Neurological deterioration within 30 days of ischemic stroke with spontaneous cervicocranial artery dissection

The objective of this study was to identify the clinical features associated with neurological deterioration within 30 days of ischemic stroke patients with spontaneous cevicocranial dissection (SCCD) and clarify the effect on outcomes. We retrospectively identified 18 patients with SCCD (1.6%, 3 wo...

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Bibliographic Details
Published inRinsho Shinkeigaku Vol. 54; no. 1; pp. 1 - 9
Main Authors Mori, Mayumi, Wakugawa, Yoshiyuki, Yasaka, Masahiro, Yasumori, Kotaro, Nagata, Shinji, Okada, Yasushi
Format Journal Article
LanguageJapanese
Published Japan Societas Neurologica Japonica 01.01.2014
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Summary:The objective of this study was to identify the clinical features associated with neurological deterioration within 30 days of ischemic stroke patients with spontaneous cevicocranial dissection (SCCD) and clarify the effect on outcomes. We retrospectively identified 18 patients with SCCD (1.6%, 3 women, 52 ± 16 years old) among 1,112 patients with acute ischemic stroke within 7 days after onset. Of the 18 patients, 13 (72%) had vertebrobasilar arterial dissection. Neurological deterioration was present in 4 patients (22%), and 2 patients (11%) died. All of them became worse within 3 days after onset. Their initial blood pressures were high. All of them had dominant side vertebral artery or basilar artery dissection. Subarachnoid hemorrahage (SAH) were not seen although the agressive anticoagulant therapy were performed except for a case who had aneurysmal change. The patients with neurological deterioration had poor outcome, but the patients without neurological deterioration had good outcome. Recurrent ischemic event or SAH did not occurred in 3 months if they had not neurological deterioration. When we see acute stroke patients with dissection at the dominant side vertebral artery or the basilar artery, we should observe carefully for neurological deterioration especially within three days of onset.
ISSN:0009-918X
1882-0654
DOI:10.5692/clinicalneurol.54.1