Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influenza B virus mouse model of Reye's syndrome was studied to learn more about the encephalopathy in Reye's syndrome. One to 3 days after intravenous influenza B/Lee virus, Balb/c mice became lethargic, seized and lapsed into a fatal coma. Wide-spread cerebral edema without inflammation developed 1-3 days after virus inoculation. Swollen astrocytic foot processes containing increased glial fibrillary acidic protein were located around capillaries. Viral particles were not seen by electron microscopy and complete viral replication did not occur. Immunohistochemical studies demonstrated influenza B viral antigen within many endothelial cells but not within other brain cells. Qualitative (Evans blue dye) and quantitative (percent brain water and technetium -99 pertechnetate) studies of the blood-brain barrier demonstrated abnormalities. This model reproduced many clinical, virologic and pathologic features of the Reye's syndrome encephalopathy. In addition, a non-permissive viral infection of brain endothelial cells occurred which may be important in the pathogenesis of the mouse encephalopathy and may participate in the encephalopathy of Reye's syndrome.
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PMID:The influenza B virus mouse model of Reye's syndrome: clinical, virologic and morphologic studies of the encephalopathy. 216 26

A case of malignant choroid plexus papilloma (choroid plexus carcinoma) originated in the third ventricle is reported. A 14-month old girl was admitted to our department with two-month history of impaired vision and gait disturbance. Neurological examination on admission disclosed a lethargy, blindness, and left hemiparesis. Computed tomographic (CT) scan and magnetic resonance imaging (MRI) demonstrated a large contrast-enhancing mass, approximately 5 cm in diameter, in the region of third ventricle, extending to the bilateral lateral ventricles. The patient had gross total removal of the tumor via lateral ventricle route, and received 40 Gy of postoperative radiation therapy. Light microscopically, the tumor was composed of epithelial cells showing both papillary and poorly differentiated pattern. There were considerable cellular pleomorphism, frequent mitoses, and occasional necroses. Immunohistochemically, anti-keratin antibody was detected within majority of neoplastic cells. Both neoplastic epithelial cells and stroma showed negative reaction to anti-GFAP antibody. Ultrastructurally, the shape of the nuclei varied from ovale to irregular with many indentations. The chromatin was clumped around the periphery of the nuclei. The neoplastic cells contained numerous free ribosomes, glycogen granules, and rough endoplasmic reticulum. The apical cell surfaces showed various size of club-like or roundish microvilli filled with glycogen granules, and rarely 9 + 2 cilia. Elongated junctional complexes were occasionally seen near the apical ends. The basal portions of the cells had a continuous basement membrane. These immunohistochemical and ultrastructural findings were comparable to the choroid plexus papilloma with malignant features.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of large malignant choroid plexus papilloma in the third ventricle--immunohistochemical and ultrastructural studies]. 248 83

A 13-month-old boy admitted with lethargy and hydrocephalus was found to have a right thalamic mass. Ventricular drainage was instituted, and the tumor mass was reduced by partial resection and local irradiation. A ventriculoperitoneal shunt was then placed. However, the tumor recurred 16 months later, with extensive ventricular seeding and peritoneal metastasis through the shunt tube. The child died 22 months after onset. Histological study of surgical specimens of the primary tumor and autopsy specimens of the brain and peritoneal metastatic tumors revealed poorly differentiated, small, round cells with numerous mitotic figures. In addition, autopsy specimens of the brain tumor contained areas of ependymal, oligodendroblastic, and spongioblastic differentiation. On immunohistochemical study, the tumor cells of each specimen were positive for anti-neuron specific enolase and anti-neurofilament antibodies, but negative for anti-glial fibrillary acidic protein antibodies. Electron microscopy revealed some zonulae adherens. These findings strongly suggest that the tumor originated from primitive multipotential cells capable of differentiating into ependymal, glial, and neuronal lines.
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PMID:[Primitive neuroectodermal tumor with peritoneal metastasis through a ventriculoperitoneal shunt. Case report]. 248 94

Chickens infected as embryos with RAV-7 developed neurological signs including ataxia, lethargy, and imbalance. Evoked spinal cord potentials for RAV-7 infected SC chickens were considerably slower (64.8 m/s) than for uninfected SC (103.4 m/s), genetically hypothyroid (OS) (93.9 m/s) or special C (95.1 m/s) chickens. Conduction velocity measurements of sciatic nerves showed normal values for all the chickens examined in this study. Histopathological studies revealed non-suppurative meningoencephalomyelitis in RAV-7 infected SC chickens. The inflammatory infiltrate consisted of lymphocytes, macrophages, and occasional plasma cells. The cells in the infiltrate reacted with mouse monoclonal antibodies directed against la and T-cell antigens. Astrocytic hypertrophy and hyperplasia, demonstrated by the use of monoclonal antibody specific for glial fibrillary acidic protein (GFAP), was associated with the CNS lesions. The results of this investigation indicate that RAV-7 causes significant central nervous system lesions and functional impairment in the infected chicken. This system may serve as a useful model for studying retrovirus-induced neurological dysfunction.
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PMID:Functional and structural alterations of the nervous system induced by avian retrovirus RAV-7. 319 74

A three-year-old boy with a progressive history of headache, vomiting and ataxia in the course of 2 months, was admitted on August 1983, when he was lethargic. Neurological examination revealed dysphagia, scanning speech and tremor in the bilateral hand. CT scan showed a very large enhanced mass in the center of posterior fossa with central necrosis in it and the dilatation of whole ventricular system. Suboccipital craniectomy was immediately performed and the tumor that occupied the vermis and invaded into both cerebellar hemisphere was subtotally removed. Postoperative irradiation was well performed: 4140 rads to the whole brain and 3162 rads to the spinal cord. However, 5 months later, facial palsy in the left side and progressive ataxia became prominent. CT scan showed multiple enhanced masses in the left trigonum and right anterior horn of the lateral ventricles and in the left cerebellopontine angle. In spite of chemotherapy, the patient had a down-hill course, especially after the ventricular hemorrhage, and died on June 9th, 1984. Histologically, the tumor had a lobulated appearance with an aggregation of tumor cells encircled by vascular septae. The cells within lobules generally had vesicular nuclei, which were arranged in parallel row. Occasionally smaller hyperchromatic cells with scant cytoplasm were present along the vascular septae. Reticulin was present within the septa, but was not observed within the lobules. Scattered astrocytic cells and processes were identified within the lobules by the immunoperoxidase technique for GFAP. The fibrillary cytoplasmic processes within the lobules were stained by immunoperoxidase technique for neurofilament (68K).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of cerebellar neuroblastoma]. 361 40

The FVB mouse is used extensively in transgenic research because of its defined inbred background, superior reproductive performance, and prominent pronuclei, which facilitate microinjection of genomic material. Seizures associated with a known mutation and seizure-susceptible inbred strains are well documented in mice; however, to the authors' knowledge, seizures in the FVB strain have not been evaluated. Affected nonmanipulated FVB/N (n = 5) and transgenic FVB/N mice generated, using eight unrelated transgenic constructs (n = 63), were submitted for pathologic examination. Most cases were detected during routine observations in animal rooms; however, seizure induction by tail tattooing, fur clipping, and fire alarms has been observed. The majority of mice were female (62 of 68), with mean age of 5.8 months (range, 2 to 16 months). Observations made during seizure presentation in 12 of 68 mice included facial grimace, chewing automatism, ptyalism with matting of the fur of the ventral aspect of the neck and/or forelimbs, and clonic convulsions that frequently progressed to tonic convulsions and death. Four mice were dead at presentation, with matting of the fur of the neck and forelimbs. The remainder of the mice had nonspecific signs of disease, such as lethargy, moribundity, or matting of the fur. Vendor and in-house animal health surveillance reports indicated that mice were seronegative to all murine pathogens. Results of gross pathologic examination were unremarkable. Microscopic findings were limited to the brain and liver. In all mice, neuronal necrosis was present in the cerebral cortex, hippocampus, and thalamus. Concurrent astrocyte hypertrophy, as evidenced by an increase in glial fibrillary acidic protein staining, was detected. Acute coagulative necrosis of centrilobular hepatocytes was present in the liver of some cases (19 of 68). Infective agents were not detected in selected brain specimens submitted for electron microscopy or in brain and liver specimens evaluated by use of special stains. Cytopathologic effect was not observed in 3T3, Vero, and BHK-21 cell lines inoculated with brain and liver specimens. The ischemic neuronal necrosis observed in these mice is consistent with lesions associated with status epilepticus in humans. The hepatocellular changes are interpreted to be agonal and associated with terminal hypoxia in seizuring animals. These results provide evidence of a previously unrecognized, often lethal epileptic syndrome in FVB mice that may have a major impact on transgenic research and other disciplines using this mouse strain.
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PMID:Neuropathologic findings associated with seizures in FVB mice. 951 87

The term "chordoid glioma" was recently introduced to denote a circumscribed, apparently low-grade neoplasm arising in or preferentially involving the third ventricle of middle-aged women. We report biopsy and postmortem findings in a 60-year-old woman with symptoms of forgetfulness, headache, and lethargy. Neuroimaging showed a contrast-enhancing third ventricular mass with obstructive hydrocephalus. The tumor was subtotally resected. Microscopically, it consisted of clusters and strands of epithelioid cells in a mucoid matrix. Its margins were remarkably discrete and showed little tendency to infiltrate surrounding brain parenchyma. The majority of neoplastic cells were glial fibrillary acidic protein (GFAP) and vimentin positive, whereas S100 protein labeled only individual cells. Stains for epithelial membrane antigen (EMA) and cytokeratin were nonreactive. There was no evidence of neuroendocrine differentiation or expression of estrogen and progesteron receptors. Lymphoplasmacellular infiltrates were noted throughout the lesion and at the tumor-brain interface. The MIB-1 labeling index averaged 1.5%. At present, chordoid glioma is considered a glial neoplasm of uncertain histogenesis with distinct clinicopathologic features.
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PMID:Chordoid glioma of the third ventricle: confirmatory report of a new entity. 1037 85

A case of pilocytic astrocytoma of neurohypophysis is presented. The clinical, pathological and MRI features of a rare tumor of the neurohypophysis are described. A 5-year-old girl presented with a 3 month history of lethargy, imbalance and visual disturbances. A MRI revealed a large suprasellar mass. Histopathological examination demonstrated a pilocytic astrocytoma. Its astrocytic nature was confirmed by positive immunostaining for GFAP and the findings of an electron microscopy.
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PMID:Pilocytic astrocytoma of neurohypophysis. 1457 Feb 90

A 4-year-old female miniature dachshund presented with a history of progressive decrease in vision, neck pain, and ataxia for which an MRI was performed 21 days after the initial consultation. The optic nerves showed isointensities on T1- (T1W) and T2-weighted (T2W) images that were enhanced by the contrast medium. The optic chiasm was swollen. Other parts of the cerebral parenchyma, not only the visual pathway, showed symmetrical hyperintensities on T2W images. Cerebrospinal fluid showed increased anti-GFAP autoantibodies. The dog received corticosteroid therapy despite which she exhibited anorexia, vomiting, and lethargy. Hence, a follow-up MRI was repeated 30 days after the initial consultation in which T2W images showed enlargement of the hyperintense area. The dog died 45 days after the initial consultation. Postmortem pathological examination confirmed a diagnosis of granulomatous meningoencephalomyelitis (GME).
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PMID:Ocular granulomatous meningoencephalomyelitis in a dog: magnetic resonance images and clinical findings. 1926 40

A 2-year-old gelding presented with a history of lethargy and anorexia. Physical examination revealed pleural and abdominal fluid, as well as several masses in the scrotum. The horse became acutely dyspneic despite 7 days of supportive care. Because of the poor prognosis, the owners elected euthanasia. Gross necropsy findings included multiple masses in the scrotum and inguinal canals and along the dorsal peritoneal cavity. The neoplasm infiltrated the kidneys, liver, spleen, mesenteric lymph nodes, mesentery, and abdominal surface of the diaphragm. Histologically, the neoplasm is composed of spindle to round cells arranged in densely cellular areas, vague streams, and rare rosettes. Neoplastic cells were immunoreactive for S-100 protein, glial fibrillary acidic protein, neuron-specific enolase, neurofilament protein, and synaptophysin. Based on gross, histological, and immunohistochemical findings, a diagnosis of peripheral primitive neuroectodermal tumor was made. Primitive neuroectodermal tumors are rarely described in horses that were associated with the eyes.
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PMID:Peripheral primitive neuroectodermal tumor in a two-year-old paint horse. 2262 43


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