Thrombosis and cerebrovascular disease.

Strokes are heterogeneous not only with respect to their presentation, but more importantly in terms of the underlying pathology. There are now a number of choices available for the treatment of ischemic stroke, and the causative mechanisms responsible for each individual stroke must be considered in choosing an appropriate form of treatment. This article explores the underlying pathophysiological mechanisms responsible for the major categories of stroke and also examines the reasons why strokes worsen or evolve.

Paraneoplastic neurologic syndromes.

Malignancies may produce indirect effects on the central and peripheral nervous systems, as well as on muscle. Certain autoantibodies have been detected in some of these paraneoplastic syndromes, and these antibodies most likely play a role in their pathogenesis. This article describes the currently accepted paraneoplastic neurologic syndromes along with current information regarding their pathogenesis.

Sensory impairment in the hands secondary to spondylotic compression of the cervical spinal cord.

In a 5-year period, 11 patients with spondylotic compression of the cervical spinal cord presented with a clinical picture dominated by glove-distribution sensory loss in the hands. Compressive lesions in each case were documented by myelography. The hand sensory loss was often global, and in some patients the involvement extended proximally as far as the elbows. Motor findings in the hands were no more than mild to moderate, as were motor and sensory findings in the legs. Nine patients improved with surgical decompression. The syndrome may result from ischemia to the intrinsic border areas of collateralization between the superficial pial network and the central arterial supply to the cervical cord, although venous stagnation may also play a role. This clinical presentation should always raise the suspicion of a cervical myelopathy, which is potentially treatable.

Imaging of acute arterial injury with 111In-labeled platelets: a comparison with scanning electron micrographs.

The relationship between degree of acute arterial injury, extent of platelet deposition, and ability to visualize arterial injury with Indium 111-labeled platelets was studied in 18 rabbits. An aortic lesion was made with a balloon catheter in each animal immediately after injection of autologously labeled platelets. Three nonlesioned rabbits with 111In-labeled platelets served as controls. An additional control study was performed in 12 lesioned rabbits in which nine were injected with 111In-labeled plasma protein and three with 111In-labeled red blood cells. A postmortem scanning electron microscope study of the aortae was made to determine the degree of injury to the intima and the amount of platelet deposition on the damaged arterial wall. The radionuclide scans and scanning electron micrographs were then compared. Lesions were seen in ten of 18 animals with labeled platelets that had extensive regions of denuded endothelium covered by a contiguous layer of platelets. Lesions consisting of patchy deendothelialization and platelet deposition could not be visualized on the scans. Red blood cells and fibrin were not conspicuous on micrographs of the lesions. No lesions were visualized in animals receiving 111In-labeled plasma protein or red blood cells before arterial injury, despite platelet deposition in the lesions.

Angiographic appearance of carotid occlusion in acute stroke.

The angiographic appearance of the proximal end of internal carotid artery occlusion is reported in 41 patients with acute stroke in the areas of the brain supplied by the carotid artery. All patients had angiography within 6 days of stroke onset, the majority within 24--48 hours. Three angiographic configurations of internal carotid occlusion were found, in descending order of frequency: a sharp, pointed stump; virtual absence of the artery; and a rounded, blunt stump. The results suggest that the angiographic appearance of the proximal occlusion alone may not accurately predict the age of the occlusion within the first 6 days from stroke onset.

Mechanisms of acute carotid stroke.

In a three-year study, the clinical course and results of intracranial angiography were compared in patients having an acute stroke in the carotid artery territory combined with angiographic abnormalities indicating severe extracranial carotid stenosis or occlusion. Two major mechanisms of stroke were delineated. In one group, the angiographic intracranial abnormalities strongly suggested the presence of embolism in the cerebral vessels supplied by the stenotic or occluded carotid artery; many of these patients had no obvious transient ischemic attacks prior to their stroke and experienced a moderate to severe clinical deficit. In the other group, evidence of embolism was absent; many showed a widespread delay in cerebral arterial perfusion, experienced a greater frequency of transient ischemic attacks before their stroke, and had a milder stroke than did those with embolism.

Symptomatic middle cerebral artery stenosis.

The clinical course of 16 consecutive patients with stenosis of the middle cerebral artery angiographically diagnosed between 1970 and 1977 was reviewed. All were managed nonsurgically with medical treatment including anticoagulation. Prior to therapy, transient ischemic attacks had occurred in 15 and cerebral infarction in 11. Initially, none exhibited more than a minor neurological deficit. Follow-up from one month to six years showed a benign course in 14 patients: 13 experienced no subsequent transient attacks or new stroke; 1 had repeated transient attacks for two years but not in the following four years. Two of the 16 developed a severe stroke early in the course, before medical therapy was started. No distinctive clinical or radiographic features were identified that permitted prediction of the outcome. This small series supports the need for a randomized study of bypass efficacy in these patients.

Case report. Simultaneous fungal and viral infection of the central nervous system.

A patient with lymphoma developed central nervous system dysfunction and the diagnosis of cryptococcal meningitis was made. Because of discordant clinical and laboratory responses to appropriate treatment, further investigations were performed and the additional diagnosis of progressive multifocal leukoencephalopathy (PML) was established. Computerized axial tomography (CT scanning) proved helpful in pointing toward the latter disorder. Clinical, neuropathological, and microbiologic features are presented. The diagnostic approach to central nervous system illness in patients with impaired immunocompetence should include consideration of simultaneous infection with multiple agents.

Influence of etiology of atrial fibrillation on incidence of systemic embolism.

Atrial fibrillation is well known to increase greatly the risk of systemic arterial embolism in patients with mitral valve disease. In light of the clinical frequency of embolism in patients with atrial fibrillation due to other types of heart disease, a study was made of embolic occurrences in 333 autopsy patients with atrial fibrillation associated with various kinds of heart disease. Considering only symptomatic emboli with pathologic or surgical confirmation, embolism occurred in 41% of patients with mitral valve disease, 35% of those with ischemic heart disease, 35% of those with coexisting mitral and ischemic heart disease and 17% of those with "other" types of heart disease. Embolism was found in only 7% of a control group of 58 autopsy patients with ischemic heart disease without atrial fibrillation. These findings suggest a high risk of embolism from atrial fibrillation of any origin, but particularly from that caused by ischemic heart disease and mitral valve disease.