Transcranial magnetic brain stimulation over the motor cortex is used to characterise the function of the human corticospinal motor system. This covers aspects like the influence of medication, of cerebello-corical connections (Meyer et al. 1994a), of diseases of the basal ganglia (Meyer et al. 1992), and of circumscript lesions outside the motor cortex on the function of the corticospinal system. Furthermore we use transcranial magnetic stimulation as an instrument to study the functional anatomy of descending tracts (Meyer et al. 1994b) and interhemispheric connections (Meyer et al. 1995) as it is illustrated by the following two abstracts.
Functional organisation of corticonuclear pathways to motoneurones of lower facial muscles in man
EMG responses were recorded from lower facial muscles of 12 normal subjects after magnetic stimulation of the motor cortex. Using a figure-of-eight stimulation coil, the largest responses were obtained from points around 8-10 cm lateral to the vertex. Usually they were bilateral, and had the same latency (11-12 ms) on both sides of the face. Patients with complete Bell´s palsy had no response in muscles on the same side as the lesion indicating that the ipsilateral component to cortical stimulation was not the result of recrossing in the periphery of nerve fibres from the contralateral side. Single unit studies showed that cortical stimulation produced two phases of motoneuronal facilitation : a short latency (central motor delay from contralateral cortex to the intracranial portion of the facial nerve, 7.6 ms), short duration (1-2 ms duration peak in the PSTH) input which was more commonly evoked by contralateral than ipsilateral stimulation, and a longer latency (central delay >15 ms), long duration input evoked equally well from either hemisphere. The former may represent activity in a predominantly contralateral oligo-synaptic cortico-bulbar pathway, the latter a polysynaptic indirect (e.g. cortico-tegmento-nuclear) pathway to lower facial muscles.
Inhibitory and excitatory interhemispheric transfers between motor cortical areas in normal humans and patients with abnormalities of the corpus callosum
Transcranial magnetic stimulation of the motor cortex was performed in ten normal subjects and ten patients with radiographical abnormalies of the corpus callosum (CC). Seven patients had a complete or partial agenesis or hypoplasia of the CC, two had a thin CC due to hydrocephalus or white matter degeneration and one had a circumscript contusion lesion of the CC. The patients served as a clinical model to investigate transcallosal influences on excitatory and inhibitory effects of motor cortex stimulation and to assess the potential diagnostic use of interhemispheric conduction studies and the contribution of interhemispheric interaction on transcranially elicited contralateral excitatory and inhibitory motor responses.
Stimulation over one motor cortex suppressed tonic voluntary electromyographic activity in ipsilateral hand muscles in all subjects with preserved anterior half of the trunk of the CC. Since this suppression was lacking or had a delayed onset latency in patients with absence or abnormalities of the anterior half of the trunk of the CC it can be concluded that it is due to a transcallosal inhibition (Ti) of the opposite motor cortex mediated by fibers passing through this part of the CC. In normal subjects Ti had an mean onset latency of 36.1±3.5 ms (SD) and a duration of 24.5±3.9 ms. The calculated mean transcallosal conduction time was 13 ms. The threshold of Ti recorded in muscles ipsilateral to stimulation tended to be higher than the one for eliciting excitatory contralateral motor responses (56±6% vs 46±10% max. stimulator output). Cortical thresholds (at rest) for contralateral excitatory hand motor responses were higher in patients with developmental abnormalities of the CC than in normals (66±17% vs 46±10% max. stimulator output), which probably reflects also a facilitatory transcallosal interaction of both motor cortices in normals. In contrast, facilitation of cortically elicited motor responses in one hand by strong contraction of the other hand was the same in the patients with agenesis of the CC and normals, which suggests that this facilitatory spread takes place on a spinal rather than on a cortical level. Central motor latencies and amplitudes of contralateral hand motor responses were the same in patients with developmental abnormalities of the CC and normals (6.1±0.7 ms vs 6.3±0.7 ms and 6.7±2.4 mV vs 6.6±2.9 mV) so that callosal transfers do not seem to influence corticospinal conduction properties. Furthermore the inhibition of tonic electromyographic activity following the cortically elicited contralateral response was investigated which we refer to as postexcitatory silent period (Pi). When about the same stimulus intensity was used the Pi was shorter in the patients with developmental defects of the CC. This could be compensated by increasing the stimulus intensity in the patients, which might hint at some callosally mediated enhancement of inhibition in the late phase of the postexcitatory silent period.
Since transcranial stimulation of one motor cortex reproducibly elicited a transcallosal inhibition of the other motor cortex in normal subjects this approach might be of diagnostic value for studying callosal conduction and intracortical inhibitory mechanisms.