Search

Background and Purpose: The ability to identify patients at increased risk for stroke from cerebral hemodynamic ischemia may help guide treatment planning. We tested the correlation between regional cerebrovascular reserve (rCVR) on acetazolamide-challenged single-photon emission CT (SPECT) brain scans and intracranial collateral pathways as well as extra- or intracranial (EC-IC) arterial stenosis on cerebral angiography., Methods: A retrospective analysis of 27 patients who underwent cerebral angiography and acetazolamide-challenged SPECT brain imaging was performed. With cerebral angiography, the anterior, middle, and posterior cerebral artery (ACA, MCA, PCA) territories were evaluated for patterns of flow, including the ipsilateral carotid or basilar arteries, the circle of Willis collaterals, the EC-IC collaterals, and the leptomeningeal collaterals. With acetazolamide-challenged SPECT, the ACA, MCA, and PCA territories were classified as either showing or not showing evidence of decreased rCVR. Statistical significance was determined by the chi(2) test., Results: Patients with decreased rCVR had significantly greater dependence on either the EC-IC or leptomeningeal collaterals (42%) than did patients without decreased rCVR (7%). Similarly, the cerebral hemispheres with decreased rCVR showed a higher prevalence of 70% or greater stenosis or occlusion of the ipsilateral EC-IC arteries in the anterior circulation (74%) than did hemispheres with no evidence of decreased rCVR (16%), and this difference was also statistically significant., Conclusion: Acetazolamide-challenged SPECT brain scanning provides additional information regarding rCVR that is not reliably provided by cerebral angiography.

We describe two cases of disseminated coccidioidomycosis that were complicated by fatal subarachnoid hemorrhage. In the first case, a left middle cerebral artery aneurysm and long-segment vasculitis occurred. In the second case, MR imaging revealed an enlarging coccidioidal granuloma at the tip of the basilar artery, and the artery subsequently ruptured. Fatal intracranial hemorrhage is a rare complication of disseminated coccidioidomycosis.

This study evaluates the effect of blood volume and hematocrit changes on brain tissue during temporary global ischemia. Normal saline was administered intravenously to 55 gerbils to achieve hypo-, normo-, and hypervolemic hemodilution and uniform 30% hematocrit reduction. Each group had unilateral carotid artery ligation and temporary (20 minute) contralateral carotid occlusion. After ten days or death, brains were harvested, preserved in formalin, sectioned in a manner which provided adequate samples of both cortex and hippocampus, and stained with H&E and luxol fast blue. They were then examined and staged microscopically for white and gray matter infarction, edema, and neuronal injury and loss. Histologic studies were performed in a randomized and blinded manner and were classified by one of four categories: normal, minimal, moderate, and severe changes. Three of ten (30%) controls survived ten days but had severe neuronal loss, minimal cerebral edema and a minimal to moderate number of white matter strokes. Survival was best in animals treated with hypovolemic hemodilution (43%). Other rates were: normovolemic (33%), controls (30%), and hypervolemic (8.3%). The degree of brain tissue damage was markedly less in the normovolemic group. In this model, normovolemic hemodilution followed by hypovolemic hemodilution offered the best overall cerebral protection during global ischemia.

From the present review it seems clear that the physiopathogenesis of the chronic subdural hematoma is far from being completely understood. However, an analysis of the known data can be summarized as follows: The development of subdural hematomas most likely occurs following minimal trauma in those patients with predisposing factors. Experimental data substantiates the fact that an accumulation of clotted blood in the subdural or subcutaneous space induced the formation of the fibroplastic neomembrane. The hypothesis that blood must come in contact with cerebrospinal fluid in order for the growth to occur, is still controversial. It has been virtually disproven that osmosis, referring to the electrolyte gradient as measured by freezing point depression, has any significance as a growth inducing factor. The protein oncotic gradient theory, having been the most widely accepted explanation as to the progressive enlargement of the subdural hematoma sac, has little experimental data supporting it. A larger body of clinical evidence exists supporting the concept that plasma and/or erythrocytes continuously penetrate into the subdural cavity, where enhanced fibrinolytic activity is present. However, this chronic rebleeding cannot fully explain the observed growth, because the composition of the hematoma fluid is smoewhat different from serum or plasma, and the protein content is also progressively diluted by fluid arising from an unknown source. There is some clinical and experimental evidence to suggest that a production-reabsorption balance may be a significant growth variable. No work has been done to define the role, if any, of local inflammatory mechanisms in the chronic subdural hematoma. Sound clinical evidence has shown that after the initial formation of the subdural clot, growth follows, than a slow, complete reabsorption usually occurs. Aside from the plausible production-reabsorption balance concept, it is not known why the evolution proceeds in this manner.

Both Doppler supraorbital examination (OSM) and oculoplethysmography (OPG) were administered to 101 patients (202 arteries) to document the presence or absence of hemodynamically significant lesions of the internal carotid artery prior to angiography. There was no significant difference between the OSM and OPG with respect to diagnostic sensitivity or specificity, incidence of false-negative or false-positive results, and overall diagnostic accuracy. The diagnostic accuracy for the OSM and the OPG were 94.2% and 91.6%, respectively. In 171/202 (84.6%) arteries, the OSM and OPG were in diagnostic agreement, and the overall diagnostic accuracy of the combined tests was 97%. However, when the OSM and OPG did not agree (31/202 arteries, 15.4%), the diagnostic accuracy of neither the OSM nor the OPG was acceptable. Although the best diagnostic accuracy was obtained using two means of noninvasive cerebrovascular testing, in those instances where only one test may be available, the OPG would appear to be the test of choice. In those laboratories in which high diagnostic accuracy is obtained with the OSM, the addition of OPG testing will increase the overall diagnostic accuracy to a very high level. The presence of a midcervical bruit was found to have a very poor correlation with the incidence of hemodynamically significant stenoses of the internal carotid artery. Although both the OSM and OPG have minimal value in patients with symptomatic cerebrovascular disease, these tests play a very important role in screening patients for asymptomatic carotid stenosis or atypical cerebrovascular symptoms.

Three unusual cases of fatal meningitis secondary to undetected bacterial psoas abscess occurred at this institution over an 11-year period. All three patients had suffered chronic debilitating disorders before the abscess formation. The superimposed variable clinical presentations led to the initial diagnosis of a progressing cerebrovascular accident in one case, herniated nucleus pulposus at the L3-4 level in another, and osteomyelitis of the hip joint in the third. Analysis of these cases revealed that before the meningeal dissemination, all of the patients had shown evidence of intraabdominal pathology with positive psoas signs. Diagnostic and therapeutic guidelines are discussed.

The dorsal subcutaneous injection in rats of 12 ml or more of autologous hemolyzed whole blood clotted in situ induced the formation of sterile, hemispheric lesions, 47% of which showed an initial decrease in volume followed by a progressive enlargement. The behavior, histology, and biochemical characteristics of the liquid contents of these lesions were found to be remarkably similar to those of subdural hematomas in man. To evaluate the role of the various blood components that may have influenced the formation and growth of these lesions, more than 150 clots composed of human platelet-free plasma, autologous hemolyzed blood, or autologous whole blood were implanted subcutaneously in rats by either surgical or injection techniques. The in vitro behavior of the different clots used was also assessed. This systematic approach led to the following conclusions: 1) the composition and volumes of the clots are critical variables; 2) plasma-fibrin provides the matrix shape of the lesions; 3) the breakdown products derived from erythrocytes, hemoglobin, leukocytes, and other solid blood elements induce neomembrane formation and contribute to the lesion's subsequent growth; and 4) inflammation mechanisms appear to be essential, while cerebrospinal fluid plays no discernable role in this process.

An elderly man presented with signs of normotensive hydrocephalus. Elevated protein content in the spinal fluid led to the diagnosis of an "asymptomatic" cauda equine neurilemoma and its removal. Within 6 weeks the patient's mental status had dramatically improved. Chronic transudation of plasma proteins including fibrinogen into the subarachnoid space had probably impeded spinal fluid reabsorption. It is suggested that the leakage of fibrinogen into the cerebrospinal fluid may be the cause of hydrocephalus in other clinical settings in which there is an elevation of the spinal fluid protein.

Over the past six years, many new agents have become available for the treatment of bacterial central nervous system (CNS) infections. Certain principles guide the use of these agents for CNS infections: first, an antimicrobial agent must be able to penetrate the CNS to be effective; second, the CNS is a "relatively immunoincompetent site" so that an antimicrobial must achieve levels within the CNS capable of killing the offending bacterium. The lack of efficacy of chloramphenicol for meningitis due to gram-negative aerobes is probably due to its failure to achieve such killing levels, whereas the success of the newer cephalosporins, such as cefotaxime and ceftriaxone, is due to their very high killing activity against these organisms. Penicillin remains the first choice for pneumococcal and meningococcal meningitis. Ampicillin plus chloramphenicol is still recommended as initial therapy for meningitis due to Hemophilus influenzae. The newer cephalosporins are now the first choice for the treatment of meningitis due to many gram-negative bacilli. Trimethoprim-sulfamethoxazole may also be useful in some of these infections and those due to Listeria monocytogenes. In the treatment of severe CNS infections, a team approach is advised to ensure optimal therapy.

A previously described experimental hematoma model, achieved by the subcutaneous injection of 12 ml of autologous hemolyzed blood clotted in situ, was made in 33 rats. Sventeen animals served as controls; the other 16 received daily intra-muscular injections of dexamethasone. After an initial decrease in size, 47% of the lesions in the control animals enlarged to a mean weight of 12.1 +/- 2.5 gm, while the lesions in the 16 steroid-treated rats weighted 3.2 +/- 0.70 gm (p less than 0.01). Histologically, lesions from the steroid group showed absence of neomembrane formation. These data offer further support to the theory that the neomembrane development and subsequent enlargement of subdural hematomas is due to inflammatory reactions of tissues in contact with large blood clots.

Three patients are described in whom optic neuritis was presumably caused by concurrent sinus infection. Aggressive treatment of the underlying sinus condition led to prompt visual improvement. Although underrecognized in clinical neurology, paranasal sinusitis is an uncommon but treatable cause of optic neuritis. Shortcomings of conventional radiological investigations and inappropriate use of corticosteroids may contribute to initial misdiagnosis.

The case of a 58-year-old white man with a history of high blood pressure and chronic obstructive pulmonary disease who developed double vision followed by right-sided facial paralysis is reported. A computerized axial tomogram (CT) scan showed an enhancing lesion in the pontine tegmentum, and the diagnoses of pontine glioma or hemorrhage were considered. Physical findings were limited to the cranial nerves. Conservative management with Decadron for 3 weeks resulted in a prompt clinical improvement, and a CT scan 1 month later showed resolution of the lesion, effectively ruling out a glioma. Total clinical recovery occurred at the end of 6 months. To our knowledge this is the first report of a case of Fisher one-and-a-half syndrome with facial paralysis correlated with computed tomography.

The effect of sucralfate on steady-state phenytoin concentrations was evaluated in 6 normal volunteers. The subjects took phenytoin at bedtime until steady-state was confirmed (8 to 9 days) and then took in addition sucralfate 1g four times daily for a further 7 days. Serum phenytoin concentrations were measured on days 1, 3, and 7 of sucralfate administration. Measured phenytoin concentrations were 10.9 +/- 3.0 mcg/ml and 11.0 +/- 3.1 mcg/ml before sucralfate and 10.8 +/- 3.1 mcg/ml, 11.4 +/- 3.2 mcg/ml, and 11.1 +/- 2.5 mcg/ml during sucralfate administration (p greater than 0.05; ANOVA). These results suggest there is not a significant drug interaction between sucralfate and phenytoin.