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Stroke. 2006;37:305-308
Published online before print January 12, 2006, doi: 10.1161/01.STR.0000200558.38774.d5
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Right arrow Cerebral Aneurysm, AVM, & Subarachnoid hemorrhage

(Stroke. 2006;37:305.)
© 2006 American Heart Association, Inc.


Advances in Stroke 2005

Advances in Subarachnoid Hemorrhage

Valery L. Feigin, MD, PhD Max Findlay, MD, PhD, FRCSC

From the Clinical Trials Research Unit (V.L.F.), Department of Medicine and School of Population Health, University of Auckland, New Zealand; and the Division of Neurosurgery (M.F.), Department of Surgery, University of Alberta, Edmonton, Alberta, Canada.

Correspondence to Valery Feigin, Clinical Trials Research Unit, University of Auckland, Private Bag 92019, Auckland, New Zealand. E-mail v.feigin@ctru.auckland.ac.nz


Key Words: subarachnoid hemorrhage


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

Although subarachnoid hemorrhage (SAH) comprises only 1% to 7% of all strokes,1 the loss of productive life years in the general population from SAH is comparable to that of cerebral infarction2 because of the relatively young age of onset and poor outcome in SAH.1,3,4 However, unlike other stroke subtypes, the incidence of SAH exhibits little geographical variation and did not significantly change over the last decades.1 In the most recent overview of 14 longitudinal and 23 case-control studies of risk factors for SAH published in English from 1966 through March 2005,5 it was concluded that smoking, hypertension, and excessive alcohol are the most important risk factors for SAH. Exposure to these risk factors individually and/or in combination promotes formation, growth, and rupture of intracranial aneurysm(s),6–8 a major cause of SAH. The consistency of the data across studies involving different designs and populations suggests that cigarette smoking and elevated blood pressure are causally related to SAH.9 There is also evidence that genetic factors play an important role in the pathogenesis of SAH.10 Accumulating evidence suggest a temporal (seasonal and diurnal) pattern in the occurrence of SAH,11,12 but reasons for these temporal patterns remain unclear. However, there is still lack of good quality population-based epidemiological studies on incidence, trends, and outcomes of SAH in different populations (especially from developing countries).

Diagnosis and Investigation

Misdiagnosis of SAH occurred in 12% of 482 SAH patients admitted to a large American tertiary care hospital and was associated with a smaller hemorrhage and normal mental status on first assessment . . . [Full Text of this Article]




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