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Recently Ugawa and co-workers reported that motor cortex excitability after magnetic stimulation in man can be reduced by coupling an electrical transcranial stimulus over the base of the skull. They hypothesised that the motor cortex inhibition observed was determined by activation of cerebellar structures. Nevertheless, the paradigm employed did not allow to exclude interference from extracerebellar structures due to spread of the electrical stimulus. In order to ascertain the role of the cerebellum in determining the modulation of the motor cortex excitability we examined, in 10 normal subjects and in 2 patients with unilateral cerebellar lesions, the effects of electrical stimuli over the base of the skull on the motor responses evoked by cortical magnetic stimulation. In both patients no inhibition of motor responses was present in the muscles ipsilateral to the lesion, whereas an inhibition, similar to that observed in controls, was evident on the opposite side. The present findings suggest the cerebellar origin of the motor effects seen after electrical stimulation of the base of the skull and further clarify the physiological cerebro-cerebellar interactions in man.

The excitability of the motor cortex to magnetic stimulation was evaluated in seven patients with cerebellar lesions (six patients with a unilateral lesion) and in 20 control subjects. Magnetic motor threshold was defined at rest. In all but one of the patients with a hemicerebellar lesion the threshold was higher in the motor cortex contralateral to the impaired hemicerebellum and the right/left threshold asymmetry was clearly greater than normal. In the patient with a lesion involving both cerebellar hemispheres the magnetic threshold was above the normal limit on both sides. The latencies of motor responses were normal in all patients. This increase in the magnetic threshold of the motor cortex functionally related to the impaired hemicerebellum suggests the existence of a facilitating tonic action of the cerebellum on central motor circuits that might act at the cortical, or spinal level, or both.