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04.12.2017 | Original Communication | Ausgabe 1/2018

Journal of Neurology 1/2018

Patterns of convexal subarachnoid haemorrhage: clinical, radiological and outcome differences between cerebral amyloid angiopathy and other causes

Journal of Neurology > Ausgabe 1/2018
Lionel Calviere, Nicolas Raposo, Victor Cuvinciuc, Christophe Cognard, Fabrice Bonneville, Alain Viguier
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The online version of this article (https://​doi.​org/​10.​1007/​s00415-017-8693-7) contains supplementary material, which is available to authorized users.



Cerebral amyloid angiopathy (CAA) is a common aetiology of convexal subarachnoid haemorrhage (cSAH) but little is known about its specific characteristics in comparison with cSAH from other causes. In this study we compared patients with CAA vs. non-CAA-related cSAH.


Retrospective review of baseline and follow-up data of consecutive patients admitted with a symptomatic acute cSAH.


Sixty-two patients were included (mean age 66.2 ± 14.1 years), of whom 31 with probable CAA. CAA patients presented more frequently with transient symptoms (83.9 vs. 19.3%; p < 0.001) usually without headache (19.0 vs. 58.1%; p = 0.002). In CAA, these were essentially positive sensory disturbance that met the criteria of transient focal neurological episodes (TFNE). CAA was more often associated with cortical superficial siderosis (cSS) (80.6 vs. 0%; p < 0.001) and lobar cerebral microbleeds (83.4 vs. 9%; p < 0.001). During a mean of 22 months of follow-up, recurrent symptomatic cSAH occurred in 4/27 (12.9%) CAA patients and in 0/27 non-CAA patients. Among 40 patients with MRI follow-up, cSAH recurrences were observed in 44% of CAA patients vs. 13.3% of other cases (p = 0.08) and extension of cSS was detected only in CAA (60%) (p < 0.001). Acute cSAH evolved to cSS in 96 and 73.3% of CAA and non-CAA patients, respectively (p = 0.06).


CAA differs from other cSAH in having TFNE as a frequent clinical presentation, a high prevalence of cSS and an increased risk of recurrent subarachnoid bleeding. However, evolution from acute cSAH to focal cSS may not be specific to CAA.

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