Funding Stroke Association.
Copyright ©Markus et al. Open Access article distributed under the terms of CC BY.
Introduction Cervical artery dissection accounts for only 1–2% of all ischaemic strokes, but in young and middle-aged people it accounts for 10–25% of strokes.1 Some studies suggest a signifi cantly increased risk of stroke in patients presenting with dissection either with local symptoms, such as headache and Horner’s syndrome, or with stroke or transient ischaemic attack, with estimates of the risk of secondary stroke after presentation of 15–20%,2–4 although other studies have reported a much lower proportion.5 These studies suggested that most strokes occurred soon after initial onset of symptoms. Embolism from thrombus forming at the dissection site is thought to play the major part in stroke pathogenesis.6 This suggestion is supported by
transcranial Doppler studies7,8 showing cerebral micro- emboli soon after dissection, and by the distribution of infarcts after dissection, which suggests an embolic pattern.9 The risk of early recurrence of stroke has led many clinicians to advocate the use of anticoagulation from presentation until 3 or 6 months after dissection. However others believe that antiplatelet drugs might be suffi cient.10 Anticoagulants might prevent embolism from a fresh thrombus but they are also more hazardous than antiplatelet drugs and can result in extension of the intramural haemorrhage, which occurs in a third of patients according to MRI.11 No data exist from randomised controlled trials assessing the relative effi cacy of the two treatments.
Funding Stroke Association.Copyright ©Markus et al. Open Access article distributed under the terms of CC BY.Introduction Cervical artery dissection accounts for only 1–2% of all ischaemic strokes, but in young and middle-aged people it accounts for 10–25% of strokes.1 Some studies suggest a signifi cantly increased risk of stroke in patients presenting with dissection either with local symptoms, such as headache and Horner’s syndrome, or with stroke or transient ischaemic attack, with estimates of the risk of secondary stroke after presentation of 15–20%,2–4 although other studies have reported a much lower proportion.5 These studies suggested that most strokes occurred soon after initial onset of symptoms. Embolism from thrombus forming at the dissection site is thought to play the major part in stroke pathogenesis.6 This suggestion is supported by transcranial Doppler studies7, 8 แสดงไมโคร emboli สมองหลัง จากชำแหละ และการกระจายของ infarcts หลังจากชำแหละ การ pattern.9 การ embolic ของช่วงการเกิดซ้ำของโรคหลอดเลือดสมองได้นำ clinicians ในการสนับสนุนการใช้ anticoagulation จากงานนำเสนอถึง 3 หรือ 6 เดือนหลังจากชำแหละ อย่างไรก็ตาม ผู้อื่นเชื่อว่า อาจเป็นยา antiplatelet suffi cient.10 Anticoagulants อาจป้องกันเครื่องจาก thrombus สด แต่พวกเขาก็ยิ่งอันตรายมากกว่ายา antiplatelet และในส่วนขยายของ haemorrhage intramural ซึ่งเกิดขึ้นในหนึ่งในสามของผู้ป่วยตาม MRI.11 ไม่มีข้อมูลที่มีอยู่จาก randomised ทดลองควบคุมประเมิน cacy effi ญาติรักษาสอง
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