Subarachnoid haemorrhage in identical twins.

Abstract

SUMMARY A pair of identical twins both of whom died of subarachnoid haemorrhage from ruptured anterior communicating artery aneurysms are reported. These twins are compared to the three other reported twins with ruptured cerebral aneurysms.The lesion underlying a cerebral aneurysm is a defect in the medial coat of the artery usually at a point of bifurcation. Despite the fact that this defect is believed to be present from birth, the vast majority of subarachnoid haemorrhages due to the rupture of intracranial aneurysms are not associated with any identifiable genetic predisposing factors. However, families have been reported'-4 in which multiple cases have occurred, suggesting the possibility that a genetic factor may play a part, at least in this minority group. This view is further supported by the well known association of certain rare hereditary disorders with an increased incidence of cerebral aneurysms; these include Ehlers-Danlos syndrome,5 pseudo-xanthoma elasticum6 and polycystic renal disease.7'8 It has been suggested that the mechanism underlying such a predisposition to aneurysm formation is a deficiency of type 3 collagen.9In this paper a pair of identical twins is reported who died of subarachnoid haemorrhage from identically sited aneurysms. There are three other twin pairs reported in the literature of which only two had proven cerebral aneurysms.

Concordant Symptomatic Intracranial Aneurysm in a Monozygotic Twin: A Case Report and Review of the Literature

“…The details of 14 monozygotic twin-pairs, including our present twins, are listed in Table 1. In eight pairs (including our case), both twins had an aSAH (Brisman & Abbassioun, 1971;Fairburn, 1973;Hagen et al, 1997;Nakajima et al, 1998;Ohno et al, 2004;Schon & Marshall, 1984;Wilson & Cast, 1973), in six pairs the other (non-symptomatic) twin was found to have one or more aneurysms after screening (Hager & Steiger, 2004;Parekh et al, 1992;Porter, 2001;Sakovich et al, 1998;Sharma & Brown, 2001;Weil et al, 1988). All except one individual had their aSAH between age 30-50 years (mean age at time of rupture: 40.5 years).…”