Cases reported "Brain Edema"

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1/9. glycogen-rich and glycogen-depleted astrocytes in the oedematous human cerebral cortex associated with brain trauma, tumours and congenital malformations: an electron microscopy study.

    PRIMARY OBJECTIVE: The anaerobic mobilization of astrocyte glycogen in anoxic-ischemic regions of the oedematous human cerebral cortex is analysed. methods and PROCEDURES: Seventeen cortical biopsies of patients with brain trauma, brain tumours and congenital malformations were examined by conventional transmission electron microscopy. RESULTS: glycogen-rich and glycogen-depleted, clear or dense astrocytes cell bodies were observed in anoxic ischaemic regions of different brain cortical areas in perineuronal, neuropilar and perivascular localization. glycogen-rich astrocytes showed clear or moderately dense cytoplasm and accumulation of both beta-type or monogranular glycogen granules and alpha-type or multigranular glycogen particles. Focal regions of translucent cytoplasm were observed in areas of glycogen degradation. glycogen-depleted astrocytes exhibited a clear cytoplasm and scarce amount or absence of beta-type glycogen granules. Coexisting glycogen-rich and glycogen-depleted neuropilar astrocytic processes were observed in the vicinity of degenerated myelinated axons and degenerated axodendritic contacts. glycogen-rich and glycogen-depleted perivascular astrocytic processes were also found surrounding injured and collapsed cerebral capillaries. CONCLUSION: The findings suggest astrocytic glycogen mobilization during anoxic and ischaemic conditions, revealing the important contribution of astrocytes on neuronal survival under conditions of energy substrate limitations.
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2/9. Edema of the cortical gray matter of the human cerebrum.

    Five cases of brain tumor are reported in which an extracellular edema of the cerebral cortex was recognized in the form of lakes of eosinophilic, PAS positive material, presumably serum proteins, permeating among the neuronal and glial cells and processes. In three, the astrocytes and their processes were stained in replicate paraffin sections by a gold sublimate technique. The astrocytic changes were variable. Most often, the astrocytes changed from protoplasmic to fibrillary, with long deeply stained processes, the cells sometimes becoming large and distorted. Many became enlarged and smudgy, with short stubby processes. Only a few showed the fragmentation and disintegration of processes. Only a few showed the fragmentation and disintegration of processes which are regularly observed in edematous white matter. The neuronal processes remained essentially normal. In comparison with edema of white matter, edema of the cortex is rare, involves only small portions of tissue, and differs in its effects on astrocytes. The edema in both cortex and white matter is extracellular. We have not been able to recognize a specific intracellular form of edema, grossly or with light microscopic techniques.
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3/9. Fatal cerebral edema from late-onset ornithine transcarbamylase deficiency in a juvenile male patient receiving valproic acid.

    OBJECTIVES: The aims of this report are to 1) present a rare case of fatal cerebral edema associated with late-onset ornithine transcarbamylase (OTC) deficiency in a juvenile male patient receiving valproic acid and 2) review the neuropathologic changes associated with the hyperammonemia. DESIGN: Case report. SETTING: A community hospital and a tertiary pediatric critical care unit. INTERVENTIONS: Carbohydrate administration, intravenous nitrogen excretion cocktail, and high-flux hemodialysis. MEASUREMENTS AND MAIN RESULTS: Despite aggressive therapy for presumed late-onset OTC deficiency, the patient rapidly developed fatal cerebral edema with tonsillar herniation. A liver biopsy confirmed OTC deficiency with approximately 3% of residual hepatic enzyme activity. Chromosomal analysis showed a normal male karyotype. A thorough molecular analysis of the coding region in the OTC gene Xp21.1 was completed, but mutations were not identified, suggesting an upstream or downstream abnormality. Severe brain swelling was evident on neuropathology, and histopathology showed Alzheimer type II astrocytes, neuronal cytoplasmic changes, and hypertrophy and eosinophilia of the small arterial walls. CONCLUSIONS: OTC deficiency is the most common urea cycle defect causing hyperammonemia. Late-onset presentations of OTC are infrequent, primarily affecting female patients. We present a rare case of a late-onset OTC deficiency in a juvenile male patient receiving valproic acid therapy who developed fatal cerebral edema. valproic acid exacerbates acute elevations in ammonia and may contribute synergistically with ammonia to cerebral mitochondrial dysfunction.
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4/9. Brain and liver pathology in a patient with carnitine deficiency.

    The ultrastructural brain and liver pathology in an infant, who died of acute encephalopathy due to systemic carnitine deficiency (CD), an important condition mimicking Reye's syndrome (RS), was reported. The major finding in the brain was swelling of astrocyte cytoplasm. Expanded mitochondria in nerve cells and myelin sheath splitting in the white matter, which have been reported to be specific to RS, were not observed. Also in contrast to findings in RS, hepatocytes were filled with macrovesicular fat droplets without expanded mitochondria. These findings suggest significant differences in the pathophysiology of acute encephalopathy in CD and RS, although the clinical and laboratory findings during an episode of acute encephalopathy in the former are usually very similar to those in the latter.
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5/9. Spongy encephalopathy in ketotic hyperglycinemia.

    Three cases of ketotic hyperglycinemia are described. Spongy encephalopathy was present in white as well as gray matter. The cell type that predominantly exhibited swelling was the astrocyte. glycine binding is required for activation of the NMDA receptor. By constant excitation a surplus of glycine could disturb the ion balance. This might provide the pathogenetic principle of seizures and cytotoxic edema in hyperglycinemia.
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6/9. Structural and vascular permeability abnormalities associated with lacunes of the human brain.

    Histopathological and immune-histochemical studies were carried out in four cases with multiple lacunes of the central grey matter and in control cases without such lesions. Routine light microscopic techniques were applied on paraffin-embedded material to identify lesions that may represent developing lacunes. In addition, polyclonal antisera to human albumin, IgG, fibrinogen and fibronectin were chosen as markers for extravasated plasma proteins. The brain tissue between lacunes contained several forms of focal injuries which may represent precursors of lacunes. Such lesions included foci of status spongiosus and status cribrosus, regions with dilated extracellular spaces and astrocytic gliosis, and multi-locular cysts. These "lacune-associated lesions" often included albumin immune-reactivity in extracellular spaces, nerve cell bodies and astrocytes. Less frequently signs of extravasated IgG, fibrinogen and fibronectin were identified. Thus, lacunes of the human brain frequently showed signs of antigenic sites to albumin. The extracellular deposits probably represent extravasated material from the blood. Vasogenic and cytotoxic oedema combined with other factors probably play important roles during the formation of some of the lacunes.
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7/9. Spongy degeneration of the central nervous system (van Bogaert-Bertrand type?) in a newborn infant. A light and electron microscopic study.

    autopsy findings on a 5 day old infant with hypotonia from birth showed extensive spongy changes of the myelinating tracts within the cerebrum, cerebellum and brain stem. The spongy changes, similar to Van Bogaert-Bertrand disease, resulted from intramyelinic edema. However, unlike the typical forms of this disease, swollen astrocytes with abnormal mitochondria were not found. The relationship of this case to typical forms of Van Bogaert-Bertrand disease is discussed. This case may represent a very early form of Van Bogaert-Bertrand disease or a new pathological entity.
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8/9. Synaptic degenerative changes in human traumatic brain edema. An electron microscopic study of cerebral cortical biopsies.

    The cerebral cortex of 9 patients with complicated brain trauma has been examined with the transmission electron microscope to study the distinctive degenerative synaptic changes induced by brain injury and associated vasogenic, moderate or severe, brain edema. The brain injury and the hematogenous edema fluid accumulated in the dilated extracellular space of cerebral cortex neuropil induced swelling and shrinkage of pre- and postsynaptic structures, increased amount of presynaptic axoplasmic granular substance and clumping, enlargement and depletion of synaptic vesicles. In severe brain edema, swollen and shrunken presynaptic endings with discontinuous limiting plasma appeared separated from the postsynaptic structures and detached from glial ensheathment (synaptic disassembly). Post-synaptic shaft dendrites and their spines showed swelling and vacuolization. Fragmen-tation and atrophic changes of spine apparatus were found in the dendritic spines. The clear and dark types of degeneration were observed in most cases examined, in both preand/or postsynaptic structures. Filamentous hypertrophy of presynaptic endings was observed only in two cases. Osmiophylic bodies, necrotic membranes, lipid inclusions and glycogen granules were seen in the synaptic terminals. Disappearance of synaptic densities was evident in some cases. phagocytosis of isolated presynaptic endings or of the entire synaptic contacts by astrocytes, microglial cells and by non-nervous invading cells, such as monocytes and macrophages, was found.
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9/9. Electron microscopic analysis of cortical biopsies in patients with traumatic brain injuries and dysfunction of neurobehavioural system.

    Cortical biopsies of eight patients with craniocerebral trauma complicated with subdural or epidural hematoma were examined with the transmission electron microscope. The patients showed post-traumatic neurobehavioural disorders and moderate or severe vasogenic brain edema. The capillary wall displayed increased vacuolar and vesicular endothelial transport, basement membrane thickening and vacuolization and swollen astrocytic end-feet. Pericapillary and parenchymatous hemorrhages were also observed. The extracellular space appeared considerably enlarged with presence of proteinaceous hematogenous edema fluid and fibrinous organization. Pyramidal and non-pyramidal neurons showed intracellular edema featured by irregular enlargement of rough endoplasmic reticulum, nuclear envelope and golgi apparatus. The myelinated axons exhibited clear or black type axoplasmic degeneration, varicose fiber swelling, myelin sheath distortion, formation of myelin ovoids and increased amount of oligodendroglial ad-axonal layer. The dendrites also showed clear or dark and beaded shape degeneration. Synaptic degeneration was characterized by swollen and shrunken pre- and postsynaptic endings, clumping, enlargement and depletion of synaptic vesicles, synaptic membrane complex disassembly and detachment of glial ensheathment. Perivascular and perineuronal astrocytes appeared remarkably swollen. Phagocytic astrocytes were also found. Oligodendrocytes displayed hydropic and reactive changes. Reactive oligodendrocytes induced myelinolysis. The brain barrier dysfunction, the vasogenic and cytotoxic edema and the subsequent neuronal and neuroglial cell reactive and degeneration processes might represent the morphological substrate responsible for the post-traumatic neurobehavioural disorders.
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