Objective: To identify patterns of clinical presentation, imaging findings, and etiologies in a cohort of hospitalized patients with localized nontraumatic convexal subarachnoid hemorrhage.Methods: Twenty-nine consecutive patients with atraumatic convexal subarachnoid hemorrhage were identified using International Classification of Diseases-9 code from 460 patients with subarachnoid hemorrhage evaluated at our institution over a course of 5 years. Retrospective review of patient medical records, neuroimaging studies, and follow-up data was performed.Results: There were 16 women and 13 men between the ages of 29 and 87 years. Two common patterns of presentations were observed. The most frequent presenting symptom in patients Յ60 years (n ϭ 16) was a severe headache (n ϭ 12; 75%) of abrupt onset (n ϭ 9; 56%) with arterial narrowing on conventional angiograms in 4 patients; 10 (p ϭ 0.003) were presumptively diagnosed with a primary vasoconstriction syndrome. Patients Ͼ60 years (n ϭ 13) usually had temporary sensory or motor symptoms (n ϭ 7; 54%); brain MRI scans in these patients showed evidence of leukoaraiosis and/or hemispheric microbleeds and superficial siderosis (n ϭ 9; 69%), compatible with amyloid angiopathy (n ϭ 10; p Ͻ 0.0001). In a small group of patients, the presentation was more varied and included lethargy, fever, and confusion. Four patients older than 60 years had recurrent intracerebral hemorrhages in the follow-up period with 2 fatalities. Conclusion:Convexal subarachnoid hemorrhage is an important subtype of nonaneurysmal subarachnoid bleeding with diverse etiologies, though a reversible vasoconstriction syndrome appears to be a common cause in patients 60 years or younger whereas amyloid angiopathy is frequent in patients over 60. These observations require confirmation in future studies. Atraumatic localized convexal subarachnoid hemorrhage (cSAH) is an unusual presentation of subarachnoid bleeding, in which the bleeding is localized to the convexities of the brain without involvement of the adjacent parenchyma or extension into the interhemispheric fissures, basal cisterns, or ventricles. Since most saccular aneurysms arise from the circle of Willis, aneurysmal rupture is an unlikely source of cSAH. Diverse etiologies have been posited for its occurrence, including cortical vein occlusions, posterior reversible leukoencephalopathy syndrome (PRES), reversible cerebral vasoconstriction syndrome (RCVS), coagulopathy, cocaine use, lupus vasculitis, cavernoma, brain abscesses, and cerebral amyloid angiopathy (CAA). 1-13Existing information about this condition is largely derived from case reports and small case series, which carry inherent referral and diagnostic biases. We undertook this study to systematically evaluate and review the potential causes and patterns of clinical and radiologic presentation of localized cSAH from the inpatient population at our institution.

Nine patients had intraluminal filling defects identifiable as clot within the internal carotid artery at angiography. Thrombus was unilateral in eight, bilateral in one. Eight of the 10 clots were attached to atheromatous plaques. Three patients had serious concurrent illness: pancreatic cancer, rheumatoid arthritis with arteritis, and chronic pulmonary disease with polycythemia. In three patients, the clot was related to severe atherosclerosis. In three other patients, all young, the carotid thrombi remained unexplained though two of these patients had coagulation abnormalities. No patient had a new stroke after surgical or anticoagulant treatment.

In two patients, lateral medullary infarcts were followed by repeated brainstem ischemia. One patient had posturally sensitive vertebrobasilar TIAs, and the other had TIAs followed by quadriparesis. Both had angiographic evidence of intracranial vertebral artery occlusion on one side and severe stenosis of the contralateral vertebral artery. Propagation or embolization of clot from the occluded vertebral artery or decreased blood flow caused by stenosis of the contralateral vertebral artery can cause a bad outcome.

PerspectiveThe role of cerebral angiography in the diagnosis of cerebrovascular disease is currently being questioned because of the increasing availability of MR angiography.The purpose of this essay is to place the use of cerebral angiography in perspective in light of these new developments.In patients with atherosclerotic cerebrovascuhar disease, MR angiography can almost entirely supplant cerebral angiography as a screening procedure in the evaluation of the carotid bifurcation. However, detection of "pseudoocclusion" still requires cerebral angiography for accurate diagnosis. Atherosclerotic stenosis or occlusion of the major intracranial vessels at the base of the brain can be detected with MR angiography, but not as accurately as with cerebral angiography. Furthermore, for detection of more distal occlusions, cerebral angiography is still needed. A number of erroneous concepts about the risks and value of cerebral angiography have prevented its optimal use for patients with cerebrovascular disease. These myths can be countered by applying several rules to optimize the use of cerebral angiography. Subarachnoid hemorrhage is best evaluated with CT followed by detailed cerebral angiography, although MR angiography can be used as a screening test for aneurysms 3 mm or larger. Cerebral angiography is still necessary to confirm the diagnosis of cerebrovascular malformations, although MR angiography is a useful screening test. Cerebral angiography is required for the definitive diagnosis of artentis, arterial dissection, or fibromuscular dysplasia.

We compared clinical and arteriographic features in 106 patients with symptomatic unilateral carotid territory occlusive disease to determine the frequency and distribution of occlusive arterial lesions in asymptomatic vessels. Among black patients who were predominantly from Chicago, young, and female, there were fewer transient ischemic attacks and myocardial infarcts, less claudication, and more asymptomatic lesions of the supraclinoid internal carotid artery, anterior cerebral artery stem, and the middle cerebral artery stem. Among white patients predominantly from New England, elderly, and male, there was more frequent and severe occlusive asymptomatic disease at extracranial carotid and vertebral artery sites. Knowledge of the distribution of asymptomatic lesions will help guide evaluation and treatment strategies for patients with occlusive cerebrovascular disease.