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Spinal cord injuries often result in irreversible loss of motor and somatosensory functions below the lesion level. Treatment is limited to physiotherapy aimed at compensating disability. We previously showed that re-establishment of tissue continuity can be achieved in animal models through nerve autografts implanted between the rostral spinal ventral horn and the caudal ventral roots. Rostral motor neuron axons could thus reach peripheral targets, leading to some return of motor function. We used a similar approach in a paraplegic patient with stabilized clinical states three years after spinal cord traumatic damage at the T9 level. Three segments from autologous sural nerves were implanted into the right and left antero-lateral quadrant of the cord at T7-8 levels, then connected to homolateral L2-4 lumbar ventral roots, respectively. Eight months after surgery, voluntary contractions of bilateral adductors and of the left quadriceps were observed. Muscular activity was confirmed by motor unit potentials in response to attempted muscle contraction. Motor-evoked potentials from these muscles were recorded by transcranial magnetic stimulation. These data support the hypothesis that muscles have been re-connected to supra-spinal centers through motor neurons located in the rostral stump of the damaged cord. They suggest that delayed surgical reconstruction of motor pathways may contribute to partial functional recovery.

Compared with cortical somatosensory-evoked potentials, neurogenic motor-evoked potential signals are well preserved in patients undergoing surgery to correct scoliosis under general anesthesia supplemented with isoflurane or desflurane in concentrations as great as 1 MAC.

Remote voluntary contraction, such as the classical Jendrassik maneuver (JM), is a procedure routinely used to increase the amplitude of tendon reflexes in the lower limb. In 8 healthy subjects we studied the effects of JM on the motor evoked potentials (MEP) recorded from tibialis anterior muscle, produced by transcranial magnetic stimulation (stimulus output of 5-10% over motor threshold). In this study, JM consisted here of a bilateral violent handgrip, preceding magnetic stimulation from 100 to 50 ms (steps of 100 ms). Compared to the control test, latencies remained unchanged. MEP amplitudes were greatly enhanced with a JM test interval from 200 to 400 ms (170% of control amplitude at 300 ms). We also studied 6 patients with severe alterations of MEPs from tibialis anterior muscle. In each case, JM preceding magnetic stimulation (stimulus output 100%) from 300 ms induced reappearance of response or marked enhancement of amplitude, allowing calculation of central conduction time. Such a technique, which is easy to perform, may be useful in clinical practice to calculate central motor conduction time, where it would otherwise be difficult or impossible.