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Query: UMLS:C0027121 (myositis)
 4,538 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report the case of a 56-years old patient with clinical symptoms of an unresolved neuromuscular disease. The light microscopic studies of a muscle biopsy from the m. triceps shows the picture of a diffuse muscular atrophy. By electron microscopy, myelin-like degeneration zones with tubular-filamentous inclusions can be shown in the cytoplasma of the atrophic muscle cells. These filamentous structures correspond morphologically to the nucleocapside of paramyxoviruses. These results lead, even without the proof of inflammatory cells, to the diagnosis of an "inclusion body" myositis also taking into account the clinical and electrophysiological findings.
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PMID:Inclusion body myositis. A "slow-virus" infection of skeletal musculature? 92 17

Nine puppies suffered from progressive paresis with muscle wasting, hyporeflexia and extensor rigidity. CK-activity in serum was elevated and electrodiagnostic findings were indicative of lower motor neuron disease. Although lesions were also found in the CNS, additional neurological signs were rare, but CSF examination revealed the presence of inflammatory lesions. On pathologic examination, all animals had a disseminated necrotizing myositis. In addition, a disseminated encephalomyelitis was found as well as, in 2 cases, a neuritis. In the lesions of 6 animals protozoal organisms were found which were immunocytochemically identified as Neospora caninum. Our results show that the protozoal myositis-encephalitis syndrome in puppies can be diagnosed in the clinic with high probability. A clinical differentiation between toxoplasmosis and Neospora caninum infection is presently difficult.
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PMID:[The clinical diagnosis of protozoal myositis syndrome (Neospora caninum) of puppies]. 188 44

Inclusion body myositis is a rare and slowly progressive myositis associated with cytoplasmic inclusions and fibrillar nuclear material. These histopathologic findings are of unknown significance. The clinical presentation of IBM has marked similarities to that of chronic polymyositis with proximal greater than distal weakness and muscle wasting more pronounced in the lower than upper extremities. In contrast to polymyositis, however, relatively few individuals report neck flexor weakness or dysphagia. Corticosteroid treatment is usually ineffective. The clinical, histopathologic and electrophysiologic findings in a patient with IBM are presented. Of particular interest in this report is the detailed motor unit recruitment frequency data. A number of previous IBM reports fail to mention specific electrophysiologic data or present evidence suggestive of a possible combined neuropathic and myopathic disease. Recruitment intervals of 150 ms or greater in combination with decreased motor unit duration and amplitudes in the involved muscles imply a myopathic pathophysiology. These findings are discussed in relation to electrophysiologic data from previously reported cases.
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PMID:Inclusion body myositis. An electrophysiologic study. 215 41

An extreme unilateral muscular atrophy of the shoulder and upper arm region was a symptom of juvenile ankylosing spondylitis in a 20-year-old female patient. No pathological patterns were found in electromyographic, bioptic, and tomographic (CT, NMR) investigations. The muscular atrophy was caused by a shoulder arthritis with severe erosive damage. The false assumption of a neurological disorder and the disregard of anamnesis and low back pain delayed for several years an accurate diagnosis. After the onset of an arthritis of hip joints a collagen disease with myositis was supposed falsely in spite of normal electromyographic results. The unusual muscular atrophy around the shoulder joint probably must be interpreted as a consequence of reflex inhibition and partly due to inactivity. A real myositis seems to not be probable, because newer investigations in contrast to earlier findings show no evidence for inflammatory muscle disease in ankylosing spondylitis.
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PMID:[Extreme atrophy of the shoulder muscles in juvenile ankylosing spondylitis as a (misleading) main symptom]. 260 97

A 38-year-old male developed a new muscle weakness in his left thigh 35 years after having acute paralytic poliomyelitis with residual right distal leg weakness and atrophy. EMG studies showed widespread denervation in proximal and distal muscles regardless the clinical involvement. Muscle biopsy from an affected muscle showed the findings of inclusion-body myositis consisting of perivascular and interstitial mononuclear infiltration, sarcoplasmic granular inclusions with membranous whorls and typical filamentous inclusions in several myonuclei. This raises the possibility of inclusion body myositis in other cases of progressive post-poliomyelitis muscular atrophy, especially those with perivascular infiltration of mononuclear cells in the muscle biopsy.
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PMID:Inclusion body myositis in post-poliomyelitis muscular atrophy. 284 1

An investigation was made into the occurrence of muscular atrophy and muscular pathology in a series of 170 patients with myasthenia gravis. The results can be summarized as follows: (1) Of the 148 patients with generalized myasthenia gravis, 14 showed local muscular atrophies. Of 10 biopsies from atrophic muscles, eight showed neurogenic changes, with or without lymphocytic infiltrations. One biopsy showed lymphocytic infiltrations only, and one showed type II-fibre atrophy (Table 1). No relationship was demonstrable between the presence of clilnical muscular atrophy and age, sex, duration of the disease, severity of the disease, presence of a thymoma, or drug resistant ophthalmoplegia. (2) In this group of patients 61 biopsies were examined from 46 individuals; 40 of these biopsies were taken from the quadriceps muscle. A thymoma was present in 17 patients. Examination disclosed neurogenic changes in 17 biopsies, lymphocytic infiltrates in 21, and myositis in one biopsy (Table 2). A distinct correlation was established between the presence of a thymoma and lymphocytic infiltrates, but none was demonstrable between thymoma and neurogenic changes (Table 3). (3) An enzyme-histochemical study was carried out in 35 cases, including 12 with neurogenic changes. A normal differentiation of type I- and type II-fibres was observed in eight instances, type grouping of type II-fibres in three, and type II-fibre atrophy in two cases. (4) In 21 patients and 19 controls, the smallest mean diameter was determined in the quadriceps muscle. Both type I- and type II-fibres proved to have a smaller mean diameter in the female patients than in the controls. In the male patients this could not be proven. (5) Of the eight patients who had died without disorders of ventilation, 90 muscle specimens were examined postmortem. Four of these patients had a thymoma. Lymphocytic infiltrations, found in 32 biopsy specimens, were mostly observed in the presence of a thymoma. Neurogenic changes were apparently unrelated to the presence of a thymoma (Tables 5 and 6). The post mortem examination included the spinal cord in five, and peripheral nerves in three cases. No abnormalities were found. (6) The muscular atrophy found in patients with myasthenia is not a myopathy but an affection of the lower motor neurone. Neurogenic changes were regularly found in the muscles of patients with myasthenia, even without muscular atrophy. The finding of these changes is no reason to reject the diagnosis. It is postulated that denervation occurs at the neuromuscular junction as a result of permanent absence of acetylcholine.
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PMID:Neurogenic muscle involvement in myasthenia gravis. A clinical and histopathological study. 470 58

A 61 year old patient presented with muscular atrophy and weakness, predominant at the shoulder girdle, as the first manifestation of a progressive systemic sclerosis with the signs of the CREST syndrome: subcutaneous calcinosis, Raynaud phenomenon, esophagus disorders, sclerodactyly, telangiectasia. The histological features were consistent with polymyositis. In spite of corticotherapy, total recovery was not obtained. The nosological relationships with Mixed Connective Tissue Disease is discussed. Myositis is infrequent in progressive systemic sclerosis and corticosteroid therapy is discussed.
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PMID:[Myositis disclosing systemic scleroderma]. 650 97

Muscle biopsies were carried out on five patients affected by a chronic neuromuscular disorder, mostly in the form of a spinal muscle atrophy. All patients had suffered from acute trichinellosis many years before, the interval between acute parasitic infection and the appearance of the slowly progressive neuromuscular syndrome being of 21, 13, 35, 26 and 16 years respectively. In biopsy specimens, morphological and enzyme-histochemical changes typical of a progressive neurogenic muscular atrophy were present; in addition, encapsulated but still living, enzyme-positive parasites and signs of focal myositis were detected. The possible pathogenetic correlations between the "chronic" trichinellosis and the "degenerative" neuromuscular disorder are discussed.
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PMID:[Chronic trichinosis and neuromuscular diseases. Morphologic and pathogenetic aspects]. 686 Jan 14

We report on a patient with an interstitial myositis in type II polyendocrine autoimmune disease (Schmidt's syndrome) showing an immunohistochemical demonstrated perifascicular expression of Leu 19 indicating perifascicular denervation, which could not be detected with classical histological methods. In neurogenic muscular atrophy, idiopathic polymyositis and normal muscle we could not find such an exclusive perifascicular expression of the Leu 19 antigen. We conclude that perifascicular denervation is a characteristic feature in IM and thus might have diagnostic value. Furthermore the interstitial myositis is characterized by a complement-mediated angiopathy (vascular deposition of the membranolytic attack complex C5b-9). This pattern is comparable to well-known changes in dermatomyositis. Interstitial myositis and dermatomyositis are evidently pathogenetically similar according to myopathological criteria, but show phenotypic differences. Additional in interstitial myositis and idiopathic polymyositis inflammatory infiltrates surrounding Leu 19 expressing myocytes are regarded as the cause of disseminated intrafascicular muscle fibre denervation.
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PMID:Myopathological findings in interstitial myositis in type II polyendocrine autoimmune syndrome (Schmidt's syndrome). 764 82

To date, 271 cases of HTLV1-associated paraplegia have been observed in Martinique (French West Indies). The clinical picture consisted mostly in a spastic paraparesis or paraplegia with sphincter disturbances (80%) and lower limbs pains (60%). The severity of the disease appeared variable: after a mean disease duration of 6.5 years, 40% of the patients could walk without help, 35% used a single crutch, and 25% used a couple of crutches or were confined to a wheelchair. A variable neuromuscular component was observed in 70 cases (25.4%). In 38 cases, the peripheral signs (SIGNS) or the myositis were only mild. In contrast, 25 patients presented with severe amyotrophy evoking amyotrophic lateral sclerosis, and 7 other had features of dermatopolymyositis. Lastly, an extra-neural spreading of the disease was extremely frequent, including lymphocytic alveolitis (76%), sicca syndrome (69%) and more rarely uveitis, arthritis or vasculitis.
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PMID:[Paraplegia associated with HTLV 1 in Martinique. Study of 271 cases including 70 with neuromuscular involvement]. 781 96


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