Biomedical subjects
R B Godwin-Austen
Publications and source records attributed to R B Godwin-Austen.
Diffuse Lewy body disease.
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Diffuse Lewy body disease: correlative neuropathology using anti-ubiquitin immunocytochemistry.
Diffuse Lewy body disease is an important pathological substrate of the common syndrome of parkinsonian dementia. The new technique of anti-ubiquitin immunocytochemistry has been used in a correlative quantitative neuropathological study of fifteen cases of diffuse Lewy body disease, showing that the severity of dementia is related to cortical Lewy body density, whilst subcortical abnormalities make a much less significant contribution. Cortical senile plaques also appear to be part of the pathology of diffuse Lewy body disease and should not therefore be used as an isolated diagnostic criterion for Alzheimer's disease. Diagnostic criteria for diffuse Lewy body disease are discussed.
Diffuse Lewy body disease: clinical features in 15 cases.
Fifteen cases of diffuse Lewy body disease were diagnosed on pathological grounds during a single year in one health district. The range and frequency of clinical features contrast strikingly with previous reports. The majority of cases presented with classical levodopa-responsive Parkinson's disease either alone (6 cases) or with mild cognitive impairment (3 cases); the remaining 6 cases presented with cognitive impairment alone. In time almost all patients developed both dementia and Parkinsonism. The dementia was cortical in type, but unusual in that most (12 cases) showed day-to-day fluctuation in severity at some point in their illness. These findings suggest that diffuse Lewy body disease is not rare, and that it presents in a range of ways from dementia with subsequent Parkinsonism to Parkinson's disease with subsequent dementia. The latter mode of presentation suggests that it should be considered as a significant pathological substrate of dementia in Parkinson's disease.
Diffuse Lewy body disease: an important differential diagnosis in dementia with extrapyramidal features.
Fifteen cases of diffuse Lewy body disease were identified in a systematic survey of all 216 brains referred to this hospital from a single health district in a single year. These cases presented with Parkinson's disease (40%), cognitive impairment (40%) and both (20%). Quantitative neuropathological studies using anti-ubiquitin immunocytochemistry revealed that dementia severity was related to cortical Lewy body density. The prevalence of diffuse Lewy body disease may have been underestimated in the past because of the neuropathological difficulties in making the diagnosis. Firstly, cortical Lewy bodies have a subtle appearance and are easy to overlook. Secondly, senile plaques are a common feature of diffuse Lewy body disease and may lead the unwary to make an erroneous diagnosis of Alzheimer's disease or "plaque-only Alzheimer's disease'. Diffuse Lewy body disease is a common and important cause of parkinsonian dementia, including the dementia of Parkinson's disease itself.
Dementia and Parkinson's disease associated with diffuse cortical Lewy bodies.
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Acute intermittent porphyria presenting as epilepsy.
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Cervical myelopathy after metrizamide myelography.
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The treatment of the choreas and athetotic dystonias.
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An unusual neurological disorder of copper metabolism clinically resembling Wilson's disease but biochemically a distinct entity.
A patient with progressive neurological disease resembling Wilson's disease but in whom Kayser-Fleischer rings were absent, was given 67Cu and 64Cu, orally and intravenously, to measure the rate of absorption of copper using a convolution integral. The data show an abnormal distribution of body copper resulting in low copper concentrations in plasma, urine and liver but with an accumulation in the lower bowel probably due to a defect in mucosal transport. The importance of differentiating this condition from Wilson's disease is stressed.
Comparison of the effects of bromocriptine and levodopa in Parkinson's disease.
The effects of bromocriptine and levodopa were compared in a blind trial in 18 patients with Parkinson's disease. Optimal doses of the two drugs were given in identical capsules: there was no significant difference between the therapeutic effects. There were wide individual differences in response to the two drugs. Side effects were more common with bromocriptine because of side effects.
The treatment of Parkinson's disease.
The treatment of Parkinson's disease is discussed. Levodopa is the most effective drug in this therapy. The place of other agents is discussed.
Osteomalacia presenting as chorea.
A 16-year-old epileptic developed chorea. He had osteomalacia, hypocalcaemia, and hyperphosphataemia, which were due not to hypoparathyroidism but to vitamin D deficiency--itself secondary to longstanding dietary deficiency and anticonvulsant drug administration.
Observations on radiation myelopathy.
Three cases of radiation myelopathy are reported. Corticosteroid therapy was associated with worth-while remissions in 2 patients. Two patients showed swelling of the spinal cord in myelograms and in one it extended below the irradiated part of the spinal cord. Demyelination of the dorsal white columns of the spinal cord unaccompanied by vascular abnormality was seen below the irradiated part of the cord. It is suggested that radiation damages the endothelial cell barrier of capillaries and arterioles after a latent interval. Proteinous oedema fluid spreads through the white matter from the capillaries and also into the arteriolar walls narrowing these vessels enough to cause local ischaemia and infarction. It is further suggested that apart from ischaemia and infarction myelin is also damaged by poor nutrition associated with oedema fluid, and that radiation damage to oligodendroglial cells is not the cause of this additional demyelination in patients with radiation myelopathy.
Proceedings: A combined clinico-pathological and radiological study of radiation myelopathy.
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Effect of age and arteriosclerosis on the response of Parkinsonian patients to levodopa.
Twenty-four patients with Parkinsonism were treated with levodopa for up to one year. Ten were aged under 65, 12 were aged 65 or over, and two were specifically included because they were considered to have arteriosclerotic Parkinsonism. These two patients showed no response to treatment. The 10 younger patients showed less clinical evidence of arteriosclerosis than the older ones, and responded significantly better to treatment with levodopa. Mean improvement was 61% in the younger group after 12 months' treatment and 28% in the older group. Improvement was greatest within three months of starting treatment. Abnormal movements which resulted from treatment with levodopa could be reduced with only slight loss of therapeutic benefit by the addition of tetrabenazine.
Persistent phenothiazine dyskinesia treated with tetrabenazine.
Six patients with persistent phenothiazine dyskinesia were treated in a double-blind controlled trial with tetrabenazine 100 mg in divided dosage. In three patients the abnormal movements were abolished and in two others there was some improvement, but this was no greater than that achieved with the diazepam control. Tetrabenazine may be useful in the treatment of some patients with persistent phenothiazine dyskinesia.
Incidence of side effects from levodopa during the introduction of treatment.
Twenty patients with Parkinsonism were investigated in order to establish whether the gradual introduction of treatment with levodopa allows a higher dose to be tolerated than can be achieved if treatment is introduced rapidly. No indication was obtained that slow introduction of treatment offers an advantage in maximum tolerated dose, and patients aged 65 and over responded similarly in this respect to those under 65. The maximum tolerated dose is slightly lower in the elderly patient. The incidence of the different side effects does not appear to be affected by the rate of increasing the dose of levodopa.