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

Aside from clinical electrophysiology, muscle biopsy is an important method regarding the diagnosis of neuromuscular diseases. Functional disturbances like myasthenia, myotonia, or paramyotonia only lead to slight and unspecific morphological alterations of the muscle tissue. In most cases, progressive muscular dystrophies, myotonic dystrophy, and myositis of various etiologies each have their own bioptic and electrophysiological characteristics. The diagnosis of these diseases should be confirmed by both methods. Some inflammatory diseases, such as panarteriitis nodosa and muscular sarcoidosis, may be diagnosed on account of histologic findings only. The same is true for rhabdomyolysis and congenital myopathies.
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PMID:[Diagnostic value of muscle biopsy in neuromuscular diseases]. 216 Jul 61

The occurrence of high-risk factors for vascular disorders was analysed in a group of 43 patients suffering from diplopia of unknown aetiology. The subjects (25 men and 18 women) were aged between 17 and 78 years. Previously excluded were patients with intracranial or orbital tumors, ocular myositis or myasthenia, multiple sclerosis, endocrine orbitopathy, head trauma, cerebral hemorrhage or aneurysms, leucaemic infiltrates or metastasising tumors. Compared to the control groups of extensive epidemiological studies, the patients showed a higher prevalence of arterial hypertension and diabetes mellitus. Adipositas, lipometabolic disturbance and cigarette smoking were also more frequent. The findings support the hypothesis of a vascular origin of eye-muscle paresis.
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PMID:[Vascular risk factors in patients with ophthalmoplegia]. 223 96

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

This study was attempted to obtain information about biological properties of junctional acetylcholine receptor (AChR) and extrajunctional AChR, and about nerve influences on muscles AChRs under the pathological conditions of experimental myasthenia and myositis. Experimental autoimmune myasthenia gravis (EAMG) was induced in Wistar rats by immunizations with AChR purified from the electric organ of Narke Japonica without using Freund's complete adjuvant experimental myositis by immunization with rat muscle extract depleted of AChR. Thirty-five days after the initial immunization, unilateral dissection of the ischiadic nerve was performed in all immunized rats. Contents of AChR in both hind limb muscles were measured by double immunoprecipitation assay method 15 days after the experimental denervation. In the control animals the amount of AChR extractable from innervated muscles was 2.7 +/- 0.5 (mean +/- s.d.) pmole/g muscle and increased about 10-fold 15 days after the denervation (30 +/- 7.9). In rats with EAMG, AChR contents was reduced in both denervated (1.1 +/- 1.0) and innervated muscles (1.3 +/- 0.9). In experimental myositis, the increase of muscle AChR was impaired in denervated muscles (2.4 +/- 0.6), but AChR contents was not reduced in innervated muscles (2.7 +/- 0.9). These results suggest that nerves may influence AChR metabolism, keeping numbers of AChR constant even in inflammatory condition. In addition, germinal centre formation in thymic medulla was detected in EAMG rats.
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PMID:Acetylcholine receptor and thymus in experimental autoimmune myasthenia gravis and experimental myositis. 716 99

The authors report on a 76-year-old woman presenting with malignant thymoma associated with myasthenia, erythroblastopenia, myositis and giant cell myocarditis. Blood examination showed antinuclear antibodies, anti-platelet antibodies and LE cells. Only one similar case and 22 cases of thymoma associated with giant cell myocarditis have been published. It seems probable that thymomas plays a part in the pathogenesis of giant cell myocarditis.
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PMID:[Thymoma associated with myasthenia, erythroblastopenia, myositis and giant cell myocarditis. One case (author's transl)]. 726 6

Case report on a patient with varying motility disturbances. He first presented with typical clinical and electromyographic symptoms and signs of ocular myositis, which subsided after immunosuppressive therapy. Three years later he developed ocular myasthenia. The diagnostic procedures (especially electromyography, immunology, differential diagnosis and possible underlying pathomechanisms are discussed.
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PMID:[Ocular myositis/myasthenia (author's transl)]. 733 57

Few comprehensive epidemiological studies of the prevalence of muscle diseases have been undertaken, and none has been carried out in our locality. The present cross-sectional study was conducted in Assiut Governorate (Upper Egypt) to estimate the prevalence of different types of primary muscular disorder in 1997. The study involved 52,203 subjects, 15,617 (30%) from the rural community and 36,586 (70%) from the urban community. Patients were identified from a door-to-door survey, and all were subjected to a full clinical examination, with confirmation of the diagnosis through electrophysiological, and biochemical investigations. Histopathological studies were performed for the classification of muscular dystrophies. Forty patients with muscular disorders were identified, with a point prevalence of 76.6 per 100,000 in the total community with no significant differences between the rural and urban communities. The creatine kinase level was abnormally high (>225 IU/l) in 80% of the cases, increased in all patients with muscular dystrophy or myositis, in 88.8% of patients with systemic myopathy and 66.6% of patients with myotonia. None of the cases of myasthenia showed an increase in the creatine kinase level. The lifetime prevalence per 100,000 was 26.8 for muscular dystrophy, 11.49 for myotonia, 11.49 for myositis, 17.24 for systemic myopathy and 9.57 for myasthenia.
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PMID:Epidemiological study of muscular disorders in Assiut, Egypt. 1621 Aug 62

Although the aging process per se can produce measurable changes in the normal oropharyngeal swallow, these changes alone are rarely sufficient to cause clinically apparent dysphagia. The causes of oropharyngeal dysphagia in the elderly are predominantly neuromyogenic, with the most common cause being stroke. The evaluation of oropharyngeal dysphagia in the elderly involves early exclusion of structural abnormalities, detection of aspiration by videofluoroscopy which might dictate early introduction of nonoral feeding, and exclusion of underlying systemic and neuromyogenic causes that have specific therapies in their own right. Such conditions include Parkinson disease, myositis, myasthenia, and thyrotoxicosis. Management is best delivered by a multidisciplinary team involving physician, speech pathologist, nutritionist and, at times, a surgeon.
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PMID:Oropharyngeal dysphagia. 1969 5

Diplopia is a frequent neuro-ophthalmologic symptom with diverse etiologies. This article describes elementary diagnostic tests and frequent causes of diplopia. Monocular diplopia persists when the other eye is closed and usually disappears when the patient looks through a pinhole. It is usually caused by errors in the optical media of the eye and has to be differentiated from spectacle-induced side effect and non-organic disorders. A sign of non-organic etiology is absence of change in image position when the head is tilted. Binocular diplopia disappears regardless of which eye is closed. Binocular diplopia occurs when the images of both eyes cannot be fused. The most frequent direct cause of diplopia is acquired strabismus. Knowledge of several specific types of strabismus enables efficient patient management. Congenital and decompensating strabismus like accommodative esotropia, pathophoria, strabismus surso- and deorsoadductorius, retraction syndrome, Brown's syndrome and esotropia in high myopia only need ophthalmologic treatment. Orbital injury, orbital tumor, ocular myositis, Graves orbitopathy and vascular disease usually require multidisciplinary management. Neurogenic paresis, superior oblique myokymia, ocular neuromyotonia, myasthenia, chronic progressive external ophthalmoplegia (CPEO), internuclear ophthalmoplegia (INO) and skew deviation require specific neurologic examination. Treatment of diplopia includes treatment of the fundamental disorder, monocular occlusion, prisms and strabismus surgery.
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PMID:How to deal with diplopia. 2298 79

This article aims to analyze the frequency and clinical characteristics of peripheral neuropathy (PN) in patients with systemic lupus erythematosus (SLE).A total of 4924 SLE patients admitted to the Peking Union Medical College Hospital, Beijing, China, from January 1995 to September 2013 were included in this retrospective analysis. The individuals designated as control patients were selected from the pool of SLE patients without PN using the systematic sampling method of 1:2 during the same time.The prevalence of SLE-associated PN (SLE-PN) in SLE patients was 1.5% (73/4924). Seventy-nine cases of PN affected 73 patients and 6 of these patients (8.2%) presented with 2 types of PN. Among the 7 types of PN, polyneuropathy was the most frequent and was diagnosed in 47 cases (59.5%); the remaining patients suffered from mononeuropathy (13.9%), cranial neuropathy (12.7%), myasthenia gravis (10.1%), autonomic neuropathy (2.5%), or acute inflammatory demyelinating polyradiculoneuropathy (1.3%). Five patients developed PN before the onset of SLE (3 out of 5 patients had myasthenia gravis). The most common PN-related symptoms were myasthenia and numbness (50.6%), followed by pain in affected regions (35.9%). PN symptoms were relieved in a majority of the patients (76.7%) after treatment. Compared with non-SLE-PN patients, patients with SLE-PN had a higher frequency of fever (65.8% vs 45.9%, P < 0.01), mucocutaneous involvement (73.9% vs 36.3%, P < 0.01), arthritis (42.5% vs 28.1%, P < 0.05), myositis (17.8% vs 5.5%, P < 0.01), and central nervous system involvement (38.4% vs 21.9%, P < 0.05) as well as being positive for the anti-Sm antibody (31.4% vs 18.8%), immunoglobulin G (IgG) elevation (53.6% vs 37.1%, P < 0.01), and reduction in complement 3 (54.8% vs 36.9%, P < 0.05). A statistically significant difference was found between the Systemic Lupus Erythematosus Disease Activity Index scores in SLE-PN patients compared with the non-SLE-PN patients (P < 0.05). Multivariate logistic regression showed that the only risk factor for PN was IgG elevation (odds ratio =2.553, 1.224-5.327, P = 0.012).The prevalence of PN in SLE occurs more frequently in patients with an active form of the disease. IgG elevation is a risk factor for SLE-PN and should be assessed in these patients. Young female patients with myasthenia gravis should be closely monitored for the development of SLE.
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PMID:Peripheral neuropathies due to systemic lupus erythematosus in China. 2578 54


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