Many patients with severe migraine remain refractory to the current treatment regimens or cannot tolerate the side effects. Since current research implicates serotonin dysregulation in migraine pathogenesis, we investigated in a double blind, placebo controlled study the prophylactic effect of the serotonergic drug fluoxetine. Sixteen subjects were randomly assigned to 8 week fluoxetine treatment and 16 to the placebo group; nine subjects in each group completed the study. Migraine headache scores were obtained for two weeks prior to commencement of treatment, and then for each successive two week period. Zung depression scores were obtained before and after completion of the study. Fluoxetine caused significant reduction in headache scores starting with weeks 3-4 of treatment; there was no significant change with placebo. Depression scores did not differ between groups before treatment, and did not significantly change with either treatment. Fluoxetine appears to be a safe and effective drug for migraine prophylaxis, and deserves further therapeutic trials with larger groups for longer periods of time.

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Somatosensory evoked potential (SEP) changes associated with selective attention were investigated. In 16 subjects, SEPs were recorded from five locations while they counted electrical stimuli to one of four randomly stimulated fingers. Sequential SEP events measured included peaks P30 (positivity at 30 msec). P45, N60, P100. N140. P190. N230, P400. Counting was associated with greater P45, P100. P190, N230, and P400 amplitudes; effects were not attributable to eye or tongue activity. Analyses designed to reveal changes associated with two conceptualized “channels” (finger class, hand) showed that the P45, P100, and P190 amplitude increases involved both channels. The P400 effect was limited to the target finger. Channel effects for N60 and N140 amplitudes resulted from decreases localized to the unattended element of one channel, suggesting “inhibition.” Latency effects involved mainly the hand channel; counted hand latencies were shorter for P30, P45, P100 and P190. The findings indicate modifications of both early and late electrocortical events with selective attention, and that changes can be of several kinds. They support the view that attention proceeds in more than one stage.

The vestibular, cerebellar, and reticular systems are central in importance, in motion sickness and habituation, to the effects of motion. Nuclear medicine single photon emission computed tomography (SPECT) studies of cerebral blood flow and power spectral electroencephalographic recordings during motion sickness were used to determine alterations in the central nervous system. The rotating chair with and without visual stimulation was used to study the rate of habituation and the effect of antimotion sickness medications on this rate. An increase of theta waves over the frontal cortex indicated a decreased activation of the higher centers during motion sickness. Motion sickness also produces an increase of blood flow in the central cerebellum that has connections to the reticular system. This increase in cerebellar activity is relayed to the reticular system whereby neural recruitment builds up to trigger the vomiting center, producing motion sickness. Habituation may be a conditioned compensatory activation of the reticular neurons that prevents this disruption of normal activation. The rate of habituation when motion sickness was prevented by scopolamine was slowed, indicating that, if the central nervous system is not challenged by disruption of normal activation, it does not produce the compensatory reactions that result in habituation.