Computerized axial tomography of the cranium has been carried out in 46 patients referred because recurring migrainous headaches. Increasing frequency or severity of headaches or a change in headache pattern were the usual reasons for referral. Abnormalities were found in 37 cases and fell into 4 categories. The most frequent (21 cases) consisted of a mild degree of oedema in the white matter of one or both cerebral hemispheres. This was usually bi-frontal (15 patients) but was more extensive in 2 patients. Varying degrees of cerebral atrophy, as determined by widening of the Sylvian, brain-stem and interhemispheric cisterns, and/or widening of the third and lateral ventricles as compared to a group of normal scans, was found in 8 cases. Areas of occipital infarction were found in 4 patients with permanent visual field defects. Unexpected small areas of infarction were found in the temporal lobe in 2 other cases. Cerebral tumours were found in 2 cases. The significance of these findings is discussed, as well as the possible role of migrainous vaso-spasm with consequent changes in cerebral blood flow in the pathogenesis of oedema and atrophy in migraine subjects.
Three cases of progressive facial hemiatrophy are presented. In all three cases there is evidence of localised scleroderma or morphea in association with the facial hemiatrophy. This would seem to support the contention that the two disorders are closely related. In two cases, ocular complications are prominent and in one Raynaud's phenomena provide clear asymmetrical dilatation of the lateral ventricle suggest that there may be a central rather than a peripheral cause for the sympathetic overactivity.
The effect of continual administration of neostigmine on the neuromuscular junction of the rat diaphragm was examined by determining the number of quanta of acetylcholine released by each nerve impulse, the effect of differing repetition rats on quantal release and the amplitude and frequency of miniature end-plate potentials. The number of quanta of acetylcholine released at a nerve impulse repetition rate of 1/sec was reduced to 51% of normal in treated animals. The reduction was greater at faster repetition rates. The amplitude of miniature end-plate potentials was reduced to 75% of normal. This reduction appears to be due to blocking of receptor sites rather than the reduction in the amount of acetylcholine in each quantum. The frequency of spontaneous miniature end-plate potentials was reduced in treated animals.
