Biomedical subjects
Publications and source records attributed to B Pentland.
Trace elements were estimated in the spinal cord, liver and bone of five patients dying of motor neuron disease and five control subjects dying of non-neurological disease. The content of selenium in cord and liver and the cord manganese level were significantly increased in the motor neuron disease patients. These findings are discussed in terms of the possible aetiology of motor neuron disease.
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The rate of intrathecal IgG synthesis and the degree of permeability of the blood-brain barrier in 5 patients with sarcoidosis involving the central nervous system are described. Intrathecal IgG synthesis was unusual but increased leakiness of the blood-brain barrier was common in these patients; a finding which may help differentiate such cases from patients with multiple sclerosis.
An unusual case of hypereosinophilic syndrome is described which presented with peripheral neuropathy with no evidence of cardiac involvement. The response to steroid therapy is documented and the literature on peripheral neuropathy in hypereosinophilic syndrome is reviewed.
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The presenting features, clinical course and outcome of 19 patients with a diagnosis of CNS sarcoidosis are described. In two-thirds of the patients the initial features of sarcoidosis were neurological; half of them had an acute monophasic illness and half a chronic progressive or relapsing course. A favourable outcome was recorded unexpectedly during a study period of one to 16 years for two-thirds of the patients. The course of the disease in four patients suggested multiple sclerosis thus emphasising the importance of considering the possibility of CNS sarcoidosis in patients with suspected demyelinating disease.
Concentrations of sodium, chlorine, potassium, chromium, iron, cobalt, zinc, rubidium, silver, caesium, and selenium in cerebrospinal fluid from 14 control subjects and 20 patients with motor neurone disease were measured by in vitro neutron activation analysis. No statistically significant correlation was found between the concentrations of any two elements other than sodium and chlorine in either the patient or control group (r = 0.9905; p less than 0.001). The mean cobalt concentration was significantly lower in the patients (p = 0.0015). No other statistically significant difference was shown. The relevance of this finding was examined in relation to current concepts of the pathogenesis of motor neurone disease and the role of cobalt in cellular metabolism.
Cultured blood lymphocytes from nine patients with Friedreich's ataxia (FrA) and nine matched controls were exposed to a series of graded doses of mitomycin C and ethyl methane sulphonate and examined for the incidence of sister chromatid exchange (SCE). The spontaneous SCE levels did not differ between patients and controls, but the cells from each of the patients showed a significantly enhanced response to the induction of SCE by both mutagens - the patients' cells being up to 50% more sensitive than controls. Cultures from five FrA patients and five controls were analysed to determine the spontaneous incidence of chromosomal aberrations and exposed to a graded series of X-ray doses to measure their response to radiation-induced chromosome damage. The spontaneous aberration incidence in controls did not differ from that found in other control series, but the background incidence of aberrations in cells from the FrA patients was significantly above control levels and appeared to reflect an enhanced response to diagnostic exposure to radionuclides. The FrA cells showed a significantly enhanced in vitro response to chromosome aberration induction by X-rays, the net aberration yields being some 60% greater than those in irradiated controls at doses up to 200 rads. It is concluded that FrA is yet another syndrome which shows hypersensitivity to the induction of chromosome damage by mutagens. Possible factors responsible for this hypersensitivity are discussed and comparisons drawn with ataxia telangiectasia, another autosomal recessive disease characterized by enhanced X-ray sensitivity.
Spontaneous and mutagen induced sister chromatid exchange (SCE) frequencies have been studied in nine patients with multiple sclerosis and in nine age and sex matched healthy controls. The incidence of spontaneous SCE in lymphocytes of the MS patients was significantly greater, by about 50%, than in those of the control subjects. When exposed to mitomycin C (MMC) or ethyl methane sulfonate (EMS) in vitro, cells from both groups showed typical dose dependent increases in SCE frequency, with yields from MS patients slightly higher than from controls. The higher SCE yields in mutagen treated MS cells relative to controls is considered to reflect initial basal differences between the cell types, so that MS cells are not intrinsically hypersensitive to mutagen treatment.
Seventeen patients with Freidreich's ataxia were investigated for cardiac abnormalities using non-invasive methods. Clinical examination, routine chest radiographs and electrocardiograms were a poor guide to underlying heart involvement but using continuous ambulatory electrocardiographic monitoring, echocardiography and isotope ventriculography all patients were found to have abnormalities, even when the neurological signs were minimal.
Serum immunoglobulin levels and C3 and C4 complement concentrations were assayed and serum tested for the presence of autoantibodies in 17 patients with pre-senile Alzheimer's disease. The majority of patients showed a reduced level of one or more of immunoglobulins IgG, IgA or IgM. No significant abnormality was found to indicate an autoimmune disorder.
The results of azathioprine therapy in five patients with chronic progressive or relapsing idiopathic inflammatory polyneuropathy are described. In four patients a sustained improvement followed treatment and in the other patient azathioprine successfully replaced corticosteroid therapy. The improvement was often delayed for up to three months. The literature on the use of azathioprine in chronic polyneuropathy is reviewed. We suggest that there is a place for azathioprine treatment in patients with chronic idiopathic polyneuropathy resistant or intolerant to corticosteroid treatment.
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The long-term results of levodopa therapy in Parkinsonian patients is described. Between January 1969 and December 1972, dopaminergic therapy was started in 186 patients with Parkinson's disease. Their progress after six months, five years and in the autumn of 1980, was assessed. The initial benefit in the majority of patients was followed by a gradual loss of efficacy in most patients with increasing side effects of central-mediated type. We suggest that it may be wise to delay the onset of levodopa therapy until progress of the disease makes treatment imperative.
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Explore the source record for details and available documents.