We performed MRI of brain and spinal cord on 80 patients with multiple sclerosis (MS). Using multi-array coils and fast spin echo, 139 intrinsic lesions were identified in 59 patients (74%). Lesions were more common in the cervical than in the thoracic cord. Cross-sectional areas of the cord, measured from axial images at four levels, showed atrophy in 40%. Clinical disability correlated with cord atrophy but not with cord lesion load. These results show that the use of multi-array coils and fast spin echo allows rapid and sensitive detection of spinal cord lesions in MS and that the cord is involved in the majority of patients. A lack of association between cord lesions and disability may relate to limitations in MR resolution but also suggests that the mechanisms of disability in MS are complex and multifactorial.

Although serial MRI studies of the brain in relapsing-remitting MS have demonstrated frequent asymptomatic disease activity, less is known about the spinal cord. We carried out monthly gadolinium-enhanced brain and spinal cord MRI scans over 1 year in 10 patients with relapsing-remitting MS. Six of the patients had a total of 11 clinical relapses, eight of which involved the spinal cord. A total of 167 active (enhancing or new nonenhancing) lesions in the brain and 19 in the spinal cord were present. Only one active brain lesion was symptomatic compares with six spinal cord lesions. Overall, one-third of new spinal cord lesions were symptomatic, and three-quarters of clinical spinal cord relapses were associated with a new MRI lesion in a location appropriate to the symptoms. Activity in both the spinal cord and brain was more common around the time of relapse. There was a strong association between the spinal cord and brain MRI activity. We did not detect progressive spinal cord atrophy from measurements of a spinal cord cross-sectional area. We conclude that, in relapsing-remitting MS, imaging of the brain alone will detect 90% of active lesions; spinal cord MRI using current technology will therefore provide only modest gains in treatment trials in which lesion activity is the primary outcome measure. The lack of ++progressive spinal cord atrophy in these patients, suggesting that significant axonal loss has not occurred, is in keeping with their good recovery after relapse. That brain and spinal cord lesions occur concurrently implies a systemic trigger for disease activity.

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Letters to the Editor roglobulin, antimicrosome, or antiskeletal muscle autoantibodies whereas the generalised type showed a high titre and incidence of autoantibodies including AChR antibody.5 Seronegative patients or those with low AChR antibody may form a low responder subgroup of myasthenia gravis distinct from the high responders, who show a high titre of AChR antibody. Twelve patients (37 5%) were of the ocular type, which is higher than the incidence in the report of Confalonieri et al.' All subjects in Cohen-Kaminsky's report had generalised myasthenia gravis of type hIa or IIb.2 Chiu et a16 reported a difference in myasthenia gravis expression between Chinese and Caucasians. The characteristic population pattern in our study may be common to east Asians and may partly cause a different correlation between sIL-2R and disease activity. 2 The study of this characteristic population may lead to the elucidation of the pathogenesis of low responder myasthenia gravis.

(3NeurolNeurosurg Psychiatry 1995;58:562-569)