Reinforcement of motor evoked potentials in patients with spinal cord injury.

Transcranial magnetic stimulation of the motor cortex has been used to investigate the putative existence of spared motor pathways in spinal cord injured patients with clinically complete paralysis. Particular consideration was given to methods of neurological reinforcement likely to minimize the risk of false negative interpretation of absent motor evoked potentials (MEPs). The principal methods of reinforcement included target and remote muscle contractions and conditioning of MEPs with a brief (20 msec) train of cutaneous stimulation (500 Hz: duration 0.1 msec) delivered 20-150 msec prior to cortical stimulation. Twelve control subjects and 26 patients with severe traumatic spinal cord injury underwent cortical stimulation delivered from a Cadwell MES-10 (70-100% intensity) through a 9-cm focal-point coil. Electromyographic responses were recorded from surface electrodes in bipolar configuration and amplified (3 dB down at 10 Hz-1 kHz) prior to storage. MEPs were recorded, following reinforcement, in muscles with clinically complete paralysis in 4/26 patients. In each case, MEPs were of low amplitude (less than 0.5 mV), polyphasic, and with variable and prolonged latencies. MEPs were evoked in severely paretic (clinically incomplete paralysis) muscles in 6/8 patients only when neurological reinforcement was employed. Conditioning of MEPs in tibialis anterior with preceding cutaneous stimulation to the plantar surface (subthreshold for evoking a flexion reflex) yielded a well-defined modulation of MEP amplitude in control subjects. An early (Conditioning-Test (C-T) intervals 20-45 msec) period of inhibition of MEPs (mean = 60% of control) was followed by a period (C-T intervals 50-90 msec) of facilitation (mean = 345%) and a subsequent (C-T intervals 90-150 msec) period of inhibition (mean = 0%). In spinal cord injured patients the same conditioning paradigm failed to reveal MEPs, but did result in the appearance of suprathreshold flexion reflexes in 2 patients at 20-55 msec C-T intervals. This summation of convergent but subliminal cortical and cutaneous inputs to the target motoneuron pool provided additional evidence of preserved cortical influence on segmental structures that was not detectable by other means. These results extend previous reports of electrophysiological evidence of spared motor pathways in spinal cord injured patients with complete paralysis, and affirm the need for neurological reinforcement as a routine procedure in cortical stimulation studies of spinal cord injuries.