The form and distribution of MRI abnormalities in 114 patients with clinically definite multiple sclerosis (MS) have been compared with observations on 53 apparently healthy individuals, 129 patients with isolated focal neurological lesions with which MS often presents (51 patients with optic neuritis, 44 with isolated brainstem lesions and 34 with isolated spinal cord syndromes) and 105 patients with disorders which may be confused clinically or radiologically with MS. The latter comprised 55 patients with cerebral vascular disease (including 7 cases of dementia with diffuse white matter disease), 24 with degenerative ataxic disorders, 8 with cerebellar tonsillar ectopia, 7 with sarcoidosis and 11 with a variety of other disorders. Periventricular abnormalities were found in all but 2 patients with MS and discrete white matter lesions in all but 12. Characteristically the periventricular changes in MS were irregular in outline. Periventricular abnormalities which were often milder and of smooth outline were seen in 37/55 patients with cerebral vascular disease, 9/24 with cerebellar degeneration, 5/7 with sarcoidosis and in 2/3 apparently healthy individuals over the age of 60. The appearances in the 7 cases of dementia resembled those with advanced MS. Cerebellar and/or brainstem atrophy characteristic of the cerebellar degenerations, in the absence of white matter abnormalities, was helpful in making the distinction from MS. Congenital anomalies and tumours in the region of the brainstem and foramen magnum were readily shown. More than half the patients with symptoms attributable to isolated focal neurological lesions had additional lesions at presentation. MS cannot be diagnosed in these cases at presentation, but repeat scans after 5 to 20 months in 25 patients with optic neuritis and 10 with clinically isolated brainstem lesions have shown new lesions in 7 (20%). The patients with new lesions fulfil the criteria for clinically probable MS (Poser et al., 1983). Measurements of T1 and T2 in vivo permitted the distinction of acute from chronic brainstem lesions. There were quantitative differences in T1 and T2 between the normal appearing white matter in MS and normal brain. Studies of postmortem brains provided convincing evidence that the MRI abnormalities in MS correspond with plaques. Evidence is adduced to support the view that an important source of the abnormal NMR signals in acute lesions is oedema, and in chronic lesions is gliosis; demyelination per se is unlikely to make an important contribution.

and Cardiff Royal Infirmary Carbazepine, Tegretol (5-carbamyl-dibenz (b,f)azepin), originally known as G.32883 and introduced in 1959 as an anticonvulsant, was first shown to have some effect in relieving the pain oftrigeminal neuralgia by Blom (1962, 1963). Since then Spillane (1963, 1964), McArdle (1963), and Taylor (1963) have confirmed that this drug has a specific effect in relieving the pain of trigeminal neuralgia in some 60 to 80 % of patients. This paper describes a controlled trial of carbazepine carried out simultaneously at

S Y N 0 P S I S Patients suffering from severe migraine, usually for many years, have been examined by the EMI scanner between attacks. Judged by criteria validated originally by comparison with pneumoencephalography, about half of the patients showed evidence of cerebral atrophy. Perhaps of more significance than generalised atrophy was the frequency of areas of focal atrophy and of evidence of infarction.Although migraine is a common disease afflicting between 5% and 10% of the population (Friedman, 1971), little is known about either the underlying pathological changes which are present during an attack or the structural changes, if any, which may occur in the brain after one or many episodes. This difficulty in obtaining information arises from the fact that migraine is rarely a fatal illness, and such information as we have is derived from studies of those vessels which are visible in the retina, from the very small number of postmortem studies which have been reported in patients dying from migraine and its complications, and from a few angiographic and cerebral blood flow studies.Computerised axial tomography (CAT) (EMI scanning) offers a new opportunity for the visualisation of pathological changes in the brain occurring in the course of non-fatal illness.Symonds (1951) suggested that slight, but cumulative structural damage may result from repeated attacks of migraine. We have therefore analysed the results of CAT in a group of patients suffering from severe migraine in an attempt to determine whether structural damage does occur.

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