A total of 101 patients (62 women; 39 men) with definite MS were treated with 1000 mg methylprednisolone (MP) intravenously for 10 consecutive days. Immediately before and after MP treatment clinical scoring (Kurtzke's Expanded Disability Status Scale) and CSF analysis were performed. Before MP treatment CSF MBP, IgG and IgM immunoglobulin levels (CSF Ig, index and intrathecal synthesis) were significantly elevated. The mean CSF MBP levels were significantly higher in the relapsing-remitting (RR) and chronic progressive MS patients with relapses (CP + RR) than in the CP group without a RR disease course, respectively 2.1, 2.3 and 1.5 micrograms/l. A weak positive correlation was found between CSF MBP level and EDSS in the RR MS group (r = 0.34). CSF MBP was significantly correlated with IgM index (r = 0.36), IgM synthesis (r = 0.26), but not with the IgG levels. Therefore demyelination seems to be related to intrathecal IgM production. After MP treatment mean (median) EDSS decreased from 4.4 (4.0) to 3.3 (3.0). Except for Q albumin and IgM index, all CSF immunoglobulin levels decreased significantly after MP. The mean CSF MBP returned to reference values. In the RR group the decrease in CSF MBP was significantly correlated with the change in EDSS (r = 0.39). CSF MBP seems to be a good parameter for disease activity in relapsing MS. Following treatment CSF MBP was found to be related with the change in IgM index (r = 0.30). MP treatment reduces CSF MBP and intrathecal IgM in a similar way indicating a relation between these 2 parameters.

A case-control study of epilepsy in multiple sclerosis (MS) is presented using magnetic resonance (MR) imaging to semiquantitatively assess cortical-subcortical lesion load. In this sample of 13 pairs of cases with MS and epilepsy and controls with MS without epilepsy we found statistically higher cumulated cortical-subcortical lesion loads in the cases than in the controls (Wilcoxon, P=0.036). Total lesion loads (cortical-subcortical plus deep white matter loads) did not differ significantly (P > 0.1) between cases and controls. The relative risk for seizures as determined by the odds ratio of a cortical-subcortical lesion load of ≥20 was. 8.8 (χ2 = 5.23, P 0.025), the odds ratio of a large (> 1 cm) cortico-subcortical lesion was 4.7 (χ2 = 4.9, P < 0.05), while the 2 MR criteria combined show an odds ratio of 19.2 (χ2 = 8.0, P < 0.005). We conclude that first, the presence of cortical-subcortical lesions in part accounts for the occurrence of seizures in MS patients; second, due to the substantial overlap of MR imaging scores between cases and controls the ultimate use of these MR imaging findings in the management of individual patients or in the organizations of trials should depend on the expected benefit of the treatment If the benefit is only moderate or not known a cautious approach with exclusion of cases showing a substantial cortical-subcortical lesion load on MR imaging seems appropriate in trials with drugs, like 4-aminopyridine, that lower the epileptic threshold.

Inhomogeneous patient samples have been used in previous studies to determine the power of magnetic resonance imaging (MRI) for trial monitoring in multiple sclerosis (MS). These power-calculations might not be applicable to the active relapsing-remitting patient who is preferably included in trials. In order to reevaluate the power-calculations for MRI in the monitoring of treatment in strictly relapsing-remitting MS and to compare the power of different trial designs we studied 12 relapsing-remitting MS patients prospectively for a median period of 12 months using monthly clinical assessments and gadolinium-enhanced MRI. A median number of two clinical relapses/patient occurred of which a median of one was treated with steroids. A median of 1.59 new lesions/scan/patient was detected (range 0-8). The total number of new active lesions correlated significantly with study period relapses (SRCC = 0.72, P = 0.023). Computer simulations using the bootstrap technique yielded mostly lower power values for a parallel groups design than in previous studies except for short follow-periods in larger samples. In this-sample the open cross-over design was found to be between 20 and 40% more powerful. Results of power-calculations are clearly sample dependent implying that for treatment trial monitoring using MRI in relapsing-remitting MS conservative sample size estimates are to be used. In an active patient group open cross-over trial designs could be a very powerful alternative to parallel groups design.

A 25 year old patient presented with recurrent prolonged episodes of life-threatening coma varying from 3 to 10 days. The clinical recovery was slow. The history and technical examinations led to the diagnosis of basilar artery migraine (BAM). The etiology of the coma episodes is thought to be related to ischemic dysfunction of the rostral part of the brainstem due to severe spasm of the basilar artery demonstrated by arteriography. Exceptional are the recurrent prolonged coma episodes of sudden onset, the severe spasm of the basilar artery, and the suppression-burst and FIRDA pattern on the EEG examinations during the coma episodes.

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