Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013362 (dysarthria)
 3,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of multiple sclerosis (MS) in a 39 year old Japanese female with high antibody titer to human T-lymphotropic virus type I (HTLV-I) in serum and cerebrospinal fluid (CSF) was reported. At the age of 15, gait and urinary disturbances accompanied by sensory impairment in the lower abdomen and lower extremities developed suddenly. The motor disturbance slowly progressed to tetraparesis over a period of 15 years with several remissions. At the age of 28 the patient suffered from an acute loss of visual acuity, unilateral initially, and became blind by the age of 34. On admission to our department in September, 1987, the patient was alert and had spastic paraparesis, the impairment of all sensory modalities below the level of Th 10 and urinary disturbance. Weakness of facial muscles, nystagmus, deviation of the tongue and dysarthria were also noted. By the PA method, the antibody titer to HTLV-I was measured x512 in the serum and x64 in the CSF. Western blotting analysis of the CSF disclosed the bands to p19, p24 and p28 of HTLV-I gag proteins. The CSF contained a few ATL-like atypical cells and showed mild lymphocytosis, but the total protein was not increased. The computed tomography revealed diffuse low density areas in the cerebral white matter. The magnetic resonance imaging disclosed high intensity signal areas in the cerebral white matter and in the dorsolateral portion of the medulla oblongata on the T2 weighted image. The link of HTLV-I infection to the pathogenesis of human demyelinating diseases was discussed.
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PMID:[A case of multiple sclerosis with high CSF antibody titer to HTLV-I]. 275 51

A 38-year-old homosexual male with AIDS suffered four neurological episodes including headaches, confusion, visual impairment, memory disturbances, and dysarthria which resolved spontaneously in a few days. He was admitted to hospital during a fifth episode. Neurological examination revealed a cerebellar syndrome. General examination was normal. CD4 count was 90. CSF contained two WBCs/mm(3) and 12.30 mg/dL protein. MRI revealed diffuse ill defined increased signal on T2-weighted images in the white matter. His condition worsened rapidly with vomiting and he died 1 month after admission. Neuropathological examination revealed diffuse brain oedema with ventricular compression, central diencephalic herniation and bilateral tonsilar herniation in the absence of a focal lesion. Microscopical examination revealed predominant involvement of the white matter with diffuse myelin pallor and massive perivascular dilatation containing an exudate expressing serum proteins and occasional macrophages. The same exudate was also diffuse in the leptomeninges. Parenchymal damage predominated around the perivascular spaces and included loosening of tissue, axonal damage with spheroids and reactive astrocytosis. There was no evidence of productive HIV encephalitis, no multinucleated giant cells; p24 immunostaining and RT-PCR for HIV genome were negative. There was neither significant inflammation nor microglial activation. In this illustrative case, the relapsing course of the neurological signs, the diffuse topography of the blood-brain barrier breakdown and the absence of local cause make it likely that the diffuse leak and axonal damage could be related to circulating factors.
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PMID:Acute, relapsing brain oedema with diffuse blood-brain barrier alteration and axonal damage in the acquired immunodeficiency syndrome. 971 86