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Biomedical subjects

J A Frith

Publications and source records attributed to J A Frith.

10 recordsLinked to original sources

Peroneal muscular atrophy with pyramidal tract features (hereditary motor and sensory neuropathy type V): a clinical, neurophysiological, and pathological study of a large kindred.

A large family with autosomal dominant inheritance of peroneal muscular atrophy, associated with extensor plantar responses in some cases, has been studied. Onset was usually in the first two decades and spasticity was not a feature. Nerve conduction studies in 21 cases and light and electron microscope findings on six sural nerve biopsies were similar to those in hereditary motor and sensory neuropathy type II.

Adolescent↗

Magnetic resonance imaging in clinically-definite multiple sclerosis.

Forty-two patients with clinically-definite multiple sclerosis were examined by magnetic resonance imaging using a 1.5-T instrument. Magnetic resonance imaging detected an abnormality in 90% of patients. In four patients, no lesions were demonstrated. The number, size and site of the lesions by magnetic resonance imaging were compared with the patients' clinical status and other variables. The Kurtzke disability status scale score increased in patients with corpus callosum atrophy, and brainstem and basal ganglia lesions, and correlated with the total number of lesions. No correlation was shown between the findings of magnetic resonance imaging and disease duration, age, sex or pattern-reversal visual-evoked potentials. This article highlights the variety of magnetic resonance images that is obtained in patients with clinically-definite multiple sclerosis.

Adult↗

Pregnancy and multiple sclerosis.

The effect of pregnancy on the relapse rate of multiple sclerosis has been investigated. Obstetric and relapse histories of 52 women with clinically definite multiple sclerosis were obtained; there were 101 pregnancies of which 85 were at risk of a multiple sclerosis relapse. By comparing the number of relapses in the pregnancy period (9 months of pregnancy and 6 months immediately post partum) with the number in non-pregnancy periods for the same women, no increased risk of relapse during the pregnancy period was demonstrated. However, of the relapses that did occur during the pregnancy period, there was a significant reduction in the number of relapses in the first and second trimesters.

Adult↗

History of multiple sclerosis. An Australian perspective.

In 1868 Jean-Martin Charcot's clinicopathological correlation of multiple sclerosis (MS) was published. Review of Australian medical journals revealed that, 7 years later, Dr Alfred K. Newman, a young physician returning from Aberdeen University, made first mention of MS in the Australian literature when he gave a dissertation entitled 'On insular sclerosis of the brain and spinal cord' which was based on Charcot's teachings. In 1886 Dr Jamieson presented the first case in Australia which fulfilled the criteria for clinically definite MS. This was followed by several other interesting case presentations of MS but it was not until 1915 that Drs Froude Flashman and Oliver Latham presented the first Australian clinicopathological correlation of this disease. Case presentations and extensive discussions regarding the cause of MS appeared in Australian medical journals over the ensuing years but no original Australian research was presented until 1933 when Dr Royle's work on division of the thoracic sympathetic trunk was published. Since that time Australians have made an ever-increasing contribution to the world literature regarding MS pathogenesis, epidemiology and treatment.

Australia↗

Chronic inflammatory demyelinating polyradiculoneuropathy associated with pregnancy.

In a series of 61 patients with the relapsing variety of chronic inflammatory demyelinating polyneuropathy, there were 16 women of childbearing age, 9 of whom became pregnant. In 4 of these women, the onset of neuropathy occurred in pregnancy and in the other 5 relapses occurred during pregnancy. There was a significant increase in the number of relapses during the year of pregnancy, and a tendency for symptoms to worsen during the third trimester or immediate postpartum period. It is concluded that there is an increased risk of relapse of chronic inflammatory demyelinating polyneuropathy in pregnancy.

Adolescent↗

Pregnancy and multiple sclerosis. An Australian perspective.

The effect of pregnancy on the relapse rate of multiple sclerosis (MS) has been investigated. Obstetric and relapse histories of 52 women from New South Wales with clinically definite MS were obtained by telephone interview. These women had 101 pregnancies of which 85 were at risk of an MS relapse. No increased risk of relapse during the pregnancy period was demonstrated. The relapse that did occur during the pregnancy period were clustered in the last trimester of pregnancy and first 3 months post partum.

Female↗

Transfer factor as a therapy for multiple sclerosis: a follow-up study.

The result of a two year, double blind, controlled trial of Transfer Factor (TF) in the treatment of multiple sclerosis (MS) were reported in 1980. It was demonstrated that TF significantly reduced the rate of progression of the disability but the benefit of therapy was not apparent until 18 months after its commencement. After the completion of the trial, TF treatment was offered to all the trial participants. Forty-five of these people accepted TF as treatment and have been followed for the subsequent three years. The twenty-three people who had received TF during the trial, and continued on TF after the trial, consistently had a slower rate of progression of their MS. Although the twenty-two patients initially on placebo had a significantly faster rate of progression during the trial, this slowed with commencement of TF treatment. After 3 years of TF, the rate of progression of disease was similar to that of the group receiving TF continuously for 5 years. In addition, 470 patients with clinically definite MS are being treated in New South Wales in an open study of TF. The rate of progression of the disease is being monitored by neurological assessments and appears to be similar to that of patients who had received TF in the original trial. The follow-up study of the 1980 TF trial patients and the open study of 470 MS patients confirm the original observation that TF has some effect on slowing the course of MS.

Clinical Trials as Topic↗

Alpha-1 antitrypsin phenotypes in demyelinating disease: an association between demyelinating disease and the allele PiM3.

Alpha-1 Antitrypsin, the major circulating protease inhibitor, has more than thirty alleles that can be identified by electrophoresis. In addition to its role as a protease inhibitor, alpha-1 antitrypsin may regulate the immune response. As there is evidence that both the inflammatory polyneuropathies and multiple sclerosis have an immune basis, and that genetic factors influence susceptibility, we have determined the alpha-1 antitrypsin phenotypes (protease inhibitor types) of 63 patients with Guillain-Barré syndrome, 52 patients with chronic inflammatory demyelinating polyneuropathy, and 178 patients with multiple sclerosis. In all 3 groups there was a significant increase in the proportion of patients with the protease inhibitor type M3 allele.

Alleles↗

Transfer factor in treatment of multiple sclerosis.

A 2-year prospective double-blind trial of the treatment of multiple sclerosis patients with the leucocyte extract, transfer factor (TF), obtained from leucocytes of relatives living with the patient, was conducted. 60 patients with definite MS, of whom 58 completed the trial, were divided into two equal groups, one of which received TF and the other placebo. The groups were evenly balanced with respect to sex ratios, disability, duration of disease, ratio of moderate to severe cases, and HLA phenotype. Neurological, electrophysiological, and immunological assessments were done at the start of the trial and every 6 months thereafter. The results indicated that (1) TF retarded but did not reverse progression of the disease; (2) a significant difference between treatment and placebo groups was not apparent with 18 months after the start of the trial; and (3) treatment was effective only in those patients with mild to moderate disease activity.

Adolescent↗