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 66-year-old female suffering from HTLV-1 associated myelopathy (HAM) for more than 30 years was hospitalized because of memorial impairment, deafness, dysarthria, dysphagia, and complete paraplegia. She first noticed stiffness and weakness of the right leg at 35 years of age. Gait disturbance was slowly progressed and complete paraplegia developed 18 years later. Neurological examinations on admission revealed that she was bedridden with decubitus, mental deterioration (pre-dementia of subcortical type), bilateral optic nerve atrophy, severe sensory-neural deafness, dysarthria, complete paraplegia, and marked neurogenic bladder. Laboratory data showed mild normocytic anemia and moderate diabetes mellitus. Anti-HTLV-1 antibody titers in serum and CSF were 78,192X and 1,024X, respectively (PA method). Serum levels of soluble IL-2 receptor was markedly elevated (2,200 U/ml). Peripheral blood lymphocytes showed spontaneous proliferation when cultured for 5 days (3H-thymidine uptake; 45,285 cpm/5 X 10(4) cells). MRI examinations of the spinal cord disclosed a predominant atrophy of lower thoracic cord without any compressive lesions. Brain MRI showed diffuse high intensity lesions of the periventricular area on T2 weighted images. Such abnormalities were predominantly found in fronto-parietal region and were quite similar to those of leuko-ariosis. Single photon emission CT using 123I-iodoamphetamine showed hypoperfusion of cerebral white matter on delayed image. It has been reported that intellectual impairment and brain atrophy are not usually seen in HAM patients. The present case, however, shows that such abnormalities of the central nervous system could occur in HAM patients with a long duration of illness.
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PMID:[A case of HTLV-1 associated myelopathy progressed in course over 30 years]. 189 70

A 41-year-old woman had radical mastectomy for breast cancer with metastasis of axial lymph nodes three years previously. In February 1990, she noticed swelling of lymph nodes in right suparclavicular region. A lymph node biopsy revealed cancer cells. Immediately, radiation therapy was performed. However, in August serum levels of CA 15-3 and LDH were markedly elevated. Two months later the patient complained of severe headache, dysarthria, shoulder pain and anorexia. Neurological examination revealed stiff neck, weakness of bilateral facial muscles, deviation of tongue to the left and no sensory disturbance. A CSF sample by lumbar puncture showed 26/mm3 in cell counts, 204 mg/dl of protein and 11 mg/dl of glucose. In addition, CSF cytology revealed malignant cells four to five times as large as lymphocytes. Immediately, and intrathecal administration of methotrexate (MTX) was started. However, one week later she developed complete paraplegia with sensory disturbance below the L1 levels and an incontinentia urine. CSF examination performed again, and showed 97/mm3 in cell counts, 792 mg/dl of protein and 91 mg/dl of glucose. On October 10, a CT scan of the head showed contrast enhancement along cerebellar folia and narrowing of quadrigeminal cistern. On November 31, sagittal T1W1 with Gadolinium revealed an enhancing stripes along the spinal cord at the Th10 to L4 levels. This finding was suggested to be meningeal carcinomatosis. On December 8, she died. At autopsy, brownish hemorrhagic mass was noticed in the bilateral cerebellar tonsils, and severe downward displacement of the tonsils.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of meningeal carcinomatosis showing myelopathy--detection of TNF-alpha in infiltrating CSF cells and brain tissue sections of cerebellum]. 831 90

A 73-year-old man with a 5-day history of continuous hiccup, fever, and rapidly progressing paraplegia was admitted to our hospital. On admission, he exhibited dysarthria, complete paraplegia, and insentience of both lower limbs. Head and spine MRI showed abnormal, asymmetric lesions in the white matter, basal ganglia, and brainstem, and multiple spinal cord lesions. Test for serum anti-AQP4 antibody was negative. Evaluation of human leukocyte antigen (HLA)-B51 was negative; however, HLA-B54 was positive. Although skin lesions were absent, we considered neuro-Sweet disease and high-dose steroid therapy was initiated. The hiccup disappeared gradually, and he regained the ability to walk with a cane 30 days after the onset. Subsequently, the patient tested positive for serum anti-myelin oligodendrocyte glycoprotein (MOG) antibody. It is important to consider MOG antibody-related disease as potential diagnosis in patients exhibiting clinical features of neuro-Sweet disease except for the absence of skin lesions.
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PMID:[A case of anti-myelin oligodendrocyte glycoprotein (MOG) antibody-related disease with human leukocyte antigen (HLA) positivity indicative of neuro-Sweet disease]. 3185 76