Migraine is not a platelet disorder.
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Biomedical subjects
Publications and source records attributed to F C Rose.
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Supernatants of cultured T lymphocytes of multiple sclerosis patients were tested for a demyelinating activity in rat cerebellum explant cultures. Supernatants of unstimulated T lymphocytes in seven out of 10 multiple sclerosis patients in relapse produced demyelination when checked by phase contrast microscopy. Supernatants of unstimulated T lymphocytes from healthy subjects did not produce demyelination, but when T cells were stimulated by phytohaemagglutinin (PHA), 50% of tested supernatants produced demyelination, which was, however, never as advanced as in multiple sclerosis supernatant treated cerebellum cultures. The demyelinating activity proved to be heat labile. Gel filtration study revealed two fractions of the demyelinating activity 12.5-29.0 kD and 43.0-66.0 kD. The results suggest that lymphokines can be directly involved in the pathogenesis of demyelination in multiple sclerosis.
The results of recent ongoing research in Parkinson's disease are outlined. Aspects discussed include histopathology, dementia, the MPTP animal model, methods of drug delivery, the new D2 agonist (+)-4-propyl-9-hydroxynaphthoxazine (PHNO) and transplantation.
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A prospective study of 230 arch and carotid arteriograms in 229 patients with symptomatic cerebrovascular disease revealed that neurological morbidity was not significantly affected by patient age, nature of neurological symptoms, duration of procedure, volume of contrast medium or degree of arterial stenosis. The total neurological morbidity of 132 examinations carried out with non-ionic contrast medium (iohexol) was slightly lower than that of 98 examinations carried out with ionic contrast medium (meglumine and sodium iothalamate) but the difference was not statistically significant. However, the morbidity of 185 examinations performed by an experienced vascular radiologist was significantly lower (p less than 0.025) than the morbidity of 45 examinations performed by a series of radiologists in training and the mean time required for the procedure was 18 min longer in the latter group (p less than 0.001). These findings suggest that the neurological morbidity of arch and carotid arteriography in patients with cerebrovascular disease depends largely upon catheter technique and will not be significantly reduced by the use of non-ionic contrast medium.
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A sensitive chemiluminescence method for assay of choline which has been developed for analysis of erythrocyte and plasma levels of choline is reported here. This method includes a charcoal purification step which yields consistent results with plasma and erythrocyte extracts. Further, choline derived from membrane phosphatidylcholine may also be measured by an extension of this method following digestion with phospholipase D. This method has been used to study abnormal levels of erythrocyte choline that occur in cluster headache patients compared to control subjects and migraine patients. In addition, the time course of changes in plasma and erythrocyte choline following a fatty meal have been monitored. Plasma choline levels rise to a maximum between 1 and 3 h after the meal and this is followed by a rise in erythrocyte choline levels which are maximal 3 h after the meal.
Previous studies have indicated that membrane structure and function may be abnormal in cluster headache. This has been further investigated by analysis of membrane phosphatidylcholine, total phospholipids, and cholesterol in erythrocytes and by assay of receptor-mediated transduction. The stimulation of lymphocyte adenylate cyclase with isoprenaline and prostacyclin was used as the test system. A significant increase in the ratio of membrane phosphatidylcholine to cholesterol without change in cholesterol was found in cluster headache patients as compared with control subjects. This indicated a reduced turnover of phosphatidylcholine, since erythrocyte choline is significantly reduced in this condition. Abnormal membrane function was also indicated from the significant depression of high-affinity prostaglandin receptor stimulation of lymphocyte adenylate cyclase and the similar trend in the beta-adrenoceptor response. Since no change in agonist affinity and beta-adrenoceptor density occurred, this depression indicates a generalized defect in coupling of receptors to adenylate cyclase. It is hypothesized that the impaired function that would result might contribute to the aetiology of cluster headache.
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The percentage of interleukin-2-receptor-positive peripheral blood lymphocytes in MS patients was significantly higher in acute relapse than in remission or in controls. After stimulation by phytohemagglutinin, the expression of interleukin-2 receptor on peripheral blood lymphocytes of MS patients was within the range of healthy controls, implying no general impairment of receptor expression. These results confirm other evidence that there is a small population of activated T lymphocytes in acute relapse of MS.
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In many patients who develop epilepsy the disease is short lived and the overall number of seizures small. The role of anticonvulsant drugs in such patients is uncertain. If treatment is merely suppressive and the disease self limiting then treatment may not be necessary in some patients. If, on the other hand, early treatment prevents the subsequent evolution to chronic epilepsy then it is imperative. To resolve this issue it is essential to undertake placebo controlled trials, in which a group of patients with newly diagnosed epilepsy is given active treatment and compared with a similar group given placebo alone.
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