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Risk of Intracranial Aneurysms in Families With Subarachnoid Hemorrhage

Published online by Cambridge University Press:  18 September 2015

Mark J. Alberts*
Affiliation:
Division of Neurology, Department of Medicine, Duke University Medical Center, Stroke Acute Care Unit, Duke Hospital
Ana Quinones
Affiliation:
Division of Neurology, Duke University Medical Center, Durham, North Carolina, USA
Carmelo Graffagnino
Affiliation:
Division of Neurology, Duke University Medical Center, Durham, North Carolina, USA
Allan Friedman
Affiliation:
Department of Medicine; Division of Neurosurgery, Department of Surgery, Duke University Medical Center, Durham, North Carolina, USA
Allen D. Roses
Affiliation:
Department of Neurobiology, Duke University Medical Center, Durham, North Carolina, USA
*
P.O. Box 3392, Duke University Medical Center, Durham, NC 27710 USA
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Abstract

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Background:

Genetic factors may be important in the etiology of subarachnoid hemorrhage (SAH) and intracranial aneurysm (IA) formation. Several studies have reported the familial occurrence of SAH and IA, although in most cases asymptomatic family members were not studied with elective angiography. The examination of data from large sibships could provide important information about the frequency of IA occurrence in at-risk individuals and the mode of inheritance for familial SAH/1A.

Methods:

We reviewed published case series of sibships with SAH and at least four siblings, in which at least one sibling underwent elective angiography. Data were collected on age-of-onset, clinical events, presence of hypertension, angiographic findings, and outcome. Patients were classified as “affected” if they had a SAH or if an IA was detected by elective angiography, and “unaffected” if they were asymptomatic and had a negative angiogram.

Results:

Seven case series with 52 individuals (26 men and 26 women) met our inclusion criteria. The sibships ranged from 6 to 13 members. Most of the siblings (32 of 52, 61%) were asymptomatic, 18 (35%) had a SAH, and 2 (4%) had focal symptoms but no SAH. Elective angiography of 34 siblings showed an IA in 11 (32%) and was negative in 23 (68%). The overall rate of affecteds (SAH or IA) was 56%.

Conclusions:

Based on data from these sibships, angiography of asymptomatic at-risk siblings demonstrated an IA in almost one-third of cases. Familial SAH/IA segregated with a pattern that was consistent with an autosomal dominant trait in this selected series of sibships, although other factors could produce these findings.

Type
Original Articles
Copyright
Copyright © Canadian Neurological Sciences Federation 1995

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