Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Medulloblastoma and acute lymphocytic leukemia patients treated by intrathecal methotrexate and radiation were investigated by means of computerized axial tomography. More than 50% of them turned out to have acquired encephalopathy. Only gross morphologic brain defects, as visualized by computerized tomography, caused manifest clinical signs of brain dysfunction, such as epilepsy, mental retardation, paresis, and apallic syndrome. Mild morphologic changes were found even in asymptomatic children. The preferred site of defects in brain substance was the paraventricular white matter.
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PMID:Findings in computerized axial tomography after intrathecal methotrexate and radiation. 28 21

Diseases of the central nervous system (CNS) occurring during treatment of acute lymphoblastic leukemia (ALL) may be of leukemic or nonleukemic origin. Well known examples for CNS disease of nonleukemic origin are somnolence following prophylactic CNS irradiation, methotrexate-induced encephalopathy and acute infections caused by bacteria, viruses and toxoplasma gondii. Less known is the fact that also subacute CNS infections may occur in patients undergoing cytostatic therapy. Progressive multifocal leukoencephalopathy and subacute sclerosing panencephalitis (SSPE) are examples of this category of disease. Up to now 11 well documented cases of SSPE were reported occurring during treatment of ALL. Main clinical features were disorders of behaviour, consciousness and speach, seizures, paresis and inappropriate secretion of ADH. Several authors were able to demonstrate a deficiency of cellular immunity in patients with SSPE. In some cases this deficiency was consistent with reduced reactivity of T-lymphocytes against measles antigen only. The presence of inhibiting factors may be responsible for this phenomenon. Other authors found a normal or increased function of cellular immunity in SSPE; In hamsters occurrence of SSPE is induced by the simultaneous injection of hamster-adapted SSPE virus and antihamster lymphocyte serum. We, therefore, conclude that also in humans SSPE appearing during treatment of ALL is due to immunosuppression.
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PMID:[Non-leukemic disease of the central nervous system in children with acute lymphoblastic leukemia. III. Subacute sclerosing panencephalitis (author's transl)]. 36 90

We reported a 62-year-old male with cerebral thrombosis presenting global aphasia without hemiparesis. The patient had an episode of aphasia 15 years ago, but recovered within 6 months. This time he had transient right sided mild hemiparesis, then he became aphasia next morning. When we examined at day 10 and day 15, his consciousness was clear, nothing he could speech, he could not understand or repeat. We diagnosed him global aphasia, but he had no hemiparesis except for right facial mild paresis and was able to walk. CT scan showed low density area in left and right posterior, left anterior watershed and left terminal zone. Cerebral angiography disclosed thrombotic occlusion of main trunk of left middle cerebral artery, and ambient segment of right posterior cerebral artery. Global aphasia without hemiparesis has been said a sign of embolic encephalopathy. This case was considered a very rare case, because he revealed global aphasia without hemiparesis by thrombotic occlusion.
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PMID:[A case of cerebral thrombosis presenting global aphasia without hemiparesis]. 169 61

Seventy-six patients with neurologic complications of cat-scratch disease are discussed. Encephalopathy occurred in 61, while 15 had either cranial or peripheral nerve involvement. The average age of the patients with encephalopathy was 10.6 years (range, 1 to 66 years), and almost twice as many males as females were affected in contrast to patients with uncomplicated cat-scratch disease, in which the ratio was almost equal. Fever was not documented in 50% of patients with encephalopathy and only 26% had temperatures higher than 39 degrees C. Convulsions occurred in 46% and combative behavior in 40%. Lethargy with or without coma was accompanied by variable neurologic signs. Results of laboratory studies, including imaging of the central nervous system, were inconsistent and nondiagnostic. Biopsy tissue from 14 patients showed histopathologic findings compatible with cat-scratch disease. The "English-Wear bacillus" was demonstrated by the Warthin-Starry stain in 10 of 14 skin or lymph node specimens. Of the 15 patients without encephalopathy, two children with facial nerve paresis displayed cranial nerve symptoms and/or signs, 10 patients had cat-scratch disease neuroretinitis, and three women had peripheral neuritis. All 76 patients recovered within 12 months; 78% recovered within 1 to 12 weeks. There were no neurologic sequelae. Treatment consisted of control of convulsions and supportive measures. Commonly used antibiotics administered to more than half of the patients were apparently ineffective.
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PMID:Cat-scratch disease. Acute encephalopathy and other neurologic manifestations. 184 21

A survey of the literature of neurological manifestations associated with the acquired immune deficiency syndrome (AIDS) shows a broad disease spectrum affecting approximately one third of the patients in large hospital series. The complications include focal cerebral lesions caused by abscesses, lymphomas, leucoencephalopathy or infarcts as well as encephalitis, meningitis and myelitis. Most opportunistic infections of the central nervous system presumably are caused by toxoplasma gondii, cytomegalovirus and cryptococcus neoformans. One tenth of all patients have neurological disease as their initial symptom of AIDS. The diagnosis should always be considered in patients at risk and in males with an unusual neurological history or with a peculiar CT scan of the brain. Besides the opportunistic complications of AIDS, LAV/HTLV-III itself probably attacks the nervous system and gives rise to concomitant lesions of the long tracts of the spinal cord with ataxia, paresis and spasticity and to subacute encephalopathy and peripheral nerve abnormalities as well.
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PMID:Neurological complications and concomitants of AIDS. 303 38

During the 3 weeks of his life, an infant born at term presented pronounced hypotonia, areflexia and generalized paresis with severe respiratory and feeding problems. He was the fourth male in two generations to die in the perinatal period, therefore suggesting an X-linked inheritance. Post-mortem examination revealed a centronuclear or myotubular myopathy. The difficulty in distinguishing the signs due to muscle disorder from those due to hypoxaemic encephalopathy is stressed. Infants with centronuclear myopathy have in any case a high risk for hypoxaemic encephalopathy. The literature concerning neonatal centronuclear myopathy with X-linked inheritance is reviewed.
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PMID:Neonatal myotubular myopathy with a probable X-linked inheritance: observations on a new family with a review of the literature. 651 77

An acute episode of encephalopathy after the infusion of 16 g methotrexate is reported in a 12-year-old girl with osteogenic sarcoma. The complication occurred during the 11th treatment course, when severe vomiting and diarrhea were followed by a low urine output with consecutive toxic concentrations of methotrexate in serum and cerebrospinal fluid leading to severe systemic and central nervous system toxicity. The onset of the central nervous system toxicity was acute with slurred speech, paresis of the external rectus eye muscles, ataxia, and hemiparesis, and symptoms resolved completely after 30 hours by treatment with calcium leucovorin and forced diuresis. After management of the cerebral and systemic toxicity, high-dose methotrexate treatment could be reinstituted, and was followed by no further complications. In contrast to the transient cerebral dysfunctions, probably caused by embolization of tumor tissue in the early course of high-dose methotrexate treatment, the acute neurologic syndrome observed in the current case after the prolonged use of methotrexate seemed to be related to direct central nervous system toxicity of the drug.
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PMID:Transient encephalopathy during the late course of treatment with high-dose methotrexate. 658 97

Disulfiram is known to produce toxic encephalopathy and peripheral neuropathy. The case of a 37-year-old alcoholic who attempted to commit suicide by taking 22.5 g disulfiram is described. During the first 6 days after the intoxication he was stuporous and had cerebellar ataxia and dysarthric speech. Then he became comatose, and as he recovered from coma, he showed peripheral neuropathy including diplegia faciei and severe tetraparesis. Denervation potentials were detected in both facial muscles and distal muscles of the upper and lower limbs, while conduction velocity was normal. Axonal degeneration was verified by sural nerve biopsy. In addition neurofilamentous axonopathy was documented. The recovery from his paresis lasted 2 years.
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PMID:[Polyneuropathy caused by disulfiram poisoning]. 686 Jan 22

Borna disease is an immunopathological virus-induced encephalopathy comprising severe inflammation and degenerative brain cell lesions which results in organ atrophy and chronic debility in rats. CD4+ and CD8+ T cells have been reported to be involved in the development of this disease of the central nervous system. A virus-specific homogeneous T-cell line, established in vitro after immunization of rats with the recombinant 24-kDa virus-specific protein, showed antigen-specific proliferation in the presence of the 24-kDa but not the 38-kDa Borna disease virus-specific protein, another major virus-specific antigen. This T-cell line, P205, was found to exhibit characteristics of a T-helper cell: CD4+ CD8- IL-2- IL-4- IFN-gamma+ IL-6+ IL-10+. Furthermore, this T-cell line expressed the alpha/beta T-cell receptor and the alpha 4 integrin (VLA-4). Adoptive transfer of this helper cell resulted in an increase of antibody titers and two different types of disease in virus-infected rats after cyclophosphamide-induced immunosuppression. (i) Rats receiving T cells between 10 and 18 days after treatment with cyclophosphamide showed an acute lymphoproliferative disease in the gut and lungs within 9 days after adoptive transfer and died. (ii) Passive transfer within the first 5 days after immunosuppressive treatment resulted in typical Borna disease associated with neurological symptoms such as ataxia and paresis starting 14 to 16 days after transfer. Immunohistological analysis of the brains of rats with Borna disease uniformly revealed the presence of CD8+ T cells in encephalitic lesions in addition to CD4+ cells that were found in the brains of recipients of the virus-specific CD4+ T-cell line, irrespective of whether neurological symptoms developed or not. However, recipient rats treated with antibodies against CD8+ T cells developed neither encephalitis nor disease. Therefore, CD4+ T cells appear to accumulate in the brain and cause perivascular inflammatory lesions which alone obviously do not cause disease. In contrast, the presence of CD8+ cells apparently directly correlates with the development of neurological symptoms.
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PMID:Immunopathogenic role of T-cell subsets in Borna disease virus-induced progressive encephalitis. 781 58

In 24 cases of multifocal necrotizing encephalopathy (MNE) in Simmental and Simmental-cross cattle, clinical features varied, consisting of mild rear limb ataxia, caudal paresis, and, less often, sudden death. Bilateral and symmetric malacic lesions were present in the brain stem (olivary nucleus) of all affected calves. Foci of malacia affecting thoracic spinal cord and additional brain stem sites were common. Neuronal cell bodies and hypertrophied capillaries were present within malacic foci. Rarefaction of neuropil, progressing to complete parenchymal loss, characterized advanced lesions. Pathologic features were similar to those of Leigh syndrome in humans, and a similar defect in aerobic metabolism is hypothesized. Occurrence of the syndrome within 1 breed over a wide geographic area suggests that hereditary factors contribute to development of MNE.
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PMID:Multifocal subacute necrotizing encephalomyelopathy in Simmental calves. 785 26


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