IPSILATERAL CORTICOCORTICAL INHIBITION OF THE MOTOR CORTEX IN VARIOUSNEUROLOGICAL DISORDERS

We used a paired-pulse magnetic stimulation technique to study ipsilat eral cortico-cortical inhibition of the motor cortex in 48 patients wi th various neurological disorders and in 20 normal volunteers, In the normal subjects, the first subthreshold conditioning stimulus suppress ed responses to the second suprathreshold test stimulus at interstimul us intervals (ISIs) of 1-5 ms (inhibition at short intervals), and fac ilitated them at ISIs of 8-15 ms (facilitation at long intervals). Pat ients with motor neuron disease, except those in whom brain stimulatio n produced control responses that were generated by direct activation of corticospinal neurons (D-waves), had normal inhibition at short int ervals. Facilitation at long intervals was not elicited in some patien ts with amyotrophic lateral sclerosis. Less inhibition at short interv als and normal facilitation at long intervals was found for all the pa tients with progressive myoclonic epilepsy, a condition in which the e xcitability of cortical inhibitory interneurons is thought to be affec ted. Inhibition at short intervals was disturbed, but facilitation at long intervals was intact in the patients with movement disorders (Par kinson's disease, corticobasal degeneration, and Wilson's disease). In these patients, positron emission tomography (PET) studies showed dec reased regional cerebral blood flow (rCBF) in the basal ganglia in the relaxed state. However, normal suppression was elicited in the patien ts with Parkinson's disease with normal rCBF. In four patients with ch orea, the time-course of inhibition and facilitation was normal, even though PET studies showed decreased rCBF in the basal ganglia in two o f them. Normal inhibition could not be elicited in patients who had a small lesion in the basal ganglia or in the pathway from basal ganglia to the primary motor cortex; the putamen, globus pallidus, and supple mentary motor cortex. In contrast, patients who had a lesion in a sens ory system (sensory cortex or sensory thalamus) or in the pontine nucl eus had normal suppression. We conclude that the results of ipsilatera l cortico-cortical inhibition with paired magnetic stimulation reflect the excitability of inhibitory interneurons in the motor cortex and t hat outputs from the basal ganglia markedly affect this inhibition, bu t outputs from somato-sensory systems or cerebellum do not. Moreover, dysfunction of the corticospinal tract or spinal motoneurons does not affect results obtained by the paired magnetic stimulation technique w hen the control responses are generated by I-waves (i.e. descending vo lleys are produced by transsynaptic activation of the corticospinal tr act neurons).