A dynamic EMG profile index to quantify muscular activation disorder in spastic paretic gait

Electroencephalography and clinical Neurophysiology, 1989, 73:233-244 Elsevier Scientific Publishers Ireland, Ltd.

233

EEG03815

A dynamic EMG profile index to quantify muscular activation disorder in spastic paretic gait J. F u n g

and H. Barbeau

School of Physical and Occupational Therapy, McGill University, Montreal, Que. H3G 1 Y5 (Canada)

(Accepted for publication: 8 March 1989)

Summary Spasticity is a complex phenomenon that interferes with motor control. Existing clinical and physiological measures of spasticity have mainly focused on the evaluation of clonus and reflexes. Subjected to the limitation of testing in a resting position, the results may not necessarily reflect the extent of functional impairment caused by spasticity. To evaluate spasticity in a dynamic, voluntary movement such as locomotion, a task-specific approach is essential. A dynamic index, I, derived from the EMG activity obtained during treadmill walking in human subjects, is therefore proposed as a functionally relevant measurement of spasticity in locomotion. I, defined as the ratio of integrated EMG in the pre-determined 'off" window of the normalized gait cycle to that in the 'on' window, would indicate the degree of abnormal activation of locomotor muscles from their normally relaxed state as compared to the total recruitment in the active state during walking. The present study done on 5 normal and 8 spastic paraparetic subjects showed that I was homogeneously low in the normal group but abnormally high and variable in the spastic group. A case study has further demonstrated that I is sensitive to the alteration in locomotor spasticity with pharmacological intervention, and the change in I parallels the improvement in the kinematics observed. This preliminary study indicates that the proposed index appears to be a functionally relevant and dynamic measurement of spastic locomotor disorder. Key words: Spasticity; Gait; Spinal cord injury; EMG; Pharmacological intervention

Spasticity, a m a j o r sequela to lesions of the central nervous system, is a n i n t r i g u i n g p h e n o m e n o n that leads to m o t o r disturbance. Clinically, spasticity is characterized b y hyperreflexia, hypertonia, clonus, a n d i m p a i r e d control of v o l u n t a r y m o v e m e n t often a c c o m p a n i e d b y various degrees of paresis ( C h a p m a n a n d W i e s e n d a n g e r 1982). I n spinal cord i n j u r e d (SCI) h u m a n s , the m a n i f e s t a tion of spasticity, being affected b y the site a n d extent of lesion, is heterogeneous i n terms of the time of onset, degree, a n d location of m u s c u l a r hypertonia. Recent findings suggest that spasticity is n o t a single pathophysiologic entity, b u t a collection of m o t o r p r o g r a m d i s t u r b a n c e s ( G r i m m

Correspondence to: H. Barbeau, Ph.D.. School of Physical and Occupational Therapy, McGill University, 3654 Drummond Street, Montreal, Que. H3G 1Y5 (Canada).

1983). However, e v a l u a t i o n of h u m a n spasticity has t r a d i t i o n a l l y focused o n hyperactive m o n o s y n aptic reflexes which comprise of o n l y o n e aspect of the multifaceted p h e n o m e n o n of spasticity. Thus, objective q u a n t i f i c a t i o n relied m a i n l y on electrophysiological testing of the H-reflex, tonic vibration, a n d stretch reflexes as well as the t e n d o n j e r k (Delwaide 1985). It is n o t a n u n c o m m o n f i n d i n g that these spastic reflexes c a n b e c o m e depressed b y various k i n d s of therapeutic intervention without any corresponding improvement in m o t o r f u n c t i o n ( K n u t s s o n 1983). As reflex testing is subjected to the l i m i t a t i o n of testing i n a resting position, the findings m a y n o t necessarily reflect the d y n a m i c muscle tone d u r i n g v o l u n t a r y m o v e m e n t or the extent of f u n c t i o n a l i m p a i r m e n t caused by spasticity. This is s u b s t a n t i a t e d b y resuits which showed that the t e n d o n jerk a n d H-reflex could actually be m o d i f i e d b y v o l u n t a r y

0013-4649/89/$03.50 © 1989 Elsevier Scientific Publishers Ireland, Ltd.

234 movement (Gottlieb and Agarwal 1973). In a recent study by C a p a d a y and Stein (1986), the human soleus H-reflex amplitude was found to be strongly task-dependent, being greater during standing than during walking at the same effective stimulus intensities. Moreover, Neilson and Andrews (1973) have shown in spastic athetotic subjects that the tonic stretch reflex measured during a resting position and during sustained voluntary contraction differed in sensitivity, pattern, duration, as well as timing of the responses. Perry (1980) has also shown that the ankle clonus frequency could markedly be enhanced by a change in b o d y posture from supine to sitting to standing. Therefore it is essential to evaluate spasticity as a m o t o r disorder in a d y n a m i c and voluntary task such as walking, in order to relate to functional outcomes. A n alternative method has been introduced by Benecke et aL (1983), employing electromyographic analysis of bicycling as a means of evaluating spastic m o t o r disorder. Although the method seemed appropriate in assessing spasticity encountered in the bicycling m o v e m e n t of the lower limbs, this task-specific a p p r o a c h m a y not be generalizable to other functional activities such as walking. Bicycling, which can involve both active and passive movements of the lower limbs, has been shown to have different muscle activation patterns from that of walking (Ericson et al. 1985). Hence the evaluation of spastic locomotor disorder needs to be performed in locomotion specifically. The manifestation of spasticity in gait is indeed an important facet that should not be neglected. Moreover, it is functionally relevant to evaluate spasticity in a dynamic and voluntary task such as locomotion, which involves a large spectrum of tonically and phasically active descending and ascending pathways acting on the segmental spinal circuitry (Grillner 1981). In contrast to the prevailing, literature on reflex testing, the few studies on spastic gait disorders (Knutsson 1980; Dietz et al. 1981; Benecke and C o n r a d 1986) are mostly descriptive-comparative in nature. It is therefore the purpose of this preliminary study to propose an index, I, derived from the electromyographic ( E M G ) activity obtained during treadmill walking, as an attempt to quantify

J. FUNG, H. BARBEAU disordered muscle activation patterns in spastic paretic gait. Preliminary results have been published ( F u n g and Barbeau 1987a).

Methods The subjects included in this study were 5 normal, healthy, male volunteers aged between 26 and 35 years, and 8 male spastic paretic patients aged between 23 and 56 years (Table I). All the spastic subjects had incomplete spinal cord lesions of traumatic origin, except for MB, who was diagnosed as having non-familial progressive spastic paraparesis. Positive clinical signs of spasticity, such as increased resistance to passive stretch, brisk jerks, ankle clonus, and spasms, were present in both lower limbs of all the spastic paretic subjects. Prior to data collection, each subject was habituated to walk on a treadmill at his maximal comfortable speed for 1 - 1 0 rain depending on the individual level of endurance. A n overhead harness suspension system provided mechanical supTABLE I Demographic data of the 5 normal male subjects and 8 spastic paretic patients. All the patients bad traumatic spinal cord injury, except for MB, who suffered from non-familial spastic paraparesis. The walking speed shown here was the maximal, comfortable speed attainable on the treadmill. Sub- Sex Age W a l k i n g Lesion Chroject (years) speed level nicity (m/sex) (years) Normal N1 M 33 1.36 N2 M 31 1.27 N3 M 26 1.35 N4 M 35 1.43 N5 M 27 1.33 Spastic MP RP MB RM BM RL SH SQ

M M M M M M M M

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EMG PROFILE INDEX TO QUANTIFY SPASTIC LOCOMOTOR DISORDER port, with force transducers determining the amount of body weight support (BWS). After individually calibrating to 0% BWS (full weight bearing) and 100% BWS (total suspension), the percentage of BWS provided during walking could be adjusted accordingly. A detailed description of this system has previously been reported (Barbeau et al. 1987). Such a suspension system together with the support from hand railings on the treadmill would minimize the non-specific compensatory effects or protective reactions that could arise due to instability, especially in spastic patients, which have been described by Conrad et al. (1983) as 'protective gait mechanisms.' Thus the system was equipped to evaluate even the severely spastic subjects, who could not normally walk full weight bearing overground. All the subjects included in this study could manage to walk at full weight (0% BWS) except for SQ and SH, who were so impaired by their spasticity that they required 40% BWS in order to walk on the treadmill, even at the minimal speed of 0.26 m / s e c . A rest period of at least 10 rain was given between the habituation trial and the actual walking trial of data collection. Blood pressure and heart rate were closely monitored in the beginning and at the end of each triM, and an emergency stop trigger control was available to the subject such that he could stop the treadmill at any time. Simultaneous E M G and kinematic data from the right lower limb as well as bilateral footswitch signals were collected during treadmill walking for analysis. E M G activity from the medial hamstrings group (MH), vastus lateralis (VL), tibialis anterior (TA) and medial gastrocnemius (GA) was detected with disposable bipolar surface electrodes after proper skin preparation, such as shaving, abrading and rubbing with alcohol to reduce skin impedance. After passing through a buffer system and preamplifiers to eliminate movement artefacts, the E M G signals were bandpass filtered (10-450 Hz), differentially amplified and recorded together with footswitch signals, time code and auditory signals on a 14-channel magnetic tape (with 12 F M channels of bandwidth 0-2500 Hz and 2 direct channels of bandwidth 100-19000 Hz, at the recording speed used. Footswitches placed bilaterally beneath the heel,

235

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%GAICYCLE T K)O Fig. 1. An illustration of the data processing procedures. A: an example of EMG record (VL of subject N1), synchronized and normalized to the ipsilateral footswitch signal depicting the gait cycle. B: the within-subject (N1) ensemble of 5 cycles of VL EMG activity normalized to 100% of the gait cycle. The arrow depicts stance-swing transition. C: the within-subject (N1) ensemble average of VL EMG activity. The dashed curves represent 1 S.D. above and below the mean activity. D: the within-subject (N1) ensemble average of VL EMG activity, normalized to 100% of the mean ensemble peak. the head of the fifth metatarsal and the big toe registered the temporal relations of the gait cycle. Each footswitch produced a distinct voltage. The stance and swing duration were defined as the period that extended from heel contact to toe-off and from toe-off to the subsequent heel contact respectively. I n f o r m a t i o n on cycle duration, stance-swing ratio, single and double limb support time could also be determined. The E M G signal was synchronized to the ipsilateral footswitch signal, to correlate muscle activity with gait sequencing (Fig. 1A). The recorded data were played back on an oscilloscope and polygraph to select portions of representative E M G and footswitch records that were free of artefacts. The selected sequence was then full-wave rectified and processed by a second order low-pass filter (cut-off frequency at 3.0 Hz) to produce an analog linear envelope. Following analog to digital conversion at a sampling rate of 1000 Hz, data analysis was performed off-line on a P D P 1 1 / 3 4 computer using interactive programs. The E M G data were normalized to the stride cycle from one foot-floor contact to the next

236 (0-100%) and averaged for each 0.4% interval of the cycle, generating a 3-dimensional plot across all the cycles (Fig. 1B). The E M G values were averaged across 5 consecutive cycles in each normal subject and 10 in each spastic subject to produce a within-subject ensemble average (Fig. 1C). The mean and peak voltage of the ensemble average were recorded for reference. For the purpose of between-subject comparison and calculation of the index, the mean E M G amplitude was further normalized to the mean ensemble peak amplitude (100%), hence the plot has 100% in both x and y axes (Fig. 1D). Sagittal motion of treadmill walking was videotaped as each subject walked with reflective joint markers affixed to anatomical landmarks at the shoulder, midline of the rib cage, hip, knee, and ankle, as well as the lateral calcaneus, fifth metatarsal phalangeal joint, and toe area of the shoe, lining the lateral border of the foot. Reference markers were also placed on a vertical and a horizontal bar. The motion could be played back on a video monitor at 60 fields/sec. Field by field viewing and selection was done by a remote search controller. Kinematics were analyzed by directly measuring the sagittal angular displacement of the trunk, hip, knee, and ankle, with a joint goniometer at each 5% interval of the stride cycle. The time code that was recorded both on magnetic tape and videotape allowed for synchronization of muscle activity with mechanical events.

Results

Definition of the index The proposed index for evaluating spastic locomotor disorder was based on the characteristic of phasic similarity in normal E M G profiles (Fung and Barbeau 1987b). It can be seen, from the between-subject ensemble averages in Fig. 2, that a relative active and silent phase of E M G activity is present in normal gait. Therefore, equal windows (totalling 50% each) of relative ' o n ' and 'off' muscular activity could be determined for each of the 4 lower limb muscles. An 'off' window of 50% gait cycle, representing the period of relative electrical silence, was predetermined to yield a minimal

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integrated E M G area within the bin and was defined as 35-85% of the gait cycle for M H and VL; 20-70% for TA; and 70-20% for G A (2 'off' bins of 70-100% and 0-20%). The predetermined windows gave rise to 3 bins (bl, b2, b3) of on-off activity for each muscle. Integrated area under the profile (al, a2, a3) could be calculated for each corresponding bin. The proposed Spastic Locomotor Disorder Index, L was defined as the ratio of the integrated E M G area in the 'off' bin(s) to that in the ' o n ' bin(s), i.e., 1 = a 2 / ( a l + a3) for M H , VL, and TA, and I = (al + a 3 ) / a 2 for GA. 1 represents the degree of abnormal activation of locomotor muscles f r o m their normally relaxed state in a defined phase of the gait cycle, as compared to the total recruitment in the active phase. Theoretically, when a muscle is activated only during the 'on' bin and relaxes during the 'off' bin, I tends to be minimal in value (approaching

EMG PROFILE INDEX TO QUANTIFY SPASTIC LOCOMOTORDISORDER 0). Any pathology in the neuromuscular skeletal system that would produce a shift in phase or increased muscular excitation throughofit the gait cycle, such as that produced by abnormal stretch reflexes or clonus, will augment the I value. The index would also indicate the state of tonus in the muscle. A high level of tonic muscular activity, such as that manifested as coactivation in spastic gait, would result in a diminished silent period during the gait cycle, thereby highly inflating the I.

Sensitivity of the index to spasticity The index, I, was calculated for each muscle in each of the 5 normal and 8 spastic paretic subjects. The I values are contrasted and summarized in Table II. It can be seen that the 1 values obtained in the normals were consistently low and subjected to only small variation, taking into account the small number of subjects (n = 5). In contrast, the 1 values measured in the spastic group were remarkably elevated and much more heterogeneous. Since the range of 1 in spastic muscles fell completely outside that of the normal, TABLE II LocomotorSpastieity Index values of individual subjects, with mean and standard deviations displayed for each of the lower extremity muscles: MH, VL, TA, and GA.

Normal

Subject

Lowerextremity muscles MH VL TA

GA

N1 N2 N3 N4 N5

0.13 0.13 0.12 0.13 0.19

0.15 0.24 0.22 0.20 0.15

0.21 0.23 0.12 0.19 0.24

0.11 0.15 0.08 0.09 0.16

0.14 0.03

0.19 0.04

0.20 0.05

0.12 0.04

MP RP MB RM

0.31 0.30 0.38 0.81

0.36 0.41 0.58 1.52

0.90 1.04 0.74 0.35

0.41 0.53 0.85 0.22

RL BM SH SQ

0.60 0.34 0.34 1.37

0.84 0.93 0.51 2.14

0.62 2.29 1.21 1.71

0.23 1.01 1.48 0.90

0.56 0.38

0.91 0.62

1.10 0.63

0.71 0.43

Mean S.D. Spastic

Mean S.D.

237

the need of statistical tests to show that the group means were significantly different in all 4 muscles was precluded. The spastic group of subjects could be divided into 2 subgroups (spastic I and II) in terms of the maximal comfortable treadmill speed at which they could manage. It could be inferred that patients in subgroup II were functionally more impaired than those in subgroup I. Patients MP, RP, MB and R M belonged to the 'spastic I' group as they could walk at a speed higher than the minimal treadmill speed of 0.26 m/sec. Patients BM, RL, SH and SQ were included in 'spastic II' since they could only walk at the minimal speed, with the latter two requiring 40% BWS. The superimposed plots of within-subject ensemble average in each subgroup, together with the range of I values, are displayed in Fig. 3. The small values of I in the normal group can be explained by the presence of minimal E M G activity in the relatively silent phase of the gait cycle among all 5 normal subjects. Fig. 3 illustrates a clear trend of increase in E M G activity in the predetermined 'off' bin of the gait cycle across the 3 groups of subjects, from normal to spastic I to spastic II, in all the muscles examined. The less affected group of spasti c I subjects were characterized by profiles of prolonged muscle activation (as in the proximal muscles M H and VL) and early stretch activation (as in the distal muscles TA and GA), hence extending the muscle activity from the normally ' o n ' bin into the 'off' bin of the gait cycle. The more affected group of spastic II subjects had, in addition, marked clonus and elevated tonic activation (as depicted especially in TA and GA), which led to a loss of the normal activation in the ' o n ' bin and resulted in a phase shift into the 'off' bin, thereby markedly elevating the upper limit of the range of ! values in all the muscles examined. Given the small number of subjects in each group, there was a trend of increase in 1 from normal to spastic I to spastic II, despite a small degree of overlap in the range of values in the 2 spastic subgroups (Fig. 3).

Sensitivity of the index to therapeutic intervention The sensitivity of the index was also examined in one severely spastic chronic SCI subject, SQ,

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EMG PROFILE INDEX TO QUANTIFY SPASTIC LOCOMOTOR DISORDER who demonstrated a remarkable decrease in spastic locomotor dysfunction as a result of pharmacological intervention. The medication investigated was cyproheptadine, a serotonergic antagonist. The effects of cyproheptadine were first reported in chronic spinal rats (Brdard et al. 1979) and chronic spinal cats (Rossignol et al. 1986), which included a decrease in spastic features such as spasms and clonus. Its action w a s proposed to be mediated through blockage of 5-HT receptors below the transection site, leading to a decrease in neuronal hyperexcitability. Hence the use of cyproheptadine was extended to humans as an antispasmodic medication (Barbeau et al. 1982). The subject, SQ, was initially functionally non-ambulatory and wheelchair-bound due to severe spasms and clonus. He had reached a plateau in his rehabilitation 1 year after his spinal cord injury and was stabilized on other antispastic medication before participating in this study. In the premedication trial, he could only manage to step on the treadmill at a minimal speed when 40% BWS was provided by the weight-supporting harness. Following administration of cyproheptadine, a serotonergic antagonist, there was, objectively, an improvement in functional outcome and, subjectively, a self-perceived reduction in spasticity. The case has been described earlier in a preliminary report by Wainberg et al. (1986). After a further 7 month administration of cyproheptadine, the patient became functionally ambulatory with crutches and a Klenzac brace on the left lower limb. He was able to walk full weight beating on the treadmill with mild assistance to the left lower limb and independent on the right. A marked decrease in flexor spasms and clonus resulted, leading to a significant decrease in mean swing duration (from 1.66 _+ 0.16 see to 1.38 _+ 0.21 see). The pictures of critical gait events at initial foot-floor contact, midstance, toe-off, midswing, and subsequent foot-floor contact in Fig. 4A demonstrated a smoother gait pattern with trunk alignment approaching neutral, and hip extension occurring at midstance and toe-off, post-medication at the same treadmill speed (0.26 m / s e e ) and BWS level (40%). With cyproheptadine, heelstrike appeared at initial contact with proper ankle dorsiflexion occurring after midstance. The foot drag disap-

239

peared with decreased plant~flexion resulting in proper foot clearance during swing. The corresponding trunk, hip, knee, and ankle angular displacement profiles (Fig. 4B) also approximated that of a normal subject (N1). Moreover, the above findings were related to a better phasing pattern in all 4 lower limb muscles studied, as slfown in the pre- and post-medication E M G ensemble averages in Fig. 5. Before medication, the abnormal burst of activity in the 'off" bin of the flexor muscles, M H and TA, that predominated due to flexor spasms, was markedly reduced after medication and replaced by a functional burst in the 'on' bin. This change corresponded with the marked decrease in the maximum hip and knee swing angle (Fig. 4B, hip: 58-33 °, knee: 90-62°). There was also a marked coactivation in the extensor muscles, VL and GA, due to frequent flexor spasms in early swing (at approximately 70% of the gait cycle) before medication, causing a shift of activity into the predetermined 'off' bin. Remarkable changes were demonstrated with medication. The prolonged activation profile of the VL muscle from midstance to midswing before medication was reduced after medication with an earlier recruitment in stance, and much less activity present in late stance to midswing (the predetermined 'off' bin of 35-85% of the cycle). Although early stretch activation of the GA was still evident post medication, the predominantly clonic discharge pattern, leading to a diminished push-off, was substituted by a more functional profile, with decreased clonus and increased activity for push-off in the 'on' bin. This was also reflected by the ankle kinematic changes as shown in Fig. 4B. These observed changes were depicted by the index values showing a marked reduction post medication (MH: 1.37-0.82; VL: 2.14-0.66; TA: 1.71-0.41; GA: 0.90-0.71). A full report on the effects of cyproheptadine on spasticity and spastic paretic gait in all the patients studied is to be further documented.

Discussion

In light of the preliminary findings of the present study, the proposed E M G profile index serves

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as a n o b j e c t i v e m e a s u r e o f d i s o r d e r e d m u s c l e a c t i v a t i o n in s p a s t i c p a r e t i c gait. T h e i n d e x , / , d e f i n e d as t h e r a t i o o f i n t e g r a t e d E M O a c t i v i t y in t h e ' o f f ' b i n o f t h e n o r m a l i z e d g a i t c y c l e to t h a t in t h e ' o n ' bin, is p o t e n t i a l l y p o w e r f u l in d e t e c t i n g the distinction between normal and spastic muscle

function during walking. I was observed to be homogeneously low in normal lower limb muscles a n d h i g h l y e l e v a t e d in the spastics. M o r e o v e r , there was a trend of increase in I values with the d e g r e e o f i m p a i r m e n t in l o c o m o t i o n , as i n d i c a t e d by the walking speed attained and the level of

Fig. 4. The effect of cyproheptadine on spastic paraparetic gait as illustrated by: (A) critical gait events of one representative gait cycle of subject SQ walking on the treadmill before and after cyproheptadine administration; (B) a comparison of the pre- and post-cyproheptadine kinematics of subject SQ with that of a normal subject (N1). N.B. The trunk and hip angles were calculated with respect to the vertical line, with the neutral position in standing being taken as 0 o displacement of the trunk and hip, flexion being positive, and extension negative. Likewise, in calculating the knee and ankle angles, the neutral standing position, with the knee at full extension, and the shank axis perpendicular to the foot, was taken as 0 o. Knee flexion and ankle dorsiflexion beyond neutral were taken as positive angular displacements, and ankle plantar flexion beyond neutral was taken as negative angular displacement.

242 body weight support required. This may reflect to a certain extent the severity of spasticity encountered, as sustained ankle clonus during walking could be elicited from all except one (RL) of the spastic group II subjects and none of the group I subjects. It was also shown, in one subject, SQ, that the index was sensitive to therapeutic intervention using an antispasmodic medication. The change in spasticity was reflected in gait outcomes such as joint kinematics and temporal distance parameters. However, caution must be exercised in relating locomotor impairment directly to spasticity as this is not the sole cause of gait disturbance. Muscle paralysis is a major confounding factor that also leads to impaired locomotion in terms of difficulty in coping with walking speed and weight bearing. The fact that paresis is often present and associated with spasticity may introduce a confounding source of variance to the muscle profiles. Hence in this study, all muscle profiles were inspected, and the mean and peak amplitude of the individual muscle burst were recorded before normalizing to the mean ensemble peak, in order to ensure that no paralysed muscle entered the analysis. It could also be argued that cerebellar or Parkinson patients may exhibit an elevated index due to gait deficits. The specificity of this index has yet to be verified. The present findings are comparable to that of Benecke et al. (1983) as an attempt to quantify spastic muscle activation disorder in a functional and dynamic task. Their quotient measured in bicycling and our index assessed in walking were both based on the phasic similarity of E M G patterns observed in a rhythmic and stereotyped voluntary movement. The normal period of relatively silent E M G activity observed in either form of motion was d i ~ s h e d and substituted by prolonged muscle activation in spastic paretic subjects. The postural influence and kinesthetic input from loading the limbs, as well as interlimb coordination in terms of timing of single limb and double limb support, are also different in the two forms of motions. Moreover, in the case of asymmetry, the more impaired extremity can readily be compensated by the less affected one in bicycfing, The extent of passive movement involved in bicycle pedalling is also greater than treadmill walk-

J. FUNG, H. BARBEAU ing. Ericson et al. (1985) have shown that quadriceps activation is much higher in cycling, whereas tibialis anterior is much more activated in walking when ergometer cycling is compared to level ground walking. The distinction of neuronal mechanisms and circuitry underlying the spasticity between bicycling and walking remains to be investigated. The original idea of assessing spasticity m bicycling (Benecke et al. 1983), in preference to gait. was to include patients who were unable to walk as a result of postural decompensation, and to avoid the non-specific 'protective gait mechanisms.' It is noteworthy that the mechanical body weight support system incorporated in the present study has a definite advantage over conventional gait analysis systems in allowing the severely spastic and non-functional walkers to be evaluated. In such cases manual assistance could be given to advance the limbs on the treadmill, in addition to decreasing the weight borne through the lower limbs. Moreover. it has been shown, in normal subjects, that body weight support did not alter the gait pattern in terms of E M G onset-offset (Finch and Barbeau 1985). In a subsequent study, Conrad et al. (1985) proposed a measure of spasticity in gait, expressed in the gastrocnemius muscle, as a ratio of the integrated E M G activity in the first half of stance phase to that in the second half. Such a measure, though capable of depicting defective recruitment and early stretch activation, could be lacking in sensitivity and validity by not taking into account the E M G activity in the swing phase of the gait cycle. It has been shown in various studies that during walking there is a phase-dependent modulation of the H-reflex in the h u m a n gastrocnemius (Garrett et al. 1984) and soleus muscle (Capaday and Stein 1986; Crenna and Frigo 1987). The predetermined 'silent' phase of normal gastrocnemius activity in the present study, spanning the last 30% (swing) of the gait cycle to the first 20% (early stance), coincided well with the phase of H-reflex depression in the afore-mentioned studies. The triceps surae myotatic reflex arc is possibly gated by presynaptic inhibition of Ia terminals as well as reciprocal Ia inhibition due to supraspinal facihtation of Renshaw cells (PierrotDeseilligny and Mazirres 1985). Hence the pres-

EMG PROFILE INDEX TO QUANTIFY SPASTIC LOCOMOTORDISORDER ence of abnormal activity in the predetermined ' o f f bin of the gait cycle in spastic subjects might be due to an ungating of Ia discharge possibly caused by decreased efficacy of presynaptic inhibition and decreased reciprocal inhibition of antagonistic muscles during voluntary movement. The gating of the stretch reflex of the human quadriceps muscles during overground walking (Garrett and Luckwill 1983) also corresponded to the predetermined 'off' bin of vastus lateralis E M G activity in the present study. Likewise the polysynaptic cutaneous reflex response in the VL muscle, evoked by noxious sural nerve stimulation during walking, was found to be strongly phase dependent (Crenna and Frigo 1984). The response was maximal when stimuli were applied toward the end of swing and in the first half of stance and, hence, appeared to be gated from midstance to toe-off. Therefore, the presence of E M G activity in the predetermined 'off' bin in a spastic SCI subject could be related to defective gating mechanisms in the spinal reflexes involved in the circuitry of locomotion. Although the existence of a normal E M G profile was questioned by Arsenault et al. (1986), a tight coupling between E M G bursts and normalized stride events was evident to suggest the possibility of preprogramming (Yang and Winter 1985). However, the control of walking speed or cadence could give rise to between-subject variation in E M G profiles. Shiavi et al. (1981) have demonstrated that the normal E M G pattern, for a range of self-selected speeds of very slow, slow, fast, and free walking, exhibited much between-subject variability, and they attributed the population difference in E M G patterns to difference in coping strategies with speed variation. A spasticity-like overlapping in timing of ankle dorsiflexors and plantar flexors was also noted in some subjects during fast speed walking. Nevertheless, Yang and Winter (1985) have reported no significant difference in the shape of the E M G ensemble profiles with mean cadence changes from 74.2 to 115 steps/rain, although there was a significant increase in mean E M G amplitude in stance and in swing. The validity of comparing pathological E M G profiles to normal profiles at each individual's free natural walking speed may seem ques-

243

tionable, as it is difficult to dissociate the effect of spasticity on E M G profiles from that caused by an alteration in walking speed. Nonetheless, when we imposed, on one normal subject, a decrease in walking speed to a level of 0.26 m / s e c , the only significant change observed was E M G amplitude. The VL burst became completely abolished, but there was no alteration in profiles or phasing that would necessitate any change in the window parameters in calculating the index. The effects of speed and temporal distance changes could not be elucidated in the present preliminary study, which is also limited by the small number of subjects in each group. The predetermined windows of on-off activities could further be verified in a larger population of normal subjects walking at their free comfortable speed and a control level comparable to that of the spastics. This preliminary study paves the way for a future full scale study to validate the use of the index in quantifying spastic motor disorder in gait. The potential application is broad, in that the index can become a great adjunct for purposes of classification, evaluation, and assessment of functional implications of various therapeutic interventions on spastic motor dysfunction. The authors appreciate the original work and essential contributions of Lois Finch and Michael Wainberg. The expertise of Dr. Patricia McKinley, in reviewing and proofreading the manuscript, is also gratefully acknowledged. J. Fung is a Croucher Foundation Scholar. H. Barbeau is a Medical Research Scholar from the FRSQ.

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