Acyclovir treatment was used in a randomized, double-blind, placebo-controlled clinical trial with parallel groups to test the hypothesis that herpes virus infections are involved in the pathogenesis of multiple sclerosis (MS). Sixty patients with the relapsing-remitting form of MS were randomized to either oral treatment with 800 mg acyclovir or placebo tablets three times daily for 2 years. The clinical effect was investigated by an extensive test battery consisting of neurological examinations, neuro-ophthalmological and neuropsychological tests, and evoked potentials. Results were based on "intent-to-treat" data and the primary outcome measure was the exacerbation rate. In the acyclovir group (n = 30), 62 exacerbations were recorded during the treatment period, yielding an annual exacerbation rate of 1.03. The placebo group (n = 30) had 94 exacerbations and an annual exacerbation rate of 1.57. Thus, 34% fewer exacerbations were encountered during acyclovir treatment. This difference in exacerbation rate between the treatment groups was not significant (P = 0.083). However, this trend to a lower disease activity in acyclovir-treated patients was supported in subsequent data analysis. If the patients were grouped according to exacerbation frequencies, i.e. into low (0-2), medium (3-5) and high (6-8) rate groups, the difference between acyclovir and placebo treatment was significant (P = 0.017). Moreover, in a subgroup of the population with a duration of the disease of at least 2 years providing an exacerbation rate base-line before entry, individual differences in exacerbation rates were compared between the 2-year pre-study period and the study period in acyclovir-treated (n = 19) and placebo (n = 20) patients and acyclovir-treated patients showed a significant reduction of exacerbations (P = 0.024). Otherwise, neurological parameters were essentially unaffected by acyclovir treatment and there were no convincing signs of reduced neurological deterioration in the acyclovir group. This study indicates that acyclovir treatment might inhibit the triggering of MS exacerbations and thus suggests that acyclovir-susceptible viruses might be involved in the pathogenesis of MS. This possibility warrants further investigation.

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Cortical evoked potentials following stimulation of the lower urinary tract have been recorded in humans. Of 26 patients investigated 9 had no urinary signs or symptoms except genuine stress incontinence, while the remaining 17 had various neurogenic bladder disorders. Monopolar and bipolar stimulation of the bladder and urethra was performed using conventional and newly designed suction-type electrodes. While no cortical evoked potentials could be obtained from patients with complete transverse spinal cord lesions polyphasic cortical evoked potentials (N45, P60, N80 and P100 msec.) were recorded in response to monopolar bladder stimulation in all patients with stress incontinence. Following bipolar stimulation a response with lower amplitude and with latencies slightly divergent could be recorded. This response is assumed to be evoked only from bladder afferent nerves, while the monopolar response could include activity from adjacent structures. The most consistent pattern was recorded at the Cz site. Cortical evoked potentials following stimulation of the urethra were more difficult to evoke but they resembled those obtained after bipolar stimulation of the bladder. The method, when fully developed, may be helpful in the clinical investigation of patients affected by various neurogenic disorders of the lower urinary tract. So far, in our limited series a delayed response at P2 has been observed in patients with uninhibited neurogenic bladders.