No abstract

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.

Low serum creatinine levels are associated with VENI, suggesting that swiftness of the efficacy of rt-PA or of neurological recovery may depend on renal function.

Introduction: Early neurological improvement (ENI) within 24 hours after fibrinolysis for ischemic stroke is strongly associated with recanalization and favourable outcome at 3 months. However, it remains unknown why some patients recover within the 1st hour after treatment (very ENI, VENI) whereas others have ENI later within 24 hours. We therefore assessed which factors were associated with timing of ENI. Methods: We retrospectively studied consecutive patients treated with intravenous rt-PA for ischemic stroke within 4h30 after onset in 4 regional hospitals. VENI assessed at 1h and ENI assessed at 24h post-treatment was defined by NIHSS improvement by 40% from baseline. We compared patients with VENI to patients with ENI. Results: Among 421 patients (mean age 70.8±15.2 years, median NIHSS 15, median onset-to-treatment time 170 minutes) 65 (15%) had VENI, and 110 (26%) ENI. Patients with VENI had significantly lower serum creatinine level than patients with ENI (79±19 vs. 91±35 μmol/L; p=0.01). After adjustment for age, sex, baseline NIHSS, High Blood Pressure and glucose level at admission, patients with low creatinine level were more likely to have VENI (lowest tertile, OR=3.8 CI95%=[1.5-9.7], intermediate tertile, OR=1.8 CI95%=[0.8-4.3]; p for trend=0.006). VENI patients were as likely as ENI patients to have a modified Rankin scale ≤ 2 at 3 months (88% vs. 84%, p=0.46). Conclusion: Low serum creatinine levels are associated with VENI, suggesting that quickness of efficacy of rt-PA, of reperfusion, or of neurological recovery may depend on renal function.