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We studied the effects of transcranial electrical stimulation (TES) and transcranial magnetic stimulation (TMS), delivered at intensities below the threshold for evoking an electromyographic response, on the disynaptic and presynaptic phases of reciprocal inhibition in 8 healthy subjects. After TES, the H-reflex evoked in the flexor carpi radialis (FCR) muscle was strongly facilitated when the cortical stimulus was given 4.0-4.5 ms after the test stimulus (median nerve stimulus). TES reduced the disynaptic phase of reciprocal inhibition most strongly when the cortical stimulus followed the test stimulus by 3.0-3.5 ms. TES also reduced presynaptic inhibition, but with a time course that was identical to that of the facilitation of the uninhibited H-reflex. After subthreshold TMS, the facilitation of the H-reflex showed at least 2 peaks, one occurring when the cortical stimulus was given 2 ms after the test stimulus and the other when the cortical stimulus followed the test stimulus by 0.5 to -1.5 ms. The effects of TMS on the 2 phases of reciprocal inhibition were similar, and in both cases the disinhibitory effects had essentially the same time course as the facilitatory effect of TMS on the uninhibited H-reflex. The different effects of TES on the 2 phases of reciprocal inhibition provide evidence of the presynaptic nature of the second phase. The absence of a difference in the effect of TMS on the 2 phases could be due to the more temporally dispersed descending volley after TMS.

F-waves are known to be highly sensitive to changes in the excitatory state of the spinal cord. This paper describes the effects of subthreshold transcranial magnetic stimulation on the F-waves evoked in hand and foot muscles. In the abductor pollicis brevis muscle, the F-wave was significantly enhanced when the cortical stimulus was given with a delay corresponding approximately to the expected time of collision, i.e., the difference between the mean latency of the F-wave and the mean latency of the motor evoked potential. A second, usually larger facilitatory phase follows the first phase after 2-3 msec, and later peaks of enhancement often occurred. After the enhancement periods, a significant inhibition of the F-wave was usually observed. In the extensor digitorum brevis muscle, the first facilitatory phase was observed some milliseconds earlier than expected in 4 of 5 subjects, and the inhibitory phase was less pronounced. We argue that the sequential arrival of I-waves at the spinal segment could be responsible for the changes observed in the F-wave recorded from the small hand muscle. In the foot muscle, anatomical and technical factors could contribute to the generation of a D-wave. The strong inhibition observed in the F-wave recorded from the hand muscle is likely to be due to the arrival on alpha-motoneurons of inhibitory postsynaptic potentials (IPSPs) generated by the cortical stimulus. Our data show that the F-wave ia a probe for changes in the spinal cord excitatory state.

We studied the effects of hyperventilation under control of the end-tidal PCO2, on the electromyographic silent period evoked by transcranial magnetic brain stimulation and by peripheral nerve stimulation. We also studied the effects of hyperventilation on the threshold, latency and amplitude of motor potentials. Hyperventilation significantly reduced the duration of the cortical silent period, but did not affect the length of the peripheral silent period. Neither did it alter the latency, amplitude or threshold of the motor potentials. These findings suggest that hyperventilation selectively depresses motor cortical inhibition in humans.

Twenty patients with hemiplegia and 13 patients with motor neurone disease were studied with electrical and magnetic transcranial stimulation. Motor evoked potentials were recorded from the biceps, thenar and tibialis anterior muscles. In both groups of patients magnetic stimulation with a Novametrix stimulator revealed fewer abnormalities than electrical stimulation with a Digitimer D180 stimulator. In patients with hemiplegia, motor evoked potentials after electrical stimulation were absent in 70% of muscles, delayed in 22% and normal in 8%; after magnetic stimulation, they were absent in 53% of muscles, delayed in 28% and normal in 19%. In patients with motor neurone disease, motor evoked potentials after electrical stimulation were absent in 62% of muscles, delayed in 10%, and normal in 29%; after magnetic stimulation, they were absent in 45% of muscles, delayed in 15%, and normal in 40%. The reason why magnetic stimulation reveals fewer abnormalities than electrical stimulation could be that magnetic stimulation repetitively discharges the pyramidal cells and, because of temporal summation mechanisms, produces more powerful excitatory potentials at the lower motoneurone synapse.