Focal cortical subarachnoid hemorrhage revealed by recurrent paresthesias: a clinico-radiological syndrome strongly associated with cerebral amyloid angiopathy

Marion Apoil, Julien Cogez, Lydie Dubuc, Mathieu Bataille, Vincent de la Sayette, Emmanuel Touzé, Fausto Viader
Cerebrovascular Diseases 2013, 36 (2): 139-44

BACKGROUND: Focal subarachnoid hemorrhage (SAH) is often revealed by transient and recurrent focal neurological episodes. This cause is important to identify because it carries a high risk of intracerebral hemorrhage (ICH). We report the clinical, imaging and prognostic data of 17 patients with focal SAH revealed by short episodes of paresthesias mimicking transient ischemic attacks.

METHODS: The medical records and imaging data of patients with focal acute SAH at the cerebral convexity and at least one episode of focal paresthesia having attended the Neurology Department of Caen University Hospital in the last 10 years were retrospectively reviewed. Hemorrhagic lesions, ischemic lesions, cerebral microbleeds (CMBs), superficial siderosis, white matter changes (leukoaraiosis) and modified Boston criteria for cerebral amyloid angiopathy (CAA) were assessed. All patients or relatives were contacted after a median delay of 16 months in order to seek for new events (death, stroke, recurrent focal symptoms, ICH and dementia) that occurred since hospital discharge.

RESULTS: Seventeen patients (12 men) aged 69-96 years were identified. All but 1 had multiple, repeated, stereotyped and brief attacks of paresthesias, associated in some of them with motor and/or speech difficulties, but only 1 had a headache. SAHs were seen on CT scans in 15/17 patients and on T2* gradient-echo magnetic resonance imaging (MRI) in all patients. They were multiple SAHs in 14/17 patients, including at least 1 SAH in the central or pre- or postcentral sulcus contralateral to the symptoms in all patients. Five patients had punctate cortical hyperintensities on diffusion-weighted MRI. Eleven patients had CMBs, and 4 of them had more than 5 CMBs. Seven patients met the modified Boston criteria for probable and 10 for possible CAA. At follow-up, 5 patients had a subsequent ICH, 4 of whom had received antithrombotic treatments. Five patients died (1 from ICH). Six patients developed dementia.

CONCLUSION: The combination of transient, repeated and stereotyped attacks of unilateral paresthesias with a contralateral sulcal SAH seems to preferentially occur in elderly people and is often indicative of CAA.

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