Austin R. T. Colohan

Cerebral vasospasm following aneurysmal subarachnoid hemorrhage.

Cerebral vasospasm following aneurysmal subarachnoid hemorrhage is one of the most important causes of cerebral ischemia, and is the leading cause of death and disability after aneurysm rupture. There are two definitions of cerebral vasospasm: angiographic and clinical. Care must be exercised to be certain that it is clear which entity is being addressed. The diagnosis of the clinical syndrome is one of exclusion and can rarely be made with absolute certainty. The pathogenesis of cerebral vasospasm is poorly understood. Most current theories focus on the release of factors from the subarachnoid clot. More attention must be given to the role of endothelial damage and alterations in the blood-arterial wall barrier. The application of modern techniques for studying vascular smooth muscle which have been developed as a result of research in the areas of hypertension and atherosclerosis must be applied to the problem of cerebral vasospasm. A stress test to select patients with angiographic arterial narrowing who have adequate cerebral vascular reserve to undergo surgery should be developed. The optimal treatment of vasospasm awaits development of agents for blocking or inactivating spasmogenic substances or blocking arterial smooth muscle contraction. Rheological or hemodynamic manipulations to prevent or reverse ischemic consequences of vasospasm are relatively effective, but complicated and hazardous, and should be viewed principally as interim measures awaiting development of more specific therapies for the arterial narrowing.

Predictors of early deterioration and mortality in black Americans with spontaneous intracerebral hemorrhage

BACKGROUND AND PURPOSE Black Americans with spontaneous intracerebral hemorrhage (SICH) may have unique clinical characteristics that affect outcome. The aim of this study was to determine the prognostic value of clinical characteristics and initial CT scan for outcome in black Americans with SICH. METHODS Clinical and demographic data were extracted from the charts of 182 consecutive black Americans admitted for SICH diagnosed by clinical criteria and initial CT scan. Hemorrhage volumes were calculated from admission CT scans by a computerized method. Univariate and multiple logistic regression analyses were performed to determine independent predictors of early deterioration (defined as a decrease from an initial Glasgow Coma Scale score > 12 by > or = 4 points within 24 hours from presentation) and mortality. RESULTS Both hemorrhage volume and ventricular extension were significant, independent predictors of early deterioration (odds ratio [OR], 6.78; 95% confidence interval [CI], 1.89 to 24.35 and OR, 4.67; 95% CI, 1.30 to 16.72, respectively) and mortality (OR, 6.66; 95% CI, 2.85 to 15.58 and OR, 4.23; 95% CI, 1.82 to 9.82, respectively). A Glasgow Coma Scale score < or = 12 also predicted mortality (OR, 3.23; 95% CI, 1.46 to 7.14). Initial mean arterial pressure was not an independent predictor of early deterioration or mortality. CONCLUSIONS Hemorrhage volume and ventricular extension are the best predictors of early deterioration and mortality in black Americans with SICH.

Cocaine-induced aneurysmal rupture: an emergent negative factor in the natural history of intracranial aneurysms?

Recent statistics from the National Institute on Drug Abuse indicate that cocaine abuse continues to be a significant public health problem. Between 1988 and 1990 at Grady Memorial Hospital in metropolitan Atlanta, Georgia, we identified 12 patients in whom subarachnoid hemorrhage was temporally related to cocaine abuse. All 12 patients had underlying cerebral aneurysms that had ruptured. Currently, the incidence of ruptured intracranial aneurysms in patients with cocaine-induced subarachnoid hemorrhage is 84.9% (mean age, 31.1 years; overall mortality, 60.5%). Hypertension is the likely precursive factor in cocaine-induced aneurysmal rupture. Cocaine abuse appears to be a significant negative factor in the natural history of cerebral aneurysms, especially in young adults. We review the epidemiology of cocaine-induced subarachnoid hemorrhage and its effects on the cerebral circulation, and suggest guidelines for patient management.

Barrier disruption in the major cerebral arteries during the acute stage after experimental subarachnoid hemorrhage.

The effects of experimental subarachnoid hemorrhage (SAH) on the blood-arterial wall barrier in the basilar arteries were studied during the acute stage after SAH. SAH was induced in rats by injecting fresh autologous blood into the cisterna magna. Horseradish peroxidase (HRP) was given intravenously before killing the animals to assess the integrity of the barrier. In the basilar arteries taken from the animals that were killed 30 minutes after the cisternal injection of either mock cerebrospinal fluid or arterial blood, HRP reaction products were diffusely observed in the subendothelial spaces and smooth muscle layers. At 5 hours after the blood injection, no permeation of HRP into the subendothelial space was observed. Endothelial cell transcytosis seemed to be the important mechanism for HRP permeation into the subendothelial space rather than the opening of interendothelial junctions. The disruption of the blood-arterial wall barrier in the major cerebral arteries after SAH may be involved in the pathogenesis of vasospasm.

Cranial migration of a lumboperitoneal shunt catheter.

We describe a patient with pseudotumor cerebri for which a lumboperitoneal (LP) shunt was placed. After a pseudomeningocele was noted at the lumbar incision site, an LP shunt revision was done, at which time migration of the catheter into the thecal sac was noted. Three months later, radiologic studies revealed cranial migration of the LP shunt into the posterior fossa. We believe no similar complication has been reported.

Bilateral persistent trigeminal arteries associated with cerebral aneurysms and aortic arch vessel anomaly

We present the case of a patient with headache who, on computed tomography, was found to have subarachnoid hemorrhage. Angiography revealed bilateral persistent trigeminal arteries, anterior communicating artery and left pericallosal artery aneurysms, and an absent left vertebral artery. An anomalous right subclavian artery, originating at a common trunk with the left subclavian artery, was also present. To our knowledge, this is the fifth case of bilateral persistent trigeminal arteries and the sixth case of bilateral persistent carotid-basilar anastomosis of any type reported in the literature. A mechanism for the pathogenesis of multiple cerebrovascular anomalies is briefly discussed.

Loss of autoregulation in patients with intracerebral hemorrhage

We evaluated cerebral vasomotor reactivity to acetazolamide in seven consecutive patients with intracerebral hemorrhage (ICH) with transcranial Doppler to evaluate autoregulation of cerebral blood flow in acute ICH. Two patients had prominent loss of vasoreactivity to acetazolamide stimulation. This suggests that autoregulation may be impaired in some patients with acute ICH. Further studies are required to determine the clinical implications of loss of autoregulation in acute phase of ICH.