Cases reported "Brain Diseases"

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11/26. An unusual late complication of Gasserian ganglion cecompression surgery. Case report.

    The authors report an unusual complication following sugery for decompression of the Gasserian ganglion. Eight years postoperatively this patient developed a left temporal lobe granuloma caused by a piece of wood used to plug the foramen spinosum at surgery. The patient's clinical and radiological findings were suggestive of a glioma involving the temporal lobe.
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12/26. Primary phycomycosis of the brain in heroin addicts.

    Two heroin addicts had fatal primary phycomycosis of the brain. The first case is unique. A 28-year-old man displayed unusual symptoms of unilateral hydrocephalus confirmed by both computed tomography (CT) scanning of the brain and craniotomy. The nature of the fungal granuloma was verified histopathologically. The second case, a 40-year-old man, possessed bilateral basal ganglionic lesions in which the CT scanning suggested abscesses. Postmortem examination confirmed the presence of phycomycotic abscesses. There was no evidence of systemic mycoses in both cases. review of the clinical features of this fatal complication in drug abusers and narcotic addicts disclosed that hemiparesis and facial weakness are common. Brain or CT scan along with brain biopsy are necessary for rapid diagnosis and prompt treatment.
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13/26. Cerebral subcortical calcification and hypoparathyroidism--a case report and review of the literature.

    Hypoparathyroidism is known to exhibit various neurological manifestations, but most of the neurological disorders seen in this condition are motor ones, and involuntary movement is rarely encountered. Basal ganglion calcification is a common feature in hypoparathyroidism. But calcification of the cerebral cortex is, to our knowledge, extremely rare with only nine previously documented cases reported. We report a case of both involuntary movement and extensive cortical calcification with some reference to the literature. Furthermore, we discuss the relationship between neurological disorders and intracranial calcification.
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14/26. frontal lobe calcification in hypoparathyroid states.

    Basal ganglion calcification is common in hypoparathyroid states. However, cerebral cortical calcification is rarely seen. Of the six cases previously recorded, five were in patients with idiopathic hypoparathyroidism and only one in a patient with pseudohypoparathyroidism. The present report is of a second case of pseudohypoparathyroidism with cerebral cortical calcification. It is stressed that cortical calcification occurs predominantly in the frontal lobes.
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15/26. Focal necrotizing brain stem encephalopathy and cranial radiculopathy in a kidney transplant recipient.

    A 48-year-old female patient developed sensory and motor palsy of the V-Xth cranial nerves immediately after kidney transplantation due to terminal uremia. A second exacerbation followed about 4 weeks later. After 46 days post transplantation she died from bronchopneumonia. autopsy showed multiple acute and subacute necrotic foci in proximal portions of the cranial nerves as well as a discontinuous necrotizing encephalopathy localized mainly in the subpial zone of the brain stem. The mechanism by which lesions of the nervous system were produced remains speculative. A possible neurotoxic role was attributed to the drugs administered after transplantation. Herpes virus hominis antigen could be demonstrated in the cells of the pons and of the trigeminal ganglion, but its presence was thought to be coincidental and probably not causally related to the described lesions.
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16/26. pathology of olivopontocerebellar atrophy with glutamate dehydrogenase deficiency.

    We report the neuropathologic findings in the first patient with recognized glutamate dehydrogenase (GDH) deficiency to come to postmortem examination. He had progressive cerebellar ataxia beginning at age 21. He died at age 47 of pulmonary emboli. Postmortem examination revealed pancerebellar, olivary, and mild pontine atrophy, demyelination of the posterior columns, degeneration of anterior horn and dorsal root ganglion cells, and reduction of myelinated fibers in the sural nerve. In addition, there was neuronal storage of lipopigment diffusely throughout the CNS and the autonomic neurons, with cell distention, atrophy, and loss in selected areas.
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17/26. Actinomycotic granuloma of the Gasserian ganglion with primary site in a dental root. Case report.

    An unusual case of cerebral actinomycosis of the Gasserian ganglion is reported. The location and the pathological diagnosis of granuloma are both extremely rare. The literature is briefly reviewed with special reference to similar reports. The manner of spread and the course of the disease are described. The present case tends to confirm the opinion that primary cerebral actinomycosis is extremely rare and probably does not exist. The case also definitely indicates that the organism reaches the central nervous system by way of nerve or perineural pathways.
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18/26. Lhermitte-Duclos disease (diffuse hypertrophy of the cerebellum). Report of two cases.

    Two cases of Lhermitte-Duclos disease or diffuse hypertrophy of the cerebellum are presented. This brings the total number of such cases reported in the literature to 42. Pathologically the disease is characterized by a circumscribed cerebellar lesion consisting of thickening of the cortex with closely packed dysplastic ganglion cells in the granular layer and with large myelinated axons in the molecular layer. purkinje cells are missing and the central white matter is greatly reduced. The first patient, a man 39 years of age, had in association to the cerebellar lesion, a megalencephalic brain (2320 g). He had suffered from epilepsy since he was 24-years-old and died with metastasizing colon carcinoma. An electron microscopic study of the cerebellar lesion disclosed perikarya containing large amounts of rough endoplasmic reticulum, cell processes filled with coated and dense core vesicles. In addition, there were numerous enlarged myelinated axons in the molecular layer. The second patient, a woman 74 years of age, had a small area of diffuse hypertrophy of the left cerebellar hemisphere measuring one centimeter in diameter. Specific symptoms were very scant in the first case and absent in the second one indicating a very slow evolution - if any - of the disease process. The etiology and pathogenesis remain unknown. However, the organoid structure of the lesion, the frequent association of megalencephaly and other congenital abnormalities, and the occurrence of familiar cases would favor the disease being basically a developmental disorder.
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19/26. Pigmentary macular degeneration with multifocal necrotizing encephalopathy.

    A previously healthy 10-year-old girl suffered sudden, binocular visual deterioration. During the next few years her neurologic and visual condition progressively worsened and she developed hypertension, seizures, ataxia, and lactic acidemia, leading to death at the age of 16 years. Bilateral optic disk pallor was followed by the loss of the foveal reflex and pigmentary maculopathy, manifested as disorganization of the retinal layers, loss of ganglion cells, degeneration of the photoreceptors and nuclei, and irregular infiltration of the retina by pigment epithelial cells. The optic nerves and tracts showed central axonal loss. Bilateral, multifocal symmetric areas of cerebral atrophy and necrosis of the neuropil and neurons in the cerebral cortex, basal ganglia, and thalamus were observed; neurons persisted in the dorsal medulla, despite neuropil degeneration.
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20/26. Hemispatial and directional performance biases in motor neglect.

    Motivationally responsive motor deficits may occur in isolation or as part of more general neglect syndromes. We describe three patients with two discrete syndromes of isolated motor neglect, differentiated primarily by their performance in motor tasks enacted within or toward the contralesional hemispace. The lesions in our patients likely disrupted attentional interactions with two separable sensorimotor processing subsystems. Physiologic data support the existence of a parietal-lateral premotor circuit that processes information encoded in spatial coordinates referenced to the extrapersonal environment and of a basal ganglionic-mesial premotor circuit that processes information mostly encoded in egocentric skeletomotor coordinates. The correlation of ischemic lesions resulting in hemispatial and directional biases in motor neglect with disruption of known physiologic subsystems may provide the basis for rational cognitive rehabilitation of these higher-order motor deficits. These observations are supported by recent PET studies that document the presence of specific attentional-motoric interactions within discrete processing components of a distributed sensorimotor attentional network.
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