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Biomedical subjects

J D Pollard

Publications and source records attributed to J D Pollard.

At least 109 records · Page 6Linked to original sources
PubMed1981

Nitrofurantoin neuropathy.

Four cases of severe peripheral neuropathy directly attributable to nitrofurantoin are reported. The neuropathy was not dose-related and not necessarily associated with abnormal renal function. Recovery was slow, and neither severity nor recovery was related to the total dose of the drug. The pathological changes seen on light microscopy and electron microscopy were those of acute, severe axonal degeneration. It is emphasised that nitrofurantoin is a neurotic drug and should not be prescribed to the elderly not to anyone with impairment of renal function.

Aged↗
PubMed1981

Effects of plasmapheresis on the course of experimental allergic neuritis in rabbits.

Experimental allergic neuritis was induced in 30 rabbits with extract of bovine peripheral nerve in complete Freund's adjuvant. Of the 22 animals that completed the study, nine animals were plasmapheresed within two weeks of inoculation and 13 animals served as controls. The plasmapheresed animals developed a less severe form of EAN than the controls. Differences were apparent in clinical weakness, weight loss, degree of dispersion of the muscle action potential and histological changes.

Animals↗
PubMed1981

Serum-induced demyelination: an electrophysiological and histological study.

Serum from rabbits with EAN in the acute phase of the disease has been injected into rat sciatic nerve, and compared to control rabbit serum and serum from patients with demyelinating neuropathy and to normal human control serum. Electrophysiological studies were performed on all rat sciatic nerves so injected, and the nerve was then removed and examined histologically. Control rabbit and human serum and neuropathic human serum, when injected in a 20 microL quantity through a 30 gauge needle, did not produce significant electrophysiological abnormalities. EAN serum, however, produced significant dispersion of the muscle action potential and conduction block. All serum produced some histological evidence of demyelination but that seen with EAN serum was quite profound compared to all other sera. It is concluded that humoral factors are present within animals with EAN which has potent demyelinating potential. We were not able to demonstrate the same effect from patients with demyelinating neuropathy in this test system.

Animals↗
PubMed1980

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↗
PubMed1980

Nerve grafts in the Trembler mouse. An electrophysiological and histological study.

Sciatic nerve grafts were inserted from normal BALB C mice into Trembler mice which have a dominantly inherited hypertrophic neuropathy. The Trembler gene had been bred onto a BALB C mouse background so that the nerve grafts were performed between isogeneic animals and no immunosuppressive agent was necessary to prevent nerve rejection. The normal Schwann cells of the donor mice survived and produced normal myelin sheaths around the Trembler axons which traversed the grafted segment. The proximal and distal segments remained poorly myelinated. Within the normally myelinated graft the mean axon area was significantly greater than that within the proximal segment, even though the graft contained axonal sprouts. Electrophysiological studies were performed and motor conduction velocity calculated across the graft, and across the proximal and distal segments. Whereas the mean conduction velocity across the demyelinated Trembler nerve in the proximal segment was 2.6 m/s the mean value across the nerve graft was 31.3 m/s, a value approximately 75% that of normal mice. These findings provide confirmatory evidence that the defect responsible for this demyelinating neuropathy resides within the Schwann cell and illustrates the importance of Schwann cell-axon interdependence.

Animals↗
PubMed1980

Current trends in the management of myasthenia gravis: plasmapheresis and immunosuppressive therapy.

In recent years a considerable body of evidence has accumulated to demonstrate autoimmune mechanisms in myasthenia gravis. This evidence has important implications for the aetiology, diagnosis and management of the disease. The primary abnormality in myasthenia gravis is related to the presence of antibody which reacts with the acetylcholine receptor. Measurement of this IgG antibody in the serum has become the most reliable diagnostic adjunct to the edrophonium test, and in an individual patient, the level of the serum antibody relates closely to the clinical indices. In cases of myasthenia where control with anticholinesterase drugs is unsatisfactory, methods to lower the antiacetylcholine receptor antibody are indicated: these may include thymectomy, immunosuppressive therapy of plasmapheresis. Two patients with very severe disease are described in whom all types of therapy were used and in whom survival depended ultimately on the use of plasmapheresis. These patients illustrate the importance of receptor antibody in the clinical manifestations of myasthenia gravis and in its management.

Acetylcholine↗
PubMed1978

HLA antigens in the Landry-Guillain-Barré syndrome and chronic relapsing polyneuritis.

Forty-four patients with inflammatory demyelinating polyneuritis (22 with Landry-Guillain-Barré syndrome, 6 with subacute polyneuritis, and 16 with chronic relapsing polyneuritis) were typed for genetic markers in and around the HLA region of chromosome 6. Patients with chronic relapsing polyneuritis showed a definite association with HLA-AW30 and AW31 and probable associations with HLA-B8, HLA-DW3, and glyoxalase I. No significant associations were demonstrated with the Landry-Guillain-Barré syndrome although an increase in glyoxalase I was significant if combined with the results of typing in chronic relapsing polyneuritis. The total patient group showed significant increases in HLA-AW30, HLA-AW31, and HLA-DW3. The results support the view that HLA-linked genetic factors influence susceptibility to chronic relapsing polyneuritis and may contribute to the differences in clinical patterns observed in inflammatory demyelination of the peripheral nervous system.

Chromosome Mapping↗
PubMed1978

Relapsing neuropathy due to tetanus toxoid. Report of a case.

A unique case history is presented, of a 42-year-old patient who has suffered three episodes of a demyelinating neuropathy, each of which followed an injection of tetanus toxoid. The clinical features on each occasion were characteristic of acute idiopathic polyneuropathy; a rapid onset of a mainly motor neuropathy with eventual recovery. Nerve conduction studies performed during the second and third episodes demonstrated grossly slowed motor conduction velocities. The sural nerve was biopsied after the third episode, and the features seen on light and electron microscopy included prominent hypertrophic changes, mononuclear cells associated with most "onion bulbs" and macrophage mediated demyelination. Studies of blastogenesis and macrophage migration inhibition, showed T lymphocyte responsiveness to both peripheral nerve myelin and tetanus toxoid. Typing for antigens of the HLA system indicated that the patient was homozygous for HLAB8.

Adult↗
PubMed1976

Human rabies encephalomyelitis.

Seven weeks after he was bitten on the lip by a puppy in the Gambia a patient showed symptons of rabies. Passive and active immunisation was begun three days after the onset of symptons. The evidence indicated that death was a direct consequence of the central nervous system disease rather than any associated complication. Our inability to alter the course of the illness appreciably emphasises the importance of immediate postexposure immunisation in rabies and draws attention to the present lack of effective means of preventing virus replication within the central nervous system.

Adult↗
PubMed1976

Acute idiopathic polyneuritis. A clinical and electrophsiological follow-up study.

Fifty patients with acute idiopathic polyneuritis have been studied clinically and electromyographically, and sural nerve biopsy was performed on 8 patients. Motor and sensory conduction studies were within the normal range in 7 patients (14%), and there was pronounced slowing of motor conduction in 25 patients (50%). There was no apparent correlation between the degree of conduction, and the clinical disability of the patient or the duration of the acute illness. Eighteen patients were re-examined at intervals up to 5 1/2 years after the onset of their illness. Eight patients (44%) were clinically normal at follow-up examination and 4 patients (22%) had a significant disability. There was no relationship between the clinical disability at follow-up examination and the results of initial or final nerve conduction studies. Electromyographic evidence of denervation, however, may indicate that complete clinical recovery will not occur. Segmental demyelination was the primary pathological change found in sural nerve biopsies and there was a significant reduction in the density of myelinated fibres in 2 nerves. It is suggested that a subacute onset of the illness,electromyographic evidence of denervation or gross slowing of conduction, and significant reduction of numbers of myelinated fibres or onion-bulb formation on sural nerve biopsy are factors which may indicate a prolonged course of the illness or incomplete recovery.

Acute Disease↗
PubMed1975

Recurrent experimental allergic neuritis. An electron microscope study.

Experimental allergic neuritis has been induced in 52 guinea pigs by the inoculation of rabbit peripheral nerve in Freund's adjuvant. The majority of the animals developed an acute monophasic illness after a mean interval of 16 days and, if they survived, recovered fully after an average period of 52 days. Two animals displayed a more chronic course and 1 animal relapsed spontaneously after clinical recovery had occurred. Twenty-three animals that recovered were re-inoculated when recovery was complete and in 4 a relapse was induced. In the remainder, no clinical response was observed, even after repeated reinoculations. The ultrastructural appearances in the animals with a monophasic illness were similar to those previously reported. The appearances differed markedly in those animals that were induced to relapse and were similar to those in the animal that relapsed spontaneously. The findings indicated persistent demyelination and remyelination with striking hypertrophic changes (onion bulb neuropathy). The possible reasons for the differences between the two groups are discussed.

Animals↗