Biomedical subjects
Publications and source records attributed to G D Perkin.
The computerized tomographic scan in a case of hypertensive encephalopathy showed widespread areas of diminished density in the white matter, mainly in the upper and posterior parts of the hemispheres. The abnormalities resolved within three months of the institution of treatment. We suggest that the low-density areas are focal collections of edema fluid extravasated through ischemic segments of the vessel wall.
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In a multicentre, randomised trial of prednisolone in acute polyneuropathy of undetermined aetiology (Guillain-Barré syndrome), 21 patients were treated with prednisolone (60 mg daily for one week, 40 mg daily for four days, and then 30 mg daily for three days) and 19 did not have steroid treatment. Patients were graded on a six-point scale by one of two neurologists who had no knowledge of the treatment schedule. Reassessment at one, three, and twelve months consistently showed greater improvement in the control than the prednisolone group but the only statistically significant result was in the improvement at three months among patients entered to the trial within a week of onset of illness. The 6 control patients had improved by 2.5 +/- 0.43 grades by three months from entry to the trial whereas the 10 prednisolone patients had only improved by 0.9 +/- 0.46 grades (P less than 0.05). There was 1 death related to the polyneuropathy in each group, and 1 suicide in a control patient during convalescence. 6 prednisolone patients were left with considerable disability compared with 1 control patient. There were 3 relapses in the prednisolone group, but none in the control group. The results indicate that steroid treatment is not beneficial and can be detrimental in acute neuropathy of undetermined aetiology.
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A new anti-spasticity agent, brolitene, has been assessed in patients with spasticity of spinal or cerebral origin. Twenty-seven patients were entered in a double-blind cross-over trial lasting 6 weeks, using a fixed dose of six tablets (1200 mg brolitene) per day. Clinical assessment failed to show any therapeutic effect in the seventeen patients completing the trial, except in one with multiple sclerosis. Ten patients had to be withdrawn from the trial, six while being treated with the active agent.
A total of 125 patients with a previous episode of optic neuritis was followed to assess the subsequent prevalence of transient visual blurring. 32.8 per cent developed this symptom and the precipitating factors were identified. No correlations were found between the development of the symptom and the parameters of optic nerve function studied.
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A patient with ergot intoxication due to medication for migraine developed lateral popliteal nerve palsy. This is attributed to recurrent ischaemia caused by ergotamine.
The effect of a 30 day course of corticotrophin gelatin injections on the natural history of acute unilateral optic neuritis in 27 patients is reported. A further 27 patients received inert injections in a double-blind control. Measurements were made on visual acuity, visual field, macular threshold, and colour vision, and the development of optic atrophy and other neurological episodes was recorded. No significant differences were found between treated and control groups at intervals up to two years from the start of the trial. The criteria for inclusion of patients are given and it is concluded that corticotrophin has no effect on the natural history of the condition as defined.
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The findings are reported of various CSF abnormalities, including IgG indices and oligoclonal IgG, in 160 patients with multiple sclerosis of differing diagnostic certainty and 146 patients with other neurological disorders. An abnormal IgG index, defined as the ratio of IgG/albumin in CSF to that in serum, has been found in 77.7% of definite MS cases, falling to a figure of 32.1% in the single lesion group. A tendency, reported previously, for IgG levels to be higher in disabled patients, particularly those with a short history or early onset, has been confirmed. Oligoclonal IgG, on the other hand, has been found in 56% of definite MS cases, less frequently than in most other reported series. Analysis of the literature suggests considerable variability in the finding of oligoclonal IgG in other than definite MS, and in other neurological disorders. The possibility that subjective factors are partly responsible for this variability, rather than discrepancies in patient selection requires consideration, and suggests that CSF electrophoresis and IgG estimations are complementary aids in the diagnosis of multiple sclerosis. Differences have been expressed regarding the relationship of oligoclonal IgG to clinical parameters of the disease. Further sequential analysis of the development and variability of the oligoclonal pattern in MS is required.
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