] The drugs tacrolimus, pimecrolimus, and sirolimus, which are used as immunosuppressants or immunomodulators, are also macrolides. They have similar activ




#Antibiotics #Antibiotiques #Macrolides #Maladies-infectieuses-et-tropicales
The primary means of bacterial resistance to macrolides occurs by post-transcriptional methylation of the 23S bacterial ribosomal RNA. This acquired resistance can be either plasmid-mediated or chromosomal, i.e., through mutation, and results in cross-resistance to macrolides, lincosamides, and streptogramins (an MLS-resistant phenotype).[16]
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Macrolide - Wikipedia
xample of an antifungal macrolide.[15] Toxic macrolides[edit] A variety of toxic macrolides produced by bacteria have been isolated and characterized, such as the mycolactones. Resistance[edit] <span>The primary means of bacterial resistance to macrolides occurs by post-transcriptional methylation of the 23S bacterial ribosomal RNA. This acquired resistance can be either plasmid-mediated or chromosomal, i.e., through mutation, and results in cross-resistance to macrolides, lincosamides, and streptogramins (an MLS-resistant phenotype).[16] Two other types of acquired resistance rarely seen include the production of drug-inactivating enzymes (esterases or kinases), as well as the production of active ATP-dependent efflux p




#Antibiotics #Antibiotiques #Macrolides #Maladies-infectieuses-et-tropicales
Les kétolides, macrolides de dernière génération, sont intéressants en raison de l'extension de leur activité au pneumocoque de sensibilité diminuée à la pénicilline (ou PSDP)
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Macrolide — Wikipédia
amydia), de certaines infections à streptocoques, staphylocoques méti-S, entérocoques. Cependant leur usage est délicat en raison de nombreux effets secondaires et interactions médicamenteuses. <span>Les kétolides, macrolides de dernière génération, sont intéressants en raison de l'extension de leur activité au pneumocoque de sensibilité diminuée à la pénicilline (ou PSDP). Leurs effets secondaires et contre-indications sont cependant les mêmes. Étymologie[modifier | modifier le code] Mot dérivé du préfixe macro- et du suffixe -olide qui désigne les lacto




#Antibiotics #Antibiotiques #Macrolides #Maladies-infectieuses-et-tropicales

Il existe plusieurs types de macrolides avec 14, 15 ou 16 atomes dans leur macrocycle. On les classe parfois en diverses générations :

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Macrolide — Wikipédia
s sont cependant les mêmes. Étymologie[modifier | modifier le code] Mot dérivé du préfixe macro- et du suffixe -olide qui désigne les lactones. Membres de ce groupe[modifier | modifier le code] <span>Il existe plusieurs types de macrolides avec 14, 15 ou 16 atomes dans leur macrocycle. On les classe parfois en diverses générations : 1re génération : cycle à 14 : érythromycine A cycle à 16 : spiramycine 2e génération cycle à 14 : clarithromycine cycle à 14 : roxithromycine cycle à 15 : azithromycine cycle à 16 : midécamycine, josamycine . 3e génération (kétolides) : cycle à 14 : télithromycine On emploie également la spiramycine (utilisée pour traiter la toxoplasmose), l'ansamycine, l'oléandomycine, la carbomycine et la tylocine. Il existe également une nouvelle classe d'anti




#Antibiotics #Antibiotiques #Macrolides #Maladies-infectieuses-et-tropicales
Les bactéries gram négatif sont généralement naturellement résistantes aux macrolides car leur membrane cellulaire externe est imperméable aux molécules hydrophobes telles que les macrolides.
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se d'un peptide) par encombrement stérique. Les macrolides sont éliminés au niveau de la bile. Antibiorésistance[modifier | modifier le code] Résistance intrinsèque[modifier | modifier le code] <span>Les bactéries gram négatif sont généralement naturellement résistantes aux macrolides car leur membrane cellulaire externe est imperméable aux molécules hydrophobes telles que les macrolides. Exemples : Escherichia coli, Salmonella typhi. Résistance acquise[modifier | modifier le code] Au moins trois mécanismes de résistance aux macrolides existent, qui sont : la modificatio




#Antibiotics #Antibiotiques #Macrolides #Maladies-infectieuses-et-tropicales
Les macrolides ont un « recyclage entérohépatique » ; c'est-à-dire que le médicament est absorbé dans l'intestin et envoyé au foie, pour être ensuite excrété dans le duodénum dans la bile du foie. Cela peut entraîner une accumulation du produit dans le système, provoquant des nausées.
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Macrolide — Wikipédia
larithromycine notamment) ont aussi un effet de classe sur l'allongement de l'intervalle QT, ce qui peut entraîner des torsades de pointe. Effets digestifs (sur le système Foie-Bile-Duodénum) - <span>Les macrolides ont un « recyclage entérohépatique » ; c'est-à-dire que le médicament est absorbé dans l'intestin et envoyé au foie, pour être ensuite excrété dans le duodénum dans la bile du foie. Cela peut entraîner une accumulation du produit dans le système, provoquant des nausées. - Chez les nourrissons, l'utilisation de l'érythromycine a été associée à une sténose du pylore[6],[7]. -Plusieurs macrolides se sont montrés capables de provoquer une cholestase (la bi




#Antibiotics #Antibiotiques #Macrolides #Maladies-infectieuses-et-tropicales
Effets sur le muscle : certains macrolides, quand ils sont combinés aux statines (traitement communément utilisé pour diminuer le taux de cholestérol) peuvent induire une myopathie débilitante ; en 2008, le British Medical Journal a recommandé de ne pas associer ces deux traitements [ 5 ] .
En effet, certains macrolides (clarithromycine et érythromycine, pas l'azithromycine) sont de puissants inhibiteurs du système du cytochrome P450, en particulier du CYP3A4.
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Macrolide — Wikipédia
que de GAS, sont ou sont devenues résistantes aux macrolides[4]. La céphalosporine est alors une autre option pour ces patients[réf. nécessaire]. Effets secondaires[modifier | modifier le code] <span>Effets sur le muscle : certains macrolides, quand ils sont combinés aux statines (traitement communément utilisé pour diminuer le taux de cholestérol) peuvent induire une myopathie débilitante ; en 2008, le British Medical Journal a recommandé de ne pas associer ces deux traitements[5]. En effet, certains macrolides (clarithromycine et érythromycine, pas l'azithromycine) sont de puissants inhibiteurs du système du cytochrome P450, en particulier du CYP3A4. Effets cardiovasculaires indésirables : Les macrolides (érythromycine et clarithromycine notamment) ont aussi un effet de classe sur l'allongement de l'intervalle QT, ce qui peut entraî




#Antibiotics #Antibiotiques #Macrolides #Maladies-infectieuses-et-tropicales
Certains sont métabolisées par le cytochrome P450 avec le risque d'interactions médicamenteuses qui en découle, l'azithromycine semblant le plus neutre sur ce point de vue [ 12 ] .
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Macrolide — Wikipédia
ella burnetii : fièvre Q Chlamydia trachomatis : trachome, pneumopathies (intracellulaire) Effets secondaires[modifier | modifier le code] Ces antibiotiques sont en règle générale bien tolérés. <span>Certains sont métabolisées par le cytochrome P450 avec le risque d'interactions médicamenteuses qui en découle, l'azithromycine semblant le plus neutre sur ce point de vue[12]. Jouant sur certains canaux ioniques, ils peuvent perturber la repolarisation de la cellule musculaire cardiaque en allongeant cette dernière, augmentant le risque de torsades de pointe,




#Antibiotics #Antibiotiques #Macrolides #Maladies-infectieuses-et-tropicales
Plusieurs macrolides sont ainsi soupçonnés d'augmenter légèrement le risque de mort d'origine cardiaque : c'est le cas de l’érythromycine [ 14 ] , de l'azithromycine [ 15 ] et de la clarythromycine [ 16 ] , la roxithromycine semblant neutre sur ce sujet [ 16 ] .
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Macrolide — Wikipédia
ques, ils peuvent perturber la repolarisation de la cellule musculaire cardiaque en allongeant cette dernière, augmentant le risque de torsades de pointe, et de trouble du rythme cardiaque[13]. <span>Plusieurs macrolides sont ainsi soupçonnés d'augmenter légèrement le risque de mort d'origine cardiaque : c'est le cas de l’érythromycine[14], de l'azithromycine[15] et de la clarythromycine[16], la roxithromycine semblant neutre sur ce sujet[16]. Voir aussi[modifier | modifier le code] Antibiotique Polycétide Notes et références[modifier | modifier le code] ↑ « MACROLIDES » [archive], sur infectiologie.org (consulté le 31 décemb




#Antibiotics #Antibiotiques #Apparentés-macrolides #Lincosamides #Maladies-infectieuses-et-tropicales #Streptogramines
Les lincosamides (ou lincosamines) sont des antibiotiques à spectre étroit représentés à l’heure actuelle par deux molécules à usage humain : la lincomycine, antibiotique d’origine natu- relle et son dérivé hémisynthétique, la clindamycine. Ces antibiotiques d’excellente biodisponibilité sont utilisés pour leur activité antistaphylococcique et antistreptococcique et, pour la clindamycine, son activité antianaérobie
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#Antibiotics #Antibiotiques #Apparentés-macrolides #Lincosamides #Maladies-infectieuses-et-tropicales #Streptogramines
En pratique, la clindamycine est utilisée de préférence à la lincomycine car mieux absorbée per os et plus active
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À partir de la lincomycine, de nombreux dérivés ont été préparés par hémisynthèse afin d’accroître le spectre antibacté- rien et l’activité. Des substituants du groupement hydroxyle en position 7 ont donné naissance à de nombreux dérivés comme la clindamycine (groupement chlore) (Dalacine ® )(Fig. 1)etla pirlimycine (à usage vétérinaire). Ces molécules sont très stables lyophilisées ou en solution
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Alors que la structure chimique des lincosamides est très différente de celle des macrolides, leur mécanisme d’action est proche
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#Antibiotics #Antibiotiques #Apparentés-macrolides #Lincosamides #Maladies-infectieuses-et-tropicales #Streptogramines
La pénétration des lincosamides dans la bactérie s’effectue probablement par diffusion passive. La diffusion est limitée chez les bactéries à Gram négatif par la présence d’une membrane externe et surtout de pompes d’efflux physiologiques, expliquant la résistance naturelle de ce groupe bactérien.
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Chez les bactéries à Gram positif sensibles, les lincosamides inhibent la synthèse protéique en se fixant sur la plus grosse des deux sous-unités du ribosome, la 50S, et en inhibant l’étape d’élongation
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Aux concentrations supérieures aux concentrations minimales inhibitrices (CMI), les lincosamides inhibent la croissance bactérienne. À concentration subinhibitrice, il est largement prouvé in vitro que la clindamycine supprime la synthèse de toxines par des souches toxinogènes de Staphylococcus aureus et de Streptococcus pyogenes (streptocoque du groupe A) [2]
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#Antibiotics #Antibiotiques #Apparentés-macrolides #Lincosamides #Maladies-infectieuses-et-tropicales #Streptogramines
De façon un peu semblable aux macrolides, la clindamycine a montré un effet immunomodulateur [3] .
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#Antibiotics #Antibiotiques #Apparentés-macrolides #Lincosamides #Maladies-infectieuses-et-tropicales #Streptogramines
Les lincosamides ont un spectre antimicrobien étroit puisque ces antibiotiques sont actifs contre les bactéries aérobies à Gram positif (sauf Enterococcus faecalis naturellement résistant) mais pas contre les bactéries aérobies à Gram négatif (résistance naturelle)
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#Antibiotics #Antibiotiques #Apparentés-macrolides #Lincosamides #Maladies-infectieuses-et-tropicales #Streptogramines
La clindamycine est très active contre les bactéries anaérobies, à part Clostridium difficile, et possède une activité contre quelques protozoaires.
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En plus de l’activité antibactérienne détaillée dans le Tableau 2, la clindamycine possède une activité antiplasmodiale et antitoxoplasmique. Chez Plasmodium falciparum, elle réduit la synthèse protéique et la synthèse des acides nucléiques. Elle réduit aussi la croissance de Toxoplama gondii et possède une bonne activité sur Pneumocystis jirovecii et sur les Babesia.
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#Antibiotics #Antibiotiques #Apparentés-macrolides #Lincosamides #Maladies-infectieuses-et-tropicales #Streptogramines
Les bactéries peuvent résister aux lincosamides par trois mécanismes : par modification de la cible via une méthylation de la cible ribosomale de l’antibiotique, par inactivation enzymatique de l’antibiotique et par efflux. En pathologie clinique, l’impact de ces trois mécanismes est inégal en termes d’incidence et d’implication clinique.
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Méthylation ribosomale C’est le mécanisme de loin le plus fréquent [4, 5] . La résistance est liée à une méthylation de l’acide ribonucléique (ARN) 23S qui est un composant de la sous-unité ribosomale 50S. C’est précisément l’adénine en position 2058 de l’ARN 23S qui est méthylée. Cette base joue un rôle clé dans la liaison des macrolides, lincosamides et du facteur B des streptogramines au ribosome
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Résistance par méthylation ribosomale
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Lorsque la résistance est inductible, la méthylase n’est produite qu’en présence d’anti- biotiques inducteurs, qui se limitent aux macrolides à noyau à 14 et 15 atomes (érythromycine, roxithromycine, clarithromy- cine et azithromycine). Les macrolides à 16 atomes (josamycine, spiramycine), les lincosamides et les streptogramines B ne sont pas inducteurs et restent donc actifs.
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Résistance par méthylation ribosomale
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Bien que des cas d’échec clinique par sélection de tels mutants lors de traitement par la clindamycine d’infections à staphylocoque aient été rapportés, ils restent rares [6] . En théorie, le risque d’échec devrait être plus important pour les infections avec un fort inoculum bactérien (abcès volumineux)
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Résistance par méthylation ribosomale
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Une autre méthyltransférase, codée par le gène cfr, modifiant l’adénine en position 2503 de l’ARNr 23s a été rapportée chez les staphylocoques chez qui elle est cependant très rare [7] . Cette résistance est responsable d’une résistance croisée à cinq antibiotiques, la clindamycine, le facteur A des streptogramines, le linézolide, le chloramphénicol et les pleuromutilines (anti- biotiques vétérinaires)
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#Antibiotics #Antibiotiques #Apparentés-macrolides #Lincosamides #Maladies-infectieuses-et-tropicales #Streptogramines
Efflux. Chez S. aureus, l’acquisition de gènes plasmidiques vga(A) et vga(Av) confère un bas niveau de résistance croisé entre la lincomycine, la clindamycine (résistance intermédiaire) et les streptogramines A. Ce phénotype est dénommé LS A . Les protéines Vga sont apparentées à des pompes fonctionnant à l’ATP, les ABC transporteurs, suggérant que la résistance est due à un efflux. L’acquisition de protéines VgA ne rend pas compte à elle seule du phénotype LS A qui peut être lié à d’autres mécanismes encore mal connus
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#Antibiotics #Antibiotiques #Apparentés-macrolides #Lincosamides #Maladies-infectieuses-et-tropicales #Streptogramines

Inactivation enzymatique des lincosamides.

L’inactivation enzymatique par nucléotidylation d’un groupement hydroxyle en position 3 ou 4 des lincosamides va conférer une résistance uniquement à ces antibiotiques, à la différence du mécanisme précédent. Les gènes de la classe lnu codent pour une lincosamide nucléotidyltransférase chez les staphylocoques, les streptocoques du groupe B et Streptococcus uberis. Ces résistances sont peu fréquentes chez S. aureus (moins de 1 %), chez les staphylocoques à coagulase négative (entre 1 % et 7 %) et chez les streptocoques (moins de 1 %)

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[unknown IMAGE 7104760515852]
Tableau 1 : Spectre d'activité des lincosamides et streptogramines
#Antibiotics #Antibiotiques #Apparentés-macrolides #Lincosamides #Maladies-infectieuses-et-tropicales #Streptogramines #has-images
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#Antibiotics #Antibiotiques #Apparentés-macrolides #Lincosamides #Maladies-infectieuses-et-tropicales #Streptogramines
Les résistances acquises aux lincosamides sont essentiellement dues à l’acquisition de méthylases Erm. Les autres mécanismes ne sont que peu représentés chez les souches résistantes.
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[unknown IMAGE 7104765496588] #Antibiotics #Antibiotiques #Apparentés-macrolides #Lincosamides #Maladies-infectieuses-et-tropicales #Streptogramines #has-images
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#Antibiotics #Antibiotiques #Apparentés-macrolides #Lincosamides #Maladies-infectieuses-et-tropicales #Streptogramines
Clindamycine [9, 10] Elle est administrée sous forme de phosphate de clindamy- cine pour un usage parentéral et sous forme de chlorhydrate de clindamycine pour la forme orale. La clindamycine sous forme phosphatée est inactive sur les bactéries. Après administration chez l’Homme, l’action de phosphatases présentes dans l’orga- nisme active la clindamycine libre.
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PK Clindamycine
#Antibiotics #Antibiotiques #Apparentés-macrolides #Lincosamides #Maladies-infectieuses-et-tropicales #Streptogramines
Forme orale. La posologie chez l’adulte est de 600 à 2 400 mg par 24 heures en 2, 3 ou 4 prises
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PK Clindamycine
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Après une dose unique de chlorhydrate de clindamycine de 150 à 450 mg, les pics sériques apparaissent en moins de 1 heure et sont compris entre 2,56 mg/l et 5,58 mg/l. La biodisponibilité, de l’ordre de 80 %, ne varie pas avec la prise alimentaire malgré une vitesse d’absorption ralentie
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PK Clindamycine
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Forme intraveineuse. La clindamycine s’administre en intraveineuse lente après dilution. La posologie recommandée chez l’adulte est de 600 à 2 400 mg/24 h en deux à trois fois par jour et chez l’enfant de plus de 30 jours, elle est de 10 à 40 mg/kg/24 h en deux à trois fois par jour
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PK Clindamycine
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Après une perfusion lente sur 1 heure, la concentration obtenue est de 5,4 mg/l et de 15,87 mg/l, respectivement pour une dose de 300 mg et de 1 200 mg. La demi-vie d’élimination estde2à3heures en moyenne. Le volume apparent de distribution est compris entre 43 et 75 l. La clindamycine s’élimine principalement par voie biliaire et partiellement par les urines.
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PK Clindamycine
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Diffusion tissulaire. La clindamycine se concentre fortement dans les macrophages et polynucléaires neutrophiles. La diffusion dans l’os est en général excellente (1,3 mg/kg en moyenne) bien que variable (0,7 mg/kg à 9,4 mg/kg). Les concentrations sont élevées dans l’œil (vitrée et humeur aqueuse). Elle pénètre bien au niveau des sites respiratoires (poumon, tissu pulmonaire et liquide pleural). Il existe un passage transplacentaire non négligeable. Elle pénètre bien dans la salive, l’ascite et dans la bile avec une élimination biliaire de l’ordre de 30%à40%deladose administrée et des taux deux à trois fois supérieurs à ceux du plasma. Sa diffusion est très faible dans le liquide céphalorachidien
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PK Clindamycine
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Métabolisme. La clindamycine est hydrolysée dans le foie. Sept métabolites ont été décrits dont un seul possède une activité antibactérienne et qui est faiblement excrétée dans les selles et les urines.
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#Antibiotics #Antibiotiques #Apparentés-macrolides #Lincosamides #Maladies-infectieuses-et-tropicales #Streptogramines
Points forts et faibles de la clindamycine. Points forts : • activité antianaérobie, • inhibition (in vitro) des toxines de staphylocoques et streptocoques, • activité bactéricide sur les streptocoques, • activité antiparasitaire, • forme orale, • bonne biodisponibilité et diffusion tissulaire, • peu d’allergie (alternative aux pénicillines). Points faibles : • inactif contre les bactéries à Gram négatifs, • activité bactériostatique contre les staphylocoques, • taux de résistance élevée chez Bacteroides fragilis, • existence de résistance chez staphylocoque et streptocoque, • effet indésirable majeur : colite pseudomembraneuse à Clostridium difficile.
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PD Clindamycine
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À dose usuelle, la lincomycine et la clindamycine montrent une activité bactériostatique. À de plus fortes concentrations, elles peuvent avoir un effet bactéricide lent et moins complet que les b-lactamines. À dose égale, la clindamycine a un effet inhibiteur quatre fois plus important que la lincomycine
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PD Clindamycine
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La clindamycine possède un effet postantibiotique correspon- dant à une inhibition prolongée de la croissance bactérienne après une exposition limitée dans le temps à l’antibiotique sur S. pneumoniae, S. pyogenes et S. aureus
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PD Clindamycine
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Peu de données sont disponibles sur les paramètres pharma- codynamiques gouvernant l’activité de la clindamycine. Cepen- dant, il semble que le temps au-dessus de la CMI (T > CMI) soit corrélé avec l’efficacité de la clindamycine. La concentration libre de clindamycine doit être au-dessus de la CMI pendant au moins 40-50 % du temps entre deux administrations pour obtenir une efficacité clinique et microbiologique suffisante [11] . Son efficacité n’est pas modifiée par la taille de l’inoculum, ni par la phase de croissance
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EI Digestifs CLINDAMYCINE
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Digestifs C’est l’effet secondaire le plus important et qui limite l’usage de la clindamycine [12] . Près de 20 % des patients traités par de la clindamycine vont présenter une diarrhée ne nécessitant habituellement pas l’interruption du traitement.
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EI Digestifs CLINDAMYCINE - Colite pseudomembraneuse
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De façon plus préoccupante, la clindamycine peut être responsable de prolifé- ration de Clostridium difficile dans l’intestin et de la production de toxine qui est à l’origine de colite pseudomembraneuse chez 0,01%à10%despatients traités par cet antibiotique.
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EI Digestifs CLINDAMYCINE - Colite pseudomembraneuse
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La colite survient8à10jours après l’initiation du traitement et cela indépendamment de la forme posologique (orale ou veineux) ou de la quantité reçue
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EI Vasculaires CLINDAMYCINE
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La perfusion de lincosamides doit être lente (minimum de 20 minutes pour 600 mg) en raison de risque d’hypotension artérielle.
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#Antibiotics #Antibiotiques #Apparentés-macrolides #Lincosamides #Maladies-infectieuses-et-tropicales #Streptogramines
Les sels et hydroxydes d’aluminium diminuent l’absorption digestive des lincosamides. D’une façon générale, il faut prendre les topiques gastro-intestinaux à distance des lincosamides (plus de 2 heures)
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#Antibiotics #Antibiotiques #Apparentés-macrolides #Lincosamides #Maladies-infectieuses-et-tropicales #Streptogramines
L’association avec la ciclosporine diminue les concentrations sanguines de l’immunosuppresseur avec risque de perte de l’activité immunosuppressive. Il faut alors contrôler les dosages sanguins de ciclosporine et augmenter éventuellement sa posologie
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La posologie ne doit pas être modifiée chez le sujet âgé
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#Antibiotics #Antibiotiques #Apparentés-macrolides #Lincosamides #Maladies-infectieuses-et-tropicales #Streptogramines
La présence de 2 mg de sodium par ampoule doit être prise en compte chez les personnes suivant un régime hypo- sodé strict
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#Antibiotics #Antibiotiques #Apparentés-macrolides #Lincosamides #Maladies-infectieuses-et-tropicales #Streptogramines
La clindamycine peut être aussi considérée dans le traitement des infections profondes (hors système nerveux central) dues à des anaérobies (sauf B. fragilis pour lequel l’étude de la sensibilité est nécessaire du fait de la fréquence de la résistance).
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En première intention, la clindamycine est indiquée dans les dermohypodermites nécrosantes, associée à une bêtalactamine. De surcroît, elle diminue la synthèse de toxine bactérienne. Et possède un effet postantibiotique plus long que les pénicillines
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La clindamycine a été récemment évaluée dans le traitement de diverses infections ostéoarticulaires à staphylocoque ou streptocoque ou Propionibacterium en association avec de la rifampicine ou des fluoroquinolones [14] . La guérison a été obtenue chez 51,1 % des 56 patients inclus. La clindamycine a été aussi évaluée en perfusion continue dans ce type d’infection avec un fort taux de succès (92 % de guérison) et une bonne tolérance [15]
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Elle est cependant moins rapidement efficace et le taux d’échec est supérieur à celui de l’association pyrimé- thamine + sulfadiazine
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Les streptogramines (ou synergistines) sont des antibiotiques à spectre étroit associant deux facteurs A et B agissant en synergie
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Deux streptogramines sont commercialisées : la pristinamycine (Pyostacine ® ) administrable per os et surtout utilisée depuis la fin des années 1960 dans les infections cutanées à staphylocoques et les infections bronchopulmonaires et la quinupristine-dalfopristine (Synercid ® ) commercialisée depuis 1999, administrable par voie intraveineuse et utilisable en milieu hospitalier contre les coques à Gram positif multirésistants
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In addition, it is now known to have a more varied clinical spectrum than previously realized.
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ypes of stroke but can be more challenging to diagnose. Due to the widespread use of magnetic resonance imaging (MRI) and rising clinical awareness, CVT is recognized with increasing frequency. <span>In addition, it is now known to have a more varied clinical spectrum than previously realized. Because of its myriad causes and presentations, CVT is a disease that may be encountered not only by neurologists and neurosurgeons but also by emergency clinicians, internists, oncolog




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The available data suggest that CVT is uncommon [1]. The annual incidence ranges from 1.16 to 2.02 per 100,000 [2-4] and is more common in females than males, with a female-to-male ratio of 3:1 [5,6].
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rognosis".) CVT in newborns is also reviewed elsewhere. (See "Stroke in the newborn: Classification, manifestations, and diagnosis", section on 'Cerebral sinovenous thrombosis'.) EPIDEMIOLOGY — <span>The available data suggest that CVT is uncommon [1]. The annual incidence ranges from 1.16 to 2.02 per 100,000 [2-4] and is more common in females than males, with a female-to-male ratio of 3:1 [5,6]. The imbalance may be due to the increased risk of CVT associated with pregnancy and puerperium and with oral contraceptives [7]. (See 'Acquired risk factors' below.) In adults, CVT affe




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In adults, CVT affects patients who are younger on average than those with arterial types of stroke. In the International Study on Cerebral Vein and Dural Sinus Thrombosis (ISCVT), the median age of patients with CVT was 37 years [5], and only 8 percent of the patients were older than 65 [8]. Compared with males, females were significantly younger (median age 34 years, versus 42 years for men) [6]
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to-male ratio of 3:1 [5,6]. The imbalance may be due to the increased risk of CVT associated with pregnancy and puerperium and with oral contraceptives [7]. (See 'Acquired risk factors' below.) <span>In adults, CVT affects patients who are younger on average than those with arterial types of stroke. In the International Study on Cerebral Vein and Dural Sinus Thrombosis (ISCVT), the median age of patients with CVT was 37 years [5], and only 8 percent of the patients were older than 65 [8]. Compared with males, females were significantly younger (median age 34 years, versus 42 years for men) [6]. There is a low risk of recurrent CVT and venous thromboembolism after a first CVT, as reviewed separately. (See "Cerebral venous thrombosis: Treatment and prognosis", section on 'Recur




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However, there are at least two different mechanisms that may contribute to the clinical features of CVT (figure 1) [9]:

● Thrombosis of cerebral veins or dural sinus obstructs blood drainage from brain tissue, leading to cerebral parenchymal lesions (eg, stroke) or dysfunction and to increased venous and capillary pressure with disruption of the blood-brain barrier.

● Occlusion of dural sinus resulting in decreased cerebrospinal fluid (CSF) absorption and elevated intracranial pressure.

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ATHOGENESIS — The pathogenesis of CVT remains incompletely understood because of the high variability in the anatomy of the venous system and the paucity of experiments in animal models of CVT. <span>However, there are at least two different mechanisms that may contribute to the clinical features of CVT (figure 1) [9]: ●Thrombosis of cerebral veins or dural sinus obstructs blood drainage from brain tissue, leading to cerebral parenchymal lesions (eg, stroke) or dysfunction and to increased venous and capillary pressure with disruption of the blood-brain barrier. ●Occlusion of dural sinus resulting in decreased cerebrospinal fluid (CSF) absorption and elevated intracranial pressure. Obstruction of the venous structures (figure 2) results in increased venous pressure, decreased capillary perfusion pressure, and increased cerebral blood volume. Dilatation of cerebral




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Obstruction of the venous structures (figure 2) results in increased venous pressure, decreased capillary perfusion pressure, and increased cerebral blood volume. Dilatation of cerebral veins and recruitment of collateral pathways play an important role in the early phases of CVT and may initially compensate for changes in pressure.
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nous and capillary pressure with disruption of the blood-brain barrier. ●Occlusion of dural sinus resulting in decreased cerebrospinal fluid (CSF) absorption and elevated intracranial pressure. <span>Obstruction of the venous structures (figure 2) results in increased venous pressure, decreased capillary perfusion pressure, and increased cerebral blood volume. Dilatation of cerebral veins and recruitment of collateral pathways play an important role in the early phases of CVT and may initially compensate for changes in pressure. The increase in venous and capillary pressure leads to blood-brain barrier disruption, causing vasogenic edema, with leakage of blood plasma into the interstitial space. As intravenous




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Elevated intracranial pressure is more frequent if superior sagittal sinus thrombosis is present, but it may also occur with thrombosis of the jugular vein or the lateral sinus. Note that the lateral sinus consists of two segments; the proximal segment is termed the transverse sinus, and the distal segment is termed the sigmoid sinus (figure 2).
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tic system, which drain CSF into the venous system. Thrombosis of the dural sinuses leads to increased venous pressure, impaired CSF absorption, and consequently elevated intracranial pressure. <span>Elevated intracranial pressure is more frequent if superior sagittal sinus thrombosis is present, but it may also occur with thrombosis of the jugular vein or the lateral sinus. Note that the lateral sinus consists of two segments; the proximal segment is termed the transverse sinus, and the distal segment is termed the sigmoid sinus (figure 2). RISK FACTORS AND ASSOCIATED CONDITIONS — Many conditions are associated with CVT. The major risk factors for CVT in adults can be grouped as transient or permanent (table 1). The most f




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The major risk factors for CVT in adults can be grouped as transient or permanent (table 1). The most frequent risk factors for CVT are [1,5]:

● Prothrombotic conditions, either genetic or acquired

● Obesity

● Oral contraceptives

● Pregnancy and the puerperium

● Malignancy

● Infection

● Head injury and mechanical precipitants

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proximal segment is termed the transverse sinus, and the distal segment is termed the sigmoid sinus (figure 2). RISK FACTORS AND ASSOCIATED CONDITIONS — Many conditions are associated with CVT. <span>The major risk factors for CVT in adults can be grouped as transient or permanent (table 1). The most frequent risk factors for CVT are [1,5]: ●Prothrombotic conditions, either genetic or acquired ●Obesity ●Oral contraceptives ●Pregnancy and the puerperium ●Malignancy ●Infection ●Head injury and mechanical precipitants In more than 85 percent of adult patients, at least one risk factor for CVT can be identified, most often an inherited or acquired prothrombotic condition [5]. In the Canadian pediatric




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In more than 85 percent of adult patients, at least one risk factor for CVT can be identified, most often an inherited or acquired prothrombotic condition [5].
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CVT are [1,5]: ●Prothrombotic conditions, either genetic or acquired ●Obesity ●Oral contraceptives ●Pregnancy and the puerperium ●Malignancy ●Infection ●Head injury and mechanical precipitants <span>In more than 85 percent of adult patients, at least one risk factor for CVT can be identified, most often an inherited or acquired prothrombotic condition [5]. In the Canadian pediatric ischemic stroke registry, a risk factor was identified in 98 percent of the children [16]. A prothrombotic state was found in 41 percent. In infants older than




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The most common risk factors in those ≥65 years old are genetic or acquired thrombophilia, malignancy, and hematologic disorders such as polycythemia [8,17].
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r than four weeks of age and in children, head and neck disorders, mostly infections and chronic systemic diseases (eg, connective tissue disease, hematologic disorder, and cancer) were common. <span>The most common risk factors in those ≥65 years old are genetic or acquired thrombophilia, malignancy, and hematologic disorders such as polycythemia [8,17]. Acquired risk factors — The most common acquired risk factors are pregnancy and the puerperium, the use of oral contraceptives, malignancy, and obesity [18,19]. (See "Cerebrovascular di




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In infants older than four weeks of age and in children, head and neck disorders, mostly infections and chronic systemic diseases (eg, connective tissue disease, hematologic disorder, and cancer) were common.
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prothrombotic condition [5]. In the Canadian pediatric ischemic stroke registry, a risk factor was identified in 98 percent of the children [16]. A prothrombotic state was found in 41 percent. <span>In infants older than four weeks of age and in children, head and neck disorders, mostly infections and chronic systemic diseases (eg, connective tissue disease, hematologic disorder, and cancer) were common. The most common risk factors in those ≥65 years old are genetic or acquired thrombophilia, malignancy, and hematologic disorders such as polycythemia [8,17]. Acquired risk factors — The




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Acquired risk factors — The most common acquired risk factors are pregnancy and the puerperium, the use of oral contraceptives, malignancy, and obesity [18,19].
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disorder, and cancer) were common. The most common risk factors in those ≥65 years old are genetic or acquired thrombophilia, malignancy, and hematologic disorders such as polycythemia [8,17]. <span>Acquired risk factors — The most common acquired risk factors are pregnancy and the puerperium, the use of oral contraceptives, malignancy, and obesity [18,19]. (See "Cerebrovascular disorders complicating pregnancy" and "Combined estrogen-progestin contraception: Side effects and health concerns" and "Risk and prevention of venous thromboembol




Acquired risk factor
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Obesity is a risk factor for CVT and other forms of venous thromboembolism. In an observational study of 186 patients with CVT and matched controls, obesity was associated with an elevated risk of CVT for females (adjusted odds ratio [aOR] 3.5, 95% CI 2.0-6.1) but not males (aOR 1.2, 95% CI 0.3-5.3) [26].
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ic acid, and cisplatin) may increase the risk of venous thromboembolism including CVT through procoagulant effects. (See "Pathogenesis of the hypercoagulable state associated with malignancy".) <span>Obesity is a risk factor for CVT and other forms of venous thromboembolism. In an observational study of 186 patients with CVT and matched controls, obesity was associated with an elevated risk of CVT for females (adjusted odds ratio [aOR] 3.5, 95% CI 2.0-6.1) but not males (aOR 1.2, 95% CI 0.3-5.3) [26]. The risk was highest for females with obesity using oral contraceptive medications (aOR 29.3, 95% CI 13.5-63.6). (See "Overview of the causes of venous thrombosis", section on 'Obesity'




Acquired risk factor
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Chemotherapeutic agents – Several medications used to treat cancer (eg, L-asparaginase, all-trans retinoic acid, and cisplatin) may increase the risk of venous thromboembolism including CVT through procoagulant effects.
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creased in the presence of a prothrombotic defect and obesity [25,26]. (See "Combined estrogen-progestin contraception: Side effects and health concerns", section on 'Venous thromboembolism'.) ●<span>Chemotherapeutic agents – Several medications used to treat cancer (eg, L-asparaginase, all-trans retinoic acid, and cisplatin) may increase the risk of venous thromboembolism including CVT through procoagulant effects. (See "Pathogenesis of the hypercoagulable state associated with malignancy".) Obesity is a risk factor for CVT and other forms of venous thromboembolism. In an observational study of 18




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Genetic thrombophilia — The risk for CVT is influenced by the individual's genetic background [27]. In the presence of some prothrombotic conditions, patients are at an increased risk of developing a CVT when exposed to a precipitant such as head trauma, lumbar puncture, jugular catheter placement, pregnancy, surgery, infection, and drugs.
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[26]. The risk was highest for females with obesity using oral contraceptive medications (aOR 29.3, 95% CI 13.5-63.6). (See "Overview of the causes of venous thrombosis", section on 'Obesity'.) <span>Genetic thrombophilia — The risk for CVT is influenced by the individual's genetic background [27]. In the presence of some prothrombotic conditions, patients are at an increased risk of developing a CVT when exposed to a precipitant such as head trauma, lumbar puncture, jugular catheter placement, pregnancy, surgery, infection, and drugs. These prothrombotic conditions include the following: ●Antithrombin deficiency [28,29] ●Protein C deficiency or protein S deficiency [16,30,31] ●Factor V Leiden pathologic variant [24,3




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These prothrombotic conditions include the following:

● Antithrombin deficiency [28,29]

● Protein C deficiency or protein S deficiency [16,30,31]

● Factor V Leiden pathologic variant [24,32,33]

● G20210 A prothrombin gene pathologic variant [24,33-35]

● Hyperhomocysteinemia [36]

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, patients are at an increased risk of developing a CVT when exposed to a precipitant such as head trauma, lumbar puncture, jugular catheter placement, pregnancy, surgery, infection, and drugs. <span>These prothrombotic conditions include the following: ●Antithrombin deficiency [28,29] ●Protein C deficiency or protein S deficiency [16,30,31] ●Factor V Leiden pathologic variant [24,32,33] ●G20210 A prothrombin gene pathologic variant [24,33-35] ●Hyperhomocysteinemia [36] In a meta-analysis of case-control studies, with over 200 neonatal and pediatric cases of sinovenous thrombosis (ie, CVT) and 1200 control subjects, the prevalence of factor V Leiden (F




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The association of CVT with hyperhomocysteinemia due to genetic variants in methylene tetrahydrofolate reductase (MTHFR) is controversial [27,38,39].
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e prevalence of the prothrombin gene variant among cases and controls was 5.2 and 2.5 percent, respectively, and carriers were significantly more likely to develop CVT (OR 3.1, 95% CI 1.4-6.8). <span>The association of CVT with hyperhomocysteinemia due to genetic variants in methylene tetrahydrofolate reductase (MTHFR) is controversial [27,38,39]. A 2010 meta-analysis of case-control studies found that the frequency of the MTHFR 677C>T polymorphism in adults was similar for 382 patients with CVT compared with 1217 controls (15




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In a review of 34,331 patients hospitalized with SARS-CoV-2 infection, the frequency of CVT was 0.08 percent (95% CI 0.01-0.5) [41]
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e been observed in the setting of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, the majority of which occurred in patient without other predisposing risk factors [41]. <span>In a review of 34,331 patients hospitalized with SARS-CoV-2 infection, the frequency of CVT was 0.08 percent (95% CI 0.01-0.5) [41]. The in-hospital mortality was 40 percent. (See "COVID-19: Neurologic complications and management of neurologic conditions", section on 'Cerebrovascular disease'.) Multiple reports des




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In cohort studies, those with vaccine-induced thrombotic thrombocytopenia (VITT) have been typically younger and less likely to have other thromboembolic risk factors than those with CVT not attributed to VITT [47,49,50]. However, patients with VITT have a higher burden of both intracranial and extracranial venous thromboses [49]. In addition, the clinical presentation is more severe and mortality is higher for those with CVT associated with VITT than other causes of CVT, ranging from 22 to 47 percent in studies, compared with 3 to 5 percent among those with other causes of CVT [46,47,49-51]
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sm including CVT associated with thrombocytopenia among patients immunized with the adenovirus-vector ChAdOx1 nCov-19 (AstraZeneca COVID-19) and Ad26.COV2.S (Janssen COVID-19) vaccines [42-48]. <span>In cohort studies, those with vaccine-induced thrombotic thrombocytopenia (VITT) have been typically younger and less likely to have other thromboembolic risk factors than those with CVT not attributed to VITT [47,49,50]. However, patients with VITT have a higher burden of both intracranial and extracranial venous thromboses [49]. In addition, the clinical presentation is more severe and mortality is higher for those with CVT associated with VITT than other causes of CVT, ranging from 22 to 47 percent in studies, compared with 3 to 5 percent among those with other causes of CVT [46,47,49-51]. Cases of CVT associated with VITT have typically occurred in patients who are between 5 and 30 days post-vaccination [42-44,52,53]. Some cases occurring after the second dose of the Ch




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Other conditions — Although infectious causes of CVT were frequently reported in the past, they are responsible for only 6 to 12 percent of cases in modern-era studies of adults with CVT [5,18]. Local infections (eg, involving the ears, sinuses, mouth, face, or neck) are typically responsible, although systemic infection is sometimes the only cause
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T is discussed in greater detail separately. (See "COVID-19: Vaccines", section on 'Thrombosis with thrombocytopenia' and "COVID-19: Vaccine-induced immune thrombotic thrombocytopenia (VITT)".) <span>Other conditions — Although infectious causes of CVT were frequently reported in the past, they are responsible for only 6 to 12 percent of cases in modern-era studies of adults with CVT [5,18]. Local infections (eg, involving the ears, sinuses, mouth, face, or neck) are typically responsible, although systemic infection is sometimes the only cause. Head injury and mechanical precipitants are less common causes of CVT [55-57]. Inflammatory diseases are also risk factors for CVT, including systemic lupus erythematosus, Behçet disea




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Inflammatory diseases are also risk factors for CVT, including systemic lupus erythematosus, Behçet disease, granulomatosis with polyangiitis, thromboangiitis obliterans, inflammatory bowel disease, and sarcoidosis.
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sinuses, mouth, face, or neck) are typically responsible, although systemic infection is sometimes the only cause. Head injury and mechanical precipitants are less common causes of CVT [55-57]. <span>Inflammatory diseases are also risk factors for CVT, including systemic lupus erythematosus, Behçet disease, granulomatosis with polyangiitis, thromboangiitis obliterans, inflammatory bowel disease, and sarcoidosis. As with venous thrombosis in other parts of the body, multiple risk factors may be found in about half of adult patients with CVT [5]. In light of this, a thorough search for additional




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Head injury and mechanical precipitants are less common causes of CVT [55-57].
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a studies of adults with CVT [5,18]. Local infections (eg, involving the ears, sinuses, mouth, face, or neck) are typically responsible, although systemic infection is sometimes the only cause. <span>Head injury and mechanical precipitants are less common causes of CVT [55-57]. Inflammatory diseases are also risk factors for CVT, including systemic lupus erythematosus, Behçet disease, granulomatosis with polyangiitis, thromboangiitis obliterans, inflammatory b




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As with venous thrombosis in other parts of the body, multiple risk factors may be found in about half of adult patients with CVT [5]. In light of this, a thorough search for additional causes should be carried out even when a specific risk factor is identified in a given patient. (See "Overview of the causes of venous thrombosis".)
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are also risk factors for CVT, including systemic lupus erythematosus, Behçet disease, granulomatosis with polyangiitis, thromboangiitis obliterans, inflammatory bowel disease, and sarcoidosis. <span>As with venous thrombosis in other parts of the body, multiple risk factors may be found in about half of adult patients with CVT [5]. In light of this, a thorough search for additional causes should be carried out even when a specific risk factor is identified in a given patient. (See "Overview of the causes of venous thrombosis".) Cryptogenic CVT — No underlying etiology or risk factor for CVT is found in a minority of children (≤10 percent) and adults (13 percent) with CVT [8,16,58]. In older adult CVT patients,




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Cryptogenic CVT — No underlying etiology or risk factor for CVT is found in a minority of children (≤10 percent) and adults (13 percent) with CVT [8,16,58].
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ht of this, a thorough search for additional causes should be carried out even when a specific risk factor is identified in a given patient. (See "Overview of the causes of venous thrombosis".) <span>Cryptogenic CVT — No underlying etiology or risk factor for CVT is found in a minority of children (≤10 percent) and adults (13 percent) with CVT [8,16,58]. In older adult CVT patients, the proportion of cases without identified risk factors is higher (37 percent) than it is in adults under age 65 (10 percent) [8]. CLINICAL ASPECTS — Cerebr




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Cerebral vein and dural sinus thrombosis has a highly variable clinical presentation [59,60]. The onset can be acute, subacute, or chronic. CVT most often presents with new headache or as a syndrome of isolated intracranial hypertension. Additional manifestations include focal neurologic deficits, seizures, and/or encephalopathy
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CVT [8,16,58]. In older adult CVT patients, the proportion of cases without identified risk factors is higher (37 percent) than it is in adults under age 65 (10 percent) [8]. CLINICAL ASPECTS — <span>Cerebral vein and dural sinus thrombosis has a highly variable clinical presentation [59,60]. The onset can be acute, subacute, or chronic. CVT most often presents with new headache or as a syndrome of isolated intracranial hypertension. Additional manifestations include focal neurologic deficits, seizures, and/or encephalopathy. Symptoms and signs — Symptoms and signs of CVT can be grouped into three major syndromes: ●Isolated intracranial hypertension syndrome (headache with or without vomiting, papilledema,




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Symptoms and signs — Symptoms and signs of CVT can be grouped into three major syndromes:

● Isolated intracranial hypertension syndrome (headache with or without vomiting, papilledema, and visual problems) [61]

● Focal syndrome (focal deficits, seizures, or both)

● Encephalopathy (multifocal signs, mental status changes, stupor, or coma) [59,62]

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. CVT most often presents with new headache or as a syndrome of isolated intracranial hypertension. Additional manifestations include focal neurologic deficits, seizures, and/or encephalopathy. <span>Symptoms and signs — Symptoms and signs of CVT can be grouped into three major syndromes: ●Isolated intracranial hypertension syndrome (headache with or without vomiting, papilledema, and visual problems) [61] ●Focal syndrome (focal deficits, seizures, or both) ●Encephalopathy (multifocal signs, mental status changes, stupor, or coma) [59,62] Less common presentations include cavernous sinus syndrome, subarachnoid hemorrhage, and multiple cranial nerve palsies. A case of CVT mimicking a transient ischemic attack has also bee




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Less common presentations include cavernous sinus syndrome, subarachnoid hemorrhage, and multiple cranial nerve palsies. A case of CVT mimicking a transient ischemic attack has also been reported [63].
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r without vomiting, papilledema, and visual problems) [61] ●Focal syndrome (focal deficits, seizures, or both) ●Encephalopathy (multifocal signs, mental status changes, stupor, or coma) [59,62] <span>Less common presentations include cavernous sinus syndrome, subarachnoid hemorrhage, and multiple cranial nerve palsies. A case of CVT mimicking a transient ischemic attack has also been reported [63]. The clinical symptoms and signs in CVT depend upon several factors, including patient age and sex, the site and number of occluded sinuses and veins, the presence of parenchymal brain l




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The clinical symptoms and signs in CVT depend upon several factors, including patient age and sex, the site and number of occluded sinuses and veins, the presence of parenchymal brain lesions, and the interval from CVT onset to presentation
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mon presentations include cavernous sinus syndrome, subarachnoid hemorrhage, and multiple cranial nerve palsies. A case of CVT mimicking a transient ischemic attack has also been reported [63]. <span>The clinical symptoms and signs in CVT depend upon several factors, including patient age and sex, the site and number of occluded sinuses and veins, the presence of parenchymal brain lesions, and the interval from CVT onset to presentation. In children, signs of diffuse brain injury, coma, and seizures are the main clinical manifestations, especially in neonates [16]. In older children, the manifestations of CVT resemble




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Females are more likely than males to have a headache on presentation and less likely to have a chronic onset of symptoms [6].
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coma, and seizures are the main clinical manifestations, especially in neonates [16]. In older children, the manifestations of CVT resemble those in adults, with headache and hemiparesis [64]. <span>Females are more likely than males to have a headache on presentation and less likely to have a chronic onset of symptoms [6]. Older adults may also have a distinctive presentation; depressed consciousness and mental status changes are more common, while headaches and isolated intracranial hypertension are less




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In children, signs of diffuse brain injury, coma, and seizures are the main clinical manifestations, especially in neonates [ 16]. In older children, the manifestations of CVT resemble those in adults, with headache and hemiparesis [64].
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on several factors, including patient age and sex, the site and number of occluded sinuses and veins, the presence of parenchymal brain lesions, and the interval from CVT onset to presentation. <span>In children, signs of diffuse brain injury, coma, and seizures are the main clinical manifestations, especially in neonates [16]. In older children, the manifestations of CVT resemble those in adults, with headache and hemiparesis [64]. Females are more likely than males to have a headache on presentation and less likely to have a chronic onset of symptoms [6]. Older adults may also have a distinctive presentation; dep




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Older adults may also have a distinctive presentation; depressed consciousness and mental status changes are more common, while headaches and isolated intracranial hypertension are less frequent than in younger patients [ 8].
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CVT resemble those in adults, with headache and hemiparesis [64]. Females are more likely than males to have a headache on presentation and less likely to have a chronic onset of symptoms [6]. <span>Older adults may also have a distinctive presentation; depressed consciousness and mental status changes are more common, while headaches and isolated intracranial hypertension are less frequent than in younger patients [8]. Cerebral edema, venous infarction, and hemorrhagic venous infarction are associated with a more severe syndrome; patients are more likely to be comatose or to have motor deficits, aphas




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Cerebral edema, venous infarction, and hemorrhagic venous infarction are associated with a more severe syndrome; patients are more likely to be comatose or to have motor deficits, aphasia, and seizures and less likely to present with isolated headache.
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stinctive presentation; depressed consciousness and mental status changes are more common, while headaches and isolated intracranial hypertension are less frequent than in younger patients [8]. <span>Cerebral edema, venous infarction, and hemorrhagic venous infarction are associated with a more severe syndrome; patients are more likely to be comatose or to have motor deficits, aphasia, and seizures and less likely to present with isolated headache. Headache — Headache is the most frequent symptom of CVT. In the International Study on Cerebral Vein and Dural Sinus Thrombosis (ISCVT) cohort, headache was present in 89 percent of pat




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Headache — Headache is the most frequent symptom of CVT. In the International Study on Cerebral Vein and Dural Sinus Thrombosis (ISCVT) cohort, headache was present in 89 percent of patients [5]. Headaches associated with CVT are more frequent in females and young patients than in males or older adults [65]. Headache is usually the first symptom of CVT and can be the only symptom [66] or can precede other symptoms and signs by days or weeks [67]
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nfarction are associated with a more severe syndrome; patients are more likely to be comatose or to have motor deficits, aphasia, and seizures and less likely to present with isolated headache. <span>Headache — Headache is the most frequent symptom of CVT. In the International Study on Cerebral Vein and Dural Sinus Thrombosis (ISCVT) cohort, headache was present in 89 percent of patients [5]. Headaches associated with CVT are more frequent in females and young patients than in males or older adults [65]. Headache is usually the first symptom of CVT and can be the only symptom [66] or can precede other symptoms and signs by days or weeks [67]. The features of CVT-related headache are quite variable. Head pain may be localized or diffuse [67]. Headache caused by intracranial hypertension from CVT is typically characterized by




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The features of CVT-related headache are quite variable. Head pain may be localized or diffuse [67]. Headache caused by intracranial hypertension from CVT is typically characterized by severe head pain that worsens with Valsalva maneuvers and with recumbency.

The site of the headache has no relationship with the localization of the occluded sinus or the parenchymal lesions [68,69]. Headache onset with CVT is usually gradual, increasing over several days [7]. However, some patients with CVT have sudden explosive onset of severe head pain (ie, thunderclap headache) that mimics subarachnoid hemorrhage [70,71].

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d young patients than in males or older adults [65]. Headache is usually the first symptom of CVT and can be the only symptom [66] or can precede other symptoms and signs by days or weeks [67]. <span>The features of CVT-related headache are quite variable. Head pain may be localized or diffuse [67]. Headache caused by intracranial hypertension from CVT is typically characterized by severe head pain that worsens with Valsalva maneuvers and with recumbency. The site of the headache has no relationship with the localization of the occluded sinus or the parenchymal lesions [68,69]. Headache onset with CVT is usually gradual, increasing over several days [7]. However, some patients with CVT have sudden explosive onset of severe head pain (ie, thunderclap headache) that mimics subarachnoid hemorrhage [70,71]. (See "Overview of thunderclap headache" and "Aneurysmal subarachnoid hemorrhage: Clinical manifestations and diagnosis".) Headache due to CVT may also resemble migraine with aura [72-74




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Headache due to CVT may also resemble migraine with aura [72-74].
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(ie, thunderclap headache) that mimics subarachnoid hemorrhage [70,71]. (See "Overview of thunderclap headache" and "Aneurysmal subarachnoid hemorrhage: Clinical manifestations and diagnosis".) <span>Headache due to CVT may also resemble migraine with aura [72-74]. (See "Pathophysiology, clinical manifestations, and diagnosis of migraine in adults" and "Pathophysiology, clinical features, and diagnosis of migraine in children".) CVT must be includ




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CVT must be included as a possible cause of persisting headache following lumbar puncture, because lumbar puncture can rarely precipitate a CVT.
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igraine with aura [72-74]. (See "Pathophysiology, clinical manifestations, and diagnosis of migraine in adults" and "Pathophysiology, clinical features, and diagnosis of migraine in children".) <span>CVT must be included as a possible cause of persisting headache following lumbar puncture, because lumbar puncture can rarely precipitate a CVT. (See "Post dural puncture headache".) Isolated intracranial hypertension syndrome — Isolated intracranial hypertension syndrome (ie, headache associated with papilledema or visual probl




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Isolated intracranial hypertension syndrome — Isolated intracranial hypertension syndrome (ie, headache associated with papilledema or visual problems) accounts for a significant proportion of CVT cases [61]. Visual obscurations may occur, coinciding with bouts of increased headache intensity.

Isolated intracranial hypertension is more frequent in patients with a chronic presentation than in those who present acutely [75]. In addition, patients with chronic course or delayed clinical presentation may show papilledema on fundoscopy, a finding that is less frequent in acute cases.

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hildren".) CVT must be included as a possible cause of persisting headache following lumbar puncture, because lumbar puncture can rarely precipitate a CVT. (See "Post dural puncture headache".) <span>Isolated intracranial hypertension syndrome — Isolated intracranial hypertension syndrome (ie, headache associated with papilledema or visual problems) accounts for a significant proportion of CVT cases [61]. Visual obscurations may occur, coinciding with bouts of increased headache intensity. Isolated intracranial hypertension is more frequent in patients with a chronic presentation than in those who present acutely [75]. In addition, patients with chronic course or delayed clinical presentation may show papilledema on fundoscopy, a finding that is less frequent in acute cases. (See "Overview and differential diagnosis of papilledema".) Seizures — Focal or generalized seizures, including status epilepticus, are more frequent in CVT than in other cerebrovascula




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Seizures — Focal or generalized seizures, including status epilepticus, are more frequent in CVT than in other cerebrovascular disorders. In the ISCVT cohort of 624 patients, seizures at presentation occurred in 39 percent, and seizures after the diagnosis of CVT occurred in 7 percent [76].
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h chronic course or delayed clinical presentation may show papilledema on fundoscopy, a finding that is less frequent in acute cases. (See "Overview and differential diagnosis of papilledema".) <span>Seizures — Focal or generalized seizures, including status epilepticus, are more frequent in CVT than in other cerebrovascular disorders. In the ISCVT cohort of 624 patients, seizures at presentation occurred in 39 percent, and seizures after the diagnosis of CVT occurred in 7 percent [76]. In a retrospective cohort of 70 children (including 25 neonates) with CVT, seizures at presentation occurred in 20 of 45 non-neonates (44 percent) [77]. Variables associated with seizur




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Variables associated with seizures include supratentorial parenchymal brain lesions, sagittal sinus and cortical vein thrombosis, and motor deficits [76].
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nosis of CVT occurred in 7 percent [76]. In a retrospective cohort of 70 children (including 25 neonates) with CVT, seizures at presentation occurred in 20 of 45 non-neonates (44 percent) [77]. <span>Variables associated with seizures include supratentorial parenchymal brain lesions, sagittal sinus and cortical vein thrombosis, and motor deficits [76]. Encephalopathy — Severe cases of CVT can cause disturbances of consciousness and cognitive dysfunction, such as delirium, apathy, a dysexecutive syndrome, multifocal deficits, or seizur




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Encephalopathy — Severe cases of CVT can cause disturbances of consciousness and cognitive dysfunction, such as delirium, apathy, a dysexecutive syndrome, multifocal deficits, or seizures.
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of 45 non-neonates (44 percent) [77]. Variables associated with seizures include supratentorial parenchymal brain lesions, sagittal sinus and cortical vein thrombosis, and motor deficits [76]. <span>Encephalopathy — Severe cases of CVT can cause disturbances of consciousness and cognitive dysfunction, such as delirium, apathy, a dysexecutive syndrome, multifocal deficits, or seizures. Focal syndrome — Weakness with monoparesis or hemiparesis, sometimes bilateral, is the most frequent focal deficit associated with CVT. In the ISCVT cohort, motor weakness was present i




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Focal syndrome — Weakness with monoparesis or hemiparesis, sometimes bilateral, is the most frequent focal deficit associated with CVT. In the ISCVT cohort, motor weakness was present in 37 percent of patients [5]. Aphasia, in particular of the fluent type, may follow sinus thrombosis, especially when the left lateral sinus is affected. Sensory deficits and visual field defects are less common
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76]. Encephalopathy — Severe cases of CVT can cause disturbances of consciousness and cognitive dysfunction, such as delirium, apathy, a dysexecutive syndrome, multifocal deficits, or seizures. <span>Focal syndrome — Weakness with monoparesis or hemiparesis, sometimes bilateral, is the most frequent focal deficit associated with CVT. In the ISCVT cohort, motor weakness was present in 37 percent of patients [5]. Aphasia, in particular of the fluent type, may follow sinus thrombosis, especially when the left lateral sinus is affected. Sensory deficits and visual field defects are less common. Syndromes associated with isolated sinus or vein thrombosis — Isolated thrombosis of the different sinuses and veins produces diverse clinical pictures. ●In cavernous sinus thrombosis,




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In cavernous sinus thrombosis, ocular signs dominate the clinical picture with orbital pain, chemosis, proptosis, and oculomotor palsies [78-81].
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d visual field defects are less common. Syndromes associated with isolated sinus or vein thrombosis — Isolated thrombosis of the different sinuses and veins produces diverse clinical pictures. ●<span>In cavernous sinus thrombosis, ocular signs dominate the clinical picture with orbital pain, chemosis, proptosis, and oculomotor palsies [78-81]. ●Isolated cortical vein occlusion produces motor/sensory deficits and seizures [82-84]. ●With sagittal sinus occlusion, motor deficits, bilateral deficits, and seizures are frequent, wh




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Isolated cortical vein occlusion produces motor/sensory deficits and seizures [82-84].
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and veins produces diverse clinical pictures. ●In cavernous sinus thrombosis, ocular signs dominate the clinical picture with orbital pain, chemosis, proptosis, and oculomotor palsies [78-81]. ●<span>Isolated cortical vein occlusion produces motor/sensory deficits and seizures [82-84]. ●With sagittal sinus occlusion, motor deficits, bilateral deficits, and seizures are frequent, while presentation as an isolated intracranial hypertension syndrome is infrequent. ●Patie




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With sagittal sinus occlusion, motor deficits, bilateral deficits, and seizures are frequent, while presentation as an isolated intracranial hypertension syndrome is infrequent.
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ns dominate the clinical picture with orbital pain, chemosis, proptosis, and oculomotor palsies [78-81]. ●Isolated cortical vein occlusion produces motor/sensory deficits and seizures [82-84]. ●<span>With sagittal sinus occlusion, motor deficits, bilateral deficits, and seizures are frequent, while presentation as an isolated intracranial hypertension syndrome is infrequent. ●Patients with isolated lateral sinus thrombosis frequently present with isolated headache or isolated intracranial hypertension [85]. Less often, they may also present with focal defic




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Patients with isolated lateral sinus thrombosis frequently present with isolated headache or isolated intracranial hypertension [85]. Less often, they may also present with focal deficits or seizures. Aphasia often follows if the left transverse sinus is occluded.
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ures [82-84]. ●With sagittal sinus occlusion, motor deficits, bilateral deficits, and seizures are frequent, while presentation as an isolated intracranial hypertension syndrome is infrequent. ●<span>Patients with isolated lateral sinus thrombosis frequently present with isolated headache or isolated intracranial hypertension [85]. Less often, they may also present with focal deficits or seizures. Aphasia often follows if the left transverse sinus is occluded. ●Jugular vein or lateral sinus thrombosis may present as isolated pulsating tinnitus [86,87]. ●Multiple cranial nerve palsies may occur in thrombosis of the lateral sinus, jugular, or p




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Jugular vein or lateral sinus thrombosis may present as isolated pulsating tinnitus [86,87].
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isolated headache or isolated intracranial hypertension [85]. Less often, they may also present with focal deficits or seizures. Aphasia often follows if the left transverse sinus is occluded. ●<span>Jugular vein or lateral sinus thrombosis may present as isolated pulsating tinnitus [86,87]. ●Multiple cranial nerve palsies may occur in thrombosis of the lateral sinus, jugular, or posterior fossa veins [88]. ●When the deep cerebral venous system (ie, the straight sinus and i




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Multiple cranial nerve palsies may occur in thrombosis of the lateral sinus, jugular, or posterior fossa veins [88].
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t with focal deficits or seizures. Aphasia often follows if the left transverse sinus is occluded. ●Jugular vein or lateral sinus thrombosis may present as isolated pulsating tinnitus [86,87]. ●<span>Multiple cranial nerve palsies may occur in thrombosis of the lateral sinus, jugular, or posterior fossa veins [88]. ●When the deep cerebral venous system (ie, the straight sinus and its branches) is occluded, the signs and symptoms of CVT are generally severe, with coma or other alterations in mental




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When the deep cerebral venous system (ie, the straight sinus and its branches) is occluded, the signs and symptoms of CVT are generally severe, with coma or other alterations in mental status and motor deficits, often bilateral [89-91]. However, more limited thrombosis of the deep venous system can produce relatively mild symptoms [92].
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teral sinus thrombosis may present as isolated pulsating tinnitus [86,87]. ●Multiple cranial nerve palsies may occur in thrombosis of the lateral sinus, jugular, or posterior fossa veins [88]. ●<span>When the deep cerebral venous system (ie, the straight sinus and its branches) is occluded, the signs and symptoms of CVT are generally severe, with coma or other alterations in mental status and motor deficits, often bilateral [89-91]. However, more limited thrombosis of the deep venous system can produce relatively mild symptoms [92]. Neuroimaging — The neuroimaging features of CVT can include focal areas of edema or venous infarction, hemorrhagic venous infarction, diffuse brain edema, or (rarely) isolated subarachn




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Neuroimaging — The neuroimaging features of CVT can include focal areas of edema or venous infarction, hemorrhagic venous infarction, diffuse brain edema, or (rarely) isolated subarachnoid hemorrhage [1].
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ith coma or other alterations in mental status and motor deficits, often bilateral [89-91]. However, more limited thrombosis of the deep venous system can produce relatively mild symptoms [92]. <span>Neuroimaging — The neuroimaging features of CVT can include focal areas of edema or venous infarction, hemorrhagic venous infarction, diffuse brain edema, or (rarely) isolated subarachnoid hemorrhage [1]. In patients with CVT, the proportion who present with intracerebral hemorrhage is 30 to 40 percent [93,94]. Small nontraumatic juxtacortical hemorrhages (image 1), which are located jus




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In patients with CVT, the proportion who present with intracerebral hemorrhage is 30 to 40 percent [ 93,94].
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g — The neuroimaging features of CVT can include focal areas of edema or venous infarction, hemorrhagic venous infarction, diffuse brain edema, or (rarely) isolated subarachnoid hemorrhage [1]. <span>In patients with CVT, the proportion who present with intracerebral hemorrhage is 30 to 40 percent [93,94]. Small nontraumatic juxtacortical hemorrhages (image 1), which are located just below the cortex in the white matter and have a diameter of <2 cm, account for up to one-fourth of intr




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Small nontraumatic juxtacortical hemorrhages ( image 1), which are located just below the cortex in the white matter and have a diameter of <2 cm, account for up to one-fourth of intracerebral hemorrhages in patients with CVT and are associated with superior sagittal sinus occlusion [95].
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us infarction, diffuse brain edema, or (rarely) isolated subarachnoid hemorrhage [1]. In patients with CVT, the proportion who present with intracerebral hemorrhage is 30 to 40 percent [93,94]. <span>Small nontraumatic juxtacortical hemorrhages (image 1), which are located just below the cortex in the white matter and have a diameter of <2 cm, account for up to one-fourth of intracerebral hemorrhages in patients with CVT and are associated with superior sagittal sinus occlusion [95]. In a minority of cases, computed tomography (CT) may demonstrate direct signs of CVT, which include the dense triangle sign, the empty delta sign, and the cord sign, described below (se




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In a minority of cases, computed tomography (CT) may demonstrate direct signs of CVT, which include the dense triangle sign, the empty delta sign, and the cord sign, described below (see 'CT' below)
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the white matter and have a diameter of <2 cm, account for up to one-fourth of intracerebral hemorrhages in patients with CVT and are associated with superior sagittal sinus occlusion [95]. <span>In a minority of cases, computed tomography (CT) may demonstrate direct signs of CVT, which include the dense triangle sign, the empty delta sign, and the cord sign, described below (see 'CT' below). Brain MRI in combination with magnetic resonance venography is the most informative technique for demonstrating the presence of dural thrombus, cortical vein thrombosis, and extent of




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In patients with clinically suspected CVT (eg, presenting with new headache, isolated intracranial hypertension syndrome, focal neurologic deficits, seizures, and/or encephalopathy), urgent neuroimaging is necessary as the first step in the diagnostic evaluation.
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he presence of dural thrombus, cortical vein thrombosis, and extent of brain injury. The imaging findings of CVT are discussed in greater detail below. (See 'Urgent imaging' below.) DIAGNOSIS — <span>In patients with clinically suspected CVT (eg, presenting with new headache, isolated intracranial hypertension syndrome, focal neurologic deficits, seizures, and/or encephalopathy), urgent neuroimaging is necessary as the first step in the diagnostic evaluation. Aside from neuroimaging, there is no simple confirmatory laboratory test that can confidently rule out CVT in the acute phase of the disease. Diagnostic approach — The diagnosis of CVT




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The diagnosis of CVT should be suspected in patients who present with one or more of the following:

● New-onset headache

● Headache with features that differ from the usual pattern (eg, progression or change in attack frequency, severity, or clinical features) in patients with a previous primary headache

● Symptoms or signs of intracranial hypertension

● Encephalopathy

● Focal neurologic symptoms and signs, especially those not fitting a specific vascular distribution or those involving multiple vascular territories

● Seizures

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in the diagnostic evaluation. Aside from neuroimaging, there is no simple confirmatory laboratory test that can confidently rule out CVT in the acute phase of the disease. Diagnostic approach — <span>The diagnosis of CVT should be suspected in patients who present with one or more of the following: ●New-onset headache ●Headache with features that differ from the usual pattern (eg, progression or change in attack frequency, severity, or clinical features) in patients with a previous primary headache ●Symptoms or signs of intracranial hypertension ●Encephalopathy ●Focal neurologic symptoms and signs, especially those not fitting a specific vascular distribution or those involving multiple vascular territories ●Seizures In addition, the diagnosis of CVT should be suspected in patients who have atypical neuroimaging features on routine CT or MRI at presentation, such as cerebral infarction that crosses




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In addition, the diagnosis of CVT should be suspected in patients who have atypical neuroimaging features on routine CT or MRI at presentation, such as cerebral infarction that crosses typical arterial boundaries, hemorrhagic infarction, or lobar intracerebral hemorrhage of otherwise unclear origin [1].
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anial hypertension ●Encephalopathy ●Focal neurologic symptoms and signs, especially those not fitting a specific vascular distribution or those involving multiple vascular territories ●Seizures <span>In addition, the diagnosis of CVT should be suspected in patients who have atypical neuroimaging features on routine CT or MRI at presentation, such as cerebral infarction that crosses typical arterial boundaries, hemorrhagic infarction, or lobar intracerebral hemorrhage of otherwise unclear origin [1]. In any of these scenarios, suspicion for CVT should be particularly high for patients with known risk factors, including prothrombotic conditions, oral contraceptive use, pregnancy and




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A number of normal anatomic variants may mimic sinus thrombosis, including sinus atresia, sinus hypoplasia, asymmetric sinus drainage, and normal sinus filling defects associated with arachnoid granulations or intrasinus septa [1].
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e findings are not always evident, and the diagnosis may rest on imaging features demonstrated by MR venography or CT venography showing only absence of flow in a venous sinus or cortical vein. <span>A number of normal anatomic variants may mimic sinus thrombosis, including sinus atresia, sinus hypoplasia, asymmetric sinus drainage, and normal sinus filling defects associated with arachnoid granulations or intrasinus septa [1]. For example, a study of 100 subjects (without CVT) with normal brain MRI found artifactual transverse sinus flow gaps on MR venography (in nondominant or codominant but not in dominant




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CT — Head CT is normal in up to 30 percent of CVT cases, and most of the findings are nonspecific [59].
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in 31 percent [96]. Another report of 100 subjects without venous pathology found asymmetric lateral sinuses in 49 percent and partial or total absence of one lateral sinus in 20 percent [97]. <span>CT — Head CT is normal in up to 30 percent of CVT cases, and most of the findings are nonspecific [59]. However, CT is often the first investigation to be performed in clinical practice, and it is useful to rule out other acute or subacute cerebral disorders. In about one-third of cases,




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In about one-third of cases, CT demonstrates direct signs of CVT, including the following (image 2) [59,98-100]:

● The cord sign is a curvilinear or linear hyperdensity from a thrombosed cortical vein typically found over the cerebral cortex.

● The dense triangle sign is a triangular or round hyperdensity reflecting a thrombosed sinus on a cross-section view.

● The empty delta sign (also called the empty triangle or negative delta sign) is a triangular pattern of contrast enhancement surrounding a central region without contrast enhancement found in the posterior part of the superior sagittal sinus on head CT performed with contrast.

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of the findings are nonspecific [59]. However, CT is often the first investigation to be performed in clinical practice, and it is useful to rule out other acute or subacute cerebral disorders. <span>In about one-third of cases, CT demonstrates direct signs of CVT, including the following (image 2) [59,98-100]: ●The cord sign is a curvilinear or linear hyperdensity from a thrombosed cortical vein typically found over the cerebral cortex. ●The dense triangle sign is a triangular or round hyperdensity reflecting a thrombosed sinus on a cross-section view. ●The empty delta sign (also called the empty triangle or negative delta sign) is a triangular pattern of contrast enhancement surrounding a central region without contrast enhancement found in the posterior part of the superior sagittal sinus on head CT performed with contrast. Indirect signs of CVT on head CT are more frequent. These can include intense contrast enhancement of falx and tentorium, dilated transcerebral veins, small ventricles, and parenchyma a




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Indirect signs of CVT on head CT are more frequent. These can include intense contrast enhancement of falx and tentorium, dilated transcerebral veins, small ventricles, and parenchyma abnormalities.
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iangular pattern of contrast enhancement surrounding a central region without contrast enhancement found in the posterior part of the superior sagittal sinus on head CT performed with contrast. <span>Indirect signs of CVT on head CT are more frequent. These can include intense contrast enhancement of falx and tentorium, dilated transcerebral veins, small ventricles, and parenchyma abnormalities. In addition, associated brain lesions may be depicted in 60 to 80 percent of patients with CVT. These may be hemorrhagic or nonhemorrhagic: ●Hemorrhagic lesions include intracerebral he




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In addition, associated brain lesions may be depicted in 60 to 80 percent of patients with CVT. These may be hemorrhagic or nonhemorrhagic:

● Hemorrhagic lesions include intracerebral hemorrhage, hemorrhagic infarcts, or rarely (<1 percent) subarachnoid hemorrhage usually limited to the convexity [101-103].

● Nonhemorrhagic lesions include focal areas of hypodensity caused by vasogenic edema or venous infarction, usually not respecting the arterial boundaries, as well as diffuse brain edema. With serial imaging, some lesions may disappear ("vanishing infarcts"), and new lesions may appear.

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ect signs of CVT on head CT are more frequent. These can include intense contrast enhancement of falx and tentorium, dilated transcerebral veins, small ventricles, and parenchyma abnormalities. <span>In addition, associated brain lesions may be depicted in 60 to 80 percent of patients with CVT. These may be hemorrhagic or nonhemorrhagic: ●Hemorrhagic lesions include intracerebral hemorrhage, hemorrhagic infarcts, or rarely (<1 percent) subarachnoid hemorrhage usually limited to the convexity [101-103]. ●Nonhemorrhagic lesions include focal areas of hypodensity caused by vasogenic edema or venous infarction, usually not respecting the arterial boundaries, as well as diffuse brain edema. With serial imaging, some lesions may disappear ("vanishing infarcts"), and new lesions may appear. CT venography — Head CT is often normal in patients with CVT, and MRI techniques for confirming the diagnosis are not readily available in some hospitals and geographic locations. In th




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The overall accuracy of head CT combined with CT venography is 90 to 100 percent, depending on the occlusion site [105]. Compared with digital subtraction intra-arterial angiography, the combination of head CT and CT venography has a sensitivity and specificity of 95 and 91 percent [106].
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ggest CT venography as a useful alternative to MR venography or digital subtraction angiography for the diagnosis of CVT, in agreement with guidelines from the United States and Europe [1,104]. <span>The overall accuracy of head CT combined with CT venography is 90 to 100 percent, depending on the occlusion site [105]. Compared with digital subtraction intra-arterial angiography, the combination of head CT and CT venography has a sensitivity and specificity of 95 and 91 percent [106]. CT venography gives a good visualization of the major dural sinuses [107,108], is readily available, and is quicker than MRI. It can be used for patients who have contraindications to M




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CT venography is often particularly helpful in subacute or chronic CVT because it can demonstrate heterogeneous density in thrombosed venous sinuses. However, its use may be limited because of low resolution of the deep venous system and cortical veins, the risk of contrast reactions, and radiation exposure [105,111,112].
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who have contraindications to MRI [1]. When combined with head CT, it may demonstrate filling defects, sinus wall enhancement, and increased collateral venous drainage (image 3) [106,109,110]. <span>CT venography is often particularly helpful in subacute or chronic CVT because it can demonstrate heterogeneous density in thrombosed venous sinuses. However, its use may be limited because of low resolution of the deep venous system and cortical veins, the risk of contrast reactions, and radiation exposure [105,111,112]. MRI — MRI using gradient echo T2* susceptibility-weighted sequences in combination with MR venography is the most sensitive imaging method for demonstrating the thrombus and the occlude




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The characteristics of the MRI signal depend on the age of the thrombus [117,118]:

● In the first five days, the thrombosed sinuses appear isointense on T1-weighted images and hypointense on T2-weighted images.

● Beyond five days, venous thrombus becomes more apparent because signal is increased on both T1- and T2-weighted images.

● After the first month, thrombosed sinuses exhibit a variable pattern of signal, which may appear isointense.

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hted sequences in combination with MR venography is the most sensitive imaging method for demonstrating the thrombus and the occluded dural sinus or vein (image 3 and image 4) [15,111,113-116]. <span>The characteristics of the MRI signal depend on the age of the thrombus [117,118]: ●In the first five days, the thrombosed sinuses appear isointense on T1-weighted images and hypointense on T2-weighted images. ●Beyond five days, venous thrombus becomes more apparent because signal is increased on both T1- and T2-weighted images. ●After the first month, thrombosed sinuses exhibit a variable pattern of signal, which may appear isointense. On T2*-weighted gradient echo and T2* susceptibility-weighted MRI sequences, the acute thrombus can be directly visualized as an area of hypointensity in the engorged sinus or cortical




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MR venography — MR venography, usually performed using the time-of-flight (TOF) technique, is useful for demonstrating absence of flow in cerebral venous sinuses, though interpretation can be confounded by normal anatomic variants such as sinus hypoplasia and asymmetric flow [1].
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can be difficult, but the use of T2* susceptibility-weighted MRI may enable a diagnosis of isolated cortical vein thrombosis by demonstrating thrombus as an area of hypointensity [84,113,119]. <span>MR venography — MR venography, usually performed using the time-of-flight (TOF) technique, is useful for demonstrating absence of flow in cerebral venous sinuses, though interpretation can be confounded by normal anatomic variants such as sinus hypoplasia and asymmetric flow [1]. Other MR techniques may be useful to distinguish these variants from venous thrombosis. Contrast-enhanced MR venography can provide better visualization of cerebral venous channels, and




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Conventional angiography — Cerebral digital subtraction angiography is typically reserved for cases when the clinical suspicion for CVT is high but CT venography or MR venography are inconclusive [1].
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n the presence of thrombus. A chronically thrombosed hypoplastic sinus will show absence of flow on two-dimensional TOF MR venography and enhancement on contrast-enhanced MRI and MR venography. <span>Conventional angiography — Cerebral digital subtraction angiography is typically reserved for cases when the clinical suspicion for CVT is high but CT venography or MR venography are inconclusive [1]. Angiography may be helpful for making this diagnosis by showing the sudden termination of a cortical vein surrounded by dilated and tortuous collateral "corkscrew veins" or by the filli




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We suggest routine blood studies consisting of a complete blood count, chemistry panel, prothrombin time, and activated partial thromboplastin time for patients with suspected CVT, in agreement with guidelines from the American Heart Association/American Stroke Association [1]
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ne (94 versus 62 percent) [123]. Laboratory tests — Aside from neuroimaging, there is no simple confirmatory laboratory test that can confidently rule out CVT in the acute phase of the disease. <span>We suggest routine blood studies consisting of a complete blood count, chemistry panel, prothrombin time, and activated partial thromboplastin time for patients with suspected CVT, in agreement with guidelines from the American Heart Association/American Stroke Association [1]. The findings from these tests may suggest the presence of conditions that contribute to the development of CVT such as an underlying hypercoagulable state, infection, or inflammatory p




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D-dimer — An elevated plasma D-dimer level supports the diagnosis of CVT, but a normal D-dimer does not exclude the diagnosis in patients with suggestive symptoms and predisposing factors.
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ions that may predispose to CVT, including use of contraceptives, at the initial clinical presentation. The utility of D-dimer testing and lumbar puncture is reviewed in the following sections. <span>D-dimer — An elevated plasma D-dimer level supports the diagnosis of CVT, but a normal D-dimer does not exclude the diagnosis in patients with suggestive symptoms and predisposing factors. The potential utility of D-dimer for the diagnosis of CVT is illustrated by the following observations: ●A 2012 meta-analysis included 14 studies that evaluated D-dimer in 1134 patients




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D-dimer performed less well in seven studies that enrolled subjects with already-confirmed CVT; the sensitivity and specificity were 89 and 83 percent, respectively. The sensitivity of D-dimer for CVT was also lower in patients with isolated headache as the presenting symptom (82 percent), in those with subacute or chronic clinical presentations of CVT (83 percent), and in those with a single affected venous sinus (84 percent).
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ated in 145 of 155 patients in whom CVT was confirmed and was normal in 692 of 771 patients in whom CVT was ruled out, yielding a sensitivity and specificity of 94 and 90 percent, respectively. <span>D-dimer performed less well in seven studies that enrolled subjects with already-confirmed CVT; the sensitivity and specificity were 89 and 83 percent, respectively. The sensitivity of D-dimer for CVT was also lower in patients with isolated headache as the presenting symptom (82 percent), in those with subacute or chronic clinical presentations of CVT (83 percent), and in those with a single affected venous sinus (84 percent). ●In a subsequent study of 233 patients with suspected CVT and symptom onset of less than seven days, D-dimer demonstrated a sensitivity and specificity of 94 and 98 percent, respectivel




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Thus, D-dimer measurement may have some value as a diagnostic screening tool for the assessment of patients with possible CVT. However, a normal D-dimer value cannot exclude CVT, especially in patients with isolated headache or with thrombosis of a single sinus. Individual assays used to measure D-dimer vary, but it is reasonable to use the same threshold levels as used in diagnostic protocols for deep venous thrombosis (eg, D-dimer >500 ng/mL of fibrinogen equivalent units).
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dy of 233 patients with suspected CVT and symptom onset of less than seven days, D-dimer demonstrated a sensitivity and specificity of 94 and 98 percent, respectively, for predicting CVT [125]. <span>Thus, D-dimer measurement may have some value as a diagnostic screening tool for the assessment of patients with possible CVT. However, a normal D-dimer value cannot exclude CVT, especially in patients with isolated headache or with thrombosis of a single sinus. Individual assays used to measure D-dimer vary, but it is reasonable to use the same threshold levels as used in diagnostic protocols for deep venous thrombosis (eg, D-dimer >500 ng/mL of fibrinogen equivalent units). (See "Clinical presentation and diagnosis of the nonpregnant adult with suspected deep vein thrombosis of the lower extremity", section on 'D-dimer'.) Lumbar puncture — Lumbar puncture




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Lumbar puncture may be useful to exclude meningitis in patients with CVT who present with isolated intracranial hypertension, a syndrome that may account for up to 25 percent of all patients with CVT [5]. In addition, lumbar puncture is valuable in such patients to measure and decrease cerebrospinal fluid (CSF) pressure when vision is threatened.
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nogen equivalent units). (See "Clinical presentation and diagnosis of the nonpregnant adult with suspected deep vein thrombosis of the lower extremity", section on 'D-dimer'.) Lumbar puncture — <span>Lumbar puncture may be useful to exclude meningitis in patients with CVT who present with isolated intracranial hypertension, a syndrome that may account for up to 25 percent of all patients with CVT [5]. In addition, lumbar puncture is valuable in such patients to measure and decrease cerebrospinal fluid (CSF) pressure when vision is threatened. However, in the absence of suspicion for meningitis, CSF analysis is usually not helpful diagnostically for patients with focal neurologic findings and neuroimaging confirmation of CVT




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However, in the absence of suspicion for meningitis, CSF analysis is usually not helpful diagnostically for patients with focal neurologic findings and neuroimaging confirmation of CVT [ 1].
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or up to 25 percent of all patients with CVT [5]. In addition, lumbar puncture is valuable in such patients to measure and decrease cerebrospinal fluid (CSF) pressure when vision is threatened. <span>However, in the absence of suspicion for meningitis, CSF analysis is usually not helpful diagnostically for patients with focal neurologic findings and neuroimaging confirmation of CVT [1]. The CSF abnormalities in CVT are nonspecific and may include a lymphocytic pleocytosis, elevated red blood cell count, and elevated protein; these abnormalities are present in 30 to 50




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The CSF abnormalities in CVT are nonspecific and may include a lymphocytic pleocytosis, elevated red blood cell count, and elevated protein; these abnormalities are present in 30 to 50 percent of patients with CVT [60,61].
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ed. However, in the absence of suspicion for meningitis, CSF analysis is usually not helpful diagnostically for patients with focal neurologic findings and neuroimaging confirmation of CVT [1]. <span>The CSF abnormalities in CVT are nonspecific and may include a lymphocytic pleocytosis, elevated red blood cell count, and elevated protein; these abnormalities are present in 30 to 50 percent of patients with CVT [60,61]. Performing a lumbar puncture is not harmful in patients with CVT, as suggested by the findings of a study that analyzed 624 patients with CVT and identified 224 who had lumbar puncture




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Performing a lumbar puncture is not harmful in patients with CVT, as suggested by the findings of a study that analyzed 624 patients with CVT and identified 224 who had lumbar puncture [126]. The groups with and without lumbar puncture did not differ on any of the outcome measures, which were neurologic worsening within 30 days of CVT onset, acute death, complete recovery at six months, or death or dependency at six months. Nevertheless, lumbar puncture is contraindicated in patients with large brain lesions because they have an increased risk of herniation.
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are nonspecific and may include a lymphocytic pleocytosis, elevated red blood cell count, and elevated protein; these abnormalities are present in 30 to 50 percent of patients with CVT [60,61]. <span>Performing a lumbar puncture is not harmful in patients with CVT, as suggested by the findings of a study that analyzed 624 patients with CVT and identified 224 who had lumbar puncture [126]. The groups with and without lumbar puncture did not differ on any of the outcome measures, which were neurologic worsening within 30 days of CVT onset, acute death, complete recovery at six months, or death or dependency at six months. Nevertheless, lumbar puncture is contraindicated in patients with large brain lesions because they have an increased risk of herniation. Evaluation for thrombophilic state — Searching for a thrombophilic state, either genetic or acquired, should be done for patients with CVT who have a high pretest probability of severe




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Evaluation for thrombophilic state — Searching for a thrombophilic state, either genetic or acquired, should be done for patients with CVT who have a high pretest probability of severe thrombophilia, a category that includes those with a personal and/or family history of venous thrombosis, CVT at a young age, and CVT in the absence of a transient or permanent risk factor (table 1) [104]. When appropriate, screening should include:

● Antithrombin

● Protein C

● Protein S

● Factor V Leiden

● Prothrombin G20210A pathologic variant

● Lupus anticoagulant, anticardiolipin, and anti-beta2 glycoprotein-I antibodies

● Homocysteine

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ery at six months, or death or dependency at six months. Nevertheless, lumbar puncture is contraindicated in patients with large brain lesions because they have an increased risk of herniation. <span>Evaluation for thrombophilic state — Searching for a thrombophilic state, either genetic or acquired, should be done for patients with CVT who have a high pretest probability of severe thrombophilia, a category that includes those with a personal and/or family history of venous thrombosis, CVT at a young age, and CVT in the absence of a transient or permanent risk factor (table 1) [104]. When appropriate, screening should include: ●Antithrombin ●Protein C ●Protein S ●Factor V Leiden ●Prothrombin G20210A pathologic variant ●Lupus anticoagulant, anticardiolipin, and anti-beta2 glycoprotein-I antibodies ●Homocysteine Acute thrombosis can transiently reduce levels of antithrombin, protein C, and protein S, so the utility of testing for these disorders in the acute phase of CVT is limited. In practice




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Acute thrombosis can transiently reduce levels of antithrombin, protein C, and protein S, so the utility of testing for these disorders in the acute phase of CVT is limited. In practice, it is preferable to test for protein C, protein S, and antithrombin at least two weeks after oral anticoagulation has been discontinued, since warfarin therapy reduces measurements of protein C and protein S and may raise plasma antithrombin concentrations into the normal range in patients with hereditary antithrombin deficiency. It is possible to test for protein C and protein S levels while receiving heparin therapy, which does not alter plasma protein C or protein S concentrations. However, testing for antithrombin should be performed when off heparin, which can lower antithrombin levels.
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clude: ●Antithrombin ●Protein C ●Protein S ●Factor V Leiden ●Prothrombin G20210A pathologic variant ●Lupus anticoagulant, anticardiolipin, and anti-beta2 glycoprotein-I antibodies ●Homocysteine <span>Acute thrombosis can transiently reduce levels of antithrombin, protein C, and protein S, so the utility of testing for these disorders in the acute phase of CVT is limited. In practice, it is preferable to test for protein C, protein S, and antithrombin at least two weeks after oral anticoagulation has been discontinued, since warfarin therapy reduces measurements of protein C and protein S and may raise plasma antithrombin concentrations into the normal range in patients with hereditary antithrombin deficiency. It is possible to test for protein C and protein S levels while receiving heparin therapy, which does not alter plasma protein C or protein S concentrations. However, testing for antithrombin should be performed when off heparin, which can lower antithrombin levels. (See "Antithrombin deficiency" and "Protein C deficiency" and "Protein S deficiency".) No underlying etiology or risk factor for CVT is found in approximately 13 percent of adult patien




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No underlying etiology or risk factor for CVT is found in approximately 13 percent of adult patients. However, it is important to continue searching for a cause even after the acute phase of CVT, as some patients may have a condition such as the antiphospholipid syndrome, polycythemia, thrombocythemia, malignancy, or inflammatory bowel disease that is discovered weeks or months after the acute phase.
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wever, testing for antithrombin should be performed when off heparin, which can lower antithrombin levels. (See "Antithrombin deficiency" and "Protein C deficiency" and "Protein S deficiency".) <span>No underlying etiology or risk factor for CVT is found in approximately 13 percent of adult patients. However, it is important to continue searching for a cause even after the acute phase of CVT, as some patients may have a condition such as the antiphospholipid syndrome, polycythemia, thrombocythemia, malignancy, or inflammatory bowel disease that is discovered weeks or months after the acute phase. (See 'Risk factors and associated conditions' above.) If abnormal results are found in assays for lupus anticoagulant, anticardiolipin, or anti-beta2 glycoprotein-I antibodies, testing




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An evaluation for paroxysmal nocturnal hemoglobinuria should be pursued if the complete blood count shows unexplained hemolytic anemia, iron deficiency, or pancytopenia.
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diagnosis of antiphospholipid syndrome requires two positive determinations of these biomarkers. (See "Diagnosis of antiphospholipid syndrome", section on 'Antiphospholipid antibody testing'.) <span>An evaluation for paroxysmal nocturnal hemoglobinuria should be pursued if the complete blood count shows unexplained hemolytic anemia, iron deficiency, or pancytopenia. (See "Clinical manifestations and diagnosis of paroxysmal nocturnal hemoglobinuria", section on 'Diagnosis and classification'.) In patients older than 40 years without identified etiol




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In patients older than 40 years without identified etiology, we suggest searching for an occult malignancy. In patients with sepsis or with fever and no obvious cause of infection, we recommend performing a lumbar puncture.
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unexplained hemolytic anemia, iron deficiency, or pancytopenia. (See "Clinical manifestations and diagnosis of paroxysmal nocturnal hemoglobinuria", section on 'Diagnosis and classification'.) <span>In patients older than 40 years without identified etiology, we suggest searching for an occult malignancy. In patients with sepsis or with fever and no obvious cause of infection, we recommend performing a lumbar puncture. DIFFERENTIAL DIAGNOSIS — The clinical presentation of CVT can be nonspecific (eg, headache, seizure, encephalopathy) and the cause may not be apparent on initial routine neuroimaging st




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For patients presenting with symptoms and signs of isolated intracranial hypertension syndrome (headache with or without vomiting, papilledema, and visual problems), the main considerations in the differential are idiopathic intracranial hypertension (pseudotumor cerebri) and meningitis.
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DIFFERENTIAL DIAGNOSIS — The clinical presentation of CVT can be nonspecific (eg, headache, seizure, encephalopathy) and the cause may not be apparent on initial routine neuroimaging studies. ●<span>For patients presenting with symptoms and signs of isolated intracranial hypertension syndrome (headache with or without vomiting, papilledema, and visual problems), the main considerations in the differential are idiopathic intracranial hypertension (pseudotumor cerebri) and meningitis. Other conditions associated with elevated intracranial pressure (eg, intracranial mass lesions from tumor or abscess) are usually apparent on neuroimaging with CT or MRI. If neuroimagin




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For patients presenting with encephalopathy (eg, multifocal signs, mental status changes, stupor, or coma), the differential includes infection (eg, bacterial and viral meningoencephalitis), inflammation (eg, paraneoplastic and autoimmune encephalitis), demyelination (eg, acute disseminated encephalomyelitis, neuromyelitis optica spectrum disorders), and toxic and metabolic disturbances.
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road and includes other vascular etiologies (eg, intracerebral hemorrhage from a variety of other causes, subdural hemorrhage, ischemic stroke), infection (eg, meningitis, abscess), and tumor. ●<span>For patients presenting with encephalopathy (eg, multifocal signs, mental status changes, stupor, or coma), the differential includes infection (eg, bacterial and viral meningoencephalitis), inflammation (eg, paraneoplastic and autoimmune encephalitis), demyelination (eg, acute disseminated encephalomyelitis, neuromyelitis optica spectrum disorders), and toxic and metabolic disturbances. ●For patients presenting with thunderclap headache, which is rare in CVT, the differential (table 2) includes subarachnoid hemorrhage, other types of intracranial hemorrhage, reversible




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For patients presenting with thunderclap headache, which is rare in CVT, the differential (table 2) includes subarachnoid hemorrhage, other types of intracranial hemorrhage, reversible cerebral vasoconstriction syndromes (RCVS), cervical artery dissection, viral and bacterial meningitis, acute complicated sinusitis, spontaneous intracranial hypotension, ischemic stroke, acute hypertensive crisis, third ventricular colloid cyst, and pituitary apoplexy.
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ation (eg, paraneoplastic and autoimmune encephalitis), demyelination (eg, acute disseminated encephalomyelitis, neuromyelitis optica spectrum disorders), and toxic and metabolic disturbances. ●<span>For patients presenting with thunderclap headache, which is rare in CVT, the differential (table 2) includes subarachnoid hemorrhage, other types of intracranial hemorrhage, reversible cerebral vasoconstriction syndromes (RCVS), cervical artery dissection, viral and bacterial meningitis, acute complicated sinusitis, spontaneous intracranial hypotension, ischemic stroke, acute hypertensive crisis, third ventricular colloid cyst, and pituitary apoplexy. If initial neuroimaging is nondiagnostic, patients with thunderclap headache should have lumbar puncture with measurement of opening pressure and cerebrospinal fluid analysis to exclude




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Cerebral venous thrombosis (CVT) is uncommon, with an estimated incidence of <2.5 per 100,000 annually. Among young adults, CVT is more common in females than males. The mean age of onset is 39 years old.
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world are provided separately. (See "Society guideline links: Stroke in adults" and "Society guideline links: Stroke in children".) SUMMARY AND RECOMMENDATIONS ●Epidemiology and risk factors – <span>Cerebral venous thrombosis (CVT) is uncommon, with an estimated incidence of <2.5 per 100,000 annually. Among young adults, CVT is more common in females than males. The mean age of onset is 39 years old. (See 'Epidemiology' above.) The major risk factors for CVT in adults (table 1) are prothrombotic (hypercoagulable) conditions, oral contraceptives, pregnancy and the puerperium, maligna




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Arterial dissections are a common cause of stroke in the young but may occur at any age
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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: Jun 22, 2022. INTRODUCTION — <span>Arterial dissections are a common cause of stroke in the young but may occur at any age. Dissection occurs when structural integrity of the arterial wall is compromised, allowing blood to collect between layers as an intramural hematoma. Dissections that occur without over




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Dissection occurs when structural integrity of the arterial wall is compromised, allowing blood to collect between layers as an intramural hematoma
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te. Literature review current through: Jun 2022. | This topic last updated: Jun 22, 2022. INTRODUCTION — Arterial dissections are a common cause of stroke in the young but may occur at any age. <span>Dissection occurs when structural integrity of the arterial wall is compromised, allowing blood to collect between layers as an intramural hematoma. Dissections that occur without overt trauma are often labeled as "spontaneous" even though there is often a triggering event or underlying predisposition contributing to the pathogenes




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Hemorrhage may be due to an intimal tear or result from rupture or other pathology in the vasa vasorum [1,2].
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rachnoid hemorrhage".) ANATOMY AND PATHOLOGY — Separation of the arterial wall layers results in dissection. A false lumen arises in the space where blood seeps into the vessel wall (figure 1). <span>Hemorrhage may be due to an intimal tear or result from rupture or other pathology in the vasa vasorum [1,2]. Subintimal dissections cause luminal stenosis or occlusion, whereas subadventitial dissections largely result in dissecting aneurysm formation (figure 2). False lumen extension back int




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Multiple simultaneous cervicocephalic dissections are found in 13 to 22 percent of cases [6-9] and may occur more often in females than males [7,8,10].
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vical transverse processes of C6 to C2 (V2 segment) or the extracranial segment between the transverse process of C2 and the foramen magnum at the base of the skull (V3 segment) (figure 3) [5]. <span>Multiple simultaneous cervicocephalic dissections are found in 13 to 22 percent of cases [6-9] and may occur more often in females than males [7,8,10]. Three or more dissections occur in approximately 2 percent of cases [10]. Although evidence is limited to observations in small numbers of patients, multiple simultaneous dissections ar




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Although evidence is limited to observations in small numbers of patients, multiple simultaneous dissections are not typically associated with a known underlying predisposition to dissection [10]. Rather, most cases may be due to a transient vasculopathy following minor trauma or infection
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halic dissections are found in 13 to 22 percent of cases [6-9] and may occur more often in females than males [7,8,10]. Three or more dissections occur in approximately 2 percent of cases [10]. <span>Although evidence is limited to observations in small numbers of patients, multiple simultaneous dissections are not typically associated with a known underlying predisposition to dissection [10]. Rather, most cases may be due to a transient vasculopathy following minor trauma or infection. Ischemia may manifest in only one of the downstream arterial territories, if at all. Histopathologic specimens of dissected arteries are rarely obtained; when done, examination may rev




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There is a high prevalence of ultrastructural connective tissue abnormalities in patients with apparently sporadic cervicocephalic artery dissection [12-14]. These abnormalities consist primarily of composite fibrils within collagen bundles and fragmented elastic fibers.
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scopic erythrocyte extravasation into connective tissue [2]. In contrast, only one of nine control arteries obtained from accident victims showed pathologic changes in the outer arterial walls. <span>There is a high prevalence of ultrastructural connective tissue abnormalities in patients with apparently sporadic cervicocephalic artery dissection [12-14]. These abnormalities consist primarily of composite fibrils within collagen bundles and fragmented elastic fibers. PATHOPHYSIOLOGY — The development of intramural hematoma with subintimal dissections causes luminal stenosis or occlusion. This may result in cerebral ischemia due to thromboembolism, h




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The development of intramural hematoma with subintimal dissections causes luminal stenosis or occlusion. This may result in cerebral ischemia due to thromboembolism, hypoperfusion, or a combination of both. Thromboembolism rather than hypoperfusion is considered the major cause of ischemic symptoms [15,16].
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pparently sporadic cervicocephalic artery dissection [12-14]. These abnormalities consist primarily of composite fibrils within collagen bundles and fragmented elastic fibers. PATHOPHYSIOLOGY — <span>The development of intramural hematoma with subintimal dissections causes luminal stenosis or occlusion. This may result in cerebral ischemia due to thromboembolism, hypoperfusion, or a combination of both. Thromboembolism rather than hypoperfusion is considered the major cause of ischemic symptoms [15,16]. (See 'Ischemic stroke or TIA' below.) Subadventitial dissections with aneurysm or hematoma formation and vessel dilatation (figure 2) may cause local symptoms from compression of adjace




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Subadventitial dissections with aneurysm or hematoma formation and vessel dilatation (figure 2) may cause local symptoms from compression of adjacent nerves and their feeding vessels, resulting in pain, partial oculosympathetic paresis (Horner syndrome), lower cranial neuropathies, or cervical nerve root involvement.
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mboembolism, hypoperfusion, or a combination of both. Thromboembolism rather than hypoperfusion is considered the major cause of ischemic symptoms [15,16]. (See 'Ischemic stroke or TIA' below.) <span>Subadventitial dissections with aneurysm or hematoma formation and vessel dilatation (figure 2) may cause local symptoms from compression of adjacent nerves and their feeding vessels, resulting in pain, partial oculosympathetic paresis (Horner syndrome), lower cranial neuropathies, or cervical nerve root involvement. (See 'Local symptoms' below.) In a minority of cases, dissection of intracranial arteries, which lack an external elastic lamina and have only a thin adventitial layer, can lead to vess




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In a minority of cases, dissection of intracranial arteries, which lack an external elastic lamina and have only a thin adventitial layer, can lead to vessel rupture with subarachnoid hemorrhage.
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s and their feeding vessels, resulting in pain, partial oculosympathetic paresis (Horner syndrome), lower cranial neuropathies, or cervical nerve root involvement. (See 'Local symptoms' below.) <span>In a minority of cases, dissection of intracranial arteries, which lack an external elastic lamina and have only a thin adventitial layer, can lead to vessel rupture with subarachnoid hemorrhage. (See 'Subarachnoid hemorrhage' below.) Head, neck, or facial pain is thought to be caused by activation of nociceptors from distension of the vessel wall due to the intimal tear and/or




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Head, neck, or facial pain is thought to be caused by activation of nociceptors from distension of the vessel wall due to the intimal tear and/or intramural hematoma formation [17,18].
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racranial arteries, which lack an external elastic lamina and have only a thin adventitial layer, can lead to vessel rupture with subarachnoid hemorrhage. (See 'Subarachnoid hemorrhage' below.) <span>Head, neck, or facial pain is thought to be caused by activation of nociceptors from distension of the vessel wall due to the intimal tear and/or intramural hematoma formation [17,18]. ETIOLOGY — Arterial dissections are generally caused by various degrees of trauma or triggering events, with or without an underlying predisposition. While major head and neck trauma ca




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While major head and neck trauma can cause dissection, most dissections occur after a mechanical trigger, which may not always be remembered [19].
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d/or intramural hematoma formation [17,18]. ETIOLOGY — Arterial dissections are generally caused by various degrees of trauma or triggering events, with or without an underlying predisposition. <span>While major head and neck trauma can cause dissection, most dissections occur after a mechanical trigger, which may not always be remembered [19]. Dissections that occur without overt trauma are often labeled as "spontaneous" even though there is often a triggering event or underlying predisposition contributing to the pathogenesi




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Observational data suggest that trauma, typically mild or trivial in nature, or other mechanical events are triggers for cervical artery dissection in up to 40 percent of cases [20]. The list of physical activities associated with dissection is long and includes the following:

● Basketball [21]

● Childbirth [22]

● Cervical manipulation therapy [23-28]

● Coughing or sneezing [29]

● Dancing [30,31]

● Minor sports injuries [32,33]

● Roller coaster or amusement park rides [34-39]

● Scuba diving [40,41]

● Sexual intercourse [42]

● Skating [43]

● Swimming [44]

● Tennis [45,46]

● Trampoline use [47]

● Vigorous exercise [29]

● Volleyball [

...
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ut overt trauma are often labeled as "spontaneous" even though there is often a triggering event or underlying predisposition contributing to the pathogenesis. Minor trauma and other triggers — <span>Observational data suggest that trauma, typically mild or trivial in nature, or other mechanical events are triggers for cervical artery dissection in up to 40 percent of cases [20]. The list of physical activities associated with dissection is long and includes the following: ●Basketball [21] ●Childbirth [22] ●Cervical manipulation therapy [23-28] ●Coughing or sneezing [29] ●Dancing [30,31] ●Minor sports injuries [32,33] ●Roller coaster or amusement park rides [34-39] ●Scuba diving [40,41] ●Sexual intercourse [42] ●Skating [43] ●Swimming [44] ●Tennis [45,46] ●Trampoline use [47] ●Vigorous exercise [29] ●Volleyball [48] ●Weightlifting [49] ●Yoga [29] While cervical manipulation therapy may trigger dissection, causality is difficult to establish, and the absolute incidence of dissection caused by spinal manipulation is unknown [28,50




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While cervical manipulation therapy may trigger dissection, causality is difficult to establish, and the absolute incidence of dissection caused by spinal manipulation is unknown [28,50-52].
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[34-39] ●Scuba diving [40,41] ●Sexual intercourse [42] ●Skating [43] ●Swimming [44] ●Tennis [45,46] ●Trampoline use [47] ●Vigorous exercise [29] ●Volleyball [48] ●Weightlifting [49] ●Yoga [29] <span>While cervical manipulation therapy may trigger dissection, causality is difficult to establish, and the absolute incidence of dissection caused by spinal manipulation is unknown [28,50-52]. Associated conditions and risk factors — Connective tissue disorders, vascular abnormalities, and other conditions have been associated with dissection. ●Connective tissue or vascular d




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Associated conditions and risk factors — Connective tissue disorders, vascular abnormalities, and other conditions have been associated with dissection.
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