Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026827 (hypotonia)
 5,860 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Myopathy may be associated with the syndrome of seroconversion in individuals infected by the human immunodeficiency virus (HIV) or may represent the initial symptom of AIDS. In 1990, 39-year old white, single homosexual who was admitted 1 month prior had experienced an episode of edema and pain in the left thigh that faded with the use of nonhormonal antiinflammatory drugs. 15 days later both forearms became enlarged accompanied by pain and erythema. Erythromycin and cefalexine were used without success. Intermittent fever started to appear before admission accompanied by dyspnea when straining. Examination showed tachypnea, oral candidiasis, and enlargement of both upper arms with pain and local erythema without articular involvement. Neurological examination revealed hypotonia and generalized hyperreflexia with intact muscle strength. Serology was positive for HIV, rheumatic activity tests were negative, and muscle biopsy indicated multifocal myonecrosis. Creatinine phosphokinase was 1019 IU (decrease to 44 IU after treatment), aldolase was 19 IU (decrease to 5.6 IU), and glutamic-pyruvic transminase was 50 IU (decrease to 22 IU). Radiography of the thorax indicated interstitial infiltration. Fiberoptic bronchoscopy indicated Pneumocystis carinii pneumonia. Sulfamethoxazole and trimetropim treatment cured the dyspnea and hypoxemia, but the enlargement of both arms progressed. Capillaroscopy indicated vasculitis that was treated without success with indomethacin (150 mg/day), for 7 days; prednisone (40-80 mg/day) for 10 days; and dexamethasone (280 mg/day) for 2 days. 6 days after methotrexate (50 mg/dose/week) treatment the fever disappeared and the enlargement in the extremities receded, but a lower dose of 7.5 mg caused the return of fever and edema in the right thigh. The myopathy remained asymptomatic for 5 months with a weekly dose of 15 mg of methotrexate.
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PMID:[AIDS and myopathy: report of a case and review of the literature]. 180 40

A 2-year-old boy suffered aphasia, hypotonia, dystonia, and loss of activity and spontaneous speech during an active stage of juvenile rheumatoid arthritis with pericarditis, fever, anemia, and a high antinuclear antibody titer. These neurologic signs slowly improved with corticosteroid treatment but fluctuated over 1 year. The neuroimaging studies revealed irregular mass lesions in the basal ganglia bilaterally mainly involving the globus pallidus. They gradually decreased in size and almost disappeared after 1 year. A stereotactic brain biopsy revealed a slight proliferation of astrocytes. Chorioretinitis was also observed during the clinical course. A chronic inflammatory process involving cerebral vessels was suspected, although angiography did not demonstrate cerebral vasculitis. The possibility of central nervous system lymphoma could not be eliminated. The type of aphasia and the relation to the lesion sites are discussed.
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PMID:Basal ganglia mass lesions in juvenile rheumatoid arthritis. 205 56

A patient developed acute phthisis bulbi and external ophthalmoplegia with herpes zoster ophthalmicus (HZO). The clinical course and ocular complications of HZO are described briefly and the cause of phthisis bulbi and external ophthalmoplegia in zoster ophthalmicus is discussed. It is suggested that the acute hypotonia in HZO is due to an ischemic necrosis of the ciliary body, resulting from an occlusive vasculitis which may also be responsible for the external ophthalmolplegia.
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PMID:Acute phthisis bulbi and external ophthalmoplegia in herpes zoster ophthalmicus. 387 92

An eleven-months-old boy with motor developmental delay, muscle weakness, hypotonia and normal tendon reflexes was diagnosed as having infantile polymyositis, histologically with a vasculitis component. Corticosteroid treatment was successful. At the age of 5 years he showed a normal motor pattern.
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PMID:[Infantile myositis]. 408 72

Twelve patients (9 women, 3 men, mean age 26.8 +/- 5.02 years) with spontaneous isolated dissection of posterior cerebral artery (PCA) were studied. Eleven patients (92%) developed ischemic stroke, 1 patient (8%)--transient ischemic attack (TIA). All patients underwent magnetic resonance imaging (MRI) of the head and magnetic resonance angiography (MRA): 9 patients--a follow-up MRA, 3 patients--a single study. Local neurological symptoms (hemianopia, hemianestesia) developed suddenly (75%) during everyday patient's activity (83%) and were combined with headache on the side of dissection in 75% of patients. The main provoked factor was alcohol (67%), 25% had preceding respiratory infection. The initial cerebral angiography carried out in most cases within the first month of stroke demonstrated the occlusion (33%) or stenosis (67%) of PCA. The repeat MRA carried out on 2-3 months or more showed the improvement or normalization of blood flow in PCA (89%). In 1 (11%) patient the occlusive process progressed that correlated with headache increasing. A single MRA carried out in 48 days--6 months (3 patients) found the prolonged irregular stenosis (1), occlusion at P2 segment (1) and normal PCA appearance (1). At the whole, the prolonged irregular stenosis at least in one study, was found in a half of patients. None of patients had atherosclerosis, vasculitis, arterial hypertension or thrombophilia. Clinical manifestations of connective tissue weakness were seen in 67% of patients, hypotonia--in 67%, headache in the past history--in 67% and mitral valve prolapse--in 75%. In conclusion, spontaneous isolated dissection of PCA is one of the causes of ischemic stroke in young adults. The diagnosis is based on characteristic clinical manifestations and follow-up MRA. The development of dissection appears to be connected with arterial wall weakness.
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PMID:[Ischemic stroke due to isolated spontaneous posterior cerebral artery dissection in young adults]. 1989 94

Necrotizing vasculitic neuropathy in polyarteritis nodosa can rarely present acutely and may mimic acute inflammatory neuropathies. A 53-year-old male presented with an acute neurological illness characterized by paresthesia and weakness of both lower limbs lasting six-days. He also had mild paresthesia of both hands. On examination, there were confluent, purpuric, and ecchymotic patches over the extensor aspects of both lower limbs, which were palpable. Neurological examination revealed grade II/V power with hypotonia and absent reflexes in the lower limbs. All modalities of sensation were decreased below the knee. Sensory impairment was also noted on the fingertips of both hands. Nerve conduction study suggested an asymmetrical sensorimotor axonal neuropathy. Sural nerve biopsy was consistent with necrotizing vasculitis. He was treated with intravenous methylprednisolone followed by oral prednisolone and monthly cyclophosphamide injection for six-months and made a good recovery.
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PMID:Acute Necrotizing Vasculitic Neuropathy due to Polyarteritis Nodosa. 2989 35