Transcallosal inhibition in patients with callosal infarction.

Recent studies in normal subjects suggested that callosal motor fibers pass through the posterior body of the corpus callosum (CC), but this has not been tested in patients with callosal infarction. The objective of this study is to define the pathways involved in transcallosal inhibition by examining patients with infarctions in different subregions of the CC. We hypothesized that patients with lesions in the posterior one-half of the CC would have greater reduction in transcallosal inhibition between the motor cortices. Twenty-six patients with callosal infarction and 14 healthy subjects were studied. The callosal lesions were localized on sagittal MRI and were attributed to one of five segments of the CC. Transcranial magnetic stimulation was used to assess ipsilateral silent period (iSP) and short- and long-latency interhemispheric inhibition (SIHI and LIHI, respectively) originating from both motor cortices. The results showed that the iSP areas and durations were markedly reduced bilaterally in patients with callosal infarction compared with normal subjects. Patients with callosal infarctions also had less IHI bidirectionally compared with normal subjects. iSP areas and durations were lower in patients with lesions than in patients without lesions in segment 3 (posterior midbody) of the CC. Lesion burden in the posterior one-half of the CC negatively correlated transcallosal inhibition measured with iSP and SIHI. Our study suggests that callosal infarction led to reduced transcallosal inhibition, as measured by iSP, SIHI, and LIHI. Fibers mediating transcallosal inhibition cross the CC mainly in the posterior one-half.