Left frontal transcranial magnetic stimulation reduces contralesional extinction in patients with unilateral right brain damage.

Abstract

It has been demonstrated previously that transcranial magnetic stimulation (TMS) of the sensorimotor cortex can induce transient suppression of the perception of cutaneous near-threshold stimuli from fingers of the contralateral hand in normal individuals. One explanation accounting for deficits in the exploration of contralateral space following a unilateral hemispheric lesion refers to a loss of the normal interhemispheric balance, with a resultant hyperactivation of the unaffected hemisphere due to the release of reciprocal inhibition by the affected one. In order to verify this hypothesis, we investigated the effects of a TMS-induced transient dysfunction of the normal hemisphere upon contralateral tactile extinctions in two groups: (i) 14 right brain-damaged patients and (ii) 14 left brain-damaged control patients. Single-pulse TMS was delivered to frontal and parietal scalp sites of the unaffected hemisphere after an interval of 40 ms from an electrical unimanual or bimanual digit stimulation. In right brain-damaged patients, left frontal TMS significantly reduced the rate of contralateral extinctions compared with controls. After left parietal TMS, the number of extinctions was comparable to the baseline. This pattern of increased sensitivity to cutaneous stimulation ipsilateral to TMS was not observed in left brain-damaged control patients. In this group, right hemisphere TMS did not significantly alter the recognition of bimanual stimuli delivered to the space contralateral to the lesion. The suggestion is made that extinctions produced by right brain damage may be dependent on a breakdown in the balance of hemispheric rivalry in directing spatial attention to contralateral hemispace, so that the unaffected hemisphere generates an unopposed orienting response to the side of the lesion. The mechanisms whereby the left frontal TMS transiently ameliorates these deficits may involve stimulus-induced removal of a left frontal-right parietal transcallosal inhibitory flow, although interactions at subcortical levels cannot be excluded.