Arthur M. Sherwood

Clinical assessment of spasticity in spinal cord injury: A multidimensional problem☆

OBJECTIVE To determine the relation between various components of spasticity evaluated clinically in persons with spinal cord injury (SCI). DESIGN Case series evaluating spasticity using clinical scales commonly referenced in contemporary literature, including the Penn Spasm Frequency Scale, the Ashworth Scale, and standard scales of tendon taps, clonus, and plantar stimulation. SETTING. A Veterans Affairs Medical Center Spinal Cord Injury Center. PATIENTS. Eighty-five spinal cord injured individuals with varying degrees of spasticity. RESULTS Correlations demonstrated weak relationships between Spasm Frequency Scale and self-report scales of interference with function (.407) and painful spasms (.312). No clinical examination score correlated with self-report scores greater than 0.4. Three clinical examination scores correlated modestly (> 0.5)-Ashworth score with patellar tendon taps (.553), ankle clonus with Achilles tendon tap (.663), and patellar tendon tap with adductor tendon tap (.512). Two other clinical scales correlated weakly (> 0.4)-Achilles tendon tap with patellar tendon tap (.417) and plantar reflex with adductor tendon taps (.423). CONCLUSIONS Clinical scales currently used to evaluate spasticity in SCI correlate poorly with each other, suggesting that they each assess different aspects of spasticity. The use of any single scale is likely to underrepresent the magnitude and severity of spasticity in the SCI population. In the absence of agreement among these various scales and with the absence of an appropriate criterion standard for evaluation of spasticity, assessments of spasticity, whether clinical or neurophysiological in nature, should be comprehensive in scope.

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.

Gabapentin for the treatment of spasticity in patients with spinal cord injury

Our serendipitous observations suggested that some patients with spasticity appeared to have improved following the administration of the anticonvulsant drug gabapentin. As some patients with spasticity are either refractory to or intolerant of established medical treatments, we conducted this study to investigate the effect of gabapentin on spasticity in patients with spinal cord injury. Twenty-five patients with spinal cord injury and spasticity received oral gabapentin (2400 mg over 48 h) in a randomized, double blind, placebo-controlled crossover study. We assessed responses by measuring the Ashworth spasticity scale, muscle stretch reflexes, presence of clonus and reflex response to noxious stimuli. Patient ratings were obtained using a Likert Scale. Administration of gabapentin, but not placebo, was associated with an 11% reduction in spasticity as measured by the Ashworth Scale (P=0.04) and by a 20% reduction in the Likert Scale (P=0.0013). Significant changes were not obtained for the other measures. The data obtained suggest that gabapentin may be useful in the management of spasticity associated with spinal cord injury.

Clinical neurophysiological assessment of residual motor control in post-spinal cord injury paralysis.

Objective. This study was designed to characterize the rudimentary residual lower-limb motor control that can exist in clinically paralyzed spinal-cord-injured individuals. Methods. Sixty-seven paralyzed spinal-cord-injured subjects were studied using surface electromyography recorded from muscles of the lower limbs and analyzed for responses to a rigidly administered protocol of reinforcement maneuvers, voluntary movement attempts, vibration, or the ability to volitionally suppress withdrawal evoked by plantar surface stimulation. Results. Markers for the subclinical discomplete motor syndrome were found in 64% of the subjects. The tonic vibration response was recorded in 37%, volitional plantar surface stimulation response suppression in 27%, and reinforcement maneuver responses in 6% of the subjects. Three subjects, 4%, produced reliable but very low amplitude surface electromyography during the voluntary movement segment of the protocol. Surface electromyography recorded during passive leg movement was related to Ashworth scores as was the tonic vibration response marker (P < 0.05). Conclusions. Multimuscle surface electromyography patterns recorded during a rigidly administered protocol of motor tasks can be used to differentiate between clinically paralyzed spinal-cord-injured individuals using subclinical motor output to identify the translesional neural connections that remain available for intervention testing and treatment planning after spinal cord injury.

Effectiveness of gabapentin in controlling spasticity : a quantitative study

The purpose of this investigation was to study the effectiveness of gabapentin in controlling spasticity in persons with spinal cord injury (SCI) using a surface EMG-based quantitative assessment technique called the brain motor control assessment (BMCA). Six men from a Veterans Affairs Medical Center with spasticity due to traumatic SCI were studied as part of a multi-center, placebo-controlled, cross-over, clinical trial of gabapentin. Spasticity was evaluated using multi-channel surface EMG recordings of muscles in the lower extremities, abdomen and low back before and during treatment with oral gabapentin or placebo. Gabapentin or placebo was given orally in doses 400 mg three times daily for 48 h. Following a 10 day wash-out period subjects were crossed-over to receive the medication not received the first time. This was followed by an elective open-label extension. Group results during the controlled trial did not reach statistical significance at the dosage used. One subject demonstrated a dramatic improvement in spasticity that was apparent both clinically and with the BMCA. Other subjects demonstrated modest improvements which were seen in the BMCA but not recognized clinically. During the open label extension, the four subjects who participated experienced important clinical improvements with higher doses (to 3600 mg/day). These improvements were often in components of spasticity in which the BMCA had detected subclinical changes during the cross-over trial. A seventh subject was studied using the BMCA at doses of 1200 mg T.I.D. gabapentin, off gabapentin and 800 mg T.I.D. gabapentin and demonstrated quantitatively a dose-related effect with higher doses of gabapentin which matched clinical observations. Gabapentin at doses of 400 mg T.I.D. may be effective in controlling some features of spasticity in persons with SCI. Higher doses provide greater control of spasticity, and controlled studies using higher doses are needed to evaluate gabapentins efficacy.

Co-activation of ipsi- and contralateral muscle groups during contraction of ankle dorsiflexors

Seventeen adult, healthy subjects, age 38.4 +/- 0.24 years (mean +/- SEM) 7 of which were females, were studied. Each subject was seated on a specially designed chair with trunk and legs fixed and the foot strapped to a rigid plate that was attached to a load cell. The position of the strap was adjusted so as to lie across the foot at the level of the metatarsal bones. The knee and ankle joints were adjusted to 90 degrees. To record EMG activity, pairs of surface electrodes were placed over the belly of both the right and left tibialis anterior, quadriceps, hamstring and contralateral triceps surae muscles. Two experimental paradigms were used, A and B. In A the subject was asked to sustain maximum voluntary contraction (MVC) of the ankle dorsiflexors until the force decreased to 50% of the initial value; in B the subject was asked to carry out contractions of the ankle dorsiflexors for 6 seconds followed by 4 sec relaxation periods. The initial contraction was 20% of MVC followed by 40, 60, 80 and 100% of MVC which represented one cycle. The subject was asked to repeat this cycle 10 times. Voluntary contraction of ankle dorsiflexors was regularly accompanied by activation of other muscles, usually first in the same leg, later in the contralateral leg during MVC of ankle dorsiflexors. When intermittent contractions with step wise increments of force developed by the ankle dorsiflexors were carried out, co-activation of ipsilateral and contralateral muscle groups occurred before the force of the contracting muscles decreased.(ABSTRACT TRUNCATED AT 250 WORDS)

Early and late lower limb motor evoked potentials elicited by transcranial magnetic motor cortex stimulation.

Transcranial magnetic motor cortex stimulation can elicit a series of responses recorded with different latencies from relaxed muscles of the lower limbs. In 7 healthy subjects, ranging in age from 16 to 62 years, stimulation was delivered by a 9 cm coil centered over Cz with the subject in the supine position. Surface polyelectromyography was used to record motor evoked potentials (MEPs) from the quadriceps (QD), hamstrings (HS), tibialis anterior (TA) and triceps surae (TS) muscles bilaterally. Three characteristic responses were identified in each muscle group on the basis of amplitude and latency criteria, identified by latencies: the direct oligosynaptic response MEP30 appeared with a latency of 24.3 msec in the QD, 26.3 msec in the HS, 30.5 msec in the TA and 31.3 msec in the TS; MEP70 with latencies of 64 msec in the QD, 59 msec in the HS, 79 msec in the TA and 72 msec in the TS; MEP120 with latencies of 115 msec in the QD, 126 msec in the HS, 117 msec in the TA and 124 msec in the TS. These 3 responses have distinct latencies, amplitudes and durations. MEP70 appears to be the result of activation of long descending tracts which end on spinal interneuronal circuits. As MEP120 has different features, it may have a different mechanism.

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.