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)

Sixteen cases of juvenile, non-progressive muscular atrophy localized in the hand and forearm were seen at our neurology out-patient clinic for the past 8 years. The analyses of these 16 cases disclosed characteristic features as follows: 1) juvenile onset 2) male preponderance 3) unique distribution of muscular atrophy and weakness in the hand and forearm. 4) insidious onset, initial progressive period and subsequent non-progressive course 5) tendon reflexes of the arms are hypoactive in half of the cases 6) no pathological reflexes 7) cold paresis 8) no definite sensory disturbance 9) no cranial nerve involvement 10) neurogenic patterns on EMG According to these features, this clinical entity carrying good prognosis must be differentiated from several diseases associated with similar muscular atrophy of extremities, especially amyotrophic lateral sclerosis which is notorious as a fetal disease.
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PMID:[Juvenile, non-progressive muscular atrophy localized in the hand and forearm. Report of 16 cases (author's transl)]. 54 13

Four Japanese cases of postpolio progressive muscular atrophy (PPMA) of late onset were clinically studied to characterize their clinical features and discussed upon the epidemiologic viewpoint. Four male patients were included with mean age of 43.5 (30-59) years on examination, diagnosed as PPMA after the criteria by Alter (1982) and Dalakas (1986). All suffered from polio at age 10 month to 8 years (mean: 3y) between 1931 and 1957 with residual motor paresis in one limb or two. Twenty-eight to 55 (mean: 40.3) years later, subsequent muscle weakness and atrophy appeared in the limb seemingly unaffected by the initial polio attack. Marked fasciculations and occasional myalgias were noticed without sensory disturbance and bulbar as well as upper motor neuron signs. Laboratory examinations revealed moderate elevations of serum CK and protein content in SCF. No significant elevation of polio virus antibody titers was found in both serum and CSF. Electromyography showed neurogenic changes of various degrees by muscle tested. Muscle CT disclosed patchy distribution of atrophied muscles with fatty replacement in all extremities. Spinal cord MRI images were unremarkable. Scatters of small grouped atrophy and fiber type grouping were noticed on muscle biopsy specimens. These findings summarized in our cases are generally compatible with those of hereby reported PPMA cases. On reviewing the western literature and the great epidemic of polio around 1960 in Japan, an increasing number of patients with PPMA can be anticipated in near future; possibly in 10 years.
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PMID:[Postpolio late progressive muscular atrophy--clinical and epidemiologic analyses in 4 Japanese cases]. 238 7

Patients with prior poliomyelitis with paresis and excessive use (n = 8) and low use (n = 6) of residual anterior tibial motor units (MUs) during walking were subjected to muscle biopsy of the anterior tibial muscle (TA). Antibodies directed against cytoskeletal proteins, spectrin and desmin, and against Leu-19, a myoblast and satellite cell related antigen, were applied. In the patients with excessive use of residual MUs there was an almost total predominance of hypertrophic type I fibres. In the hypertrophic fibres, staining for spectrin and desmin was normal while staining for Leu-19 was seen in a few fibres. Scattered atrophic fibres seen in the patients with excessive use showed staining for spectrin, desmin and Leu-19. In the patients with low use of residual MUs there were extensive pathological muscle fibre changes. Increased staining for spectrin, desmin and Leu-19 was found in most of the atrophic fibres. The predominance of type I fibres in the patients with excessive use of residual MUs is suggested to be due to muscle fibre transformation. The normal staining pattern for spectrin and desmin in the hypertrophic fibres indicates a normal cytoskeletal structure which might suggest that the adaptive muscle fibre changes are adequate to meet the increased demand. The increased staining for spectrin, desmin and Leu-19 in the atrophic fibres might indicate an ongoing denervation process which earlier has been suggested as an important factor for the development of postpolio progressive muscular atrophy.
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PMID:Prior poliomyelitis: an immunohistochemical study of cytoskeletal proteins and a marker for muscle fibre regeneration in relation to usage of remaining motor units. 768 Jan 80

Increased weakness during cold (cold paresis) was reported in single cases of multifocal motor neuropathy (MMN). This was unexpected because demyelination is a feature of MMN and symptoms of demyelination improve, rather than worsen, in cold. It was hypothesized that cold paresis in MMN does not reflect demyelination only, but may indicate the existence of inflammatory nerve lesions with permanently depolarized axons that only just conduct at normal temperature, but fail at lower temperatures. We investigated symptoms of cold paresis in 50 MMN patients, 48 chronic inflammatory demyelinating polyneuropathy (CIDP) patients, 35 progressive spinal muscular atrophy (PSMA) patients, and 25 chronic idiopathic axonal polyneuropathy patients. We also investigated symptoms of increased weakness during warmth (heat paresis). Cold paresis was reported more often than heat paresis. Cold paresis was most frequently reported in MMN. Multivariate analysis indicated that MMN patients had a 4- to 6-fold higher risk of reporting cold paresis than CIDP or PSMA patients. Because cold paresis is not consistent with demyelination, the lesions in MMN may involve other mechanisms than demyelination only. In conclusion, symptoms of cold paresis are common in peripheral nervous system disorders, particularly in MMN. This supports the above-described hypothesis.
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PMID:Cold paresis in multifocal motor neuropathy. 2080 25

Progressive muscular atrophy (PMA), or the lower motor neuron disease, is a sporadic disorder characterized by onset in adulthood, pure lower motor neuron involvement and relatively benign course. Muscle atrophy and weakness may be symmetrical or asymmetrical, but they are always bilateral. We present a male patient with exclusively left-side flaccid paresis due to lower motor neuron disease without electromyographic evidence of neurogenic lesion of contralateral muscles and with no signs of corticospinal tracts involvement. The rapid disease progression was typical of the generalized phenotype of PMA and it suggested the relation to the aggressive course of classical ALS.
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PMID:Unilateral progressive muscular atrophy with fast symptoms progression. 2685 91