New Rehabilitation Strategies for the Treatment of Spastic Gait Disorders

ADAFTABILlTY OF HUMAN GAIT / A.E. Patla (Editor) 0 Elsevier Science Publishers B.V. (North-Holland), 1991

3 87

NEW REHABILITATION STRATEGIES FOR THE TREATMENT OF SPASTIC GAIT DISORDERS

Carol L. RICHAFtDS", Francine MALOUIN', Francine DUMAS1, and Sharon WOOD-DAUPHINEE2 'PhysiotherapyDepament, Faculty of Medicine,Laval University, Quebec City and 2Schoolof Physical and Occupational Therapy, McGill University, Montreal

ABSTRACT Advances in basic neurobiology and motor learning theory in the past 10 years have revealed key factors for the optimization of sensorimotor recovery. This chapter argues that principles of treatment derived from these studies should be incorporated into the development of new rehabilitation strategies for the treatment of spastic gait disorders. These therapy principles include: early intervention, task specificity in the choice of exercises, exercising at an optimal intensity level, the use of weight support as an integral part of the gait training and ensuring that the therapy strategy motivates the patient. The next step in the development of new therapy strategies is the testing of their impact on selected groups of patients using appropriate clinical research methodology. This chapter thus also briefly addresses some issues related to the planning and execution of clinical trials, including the choice of outcome measures and the confounding effect of natural sensorimotor recovery. This theoretical framework has been applied to clinical studies designed to evaluate the effects of new therapy strategies. In the first section, the methodological aspects of a pilot randomized clinical trial designed to evaluate the effects of three physical therapy treatment strategies on qualitative and quantitative parameters of gait outcome are described. Individual results in six hemiplegic patients are used to illustrate points related to the interpretation of the results. The second section describes the effects of two therapy strategies directed at improving the motor control of the ankle in children with spastic cerebral palsy. The first is the use of prolonged muscle stretch imposed

'Address correspondence to: Carol L. Richards, Physiotherapy Department, Faculty of Medicine, Laval University, Quebec City, P. Que., G1K 7P4,Canada

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by an ankle foot orthosis and the use of a walker to reduce the need for weight support and equilibrium control. This chapter concludes with a note of caution for the interpretation of the promising results presented. Before such findings can be generalized to other patients, they must be confirmed in studies that include control groups with randomly assigned patients. Such studies are presently underway. INTRODUCTION Rehabilitation treatment strategies for gait disorders of neurological origin have not evolved as fast as knowledge in the basic neurological and behavioral sciences over the past 40 years. In fact, treatment strategies used today remain largely based on empirical treatment approaches outlined by expert clinicians about 30 years ago. For example, the neurodevelopmental Bobath (1970) approach combines the control of postural and hypertonic responses while encouraging appropriate voluntary movements. This approach was inspired by the work of Magnus (1926) and Sherrington (1947) on reflexes and postural responses in cats. Other widely used therapies include the proprioceptive and neuromuscular facilitation (Knott & Voss, 1968) and Brunnstrom (1970) methods which use normal and abnormal reflex responses to encouragevoluntary movement. All of the above-mentioned treatment approaches have been reported to give immediate beneficial effects, especially in the hands of a skilled practitioner. What remains unknown, however, is whether these therapies can induce motor improvement on a long-term basis that is superior to that obtained by spontaneous motor recovery or non-skilled home therapy. This question is not easy to answer both because of ethical issues which preclude scientifically rigorous trials with a non-treatment group, and the heterogenous nature of brain lesions which produce spastic gait disorders in hemiplegia or cerebral palsy (CP).

Over the past decade, research on motor recovery after experimental lesions in animals (Black et al., 1975; Goldberger et al., 1978; Finger & ALmli, 1985), development of sensorimotor skills in normal human infants (Zelaso et al., 1972; Thelen et al., 1986; 1989;) and the acquisition of cognitive and motor skills (Schmidt, 1982; Carr & Shepherd, 1987; Gentile et al., 1987) has elucidated key principles for the development of new treatment strategies for spastic gait disorders. The first principle is early intervention. Spinalized cats receiving delayed locomotor training never achieve the same quality of recovery as cats with more precocious therapy (Barbeau & Rossignol, 1987; Lovely et al., 1986).

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For the treatment of adult hemiplegics or children with CP, "early" remains to be defined. A second principle is task specificity. Maximal improvement is gained in the task that is practised. By inference this means that therapeutic strategies for alleviating gait disorders should include exercises preparatory to walking as well as specific walking exercises. Optimal intensity is a third principle. This is well understood for cardiovascular training but is relatively unknown for locomotor training. Is 30 minutes a day sufficient or is a minimum of 60 minutes required for a training effect? A fourth principle is weight support. Thelen et al (1989) have shown that a more mature walking pattern emerges when very young infants are supported and Visintin and Barbeau (1989) have demonstrated that partially supporting the weight of paraparetic patients walking on a treadmill permits the expression of a more normal muscle activation pattern. These findings are in agreement with the concept of "protective reactions" which may interfere with the expression of a more normal underlying gait pattern (Conrad & Benecke, 1983). From these studies, it stands to reason that progressive weight support should be included in therapy strategies. A fifth principle that should not be overlooked is the motivational character of the treatment strategy which will involve weeks and months of repetitious work by the patient (Carr & Shepherd 1987; Gentile et al., 1987). Before adequate studies of the effects of therapy can be carried out, two questions must be addressed. First, the natural course of recovery following stroke and secondly, the choice of outcome measures to represent sensorimotor recovery. A major problem encountered when trying to measure impact of therapy is the confounding effect of spontaneous, post stroke, sensorimotor recovery over time. Recovery is largely complete by three months (Twitchell, 1951) and reaches a plateau at about six months (Katz et al., 1966; Brocklehurst et al., 1978), although signs of recovery have been documented up to 5 years post stroke (Bach-y-Rita, 1980). These recovery profiles, derived from clinical evaluations, have usually not been correlated with pathophysiological changes which might explain the improvement. For example, BogArdh and Richards (1974) were able to relate the new-found ability to control stance phase knee hyperextension following gait therapy to an acquired burst of quadriceps activation, but little information of this nature is available. Further studies are required to better understand how the biomechanical variables obtained in sophisticated gait analyses (eg. EMG, movements, muscle moments, forces) signal recovery. It is thus not surprising that the choice of outcome measures remains a problem when evaluating therapy efficacy on gait. Functional clinical tests such as the Barthel (Mahoney & Barthel, 1965) and Fugl-Meyer (Fugl-Meyer et al., 1975; Kusoffsky et al., 1982) assessments, which have been validated for stroke patients, include locomotion components, but do not

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specifically measure changes in gait movements or muscle activations. These can only be studied by measures of sophisticated laboratory evaluations. Further, because accepted and potentially beneficial therapy cannot be withheld, the natural course of recovery is unknown. Consequently, when evaluating impact, carefully conceived control groups are essential and factors such as time post-stroke, and type, intensity and duration of therapy must be considered in addition to the cerebral lesion. The purpose of this paper is to report preliminary results from ongoing studies designed to evaluate new physiotherapy treatment strategies for adult hemiplegics and children with spastic cerebral palsy (CP). These studies represent efforts to apply the principles mentioned above and in addition, to evaluate outcome by both qualitative clinical scales and quantitative laboratory methods in an attempt to identify the EMG and movement correlates of locomotor recovery. TREATMENT STRATEGIES FOR ADULT HEMIPARETIC GAIT The development of new strategies for the treatment of spastic hemiparetic gait has been immensely hampered by the heterogeneity of the pathophysiological disorder (Knutsson & Richards, 1979). For example, some hemiparetic patients can be expected to improve with antispastic medication (Knutsson et al., 1973; 1976) while others in whom paresis is the dominant syndrome, will not be helped and may even deteriorate. These findings emphasize the need to fully understand the dominant component of the motor disorder of each patient prior to selecting an appropriate therapy (Bogkdh & Richards, 1974; Knutsson & Richards, 1979). Surprisingly, the issue of chronicity is not often raised when evaluating therapeutic effects, although some controversy has arisen when "acute" hemiplegics (less than 3 months post-stroke) have been included with "chronic" patients (Basmajian et al., 1975). In general, physical therapy is seen to be benign and necessary at any stage of stroke (Quin, 1971;Dickenstein et al., 1986; Lord et al., 1986), although guidelines for precocity of intervention and its intensity are unclear (Truscott et al., 1974; Feigenson et al., 1977; Smith et al., 1982; Novak et al., 1984; Henley et al., 1985; Dombovy et al., 1986; Hayes & Carrol, 1986). Many types of physical therapy have been advocated for the treatment of hemiparetic gait disorders, some more specific to the walking problem and others as part of a more global approach. The traditional physical therapy approach usually involves a form of sensorimotor facilitation (Knott & Voss, 1968,Bobath, 1970; Brunnstrom, 1970) practised alone or in combination

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with functional electrical stimulation or biofeedback (Liberson, 1%1;Basmajian et al., 1975; Cozean et al., 1988). These approaches appear to enhance functional recovery, despite the lack of emphasis on early and intensive therapy. It should be mentioned, however, that none of these therapies have been compared to natural recovery without professional intervention, most likely because of ethical issues (Wood-Dauphinee, 1985). Much work on motor learning theory in the last 10 years has pointed to the need for task-specific training (for a review see Carr & Sheperd, 1987) to promote motor recovery. Additionally, it is known that such training must be sufficiently intense and motivational (Bach-y-Rita, 1980; Schmidt, 1982). These findings as well as new information concerning the heightened potential for plasticity soon after a lesion (Black et al., 1975; Barbeau & Rossignol, 1987), led us to propose a gait therapy for stroke patients. This approach combines the principles of early (initiation 1week post-stroke) and intensive @/day for a total of 2 hours as soon as tolerated) with task specificity. The patient is encouraged to stand with the assistance of a tilt-table and the use of biofeedback (limb load monitor) to gauge weight bearing on the affected side early in the post-stroke period. Reciprocal and resisted leg exercises with speed control are started with progressive weight-bearing using the Kinetron system. As soon as possible, with the help of airsplints if necessary to stabilize the leg while weight-bearing, the patient is encouraged to stand and to walk in parallel bars. Treadmill walking while wearing a specially designed suspended harness for safety is initiated as soon as possible at a low treadmill speed which is gradually increased as the patient improves. The difficulty of locomotor-directed tasks are progressively increased over a 5 week period (about the maximum length of stay for a hemiparetic patient in an acute care hospital), without forgetting to give conventional care to the accompanying upper extremity disorder. The following section presents preliminary results of an ongoing study to evaluate the effects of this new therapy on qualitative and quantitative measures of gait outcome in stroke patients. EVALUATION OF EARLY AND INTENSIVE GAIT-SPECIFIC PHYSICAL THERAPY IN STROKE PATIENTS Using a randomized control trial (RCT) design, the effects of early versus later therapy initiation as well as the type of therapy are being evaluated in three groups of patients with similar lesions of the middle cerebral artery confirmed by CAT scan. All stroke patients admitted to l'H6pital de l'Enfant-JCsus are screened and if judged to fulfill specific inclusion criteria are requested to sign an informed consent prior to being recruited into the study. Within one week

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post-stroke the patient's functional capacity is assessed by an independent trained evaluator using the Barthel (Mahoney & Barthel, 1965) and Fugl-Meyer (1975) tests. The Barthel scores are then used to stratify the patients into good (= >20) and poor (cu)) prognostic strata prior to their random assignation to three therapy groups for 5 weeks: 1. early (initiated 1week post stroke) and intensive (2 hours/day as soon as tolerated) task-specific gait training (briefly described above), 2. early and intensive traditional therapy which does not concentrate on gait and 3. conventional physical therapy as practised in the hospital (initiated later, traditional in approach and not as intensive since it usually includes only 1 therapy session per day). At 6 weeks, and 3 and 6 months post-Stroke functional (qualitative) evaluations using the Barthel, Fugl-Meyer and' Berg Balance (Berg et al., 1989) tests were carried out by an independent evaluator and laboratory gait analyses (movements and muscle activations) were made. Because this trial has just been completed, group results are not available. Preliminary results in selected patients chosen on the basis of the Barthel scores obtained 5-7 days post-stroke are given in Table I and Figures 1-4. The results of these patients were chosen to illustrate the interplay of factors which affect outcome: heterogeneity of the gait disorder despite a similar lesion site, relationship of early prognostic strata, early vs late therapy initiation, therapy choice and intensity. In addition, for the first time, scores on tests of functional performance will be correlated to parameters derived from the results of the gait analyses. The figures give the results of a group of patients in the good prognostic strata (Figures 1 and 2) and a second group in the poor prognostic strata (Figures 3 and 4). Each patient in a given group received a different therapy, the most intensive and task-specific represented on the left and the later, less intensive, conventional therapy on the right of the figures. The most obvious finding is the relationship of gait capacity at 6 weeks and 3 months post-stroke to the Barthel scores at 1week post-stroke. Indeed, all the patients in the good prognostic group (Figs. 1 and 2) were able to walk at 6 weeks post stroke; 2 with minimal assistance (light touch for assurance) and patient 3 with much support. In contrast, the patients in the poor prognostic group (Figs. 3 and 4) required maximal assistance to remain upright and in some cases even to guide the foot placements. In the poor prognostic group there was little change in the walkiig capacity at 3 months post-stroke and it still was not possible to make an electrogoniometric record of the gait movements (Fig. 4). The spatiotemporal gait characteristics in Table I confirm the extremely low walking capacity of the poor prognostic group as well as the small improvement, if any, with time.

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TABLE 1: Spatiotemporal gait characteristics of 6 hemiplegic patients 6 weeks and 3 months post-stroke Group Patient

Cycle Duration

Stride Length (m)

Stance

Cadence

(%)

(steps/min)

2.1 (0.1) 1.8

0.73

69

57

1.00

66

65

2.7 (0.2) 1.4 (0.5) 2.0 (0.2) 1.4 (0.7)

0.46

85

45

0.81

67

87

0.38

86

61

0.82

74

89

3.6 (0.8) 3.9 (0.4) 4.7 (0.2) 4.9 (0.8) NA 3.5 (0.5)

NA

87

33

0.49

81

31

NA

89

25

NA

84

24

NA 0.49

NA 77

NA 34

(4

la b

2a

A

b 3a

b la

b B

2a b 3a

(0.7)

Values give mean of 3-10 gait cycles (see Figs. 1 and 4); duration. A: B:

a

=

NA

+. 1 SD for

cycle

Good prognostic group with initial Barthel score = > 20; Poor prognostic group with initial Barthel score c 20 evaluations at 6 weeks post-stroke; b = evaluations 3 months post-stroke not available because unable to walk.

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GAITCYCLE ( % I Figure 1: Comparison of movement (derived from electrogoniometric records) and muscle activation profiles (rectified, time averaged surface EMGs) during free gait in 3 hemiplegic patients in the good prognostic group (patients 1, 2 and 3) taken 6 weeks and 3 months post stroke with normal mean values (mean age=58, n=10). Patient 1,a 60-yrold man received early and intensive

task specific gait therapy, patient 2, a 85-yr old woman, early and intensive conventional therapy while patient 3, a 69 yr-old man, conventional therapy for 5 weeks. Values represent mean of 9 or 10 gait cycles for patients and 100 gait cycles for normals. End of stance indicated by a star for normal subjects and k o w s (short=6 weeks, long=3 months) for patients.

Spastic Gait Disorders FUGL --

395

SENSATION

B

0

C

LOWER EXTREMIW

1

2

3

66

2

3

UPPER EXTREMITY

0

1

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loo

1

D

2

3

BARTHEL

F

0 1

2

3

SUBJECTS

Figure 2: Comparison of scores obtained in functional evaluations before therapy (5-7 days) and 6 weeks and 3 months post-therapy for the same 3 hemiplegic patients represented in figure 1.

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C. L. Richards et al. FUGL-MEYER EVALUATION A

SENSATION

BALANCE 6WEEKS

JMONTHS

LOWER EXTREMITY

C

1

2

UPPER EXTREMITY

D

3

1

2

3

1

2

3

SUBJECTS

100

E

1

2

3

F

0

SUBJECTS

Figure 3: Comparison of the scores obtained in the functional evaluations before therapy (5-7 days) and 6 weeks and 3 months post-therapy of 3 hemiplegic patients placed in the poor prognostic group. Patient 1, a 73 yr-old man, received early and intensive task specific gait therapy, patient 2, a 70 yr-old woman, early and intensive conventional therapy and patient 3, a 71 yr-old man, conventional therapy for 5 weeks.

Spastic Gait Disorders

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300i H A M S 1

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397

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GAITCYCLE ( % ) Figure 4: Comparison of the muscle activation profiles (rectified, time-averaged surface EMGs) during gait of the same 3 hemiplegic patients represented in figure 3 with normal values. Mean activation profiles in patients derived from 3-4 gait cycles. End of stance indicated by star for normal subjects and arrows (short=6 weeks, long=3 months) for patients.

A second obvious finding was that most of the recovery occurred in the first 6 weeks post-stroke in both groups of patients, regardless of their therapy. This 6 week window is thus a critical time for change and it emphasizes the need to guide this recovery with an appropriate therapy. As expected, there was a good correlation between increases in the functional test scores (Figs. 2 and 3) over time and the EMG and movement correlates (Figs. 1and 4) of this recovery. As

with the gait analyses results, the greatest change in functional scores occurred in the first 6 weeks. In the poor prognostic group the Barthel and sensation scores tended to improve at 3 months but balance capacity remained about the same (Fig. 3), while in the good prognostic group (Fig. 2), the general trend was for a further step toward recovery for all the items except sensation at 3 months. Given the remarkable difference in sensation between the groups (Figs. 2 and 3), its role in recovery may be underestimated.

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These comparisons also provide some preliminary insight into the effects of the different therapies. These findings suggest that the differences in performance of the patients in the good prognostic group are therapy related; keeping in mind that many other factors such as age and severity of initial insult affect outcome (Wood-Dauphinee, 1985;Lindmark, 1988). Similarly because the type of therapy for patients 2 and 3 is the same, differences in performance between these patients hint at the effect if any of precocity and intensity of therapy. When comparing the 6 week and 3 month evaluations in the good prognostic group (Fig. l), it appears that the recovery in the muscle activation and movement profiles of patient 1 (Fig. 1, A-F) is largely complete at 6 weeks, while in patients 2 (Fig. 1,G-L)and 3 (Fig. 1,M-R) the recovery process results in a remodelling of the activation profiles (Fig. 1, I, J, L, 0, P and R) between 6 weeks and 3 months. At 3 months post stroke, patient 1 (Fig. 1, A-F) has improved even more and his knee and ankle movements are much closer to normal than the other 2 patients. The distal recovery of this patient is remarkable at 6 weeks and is related to low but well-timed activations of the TS and TA. Patient 2 (Fig. 1, G-L)also attains good distal recovery, but not until 3 months. It is interesting to note that the functional scores (Fig. 2) also show the apparent earlier recovery of patient 1who was in the early and intensive gait specific therapy group. In the poor prognostic group (Figs.3 and 4) the low Barthel scores (Fig. 3, F) are correlated with low scores on the Fugl-Meyer test items (Fig. 3, A-D) at the first evaluation. Note in particular the deficits in sensation and in the upper extremity (Fig. 3B and D). Improvement in scores for sensation during the follow-up period may be related not only to recovery but also to better comprehension and cooperation of patients at these assessments. In general, the 3 month functional scores in this group of patients did not attain the initial scores of the good prognostic group. Again, most of the recovery had occurred by 6 weeks, except for sensation (Fig. 3B). Of particular interest to the prediction of gait capacity are the Fugl-Meyer balance and lower extremity item scores (Fig. 3A and C) and the Berg balance score (Fig. 3E).

As explained above, movement profiles are absent in Figure 4 because the poor gait capacity of these patients made it impractical to attempt to make movement records of independent gait with the electrogoniometer system. At 6 weeks it was possible to record muscle activations during gait with much-manual-supportfor patients 1and 2 but not for patient 3. For the 3 month evaluations, all 3 patients could walk with similar manual support, The most obvious finding is the very low amplitude of activations in the distal muscles (Fig. 4, C,D, G, H, K and L). In patient 1, at 6 weeks the Quad, Hamst, and TS are coactivated in mid-stance

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phase and there is little change at 3 months. Recovery in patient 2 (Fig. 4, E-H) appears to regress at 3 months. Finally, patient 3 who could only be evaluated at 3 months, had an activation burst in the Quad, Hamst and TS as the lower extremity collapsed, activations suggestive of activation initiated by stretch reflexes in the lengthening muscles during hip, knee and ankle flexion (Knutsson & Richards, 1979). Comparison of the performance of these 3 severely involved patients (Figs.3 and 4) demonstrates little difference. Obviously in patients with such severe deficits, information on more subjects is required before conclusions are drawn about the slight difference apparent in Fig. 4. The movement and activation profiles illustrated in Figure 1 also raise many questions: What is the significance of the amplitude differences of the activation profiles? Is the marked Quad and Hamst activation of patient 1 (Fig. 1, C and D) induced by the early treadmill gait training? Is the excessive late stance Hamst activation (Fig. 1,D and P) related to the prolonged Quad activation? Is there a proximal to distal gradient in the recovery process? Can early and intensive therapy alter the recovery process post stroke so that muscle activations during gait characterized by excessive muscle coactivations or very Iow muscle activations (Knutsson & Richards, 1979) are suppressed? Analysis of the group results of the pilot trial should provide clues to some of these questions. The results summarized in figures 1-4 clearly show that lesions of the same artery can result in quite different functional deficits, making the stratification of patients on the basis of functional scores such as done in the present study essential for comparative purposes. Functional scores reflect the severity of the initial insult which in turn predicts outcome (Mahoney & Barthel, 1954; WoodDauphinee, 1985). These preliminary results show promise for the differentiation of the effects of the early and intensive specific gait therapy under investigation. On the basis of these preliminary findings, it appears that early and intensive specific gait therapy may offer the possibility of promoting earlier recovery in both proximal and distal muscles than conventional therapy. It may be that the recovery potential attained by 6 weeks does not progress further because the specialid therapy is replaced by conventional therapy on a much less intensive basis when the patients are transferred from the acute-care hospital to a setting specialized for chronic care.

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TREATMENT APPROACH OF SPASTIC GAIT DISORDERS IN CEREBRAL PALSY Spastic gait disorders in children with CP are compounded by the confounding interaction of maturation which makes the differentiation of the motor disturbance more difficult (Richards & Knutsson, 197% Knutsson, 1980) and emphasizes the need for age-matched normal controls (Richards et al., 1987). Further, in addition to problems related to documenting therapy effects by appropriate outcome measures and the use of control groups, therapy strategies must contend with the capacity of the child to follow directions and/or parental compliance to therapy. The most common physical therapy approach to spastic gait disorders in CP children is some form of neurodevelopmental therapy (Bobath, 1970)which includes a locomotion component but does not concentrate on the walking disorder. Although extensively practised, the few controlled clinical trials (Wright & Nicholson, 1973; Scherzer et al., 1976) have failed to document the benefits of this approach over others either in CP infants or those of high risk infants (Piper et al., 1986; 1988, Palmer et al., 1988). During the past decade, the use of prolonged muscle stretch in various forms has been advocated to encourage mobility or to provide stability. For example, casts (Tardieu et al., 1982; Watt et al., 1984; Bertoti, 1986) or ankle-foot-orthoses (Simon et al., 1978), have been used to stretch out hypertonic ankle plantarflexors. A recent controlled study in our laboratory has shown that a single session of prolonged TS stretching for 30 min by standing CP children on a tilt table significantly reduces spasticity (EMG and mechanical responses to passive movements) and leads to improved voluntary activation of the stretched TS (Malouin et al., 1987; Tremblay et al., 1990). During gait, however, the typically spastic early activation of the TS was not changed by such a procedure (Richards et al., 1987; Richards et al., 1990),suggesting that the inhibitive effects of a single session of PMS were not strong enough to induce change in the more complex muscle activation control systems of gait. To further investigate the potential effects of long-term PMS, an ankle foot orthosis (AFO) is being used to stretch (ankle position maintained in 5 degrees of dorsiflexion) the spastic plantarflexors while the child engages in functional activities for about 4 hours/day; 5 days/week for months. PROLONGED MUSCLE STRETCH Figure 5 compares the gait movements and muscle activationsof an age-matched normal girl with those of a 32 month old (at therapy initiation) CP (spastic hemiplegic) girl before (Fig. 5-A) and after 10 months (Fig. 5-B) of AFO-wearing. These records which illustrate changes in the TS and TA

Spastic Gait Disorders

401

h

M al

a

v

1 0 -

A N K L E

-04-

“1‘

5i w

8001

T S

I T A

T A

100

0

100

GAITCYCLE ( % ) Figure 5: Comparison of movements (derived from electrogoniometric records) and activation profiles (surface electrodes, rectified, time averaged EMG) of a 32 month-old hemiplegic child with those of a normal child also 32 months old before and after wearing an ankle-foot orthosis for 10 months. Profiles give mean of (5-10) gait cycles -C 2 SE. Cadence was 134 stepslmin in normal child and 144 stepsbin in CP child. End of stance indicated by star in normal child and arrow for CP child.

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C A D E N C E

F A S T

C A D E N C E

400

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>

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100

0

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GAITCYCLE ( % ) Figure 6: Comparison of the effects of AFO-wearingon activation profiles of the TS and TA (when the AFO is removed) at slow (123-129 stepshin) and fast ( 152-155 steps/min) cadence. Values give mean of 5 gait cycles f 2 SE obtained in a hemiplegic child 32 months old when she began to wear the AFO. Arrow indicates end of stance phase.

activation profiles over time post-AFO wearing were obtained when the child had removed the AFO in the laboratory for the gait tests. After AFO-wearing the shape and amplitude of the TS activation (rectified, time averaged) profile of the CP child have become similar to the normal values. In contrast, in the TA which was not stretched by the procedure, the activation profile remains abnormal and similar to the pre-AFO profile. These marked changes in the TS activation profiles were accompanied by more ankle plantarflexion, especiallyin late stance and swing and knee hyperextension in late stance. The knee hyperextension was an unexpected consequence of AFO-wearing since it is often prescribed to control knee hyperextension (Simon et al., 1978). This finding emphasized the need to combine the wearing of an AFO with specific gait physical therapy aimed at increasing the stance phase TA activation and controlling the knee hyperextension. General conclusions can be drawn from the results illustrated in Figs. 5 and 6. First,,the effects of the stretch imposed by the AFO on the TS as well as other unspecified effects of the AFO appear to be cumulative. A minimal time and/or

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intensity level must be reached before changes in the TS activation become evident; in this case more than 2 months. Secondly, the beneficial effect is specific to the stretched muscle (Figs. 5 and 6), is specific to a segment of the activation profile (Fig. 6 A) and is cadence dependent (Fig. 6 A and B). These findings can be explained if the oscillations in the TS profile are related to abnormally sensitive reflex activations which resemble clonic bursts (Stein et al., 1990) and are dependent on TS stretch by the gait movements (Knutsson & Richards, 1979). On the other hand, the increased amplitude of the TS and TA activation with higher cadence is expected (Yang & Winter, 1985). EFFECTS O F WEIGHT SUPPORT It has long been known to the clinician that the gait pattern of a CP child will change if support is given by holding the child’s hands or using a walker. Recent work with normal infants now suggests that weight support may play a even more important role than realized in the expression of gait muscle activations and the resulting movement patterns. While studying factors involved in the attainment of independent gait in normal infants, Thelen et al. (1989), have shown that a more mature pattern emerges when 6-8 months old infants are supported on a treadmill. They interpreted their findings in light of a reduced need for equilibrium. Similarly, when support is given to normal infants beginning to acquire independent gait, the excessive coactivation of antagonist leg muscles, characteristic of early walkers, is much reduced so that a more mature activation pattern is revealed (Okamoto & Kumamoto, 1972; Kazai et al., 1976). In children with spastic CP one would expect weight support to play an even more important role than in normal children. Figure 7 illustrates the effects of a walker support (controlled by the child) on the TS and TA activations of a 48 month-old spastic diplegic child during gait. Since the cadence was identical (118 steps/min) when walking with and without the walker, cadence was not a factor (Yang & Winter, 1985) in the decreased abnormal early stance activation peak and the improved shape and amplitude of the mid stance phase TS activation burst, nor of the swing phase increased TA activation. It appears that a walker improves this child’s equilibrium so that abnormal reflex activations are reduced and a more normal EMG pattern emerges even though the lower limb movements do not change markedly and most cycle initiations are made with foot-contact. Such findings clearly point to the importance of dissociating equilibrium and weight support requirements to train more appropriate muscle activation patterns (Conrad et al., 1983; Visintin & Barbeau, 1989). Perhaps we should look at

404

C. L. Richards et al.

500 -

h

>

400__

T S

NORMAL

El WITHOUT WALKER

-

r

W

-

WITH WALKER

300

c3

= 200 W

100

0

"""l

n

T A

500

>

5 400

"I 300 200 100

0 DDC

0

20 40 60 G A I T C Y C L E

80

(X)

100

Figure 7: Comparison of the activation profiles of the TS and TA of 48 month-old diplegic child walking with and without the support of a walker with those of a normal child (age= 32 months). Values give mean of 5 gait cycles 2 2 SE. Cadence was 134 steps/min in normal child and 118 steps/min with and without walker for diplegic child. End of stance indicated by star for normal child and arrow for CP child.

weight support as a prerequisite of independent gait and an essential step in gait therapy. The question then arises as to whether long-term support with canes or tripods should be encouraged instead of eliminating external supports as soon as possible?

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