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Biomedical subjects

J D Pollard

Publications and source records attributed to J D Pollard.

At least 91 records · Page 5Linked to original sources
PubMed1987

Peripheral sensorimotor and autonomic neuropathy associated with systemic lupus erythematosus. Clinical, pathological and immunological features.

The clinical features and pathological findings in the sural nerves are described of 7 patients with peripheral neuropathy; in 4 cases the criteria for diagnosis of systemic lupus erythematosus (SLE) were satisfied and in 3 other cases there was serological evidence of an undifferentiated connective tissue disease, most probably SLE. The peripheral neuropathy was of a chronic sensorimotor type with predominantly sensory features and gradual onset. In 2 cases the presentation was asymmetric. One patient had autonomic dysfunction. The pathological findings in the biopsied sural nerves were those of axonal degeneration and vasculitis. In 6 nerves there was increased expression of Class II (Ia) antigen within the nerve fascicle, perineurium and within endothelial cells.

Adolescent↗
PubMed1987

Chronic inflammatory demyelinating polyradiculoneuropathy. A clinical and electrophysiological study of 92 cases.

Ninety-two patients with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) have been studied in order to define better the clinical features, course and prognosis of the condition and to identify possible aetiological factors. Sural nerve biopsy was performed on 87 subjects. Electrophysiological studies were undertaken on all patients and demonstrated marked slowing of motor conduction and impairment of sensory conduction. The onset was usually gradual but there was a rapid rate of onset in 15 (16%) patients. Males were more commonly affected than females. Weakness and paraesthesiae were the most common symptoms but pain was frequently a feature. Age of onset ranged from 2 to 72 years. Sixty patients (65%) had a relapsing course and 32 patients (35%) a progressive or monophasic course; there was a significantly earlier age of onset in patients with relapsing disease. Thirty-two patients (35%) gave a history of preceding infection or some other possible antecedent precipitating event and there was a significantly higher titre for cytomegalovirus antibodies in the serum of patients with CIDP than in controls. The patients were followed up for an average time of approximately ten years. Most patients (73%) had made a good recovery and were independent, but 7 patients had either died or were completely immobilized as a result of their disease. The value of treatment with corticosteroid therapy, immunosuppressive agents and plasma exchange is discussed.

Adolescent↗
PubMed1987

Cytotoxic response of serum from patients with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP).

The serum of 8 patients with chronic inflammatory demyelinating polyneuropathy (CIDP) was tested using a chromium release cytotoxicity assay and cultured Schwann cells. Serum was obtained from all patients prior to treatment by plasma exchange, which was beneficial in some patients only. Those patients with high serum cytotoxicity (high chromium release) were those who showed a positive response to plasma exchange.

Adult↗
PubMed1986

Microwave fixation of whole peripheral nerve for rapid and efficient enzyme-linked immunosorbent assay (ELISA) screening of monoclonal antibodies.

Testing hybridoma supernatants for antibodies of interest involves extensive screening, particularly when the immunogen comprises whole cells. The number of different screening procedures is often large and unmanageable and depends on whether one is interested in, for example, cell surface or intracellular binding. This paper describes an initial screening technique using whole tissue homogenate rather than the individual tissue components. The tissue is fixed to the surface of 96-well microtitre plates by microwaves using a conventional microwave oven. This technique provides a rapid and cost-effective means of screening large numbers of monoclonal antibodies.

Animals↗
PubMed1986

Peripheral neuropathy associated with mitochondrial myopathy.

Twenty patients with mitochondrial myopathy were investigated for the presence of peripheral neuropathy. There were clinical features of a mild sensorimotor neuropathy in 5 patients (25%) and nerve conduction studies were abnormal in 10 patients (50%). Electrophysiological studies of the whole group showed significant impairment of motor and sensory conduction, compared with controls. Sural nerve biopsy and morphometric studies were performed on 4 patients with clinical neuropathy. There was a reduction in density of myelinated fibers and electron microscope features of axonal degeneration affecting myelinated and unmyelinated fibers. Abnormal mitochondria containing paracrystalline inclusions were seen in the Schwann cell cytoplasm of two nerves.

Adolescent↗
PubMed1986

Class II antigen expression and T lymphocyte subsets in chronic inflammatory demyelinating polyneuropathy.

The inflammatory infiltrate within human sural nerve, biopsied from six patients with active chronic inflammatory demyelinating neuropathy (CIDP) was studied for T lymphocyte subsets and Class II antigen (Ia)-expressing cells. Immunohistochemical staining with mouse monoclonal antibodies, acid phosphatase staining, and electron microscopy were used to provide an alternative assessment of macrophage and other mononuclear cell numbers. In normal control nerves Class II antigen was present upon endothelial cells, very occasional mononuclear cells and sparsely within the perineurium. In CIDP nerve dense Class II antigen staining was prominent within nerve fascicles, in capillary endothelial cells and within the perineurium. T lymphocytes of suppressor and helper type were present in small numbers only. Moderate numbers of macrophage-monocytes were found in the patients within nerve fascicles but these cells accounted for only part of the dense Ia staining. Since two nerves with hypertrophic changes, Schwann cells forming 'onion bulbs', were clearly Ia positive, the dense and widespread staining in all nerves studied is best explained by Ia antigen expression upon mononuclear and some Schwann cells.

Antibodies, Monoclonal↗
PubMed1986

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↗
PubMed1985

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↗
PubMed1985

Glue sniffing neuropathy.

Three young men are described in whom a severe, subacute, predominantly motor peripheral neuropathy resulted from the deliberate inhalation of glue vapour. Weakness began after several years of daily glue sniffing and was marked in proximal as well as distal muscles. Muscle wasting was prominent at the time of presentation. Deterioration continued for several weeks after glue sniffing ceased. Peripheral nerve conduction was markedly slow and there was extensive denervation in the muscles. Characteristic changes were seen on sural nerve biopsy. The habit of glue sniffing is now widespread amongst Australian adolescents and this factor should be considered when any young person presents with a peripheral neuropathy.

Adult↗
PubMed1984

Pattern of Schwann cell remyelination in a spinal cord lesion.

Intraspinal injection of mitomycin C into the rat dorsal columns produced extensive demyelination, axonal degeneration and glial cell death. Five weeks post-injection Schwann cell remyelinated fibers were present along the surface of the dorsal columns and around blood vessels within the lesions. Axons near these sites either were enclosed within a Schwann cell but not myelinated or were completely devoid of any cellular ensheathment. Schwann cells were associated only with those blood vessels which no longer retained astroglial end-feet. It is concluded that Schwann cells migrate into spinal cord lesions along such vessels. The marked sub-pial and perivascular distribution of Schwann cell remyelinated fibers may reflect a failure of Schwann cells to disperse quickly elsewhere within the lesion.

Animals↗
PubMed1984

Demyelination induced by serum from patients with Guillain-Barré syndrome.

Sera from 16 patients with acute Guillain-Barré syndrome (GBS) and 14 healthy control subjects were injected into rat sciatic nerve and assessed for demyelinating activity by electrophysiological and histological techniques. Only fresh GBS serum, and not GBS serum stored at -20 degrees C or -70 degrees C, blocked conduction to a significantly greater extent than did fresh control serum. Conduction block developed gradually, starting within 24 hours of injection and reaching a maximum between days 3 and 6. Recovery of conduction commenced thereafter, and conduction returned to normal by day 33. Quantitative histological studies on day 6 showed that fresh GBS serum produced significantly more widespread demyelination than did stored GBS serum (p less than 0.01). Stored GBS serum showed residual demyelinating activity when compared with fresh control serum (p less than 0.01). Fresh serum obtained from 4 patients after recovery from GBS did not produce conduction block, despite it having done so during the acute phase of the disease.

Animals↗
PubMed1984

Chronic polyneuropathy of undetermined cause.

The case histories of 519 patients with peripheral neuropathy on whom sural nerve biopsy had been performed were reviewed. In 67 patients (50 males, 17 females) (13%) who had symptoms of a symmetrical polyneuropathy for more than one year, the cause remained undiagnosed in spite of intensive investigation. Patients with inflammatory neuropathy were not included, but represented 17% of the whole series. The mean age of onset of symptoms was 50.6 years, and the median time from onset of symptoms to initial investigation was 2 years. Males were affected more commonly than females in a ratio of 3:1. The clinical features in 43 patients were those of a mixed motor and sensory neuropathy, in 17 patients a predominantly sensory neuropathy and in 7 patients a predominantly motor neuropathy. The mean CSF protein was 0.73 g/l and in only six patients was it greater than 1 g/l. Nerve conduction studies most commonly demonstrated mild slowing of motor conduction and impairment of sensory conduction. The usual pathological changes on sural nerve biopsy were those of chronic axonal degeneration. Forty seven patients (70%) were re-examined at intervals of time which ranged from 4 months to 12 years after their initial presentation and nerve biopsy (median, 3 years). As a group, they were only mildly disabled, the condition had a very slowly progressive course and there had been little change in their disability. A possible aetiological factor was found in 17 of the 47 patients (36%) and included malignancy, alcoholism, and benign paraproteinaemia. It is concluded that with intensive investigation the cause of chronic polyneuropathy of duration greater than one year remains undetermined in only about 13% of patients and that continued follow-up is worthwhile since a diagnosis may be established on re-examination.

Adult↗
PubMed1983

Prediction of response to plasma exchange in chronic relapsing polyneuropathy. A clinico-pathological correlation.

The clinical features, results of nerve conduction studies and sural nerve biopsy findings have been compared in 5 patients with chronic relapsing polyneuropathy in whom plasma exchange was used in treatment. In 2 patients who consistently responded to plasma exchange, the dominant pathological findings was segmental demyelination without prominent onion bulb formation, whereas axonal degeneration was more prominent in the cases which did not respond. It is concluded that in cases of chronic relapsing polyneuritis where the clinical, electrophysiological and histological features suggest primary demyelination, plasma exchange may provide a useful adjunct to therapy.

Adult↗
PubMed1982

Hypothyroid polyneuropathy. Clinical, electrophysiological and nerve biopsy findings in two cases.

Two patients in whom polyneuropathy was associated with hypothyroidism have been studied clinically and electrophysiologically. Sural nerve biopsy was performed on both patients and the nerve studied by light and electron microscopy. Both patients had symptoms of paraesthesiae and muscle pain and there was distal weakness, sensory impairment and incoordination in both upper and lower limbs. Gait was impaired and tendon reflexes were depressed. Electrophysiological studies demonstrated moderate slowing of motor conduction velocity and absent sensory potentials. Microscopic studies of the sural nerves revealed a loss of myelinated fibers of all diameters but particularly those of large diameter. On teased fibre examination, the predominant abnormality was axonal degeneration and electron microscopy showed degenerating fibres, prominent cluster formations, abnormalities of mitochondria and prominent glycogen deposits within Schwann cells. Quantitative study of unmyelinated fibres indicated a relative increase in fibres of small diameter. It is concluded that the polyneuropathy associated with hypothyroidism is due largely to axonal degeneration.

Adult↗
PubMed1982

Specificity of plasmapheresis in the treatment of chronic relapsing polyneuropathy.

A 27-year-old woman with an eight year history of chronic relapsing polyneuropathy presented in her fifth relapse. Raised immune complexes prompted a trial of plasmapheresis. Remarkable clinical improvement was seen after the second exchange. Complete remission was obtained after ten treatments. Subsequently, further relapses have occurred, each responsive to plasmapheresis. The effect of plasma exchange in this patient appears to be unique as neither charcoal perfusion nor plasma infusion per se proved efficacious. The patient is currently maintained with weekly plasma exchanges, her course complicated by supervening hepatitis B antigenemia. The clearance of immune complexes observed during plasmapheresis raises the possibility that removal of a serum factor is responsible for her clinical improvement and that patients with such a factor may benefit from plasmapheresis.

Adult↗
PubMed1981

Autonomic neuropathy in experimental allergic neuritis: an electrophysiological and histological study.

Electrophysiological and histological studies have been performed on the vagus and splanchnic nerves of guinea pigs with experimental allergic neuritis. Slowing of conduction and dispersion of the compound action potential were consistent with the pathological changes of demyelination. In teased single fibre preparations, axonal degeneration was found more frequently than was expected and in the splanchnic nerves, the unmyelinated fibres appeared to have been indirectly involved. These findings in experimental allergic neuritis are relevant to the pathogenesis of autonomic dysfunction in the Landry-Guillain-Barré syndrome.

Animals↗