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Biomedical subjects

P Hudgson

Publications and source records attributed to P Hudgson.

At least 37 records · Page 2Linked to original sources
PubMed1983

Writer's cramp.

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Hand↗
PubMed1982

Tizanidine in the treatment of spasticity.

A double-blind crossover trial compared tizanidine with baclofen in 36 patients with spasticity. Tizanidine appeared to reduce lower limb spasticity more effectively and to have fewer side effects, but no statistically significant differences emerged when the two drugs were compared. An additional open study of tizanidine confirmed the beneficial action in a selected minority of patients with spasticity. This drug may have an important role in the management of spasticity, but further studies are required.

Adult↗
PubMed1982

Immunocytochemical localization of immunoglobulins in the inflammatory lesions of polymyositis.

Biopsy material from the muscles of 40 patients with either polymyositis or dermatomyositis was examined with the immunoperoxidase method to compare the distribution of immunoglobulin (Ig)-containing cells in the inflammatory infiltrates and elsewhere in the muscle tissue. Large numbers of IgG-positive and occasional IgM-positive cells were found in the infiltrates in 23 of these biopsies in contrast to the rather sparse representation of plasma cells. It is suggested that the Ig-containing cells may either represent local B-cell differentiation and proliferation or that the cells are involved in antibody-dependent cell-mediated tissue damage.

Adult↗
PubMed1981

Morphometric comparison of Duchenne's muscular dystrophy and experimental bupivacaine myopathy.

The findings of this study confirm the role of the hyaline fibre in D.M.D. and support the concept of continuing necrosis with progressive failure of regeneration as the major factor in the aetiology of the pathological changes. The persistence of internal nuclei , "split" fibres and progressive fibrosis are secondary phenomenon. Comparison of the changes in D.M.D. with those seen in experimental Bupivacaine myopathy shows that the changes in the experimental myopathy are comparable to those seen in D.M.D. between the ages of 4 and 6 years. It is suggested that Bupivacaine myopathy is an acceptable animal model for D.M.D.

Animals↗
PubMed1981

Mitochondrial myopathy.

Six clinically affected and 18 asymptomatic members of a six-generation family were investigated clinically, by estimation of serum CK levels, and in some cases by quantitative electromyographic techniques and muscle biopsy. It was concluded that the myopathy was probably inherited as an autosomal dominant trait with variable expression and incomplete penetrance although the possibility of mitochondrial inheritance could not be excluded in view of the almost exclusive transmission through the female line. Eight members of the family with myopathy also had diabetes mellitus, and 2 of these also had cerebellar ataxia. It is suggested that the myopathy, the cerebellar disorder and the diabetes may all be manifestations of the same underlying metabolic defect.

Cerebellar Ataxia↗
PubMed1980

Cardiac complications of polymyositis.

We report 3 cases of polymyositis, confirmed by enzyme assay and muscle biopsy, complicated by serious cardiac disease. They showed progressive fascicular block, despite immunosuppressive therapy sufficient to control the skeletal muscle disease, culminating in complete heart block with syncope, requiring the implantation of a pacemaker. In addition, all 3 showed echocardiographic evidence of dilated cardiomyopathy.

Adult↗
PubMed1980

Procainamide-induced myositis.

The risk of developing a syndrome resembling lupus erythematosus when taking procainamide has been well recognized for over 15 years, although the development of myopathy has been reported on one occasion only, in this instance without histopathological evidence of muscle inflammation. The patient reported in this paper developed a severe, rapidly progressive vasculitis, apparently limited to muscle, after taking procainamide for 42 months, his myopathy remitting rapidly after withdrawal of the drug and a short course of treatment with azathioprine. Although this man had no clinical evidence of SLE, he had impressive immunological evidence to support this diagnosis.

Aged↗
PubMed1979

Distal spinal muscular atrophy. A clinical and genetic study of 8 kindreds.

Twelve patients (8 kindreds) with distal SMA are described, and an analysis presented of their clinical and genetic features. Distal SMA accounted for 10% of all patients with SMA in a total population survey of this disease in North-East England. The parental consanguinity rate is high, occurring in 3 of the 8 kindreds reported; the sex ratio was 1.0; the segregation ratio of sibs did not differ from 0.25. Intrafamilial concordance for clinical features of the disease is high. This current data is consistent with a suggested aetiology of two separate autosomal recessive genes. Clinical features are discussed and a review of the literature presented. The disease is only slowly progressive, but one of the genetic types may present with infantile or early juvenile onset; there is no evidence that it shortens life. 50% of cases did not have a normal gait after 4 years of age; 50% could not run after 17 years of age; and 50% could not walk unaided after 28 years of age. Details of prognosis, and principles of genetic counselling in this disease are discussed.

Adolescent↗
PubMed1978

Syringomyelia.

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England↗
PubMed1978

Anterior-horn cell degeneration and gross calf hypertrophy with adolescent onset. A new spinal muscular atrophy syndrome.

A new variant of spinal muscular atrophy (S.M.A.), characterised by adolescent onset, gross hypertrophy of calves, and a slowly progressive clinical course, was found in 5 patients, 3 of them in a series of 102 cases being studied in North-East England. Biopsy and electrophysiological studies indicated the presence of chronic progressive degeneration of anterior-horn cells.

Adolescent↗