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At least 559 records · Page 31Linked to original sources
PubMed1990

Histopathological changes in paravertebral muscles by chronic discopathies.

Samples of paravertebral muscles were obtained from the lesion sites of forty patients operated on for recurrent lumboischiadic syndrome of discogenic etiology. None of the specimens was physiological. All of them were pathologically altered in various grades of involvement. The histopathological changes were highly varied. The findings included muscle fibre atrophy of a nonspecific type, neurogenic atrophy of typical fascicular distribution. Apart from atrophic fibres there were hypertrophic ones either at the same time or in connection with another histopathological process. Changes of myopathic nature were also present with rounded up muscle fibres and shift of nuclei from the subsarcolemnic spaces into the centre of the muscle fibre, multiplication of the connective tissue and vicarious growth of adipose tissue. The visible neuromuscular spindles contained thickened connective tissue capsules and atrophied intrafusal fibres. The present authors' conclusion of their interpretation of these histopathological changes is that they are not produced by one but by a whole set of factors. What results is a cyclic nature of the changes, when it is hard to decide whether we are facing a primary cause or its sequela. The regular company of discopathies are repeated microtraumas during recurrent paravertebral contractures and spinal blocks. A not negligible part can be played also by primary muscle diseases affecting, among others, back muscles, e.g. progressive muscular dystrophy of Duchenne's and Becker's type, various myopathies, nonspecific myositis and paravertebral polymyositis, and other rheumatological involvement. These muscular diseases with disturbed proprioception causing unphysiological posture and loading the spine can share in the origin degenerative processes on intervertebral disks.

Adult↗
PubMed1989

[Analysis of 4628 cases in the genetic counseling clinic].

An analysis of 4628 cases in the genetic counseling clinic of the PUMC Hospital is reported. Altogether 966 cases (20.89%) were diagnosed as genetic diseases, among which were 436 cases (45%) with chromosomal aberrations, 161 (16.70%) with inherited metabolic diseases, 111 (11.50%) with constitutional bone diseases, 103 (10.70%) with various kinds of genetic muscular diseases, 109 (11.30%) with different dysmorphic syndromes, and 46 (4.80%) with different kinds of genetic dermatoses and oculopathies. 973 cases (21.00%) were suspected to be genetic diseases but could not be proved due to a lack of specific diagnostic methods. Some of the experiences gained and the key role of genetic counseling in preventing the birth of babies with congenital defects are briefly discussed.

Adolescent↗
PubMed1969

[Myopathies].

Explore the source record for details and available documents.

Electrophysiology↗
PubMed1997

[Cardiac involvement in neuromuscular diseases].

Many neuromuscular disorders involve the heart, occasionally with overt clinical disease. Muscular dystrophies (dystrophinopathies, limb girdle muscular dystrophy, Emery-Dreifuss muscular dystrophy, Steinert's myotonic dystrophy), congenital myopathies, inflammatory myopathies and metabolic diseases (glycogenosis, periodic paralysis, mitochondrial diseases) may produce dilated or hypertrophic cardiomyopathy and heart rhythm or conduction disturbances. Furthermore the heart is commonly involved in some hereditary and degenerative diseases (Friedreich's ataxia and Kugelberg-Welander syndrome) and acquired (Guillain-Barré syndrome) or inherited (Refsum's disease and Charcot-Marie-Tooth syndrome) polyneuropathies. A cardiologist's high clinical suspicion and a simple but systematic skeletal muscle and peripheral nerve investigation, including muscle enzymes quantification, neurophysiological study and muscle biopsy, are necessary for an accurate diagnosis. In selected patients, more sophisticated biochemical and genetic analysis will be necessary. In most cases, endomyocardial biopsy is not essential for the diagnosis.

Adolescent↗
PubMedDate not supplied

[Epidemiology of progressive muscular dystrophy in selected regions of Poland].

On the basis of the cases registered in the Outpatient Clinic for Muscular Diseases, Medical Academy in Warsaw including patients with progressive muscular dystrophy, and after an analysis of follow-up data the epidemiological indices and mutation indices were estimated in the population of Warsaw, Province of Warsaw and Province of Radom for the years 1960-1976. The calculated indices of incidence and prevalence of dystrophy and mutation were at the upper range of values reported in world literature. They were, however higher than those estimated in previous years in the same regions by Prot. The calculated index of natural abortions in mothers of patients with Duchenne's dystrophy was slightly higher than in the control group of women. Follow-up investigations show that the genetic counselling in this disease was insufficient in that time period.

Adolescent↗
PubMed2006

Atypical presentations of spinal muscular atrophy type III (Kugelberg-Welander disease).

Spinal muscular atrophy type III (SMA III, Kugelberg-Welander disease) typically presents with symmetric proximal weakness, areflexia, and hypotonia. We present four children with spinal muscular atrophy type III who had atypical phenotypes. Three patients clearly had asymmetric weakness at presentation and two had upper motor neuron signs in the lower extremities (one patient had both features). Two of the patients had prolonged evaluations before the diagnosis was made. All patients had Gowers signs and two had pes planus. In patients with proximal muscle weakness the presence of asymmetrical weakness, upper motor neuron signs, or both, may be compatible with spinal muscular atrophy type III. The diagnosis of spinal muscular atrophy should be considered when other possibilities have been excluded.

Brain↗