Systemic vascular responses to increased intracranial pressure. 1. Effects of progressive epidural ballon expansion on intracranial pressure: and systemic circulation.
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This paper details the results of experimental studies, on 16 dogs with artificially-induced intracranial space-occupying lesions, of the systemic vascular responses and the intracranial pressure changes (both in the supratentorial and infratentorial compartments) induced by increasing intracranial pressure. The changes produced were divided into two phases such that phase 1 detailed the alterations observed from the start of the balloon inflation up to the initiation of the systemic pressor response. Phase 2 recorded those alterations which occurred during, and immediately after, the period of systemic hypertension (see Fitch et al., 1977). The changes observed during phase 1, and presented in this communication, were those of increasing intracranial pressures and decreasing mean arterial pressure and heart rate. These alterations were associated with decreases in supratentorial perfusion pressure and increases in transtentorial pressure gradient and arrhythmia index. (+info)
Arachnoid cyst with rupture into the subdural space.
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Arachnoid cysts which develop in relation to the cerebral hemispheres are usually found in the middle cranial fossa. These cysts are usually asymptomatic but can produce symptoms if there is haemorrhage into the cyst or the development of an associated subdural hematoma. Recent publications have emphasised the association of arachnoid cysts of the middle fossa with subdural haematomas. This report describes a case of an asymptomatic arachnoid cyst which ruptured into the subdural space. This event was followed by the development of symptoms despite the lack of haemorrhage. (+info)
Calcified congenital arachnoid cyst with heterotopic neuroglia in wall.
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Two unique findings, advanced calcification and ectopic neuroglia, were encountered in the wall of a giant congenital arachnoid cyst occurring in a 40 year old woman. The cyst almost totally filled the supratentorial subdural space of the left hemicranial cavity, was not connected with the subarachnoid space, and thus developed intra-arachnoidally. Its congenitally derived nature was supported by the unique finding of heterotopic neuroglia in the wall. Congenital arachnoid cyst must be distinguished from various cystic lesions within the central nervous system, including the neuroepithelial cyst which can arise throughout the neuraxis. It is suggested that pathogenesis of the congenital arachnoid cyst is related to aberrant flow of the ventricular cerebrospinal fluid into the developing leptomeninx in the process of differentiation of the subarachnoid space. The tract or pouch may occur within the arachnoid mater, and the cyst is formed intra-arachnoidally when the former filled with fluid is closed off from the subarachnoid space. (+info)
Cefuroxime treatment of bacterial meningitis in infants and children.
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Recently, ampicillin- and chloramphenicol-resistant strains of Haemophilus influenzae type b and multiply-resistant Salmonella strains have appeared in some areas of the world. Therefore, alternative drug therapy for infections caused by these organisms is being sought. We used cefuroxime to successfully treat five children with H. influenzae type b meningitis and two children with Salmonella meningitis. Four H. influenzae type b isolates and one Salmonella isolate were resistant to ampicillin, chloramphenicol, and cotrimoxazole. Each of the patients received 200 to 250 mg of cefuroxime per kg per day in four divided doses for 14 to 21 days. The concentrations of cefuroxime in cerebrospinal fluid at 2 h after intravenous 50-mg/kg doses were 6.4 +/- 1.7 (mean +/- standard deviation) and 3.6 +/- 2.2 micrograms/ml on days 2 and 14 of treatment, respectively. The level of drug in cerebrospinal fluid was 1.34 +/- 1.3 micrograms/ml in children without meningitis. The mean cefuroxime concentration in subdural fluid samples from each of three patients was 12.6, 15, and 25.2 micrograms/ml. Cefuroxime is recommended as an alternative drug for the treatment of H. influenzae type b meningitis, but additional information is necessary before cefuroxime can be recommended for therapy of Salmonella meningitis. (+info)
The origin of subdural neomembranes. I. Fine structure of the dura-arachnoid interface in man.
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A method for the in situ fixation of human meninges for electron microscopic examination is described. It was found that the cranial meninges of humans do not include a subdural space. Instead there is a complex, tight layer of cells, the interface layer, composed in the innermost portion of the dura mater (the dural border cells) and the outermost portion of the arachnoid (the arachnoid barrier layer). The fusion of these components within the interface layer is much more intimate than is either the attachment of the dural border cells to the dura proper or that of the arachnoid barrier layer to the rest of the arachnoid. The fine structural characteristics of these layers are defined. The erroneous macroscopic impression of a subdural space results from an extraordinary lack of cohesion within the dura-arachnoid interface layer conditioned by a) a complete absence of a collagenous reinforcement within this zone, b) the presence of large extracellular cisterns between the dural border cells, and c) a paucity of intercellular contacts within that latter layer. An understanding of the fine structural organization of the interface layer is essential to any consideration of the pathogenesis of subdural lesions: these form within a sheet of torn dural border cells and not within a preexistent tissue compartment. (+info)
The origin ofsubdural neomembranes. II. Fine structural of neomembranes.
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A comparison of the fine structure of subdural neomembranes with the fine structural organization of the normal human dura-arachnoid interface discloses that neomembranes are not de novo proliferations of tissue from a smooth inner dural surface. Rather, a neomembrane is the result of proliferation and excessive thickening of the normal layer of dural border cells. On proliferation, the dural border cells form multilayered tiers and clusters of cells, transfixed by capillaries, with collagen fibrils and elastic fibers between them. Capillaries and collagen fibrils are absent from the normal interface layer. Pathogenetic concepts of chronic subdural hematoma need to be revised. Any pathologic condition inducing cleavage of tissue within the dural border layer at dura-arachnoid interface will be followed by proliferation of fural border cells with production of a neomembrane. There is no compelling reason to postulate that proliferation of the border cell layer is always secondary to traumatic hemorrhage. (+info)
The linearity of the volume/pressure response during intracranial pressure "reserve" testing.
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The intracranial pressure "reserve" test seems to be the most reliable method of determining when the brain's natural mechanisms for pressure compensation for added intracranial volume have been compromised or exhausted. The test employs a timed sequence of intracranial fluid injections, but as a safety precaution injections are discontinued if intracranial pressure remains elevated more than 10 Torr over baseline. In this case, a linear extrapolation is then calculated to determine the elevation which might have been achieved by a full series of injections. However, this linear extrapolation has been criticised on the expectation that an exponential response should be expected. A series of experimental observations in dogs and baboons and a review of clinical records in humans have been made to determine the observed slope of increase following aliquot injection during performance of the intracranial pressure reserve test. In these species the observed response was actually linear in shape rather than exponential. This held true even for different initial baseline values and with different volumes of "lesion" balloon inflations in experimental animals. A theoretic explanation is proposed. (+info)
Central retinal vein occlusion: a prospective histopathologic study of 29 eyes in 28 cases.
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The clinical and histopathologic features of 29 eyes from 29 patients with central retinal vein occlusion (CRVO) are reported. A fresh or a recanalized thrombus was observed in each eye. This study considers the temporal aspects of the cases, and it notes the different morphologic features of the occlusion. These observations explain most of the variability of the changes observed in previous reports. We believe that these different features represent the various stages in the natural evolution of such a thrombus. The interval between CRVO and histopathologic study in our series ranged from six hours to more than 10 years. Local and systemic factors were reviewed and were found to be important in the pathogenesis of thrombus formation. Local diseases with a predisposing effect on CRVO included: glaucoma, papilledema, subdural hemorrhage, optic nerve hemorrhage, and drusen of the optic nerve head. Associated systemic diseases included: hypertension, cardiovascular and cerebrovascular disease, diabetes mellitus, and leukemia with thrombocytopenia. A fresh thrombus in the CRVO was observed in three (10.3%), and a recanalized thrombus in 26 eyes (89.7%). Endothelial-cell proliferation was a conspicuous feature in 14 (48.3%) of the eyes. Chronic inflammation in the area of the thrombus, and/or vein wall or perivenular area was observed in 14 (48.3%) of the eyes. Arterial occlusive disease was observed in seven eyes (24.6%). Cystoid macular edema was found in 26 (89.7%) of the eyes. (+info)