W. Barry McKay

Evidence of subclinical brain influence in clinically complete spinal cord injury: discomplete SCI

Previous studies of the neurocontrol of movement in spinal cord injury (SCI) subjects revealed that even those without volitional movement may retain some degree of preservation of distal brain influence. We previously defined a discomplete lesion as one which is clinically complete but which is accompanied by neurophysiological evidence of residual brain influence on spinal cord function below the lesion. In order to document the nature and extent of such neurocontrol, we recorded surface EMGs from multiple muscle groups to study patterns of motor unit activity in response to tendon vibration, activation of muscles below the lesion by reinforcement maneuvers above the lesion and by voluntary suppression of plantar withdrawal reflexes. We analyzed data from this brain motor control assessment (BMCA) procedure in order to describe the frequency of occurrence and characteristics of residual control in discomplete SCI subjects, comparing with findings in (clinically and neurophysiologically) complete and in (clinically and neurophysiologically) incomplete SCI subjects. From a group of 139 SCI subjects seen for management of spasticity, 88 had clinically complete lesions. Of these, 74 (84%) were discomplete as defined by responses to the above maneuvers. The selection of management and intervention strategies, whether physiological, pharmacological, behavioral or surgical, should give consideration to the high likelihood that clinically complete subjects may be neurophysiologically incomplete.

Focal depression of cortical excitability induced by fatiguing muscle contraction: a transcranial magnetic stimulation study

Motor evoked potentials (MEPs) elicited by transcranial magnetic stimulation (TMS) and transcranial electrical stimulation (TES) of the motor cortex were recorded in separate sessions to assess changes in motor cortex excitability after a fatiguing isometric maximal voluntary contraction (MVC) of the right ankle dorsal flexor muscles. Five healthy male subjects, aged 37.4±4.2 years (mean±SE), were seated in a chair equipped with a load cell to measure dorsiflexion force. TMS or TES was delivered over the scalp vertex before and after a fatiguing MVC, which was maintained until force decreased by 50%. MEPs were recorded by surface electrodes placed over quadriceps, hamstrings, tibialis anterior (TA), and soleus muscles bilaterally. M-waves were elicited from the exercised TA by supramaximal electrical stimulation of the peroneal nerve. H-reflex and MVC recovery after fatiguing, sustained MVC were also studied independently in additional sessions. TMS-induced MEPs were significantly reduced for 20 min following MVC, but only in the exercised TA muscle. Comparing TMS and TES mean MEP amplitudes, we found that, over the first 5 min following the fatiguing MVC, they were decreased by about 55% for each. M-wave responses were unchanged. H-reflex amplitude and MVC force recovered within the 1st min following the fatiguing MVC. When neuromuscular fatigue was induced by tetanic motor point stimulation of the TA, TMS-induced MEP amplitudes remained unchanged. These findings suggest that the observed decrease in MEP amplitude represents a focal reduction of cortical excitability following a fatiguing motor task and may be caused by intracortical and/or subcortical inhibitory mechanisms.

Motor control after spinal cord injury: Assessment using surface EMG

The brain motor control assessment (BMCA) protocol is a comprehensive multichannel surface EMG recording used to characterize motor control features in persons with upper motor neuron dysfunction. Key information is contained in the overall temporal pattern of motor unit activity, observed in the EMG (RMS) envelope. In paralysis, a rudimentary form of suprasegmental control of tonic and phasic reflexes can be demonstrated. EMG patterns evoked by voluntary and passive maneuvers and by volitional modulation of reflex responses reveal features of motor control not apparent in the clinical examination. Such subclinical findings may explain paradoxically different responses in apparently similar SCI subjects, and may be used to monitor spontaneous or induced changes. The recording protocol, examples of EMG patterns, and their prevalence in 40 spinal cord injured (SCI) subjects are presented, and compared with 5 healthy subjects.

Intracortical inhibition of lower limb motor-evoked potentials after paired transcranial magnetic stimulation

Abstract The aim of the present study was to determine the characteristics of intracortical inhibition in the motor cortex areas representing lower limb muscles using paired transcranial magnetic (TMS) and transcranial electrical stimulation (TES) in healthy subjects. In the first paradigm (n=8), paired magnetic stimuli were delivered through a double cone coil and motor evoked potentials (MEPs) were recorded from quadriceps (Q) and tibialis anterior (TA) muscles during relaxation. The conditioning stimulus strength was 5% of the maximum stimulator output below the threshold MEP evoked during weak voluntary contraction of TA (33±5%). The test stimulus (67±2%) was 10% of the stimulator output above the MEP threshold in the relaxed TA. Interstimulus intervals (ISIs) from 1–15 ms were examined. Conditioned TA MEPs were significantly suppressed (P<0.01) at ISIs of less than 5 ms (relative amplitude from 20–50% of the control). TA MEPs tended to be only slightly facilitated at 9-ms and 10-ms ISIs. The degree of MEP suppression was not different between right and left TA muscles despite the significant difference in size of the control responses (P<0.001). Also, conditioned MEPs were not significantly different between Q and TA. The time course of TA MEP suppression, using electrical test stimuli, was similar to that found using TMS. In the second paradigm (n=2), the suppression of TA MEPs at 2, 3, and 4 ms ISIs was examined at three conditioning intensities with the test stimulation kept constant. For the pooled 2- to 4-ms ISI data, relative amplitudes were 34±6%, 61±5%, and 98±9% for conditioning intensities of 0.95, 0.90, and 0.85× active threshold, respectively (P<0.01). In conclusion, the suppression of lower limb MEPs following paired TMS showed similar characteristics to the intracortical inhibition previously described for the hand motor area.

Voluntary supraspinal suppression of spinal reflex activity in paralyzed muscles of spinal cord injury patients

Having previously demonstrated that residual facilitatory brain influence on segmental structures occurs in paralyzed spinal cord injury patients, we sought evidence of suprasegmental suppression in such patients. By recording EMG activity from leg muscles, we studied changes in segmental excitability of the plantar reflex elicited by cutaneous stimulation of the plantar surface. Using surface EMG recordings, 50 paralyzed spinal cord injury patients were examined for their ability to volitionally suppress the plantar reflex on three repeated trials after three baseline trials. The patients, who had no voluntary EMG activity in the monitored muscles, were able to volitionally suppress the plantar reflex responses by 45% in the tibialis anterior, hamstring, and triceps surae muscles and to suppress the quadriceps response by 72%. In this patient group, 73 of 100 tibialis anterior muscle groups showed suppression of more than 20% compared with the control response. On reexamination, these findings were consistent during a period of 2 years in six patients. We conclude that suprasegmental suppression of segmental activity does occur in paralyzed spinal cord injury patients, and that in clinically complete patients, neurological evaluation should include assessment of the degree of preservation of suprasegmental neurocontrol on segmental activity below the lesion.