PubMed · 4325666
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E E Clizer, G Ioannides. 1971. Herpes simplex encephalitis.. https://doi.org/10.2214/ajr.112.2.273
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To determine the incidence of, and risk factors for, the occurrence of rebleeding between admission and early operation (ultra-early rebleeding) in patients with spontaneous subarachnoid hemorrhage (SAH), the authors reviewed the cases of 179 patients admitted within 24 hours after their last attack of SAH. Thirty-one (17.3%) of these patients had ultra-early rebleeding despite scheduling of early operation (within 24 hours after admission). The incidence of rebleeding significantly decreased as the time interval between the last attack and admission increased. Patients with rebleeding before admission, high systolic blood pressure, intracerebral or intraventricular hematoma, those in poor neurological condition on admission, and those who underwent angiography within 6 hours of the last SAH were significantly more likely to have ultra-early rebleeding than those without these factors. The incidence of rebleeding also significantly increased as levels of enhancement of platelet sensitivity and thrombin-antithrombin complex increased. Multivariate analysis revealed that the following three factors were independently associated with ultra-early rebleeding: the level of enhancement of platelet sensitivity; the time interval between the last attack and admission; and the level of thrombin-antithrombin complex. On the basis of these findings, the authors suggest that many of the risk factors for ultra-early rebleeding are interrelated. A particularly high risk of ultra-early rebleeding was observed in those patients 1) who had platelet hypoaggregability; 2) who were admitted shortly after their last SAH; and 3) whose thrombin-antithrombin complex levels were extremely high and were thus in severe clinical condition.
The authors report a unique case involving a 2-year-old child with idiopathic moyamoya disease who presented with cerebral infarctions and seizures. On initial evaluation, computerized tomography (CT) showed a left parietal infarct and angiograms demonstrated early moyamoya disease with no evidence of arteriovenous malformation (AVM). Approximately 9 years later, angiography and magnetic resonance (MR) imaging revealed an AVM centered on the same region of the left parietal lobe. Angiographic, CT, and MR images are presented that demonstrate the progression of moyamoya disease and de novo development of the AVM in the infarct site. The possible role of angiogenesis in the etiology of acquired AVMs and moyamoya disease is discussed.