Growing evidence points toward involvement of the human motor cortex in the control of the ipsilateral hand. We used focal transcranial magnetic stimulation (TMS) to examine the pathways of these ipsilateral motor effects. Ipsilateral motor‐evoked potentials (MEPs) were obtained in hand and arm muscles of all 10 healthy adult subjects tested. They occurred in the finger and wrist extensors and the biceps, but no response or inhibitory responses were observed in the opponens pollicis, finger and wrist flexors and the triceps. The production of ipsilateral MEPs required contraction of the target muscle. The threshold TMS intensity for ipsilateral MEPs was on average 1.8 times higher, and the onset was 5.7 ms later (in the wrist extensor muscles) compared with size‐matched contralateral MEPs. The corticofugal pathways of ipsilateral and contralateral MEPs could be dissociated through differences in cortical map location and preferred stimulating current direction. Both ipsi‐ and contralateral MEPs in the wrist extensors increased with lateral head rotation toward, and decreased with head rotation away from, the side of the TMS, suggesting a privileged input of the asymmetrical tonic neck reflex to the pathway of the ipsilateral MEP. Large ipsilateral MEPs were obtained in a patient with complete agenesis of the corpus callosum. The dissociation of the pathways for ipsilateral and contralateral MEPs indicates that corticofugal motor fibres other than the fast‐conducting crossed corticomotoneuronal system can be activated by TMS. Our data suggest an ipsilateral oligosynaptic pathway, such as a corticoreticulospinal or a corticopropriospinal projection as the route for the ipsilateral MEP. Other pathways, such as branching of corticomotoneuronal axons, a transcallosal projection or a slow‐conducting monosynaptic ipsilateral pathway are very unlikely or can be excluded.

We used transcranial magnetic stimulation (TMS) to study the time course of corticospinal excitability before and after brisk thumb abduction movements, either in a simple reaction time (RT) paradigm or self-paced. Premovement increase in corticospinal excitability began about 20 msec earlier for self-paced compared with simple RT movements. For both simple RT and self-paced movements after electromyographic (EMG) offset, there was a first period of increased excitability from 0 to 100 msec, followed by a second period from 100 to 160 msec. Corticospinal excitability was decreased from about 500 to 1,000 msec after EMG offset for both types of movements. Our results show that motor preparation that begins 1.5 to 2 seconds before self-paced movement is not associated with increased corticospinal excitability. The first phase of increased corticospinal excitability after EMG offset may be due to activity of motor cortex neuron subthreshold for activating spinal motor neurons, and the second phase may reflect a subthreshold second agonist burst. The period of decreased corticospinal excitability after movement corresponds to the onset of event-related synchronization (ERS) of electroencephalographic signals in the 20-Hz band, and supports the hypothesis that ERS may be related to an inactive, idling state of the motor cortex.

The human motor system undergoes reorganization after amputation, but the site of motor reorganization and the mechanisms involved are unknown. We studied the site and mechanisms of motor reorganization in 16 subjects with traumatic lower-limb amputation. Stimulation at different levels in the CNS was used to determine the site of reorganization. The mechanisms involved were evaluated by measuring the thresholds for transcranial magnetic stimulation (TMS) and by testing intracortical inhibition and facilitation. With TMS, the threshold for muscle activation on the amputated side was lower than that of the intact side, but with transcranial electrical stimulation there was no difference in motor threshold between the two sides.TMS at the maximal output of the stimulator activated a higher percentage of the motor neuron pool (%MNP) on the amputated side than on the intact side. The %MNP activated by spinal electrical stimulation was similar on the two sides. Paired TMS study showed significantly less intracortical inhibition on the amputated side. Our findings suggest that motor reorganization after lower-limb amputation occurs predominately at the cortical level. The mechanisms involved are likely to include reduction of GABAergic inhibition.Key words: amputation; motor reorganization; mechanisms of plasticity; human; transcranial magnetic stimulation; motor cortexThe motor system undergoes reorganization after peripheral nerve lesions Sanes et al., 1990), spinal cord injuries (Lev y et al., 1990;Topka et al., 1991), cortical lesions (Jenkins and Merzenich, 1987;Benecke et al., 1991;Cohen et al., 1991b;Weiller et al., 1992;Nudo et al., 1996), amputations (Hall et al., 1990;Cohen et al., 1991a;Fuhr et al., 1992;Kew et al., 1994;Ridding and Rothwell, 1995), and transient deafferentation induced by ischemia (Brasil-Neto et al., 1992, 1993. The changes after spinal cord injury and transient deafferentation are more prominent with the target muscle at rest than during voluntary activation (Topka et al., 1991;Ridding and Rothwell, 1995). Using ischemic deafferentation of the forearm as a model for short-term plasticity in humans, we recently showed that plastic changes in the deafferented motor cortex can be upregulated by transcranial magnetic stimulation (TMS) to the deafferented cortex and downregulated by TMS to the contralateral motor cortex (Z iemann et al., 1998). Although experiments in animals have shown that reorganization can occur at multiple levels, including the cortex (Pons et al., 1988;Recanzone et al., 1992;Merzenich and Jenkins, 1993; Gilbert, 1994, 1995), thalamus (Garraghty and Kass, 1991;Pons et al., 1991;Nicolelis et al., 1993), brainstem (Pons et al., 1991;Florence and Kaas, 1995), and spinal cord (C arp and Wolpaw, 1994;Florence and Kaas, 1995), the site of motor reorganization in humans is not known. Whereas animal studies have shown that GABAergic (Hendry and Jones, 1986;Welker et al., 1989;Jacobs and Donoghue, 1991), glutaminergic (Anw yl, 1991;Garraghty et al., 1993;Conti et al., 1996), and...