Cases reported "Seizures"

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1/13. Human herpesvirus 6 limbic encephalitis after stem cell transplantation.

    central nervous system complications are common in stem cell transplant recipients, but selective involvement of the medial temporal area is unusual. The 5 patients reported here presented after stem cell transplantation with increased hippocampal T2 signal on magnetic resonance imaging and increased hippocampal glucose uptake on [F-18]fluorodeoxyglucose-positron emission tomography (FDG-PET) associated with short-term memory loss, insomnia, and temporal lobe electrographic seizure activity. The initial scalp electroencephalograms (EEGs) failed to detect seizure activity in these patients, although the memory dysfunction along with the magnetic resonance imaging and FDG-PET findings suggested subcortical seizure activity. However, extended EEG monitoring revealed repetitive temporal lobe electrographic seizure activity. Follow-up MRIs in 2 patients and postmortem findings on 1 patient suggested that hippocampal sclerosis had developed following the clinical syndrome. cerebrospinal fluid studies revealed the presence of human herpesvirus 6, variant B, dna in all of 3 patients who had lumbar punctures. Immunohistochemical staining for the P41 and P101 human herpesvirus 6 protein antigens showed numerous immunoreactive astrocytes and neurons in the hippocampus of 1 of the patients who died from other causes. Because of its subtle clinical presentation, this syndrome may be underrecognized, but can be diagnosed with appropriate magnetic resonance imaging techniques, EEG monitoring, and cerebrospinal fluid viral studies.
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2/13. Mental retardation, hypotonia, and generalized seizures associated with astrocytic "residual" bodies. An ultrastructural study.

    Two siblings suffering since birth from convulsions, hypotonia, and mental retardation are presented. In the older sibling (eight and one-half years of age) frontal lobe biopsy revealed abnormal cytosomes with lamellar profiles in astrocytes, macrophages, and to a lesser degree in neurons. Similar cytosomes have not yet been reported in cases of sphingolipidoses or in late infantile-juvenile amaurotic idiocy. These cytosomes stained intensely with silver proteinate, an ultrastructural cytochemical stain for carbohydrate moieties. In contrast, lipofuscin did not stain with silver proteinate. Multilamellar (crescentic curvilinear) cytosomes from a reported case of late infantile amaurotic idocy (Batten-Vogt-Spielmeyer disease) did not stain with silver proteinate. Abnormal cytosomes were not found in blood cells, liver, and peripheral nerve. In the younger sibling (14 months old) postmortem ultrastructural studies of cerebral tissue showed very few abnormal cytosomes. On the basis of the clinical and ultrastructural findings, we conclude that these two cases can be distinguished from those with multilamellar (crescentic-curvilinear) inclusions and from cases of the so-called "neuronal ceroid-lipofuscinosis" syndrome.
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3/13. Nonketotic hyperglycinemia in two siblings with neonatal seizures.

    seizures are a common problem in neonates. Differential diagnoses include infection, trauma, hypoxia and congenital metabolic disorders. Among these, congenital metabolic disorder is less familiar to general pediatricians. We report two patients with nonketotic hyperglycinemia (NKH), a rare and lethal congenital metabolic disease. Transient hyperammonemia and transient hypouricemia, uncommon features found in NKH, were detected in one patient. High doses of sodium benzoate and dextromethorphan failed to modify the clinical course. Neuropathology denoted characteristic diffuse vacuolization and changes in reactive and gliotic astrocytes. The clinical course, biochemical findings, diagnostic approaches and diagnostic tests are discussed in detail. Recent modalities of treatment are reviewed. Because of its rarity and rapidly progressive course, it maybe underdiagnosed resulting in death before being recognized. awareness of the possibility of congenital metabolic disorder in early neonatal catastrophe will increase the diagnostic rate.
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4/13. Neonatal status convulsivus, spongiform encephalopathy, and low activity of Na /K( )-ATPase in the brain.

    The first and second child of a family died from neonatal seizures with no detectable brain malformation, metabolic, infectious, or chromosomal etiology. Neuropathological examination of the brain of the second child who died at 11 days revealed a widespread spongy state and a selective vulnerability of the astrocytes characterized by numerous enlarged bare astrocytic nuclei and different forms of astrocyte degeneration. The glial cells were strongly positive for glial fibrillary acidic protein and vimentin immunocytochemical reaction. Cortical measurement of Na /K( )-ATPase revealed very low enzyme activity. We hypothesize that a defect of Na /K( )-ATPase of the astrocytes could be the common pathogenetic factor for the congenital status convulsivus and for the spongy state.
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5/13. inclusion bodies in cerebral cortical astrocytes: a new change of astrocytes.

    A unique pathological finding of astrocytes was observed in the brain of a 20-year-old man who had severe physical and mental retardation. The brain was malformed showing micropolygyria in several cortical areas. A large number of hypertrophic astrocytes with eosinophilic granular substances in their cytoplasm were found throughout the cerebral cortex. Several staining procedures and electron microscopical examinations were carried out on these intracytoplasmic inclusion. It was found that the appearance and staining character of these inclusions were different from other astrocytic changes, especially the Rosenthal fiber, described so far. The authors consider that these inclusion bodies in cerebral cortical astrocytes represent new pathological changes of astrocytes that appear to be associated with malformation of the brain.
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6/13. Gangliogliomas: A report of five cases.

    Gangliogliomas are rare tumors of the central nervous system. Five gangliogliomas were diagnosed out of 1560 brain tumours surgically resected out in a period of 5 years accounting for 0. 32%. We have tried to discuss in detail the pathological features of these tumours and have mentioned the clinical and radiological features associated with them. All the slides, tissue blocks and pathology reports of the surgical specimens of gangliglioma were reviewed and the clinical and radiological data reviewed. The ages of the patients ranged from 7-65 years with 4 males and 1 female. The tumors were located in the lateral ventricle (a rare site), temporal, parietal and the frontal lobes with duration of seizures varying from 1-9 years. The tumors were diagnosed by the presence of a dual population of neoplastic ganglionic and glial components. The glial components consisted of pilocytic astrocytes (l case), fibrillary astrocytes (2 cases), oligodendrocytes (1 case) and anaplastic astrocytes and oligodendrocytes (1 case). There was one-grade I GG, three-Grade II GGs and one-grade III GG. astrocytes were the commonest glial component of GGs, either pilocytic or fibrillary. Oligodendrocytes as the glial component of GGs was seen in 2 cases one of which was anaplastic and this is a rare finding.
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7/13. Early cerebral images of alexander disease: report of one case.

    alexander disease is a neurodegenerative disorder characterized pathologically by demyelination and accumulation of eosinophilic hyaline bodies (Rosenthal fibers) within astrocytes. Demonstration of Rosenthal fibers on histological examination is considered a prerequisite for a definitive diagnosis. However, the CT and MRI scans may be highly suggestive of the disorder. We describe a patient who presented with subtle seizures at the age of 4 months. On examination, he was floppy with evident head lag. There was no visual following or social smiling. At that time, the brain MRI showed abnormal findings, with more white matter involvement and a characteristic periventricular rim. A diagnosis of alexander disease was not made until he was one year old, when a repeated MRI showed the full-blown pictures typically seen in alexander disease. The images fulfilled the diagnostic criteria proposed by van der Knaap in 2001. The early brain MRI findings in alexander disease can be very characteristic and greatly different from those in the late stage.
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8/13. Complex choristoma of the gyrus rectus: a distinct clinicopathologic entity?

    We report 2 cases of an unusual central nervous system lesion involving the gyrus rectus and characterized by well-differentiated epithelial and mesenchymal components. One patient was a 30-year-old woman, and the other was a 42-year-old man. Both presented with seizures. Radiologically, the lesions were solid, with ill-defined margins and increased signal on T2-weighted MRI. Both were contrast enhancing. There was no significant mass effect or edema. Histopathologically, the epithelial component was characterized by a tubule-forming, stratified epithelium. The lumina of the tubules were lined, in some areas, by a distinct layer of mature keratinocytes. Smooth muscle actin-immunoreactive myoepithelial cells were present in the basal layer, indicating glandular differentiation. Some lumina were cystically dilated and contained anucleate squames and/or PAS-positive material. In some areas, the epithelial structures were separated by reactive glial tissue resembling pilocytic astrocytoma, with prominent, piloid processes, Rosenthal fibers, and gemistocytic astrocytes. In other areas, glial nuclei formed small clusters reminiscent of subependymoma, but no glioma was identified in either case. Tissue resembling mature adipose was present focally. No mitotic figures were identified. Follow-up interval of up to 2 years showed no evidence of recurrent tumor. By location and histologic features, this lesion appears to represent a rare, distinct clinicopathologic entity, perhaps derived from misplaced cranial neural crest cells.
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9/13. Encephalopathy with astrocytic residual bodies. Report of a case and review of the literature.

    biopsy and autopsy findings in a girl who died at 7 1/2 months after having suffered from progressive axial hypotonia, myoclonus, EEG changes and retarded psychomotor development. Inclusions consisting of lamellar profiles, situated in membrane-bound cytosomes were found mainly in astrocytes, but also in neurones and in axons of peripheral nerves. lipofuscin bodies were also increased in number. The patient belongs in the same category as cases studied by Towfighi et al. (1975) and Martin et al. (1977). Etiology and pathogenesis of this syndrome remain unknown. It is suggested, however, that the pathological changes observed might have been caused by the administration soon after birth of anti-epileptic drugs (diphenylhydantoin, clonazepam and nitrazepam).
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10/13. Unilateral hemispheric cerebral changes similar to Creutzfeldt-Jakob disease in a case of hemiconvulsion.

    A 77-year-old man suffered intermittent hemiconvulsions of unknown etiology on the left side for a period of about 5 weeks. At the autopsy, there was marked neuronal loss, severe proliferation of astrocytes and spongiform changes in the right cerebral cortex. The cerebral white matter showed loosening with astroglial proliferation in areas on the same side. These neuropathological changes were slight or absent in the left cerebral hemisphere. Histopathological changes were similar to those seen in unilateral Creutzfeldt-Jakob disease (CJD). Although unilateral CJD can not be ruled out, these unilateral hemispheric changes might be induced by intermittent hemiconvulsions.
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