Oxygen costs using a reciprocating gait orthosis in a paraplegic (T9) patient with a bilateral below-knee amputation: case report.

The Reciprocating Gait Orthosis (RGO) is a useful aid to ambulation for patients with paraplegia. Its use has been described previously though not in conjunction with limb prostheses. We report here the energy costs of ambulation of a patient, disabled by paraplegia at T9 and bilateral below-knee amputations, walking at her preferred rate using an RGO while gas exchange was measured by the Douglas bag method. Oxygen uptake (VO2) rose from 0.198 1 min-1 at rest to 0.582 1 min-1 in the last minute of exercise, representing a VO2 of 14.3 ml kg-1 min-1. During the fourth minute of ambulation, energy consumption was 30.44 J kg-1 s-1 with an energy cost of 4.17 J kg-1 m-1 at a velocity of 0.13 m s-1, Ambulation with this combination of disability is possible with the aid of limb prostheses and an RGO though it is slow and the energy expenditure as consumption per second and cost per metre are high.

Preclinical trial of 4-aminopyridine in patients with chronic spinal cord injury.

4-Aminopyridine (4-AP) is a K+ channel blocking agent that enhances nerve conduction through areas of demyelination by prolonging the duration of the action potential and increasing the safety factor for conduction. We have investigated the effects of 4-AP (24 mg total dose-intravenous) in 6 patients with spinal cord injury (3 complete, 3 incomplete) with the intent of overcoming central conduction block, or slowing, due to demyelination. Vital signs remained stable and only mild side effects were noted. The 3 patients with incomplete injuries all demonstrated enhanced volitional EMG interference patterns and one patient exhibited restored toe movements. The changes were reversed on drug washout. There were no changes in segmental reflex activities. These results are consistent with those obtained from 4-AP trials with animal models of spinal cord injury, showing modest therapeutic benefit attributable to enhanced central conduction.

Reinforcement of subliminal flexion reflexes by transcranial magnetic stimulation of motor cortex in subjects with spinal cord injury.

A 20 msec train (500 Hz; 0.1-0.2 msec duration) of percutaneous electrical stimulation (ES) applied to the plantar surface was used to condition muscle responses evoked in tibialis anterior (TA) by transcranial magnetic stimulation of the motor cortex in 8 subjects with traumatic spinal cord injury (SCI). The intensity of conditioning ES was adjusted to just subthreshold for evoking flexion reflexes in TA and was delivered at conditioning-test (C-T) intervals of 15-60 msec prior to cortical stimulation. Four subjects with clinically complete SCI revealed no muscle response to cortical stimulation or following combined subliminal percutaneous ES and cortical stimulation. Four subjects (3 clinically incomplete and 1 complete injury) demonstrated muscle responses with a latency of 70-80 msec time-locked to the percutaneous ES when the conditioning subliminal stimulation was delivered at C-T: 15-40 msec. These responses, resembling suprathreshold flexion reflexes, reflect the convergence of excitatory afferent and cortical inputs and provide evidence of preserved corticospinal innervation to the L4-5 segmental motoneuron or interneuron pools. In 3 of the subjects this preserved corticospinal influence was evident despite absence of motor evoked potentials (MEPs) following cortical stimulation. The effect of the combined electrical and cortical stimulation in yielding suprathreshold flexion reflexes, instead of the facilitated MEPs seen in control subjects, appears to be related to slowed central conduction, prolonged temporal dispersion of the motoneuron facilitation following cortical stimulation and segmental reflex changes associated with disrupted modulation of interneuronal pathways. The results show this conditioning paradigm to be useful in revealing preserved corticospinal innervation in some SCI subjects with absent MEPs.

Afferent conditioning of motor evoked potentials following transcranial magnetic stimulation of motor cortex in normal subjects.

The present study determined the effects of percutaneous electrical stimulation of the plantar surface on motor evoked potentials (MEPs) in tibialis anterior (TA) and soleus (SOL) of normal subjects following transcranial magnetic stimulation of motor cortex. The conditioning stimulation consisted of a 20 msec train of electrical pulses (500 Hz; 0.1 msec rectangular) delivered to the medial border of the sole of the foot at an intensity just subthreshold for evoking a flexion reflex. The conditioning (C) stimulation preceded the test (T) cortical stimulation by intervals of 20-130 msec. Magnetic stimulation of motor cortex (Cadwell MES-10) was delivered through a 9.5 cm focal point coil positioned tangential to the scalp and located with the rim over vertex. Five healthy adults served as subjects and each was investigated on at least 2 occasions. At C-T intervals 20-50 msec there was a mild inhibition of MEPs in both TA and SOL. This was followed by marked facilitation (greater than 300%) of MEPs at C-T intervals 50-85 msec in both TA and SOL in all subjects. At longer C-T intervals greater than 110 msec, there was an inhibition of MEPs in TA but not in SOL. Based on the time course of these 3 phases of MEP amplitude modulation, and different stimulation thresholds for each phase, it appears that separate neurophysiological processes underlie each phase of MEP modulation. These observations also suggest that percutaneous electrical stimulation may be useful as a means of enhancing low amplitude or subliminal MEPs in normal subjects or patients with myelopathy.

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.

Reinforcement of motor evoked potentials by remote muscle contraction.

We investigated the effects of remote muscle contraction on the amplitude and latency of motor-evoked potentials (MEPs) recorded from tibialis anterior and lateral gastrocnemius after transcranial magnetic stimulation of the motor cortex. In particular, consideration was given to the effects of unilateral handgrip of different strengths, jaw clench, and combined bilateral handgrip (Jendrassik maneuver) and jaw clench. Eight healthy adult volunteer subjects (six women, two men) participated in the main study. The clinical usefulness of this form of facilitation was subsequently demonstrated in three patients with myelopathy. Transcranial magnetic stimulation of the motor cortex was delivered from a Cadwell MES-10 (100% intensity) with a 9.5-cm circular coil positioned with the rim over the vertex. Stimuli were delivered ∼ 1 s after initiation of reinforcement. In the main study of normal subjects, surface recordings of the evoked compound muscle action potentials were made bilaterally from anterior tibialis and lateral gastrocnemius. In the individual studies of patients, MEPs were also recorded from abductor pollicis brevis and other muscles innervated from roots below the level of lesion. The principal results showed that unilateral handgrip (50 and 100% maximum voluntary contraction, MVC) of either hand enhanced the amplitude of MEPs bilaterally in both tibialis anterior and lateral gastrocnemius in all normal subiects (p < 0.05). The mean increase in amplitude associated with 100% MVC unilateral handgrip was >300% of the control value when the subject was relaxed (p < 0.01). The bilateral Jendrassik maneuver and jaw clench were also effective in increasing (p < 0.05) MEP amplitude in both muscle groups. These two procedures did not yield the same degree of reinforcement as 100% unilateral handgrip. Remote muscle contractions induced a reduction in MEP latency of 1-2 ms (p < 0.05). The clinical importance of these observations was demonstrated by the fact that remote muscle reinforcement enabled identification of low-amplitude MEPs that might otherwise have been missed in the three patients with spinal cord trauma.