746

The Quantitative Measurement of Spasticity: Effect of Cutaneous Electrical Stimulation

Thomas P. Seib, BS, Robert Price, MSME, Maria R. Reyes, MD, Justus F. Lehmann, MD

ABSTRACT. Seib TP, Price R, Reyes MR, Lehmann JF. The quantitative measurement of spasticity: effect of cutaneous electrical stimulation. Arch Phys Med RehabilI994;75:746-50.

• The goal of this research was to determine if cutaneous electrotherapy would temporarily reduce muscle spasticity. Five traumatically brain injured (TBI) and five spinal cord injured (SCI) subjects, all with clinically evident spasticity, received surface electrical stimulation over the tibialis anterior muscle. Using the Spasticity Measurement System, stiffness around the ankle was measured before, immediately after, and 24 hours after treatment. With stimulation, ipsilateral ankle viscoelastic stiffness immediately decreased in 9 of 10 subjects and remained significantly depressed for up to 24 hours. Contralateral ankle spasticity did not significantly change. Using the same subjects under sham conditions, no significant decrements in spasticity occurred. In a subjective survey, only SCI participants reported functionally evident spasticity reductions. Also within this subgroup, efficacy of treatment was directly proportional to the severity of pre-stimulation clonus. We conclude that (I) cutaneous electrotherapy transiently decreases both TBI and SCI related spasticity and (2) pre-stimulation clonus may function as a clinical indicator of SCI patients most likely to benefit from this process.

© 1994 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation

Spasticity is a debilitating outcome of upper motor neuron lesions'? affecting approximately 6 million people each year." This complex phenomenon, characterized by hypertonia and velocity-dependent hyper-reflexia, disrupts activities of daily living, and limits the efficacy of physical therapy. Although several strategies to alleviate spasticity exist, current methods are generally inadequate.

In 1950, Lee, McGovern, and Duvall" applied cutaneous electrical stimulation to the spastic muscles of 27 spinal cord injured subjects noting up to 14 hours of significant spasticity relief. Levine, Knott, and Kabat6 conducted a related study in 1952 in which tetanizing current was directed at the muscle antagonistic to the spastic muscle. Again, reductions in spasticity resulted. Recent studies by Alfieri," Vodovnik,":" Bajd,ll and others'v" support these results. Still, the use of cutaneous electrotherapy for spasticity reduction is a controversial, seldom used practice. Those agreeing to the effectiveness of this treatment do not concur on stimulation parameters. An even stronger deterrent are reports that various forms of electrotherapy increase spasticity'v" and should be avoided,

A former problem in determining the validity, and most effective application of this therapy was the inability to objectively quantify spasticity. Now, using the Spasticity Measurement System (SMS) developed at the University of Washington, neurophysiological and biomechanical responses, which vary with the intensity of spasticity, are measurable.P:'" This

From the University of Washington School of Medicine (Mr. Seib), and the Department of Rehabilitation Medicine (Mr. Price, Drs. Reyes, Lehmann), Seattle, W A.

Submitted for publication October 14, 1993. Accepted in revised form February 9, 1994.

This research supported in part by Research and Training Center grant H133B80081, National Institute on Disability and Rehabilitation Research, US Department of Education, Washington, DC.

No commercial party having a direct financial interest in the results of the research supporting this article has or will confer a benefit upon the authors or upon any organization with which the authors are associated.

Reprint requests to Justus F. Lehmann, MD, Department of Rehabilitation, RJ-30, University of Washington, Seattle, WA 98195.

© 1994 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation

0003·9993/9417507·0019$3.0010

Arch Phys Med Rehabil Vol 75, July 1994

. system allows small variations in muscle spasticity to be recognized, enabling more accurate therapy evaluation.

The purpose of this research was to precisely measure the effects of cutaneous electrical stimulation on spasticity. Specifically, we examined whether spasticity of the gastrocnemius-soleus-Achilles tendon unit would decrease with the application of electrotherapy over the tibialis anterior (T A) muscle. This site of stimulation was chosen based on previous studies=? suggesting reciprocal inhibition as the likely cause for spasticity decrements. We attempted to determine the quality, quantity, and duration of change in spasticity using both the SMS and a subjective spasticity assessment form. It was our hypothesis that ipsilateral ankle spasticity would decrease with stimulation, whereas hypertonia in the corresponding contralateral limb would be unaffected.

METHODS

Subjects

Five traumatically brain injured (TBI) and five spinal cord injured (SCI) people with clinically evident spasticity volunteered to participate in this study via an Institutional Review Board approved informed consent procedure. The mean age of the subjects was 38 years (SD 15) with the range extending from 19 to 73 years old. Mean duration of injury for SCI subjects was 8.6 years (SD 5.8) with a range of 3 to 16 years, and for TBI subjects 4.0 years (SD 1.9) with a range from Ito 6 years. Overall, mean duration of injury was 6.3 years (SD 4.7) with a range of 1 to 16 years. Participants in the study were not required to stop taking previously prescribed anti-spasticity medications, which included baclofen, doxepin, and diazepam, but were asked to maintain stable dosages throughout the length of the testing period, A passive range of motion of 5°, with at least 2.5° of dorsiflexion was required (table 1),

Procedures

Prior to the start of each testing session, participants received a clinical evaluation of their spasticity. This included

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Table 1: Subject Profiles
No. of Beats of
Spasticity Clonus
Subject Sex Age Injury Onset Medications (prestimulation)
LB F 28 SCI 1979 None 6
LC F 19 SCI 1989 None 0
AW F 45 SCI 1989 None 0
MH M 35 SCI 1976 Diazepam 6
DB M 45 SCI 1984 Diazepam 10+
BT M 27 TBI 1988 None 5
LP M 73 TBI 1987 None 0
LM F 38 TBI 1991 Baclofen, 0
Doxepin
RP M 39 TBI 1988 None 0
JB M 28 TBI 1986 None Not tested measuring passive range of motion and evaluating for dorsiflexion-induced clonus. SMS measurements were then conducted on both ankles in a manner previously described by Lehmann et al.'" Ten warm-up measurements (one at each frequency) were given to acquaint the subject with the procedure and allow them to find a comfortable position. Testing consisted of 30 measurements (three trials per frequency) each consisting of a 20 second speed stabilization period followed by 1 second of data collecting.

Baseline spasticity measurements were conducted beginning with the least spastic (contralateral) ankle, followed by the more spastic (ipsilateral) ankle. Upon completion of these preliminary measurements, a Respond IIa electrical stimulator with NeurnAid" reusable electrodes was used to deliver electrical stimulation to the ipsilateral tibialis anterior. This was accomplished by placing the active electrode proximal and lateral on the lower leg over the belly of the tibialis anterior. The indifferent electrode was placed distal on the lower leg and over the peroneal tendons. 18 Electromyograph electrodes in this area were removed prior to stimulation and replaced upon its completion. Stimulation parameters were as follows: 2 sec rise time, 15 seconds on, instant fall, 20 seconds off. The rate of the stimulation was 30 pulses per second, with the intensity varying based on subject tolerance. These parameters mimick normal timing of the gait cycle. They are recommended settings in the Respond II gait training protocol" based on previous studies involving Functional Electrical Stimulation and gait redevelopment.20•22 Sham testing was conducted in a nearly identical manner, the only difference being that the stimulator was not turned on during the "stimulation" period. Criteria for effective stimulation was a strong contraction of the tibialis anterior in response to the electrical impulses.

After 20 minutes of stimulation, subjects were instructed to resume a prone position. SMS spasticity measurements were again taken, starting with the ipsilateral ankle first, followed by measurement of the contralateral ankle. We chose this test pattern so that the immediate effects of electrotherapy on the stimulated ankle could be determined. During the 6 hours directly following stimulation, participants were asked to do hourly SUbjective ratings of their spasticity level. All participants returned at approximately the same time the following day for evaluation of effects lasting over 24 hours. At this time both ankles were retested using the

747

SMS. In order to limit variability within the data, all participants functioned as their own control. Spasticity was not measured on the contralateral side of one subject. A W, due to a limited range of motion. No 24 hour measurements were acquired on LP due to technical difficulties.

Spasticity Evaluation

The SMS quantifies spasticity based on frequency-dependent changes in viscous and the elastic ankle stiffness.l'-!" Torque values representing ankle resistance in phase (elastic stiffness), and 90° out of phase (viscous stiffness) with ankle displacement were measured at the various oscillation frequencies. The vector sum of these two stiffness components is the total ankle stiffness for the given frequency." A final path length value representing the overall degree of ankle spasticity was determined by plotting the total stiffness vectors for all 10 frequencies then adding together the distance between each consecutive vector apex (fig 1). Longer path lengths result from frequency-dependent variations in ankle stiffness, a characteristic found in spasticity.F

A subjective Spasticity Assessment Form was also used to track changes. Participants rated their spasticity on a scale of "-4" to "+4" every hour for 6 hours directly after electrical stimulation, (Negative values represented decreased spasticity, a score of "0" represented baseline spasticity levels for that individual, and positive values indicated increased spasticity.)

Statistical Analysis

Data were statistically analyzed to determine any significant ipsilateral, or contralateral changes in path length resulting from electrical stimulation. A one-tailed Wilcoxon Matched Pairs Signed Ranks test was used to compare ipsilateral prestimulation and immediate post-stimulation path lengths. Ipsilateral 24 hour post -stimulation path lengths, contralateral path lengths, and sham therapy path lengths were evaluated using a two-tailed Wilcoxon Matched Pairs Signed Ranks test. Subjective data were not statistically evaluated.

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Fig 1-Nyquist diagram of stiffness, its components, and a demonstration of pathlength generation. (Reprinted with permission.")

Arch Phys Med Rehabil Vol 75, July 1994

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SPASTICITY AND ELECTRICAL STIMULATION, Seib

Table 2: Ipsilateral Effect
Path Lengths
(nmlrad) Stimulation Sham
Subject Diagnosis Pre Post 24Hr Pre Post 24Hr
LB SCI 50 20 32 35 25 34
LC SCI 104 71 37 55 116 52
AW SCI 87 65 49 72 47 38
MH SCI 57 24 65 34 27 10
DB SCI 45 14 44 25 30 20
BT TBI 48 103 35 25 25 57
LP TBI 66 27 18 19 21
LM TBI 136 84 118 238 151 121
RP TBI 98 35 32 50 82 42
JB TBI 82 73 61 81 41 60
Median 74 50 41 43 36 42
Range 91 89 100 219 130 111
RESULTS
Ipsilateral Effect Immediate post-stimulation (n = 10). Nine of ten participants had decreased path lengths immediately after electrical stimulation (table 2). This represents a significant reduction (p < 0.05) in spasticity (fig 2). Median prestimulation path length was 74nm/rad with a range of 91. Median path length immediately post-stimulation was SOnm/rad and had a range of 89. Examining SCI subjects, median prestimulation path length was 57nm/rad. SCI participants had a significant post-stimulation decrease in path length to a median of 24nm/rad (p < 0.05). Median TBI prestimulation path lengths were 82nm/rad. Post-stimulation, this decreased to 73nmlrad. This change was not significant. The immediate post-sham path lengths were decreased in five subjects, increased in four subjects, and unchanged in one person. Overall, sham stimulation produced no statistically significant changes as a whole, or when evaluated in the SCI or TBI subcatagories.

24 hours post-stimulation (n = 9). Overall, eight of nine subjects had decreased ipsilateral path lengths relative to prestimulation (p < 0.01). Median value at this time was 41nm/rad with a range of 100. Median SCI path length was 44nmlrad, representing no significant change. TBI path length did change significantly, to a median value of 35nm/ rad. Sham therapy produced decreased path lengths in eight of nine participants. This trend was not statistically significant except in the SCI subcatagory.

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Arch Phys Med Rehabil Vol 75, July 1994

Contralateral Effect

Immediate post-stimulation (n = 9). Six of nine subjects showed increased contralateral path lengths after stimulation to the ipsilateral tibialis anterior muscle (table 3). Overall prestimulation median path length was 52nm/rad. Post-stimulation median path length was 49nmlrad. Median path length for SCI subjects decreased from 75nmlrad to 74nm/rad whereas the median TBI path length increased from 14nm/rad to 34nmlrad. These trends were not statistically significant. Sham therapy produced no significant changes, with increased path lengths in four subjects, decreased path lengths in four subjects, and no change in one subject (fig 3).

24 hour post-stimulation (n = 8). Twenty-four hours after stimulation the median contralateral path length was 50nm/rad. This represents decreased spasticity in four subjects, increased spasticity in three subjects, and no change in one person relative to prestimulation measurements. SCI median path length was 54nmlrad. Median TBI path length was 38.5nmlrad. No significant trends were evident. The median path length of the contralateral sham was 34nm/ rad. Four subjects had increased path lengths and four had decreased. Again this result was not significantly different from presham path lengths as a whole, or when evaluated by subcatagories.

Subjective Spasticity Assessment (based on patient self-evaluation)

Immediate post-stimulation (n = 9). The subjective spasticity rating revealed a perceived decrease in spasticity bilaterally by five of the nine persons receiving electrical stimulation (table 4). All subjects reporting notable changes were spinal cord injured. The mean rating given 1 hour after stimulation by those who noticed a decrease was a "-3" on the scale of -4 to +4 (0 = no change). These subjects reported decreased spasticity for up to 6 hours (mean 4.4 hours, range 2 to 6 hours) after stimulation. The remaining four participants (all TBI subjects) reported no noticeable change in spasticity after stimulation. No person indicated having increased spasticity during this time.

DISCUSSION

Spasticity reduction has been cited repeatedly as a product of direct electrotherapyS-7.9.12,14 and as a beneficial secondary

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Path Lengths
(nmlrad) Stimulation Sham
Subject Diagnosis Pre Post 24Hr Pre Post 24Hr
LB SCI 29 48 48 30 15 46
LC SCI 109 143 94 93 46 48
MH SCI 98 80 60 43 II 10
DB SCI 52 68 15 32 42 23
BT TBI 14 16 25 16 36 20
LP TBI 11 34 11 19
LM TBI 147 287 121 170 162 88
RP TBI 11 11 11 12 12 13
JB TBI 74 49 52 39 31 44
Median 52 49 50 32 31 34
Range 136 276 110 159 151 78 Su

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effect of other rehabilitation regimens+P:" Unfortunately, a review of current literature is most notable for a wide variety of stimulation patterns, methods of application, and spasticity measurement techniques. Alfieri? reports between 85% and 100% efficacy in decreasing spasticity using stimulation on hemiplegic subjects. He also notes that permanent reductions in hypertonicity occurred with repeated application. Stimulation was administered 10 minutes a day for 5 to 16 days. Bajd et afs found decreased spasticity in 50% of test subjects after a single session of electrotherapy. These effects lasted less than 2 hours. Robinson et al'" describes increased spasticity after stimulating spinal cord injured subjects for 20 minutes, twice a day, for 4 weeks. All three of these studies used differing stimulation parameters, and criteria for subject selection. In addition, highly subjective spasticity evaluation systems such as the Ashworth Scale" used by Alfieri, or ratings of "excellent, good, fair, poor," and "no relaxatiorr" are used throughout most of the existing research. Newer measurement techniques, such as the pendulum drop tesr" used by Bajd et aI, are more precise, and have less inter-rater variability, but are still not free of external influences.P:"

Spasticity, by nature, is also highly variable. Size and location of CNS injury can influence its presentatiorr" and may alter the effectiveness of a particular treatment. This author is unaware of previous studies comparing the efficacy of electrotherapy for spasticity reduction in SCI and TBI subjects.

In our testing, SCI participants showed consistent decreases in spasticity across multiple methods of spasticity

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Fig 4-(A) Prestimulation clonus. The duration of ankle clonus caused by rapid dorsiflexion was assessed prior to the initial stimulation session. Sustained clonus was recorded as 10 beats . (B) Subjective spasticity rating. Each hour after stimulation participants evaluated their level of spasticity on a scale of -4 to 4. A score of 0 represented a baseline level of spasticity for that individual. Negative values indicate decreased spasticity. The results for the first 5 hours have been combined. (C) SMS spasticity rating. Change in ipsilateral spasticity as measured by the SMS. Values represent the percent reduction in spasticity determined by comparing prestimulation and post-stimu-

lation measurements.

Table 4: Subjective Spasticity Rating evaluation. The mean drop in path length for this subgroup
Hours Post-Stimulation was 40%. On an individual basis, the change in path length
ranged from approximately 30% to 70%. Individual SCI
Subject Diagnosis 1 2 3 4 5 6 subjects with the greatest reductions in path length also re-
Ir ported the most evident and long-lasting spasticity reduc-
LB SCI -4 -4 -4 -3 -1 0 tions on self evaluation (fig 4) and had the most persistent
LC SCI -2 -2 -1 0 0
AW SCI -2 -2 0 0 0 clonus on initial evaluation. In future applications of electro-
MH SCI -4 -4 -4 -2 -1 0 therapy, significant levels of clonus could possibly be used
DB SCI -3 -3 -3 -3 -3 -3 as an initial indicators for candidates most likely to benefit
BT TBI 0 0 0 0 0 0 from this treatment. Upon completion of this study most SCI
LP TBI 0 0 0 0 0 0
LM TBI 0 0 0 0 0 0 participants were greatly interested in continuing electrother-
RP TBI 0 0 0 0 0 0 apy as a method of spasticity reduction. The ease of use,
JB TBI No data available immediacy, effectiveness, and nonsystemic nature of electro-
Negative values represent decreased spasticity, a score of "0" represents therapy were given as benefits of this mode of treatment.
normal spasticity level, and positive values indicate increased spasticity. Four of five TBI subjects had decreased ipsilateral ankle Arch Phys Med Rehabil Vol 75, July 1994

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SPASTICITY AND ELECTRICAL STIMULATION, Seib

stiffness immediately following stimulation. The average drop in path length was 54%. This reduction was of greater magnitude than occurred in SCI subjects but was not evident to any TBI patient on self-assessment, and did not correspond to prestimulation levels of clonus. We presently have no explanation for the disparity in results between SCI and TBI participants. It is possible that changes measured by the SMS were not large enough to have a significant mechanical effect recognizable to the TBI patient. The validity of selfassessment by TBI individuals can also be argued. Our resuIts suggest electrical stimulation reduces ankle stiffness in TBI patients but the clinical benefit of electrotherapy for this population remains in question.

Subject BT (TBI), was the lone person in this study with increased ipsilateral stiffness as a result of stimulation. His path length increased from 48nmlrad to 103nmlrad. BT was one of five participants sensate below the waist, and the only person to become aggravated by the stimulation procedure. The association between emotional stress, irritants, and spasticity is well documented." It is possible that increased discomfort and anxiety from the testing process negated any beneficial results from stimulation.

Disagreement exists throughout the literature as to the duration of spasticity reduction produced by a single episode of cutaneous electrical stimulation. Our SMS results indicate that 24 hours after stimulation statistically significant decrements in spasticity still exist in both head and spinal cord injured subjects. Subjectively, on self assessment, these effects were noted for 6 hours or less. These numbers again suggest the sensitivity of the SMS exceeds what is perceived by the subject. In light of these results, electrotherapy appears most useful as an immediate source of short-term spasticity reduction. These qualities make it especially useful for decreasing spasticity prior to stretching/range of motion exercises, before sleep, or as an adjunct therapy during times of increased hyper-reflexive activity.

CONCLUSION

From this study we conclude that cutaneous electrical stimulation applied over the tibialis anterior will decrease gastrocnemius muscle spasticity for 6 or more hours. This decrease in stiffness occurs in both head and spinal cord injured subjects, but is most notable to the SCI population. Significant pretreatment clonus can be used as a clinical indicator of SCI patients likely to benefit from this process. Contralateral spasticity may increase slightly with ipsilateral electrical stimulation, although this appears to have little clinical relevance.

References

1. Clemente C. Neurphysiological mechanisms and neuroanatomic substrates related to spasticity. Neurology 1978;28:40-5.

2. Little JW, Merritt JL. Spasticity and associated abnormalities of muscle tone. In: DeLisa I, editor. Rehabilitation medicine: principles and practice. Philadelphia: Lippincott, 1988:432.

3. Nathan PW. Factors effecting spasticity. International Rehabilitation Medicine 1980;2:27-30.

4. Bishop B. Spasticity: its physiology and management: part II. neurophysiology of spasticity: current concepts. Physical Therapy 1977;57:377-83.

5. Lee W, McGovern JP, Duvall EN. Continuous tetanizing (low voltage) currents for the relief of spasm. Arch Phys Med 1950;Dec:766-70.

Arch Phys Med Rehabil Vol 75, July 1994

6. Levine M, Knott M, Kabat H. Relaxation of spasticity by electrical stimulation of the antagonist muscles. Arch Phys Med Rehabil 1952; 33:668-73.

7. Alfieri V. Electrical treatment of spasticity. Scand J Rehabil Med 1982; 14:177-82.

8. Vodovnik L. Therapeutic effects of functional electrical stimulation.

Med BioI Eng Cornput 1981; 19:470-8.

9. Vodovnik L, Rebersek S, Stefanovaska A, Zidar I, et al, Electrical stimulation for the control of paralysis and therapy of abnormal movement. Scand J Rehabil Med Suppl 1988;17:91-7.

10. Vodovnik L, Bowman BR, Hufford P. Effects of electrical stimulation on spinal spasticity. Scand J Rehabil Med 1984; 16:29-34.

11. Bajd T, Kralj A, Turk H, Benko H, Sega J. Use of functional electrical stimulation in the rehabilitation of patients with incomplete spinal cord injuries. I Biomed Eng 1989; 11 :96-102.

12. Franek A, Turczynski B, Opara 1. Treatment of spinal spasticity by electrical stimulation. J Biorned Eng 1988;10:266-70.

13. Stefanovska A, Vodovnik L, Gros N, Rebersek S, Acimovic-Janezic R. FES and spasticity. IEEE Trans Biomed Eng 1989;36:738-45.

14. Robinson C, Kett N, Bolam 1. Spasticity in spinal cord injured patients: 2. initial measures and long term effects of surface electrical stimulation. Arch Phys Med Rehabil 1988;69:862-8.

15. Dimitrijevic M, Illis L, Nakajima K, Sharkey P, Sherwood A Spinal cord stimulation for the control of spasticity in patients with chronic spinal cord injury: II. neurophysiological observations. CNS Trauma 1986; 3: 145-52.

16. Price R. Mechanical spasticity evaluation techniques. Crit Rev Phys Rehabil Med 1990;2:65-73.

17. Lehmann IF, Price R, de Lateur B, Hinderer S, Traynor C. Spasticity: quantitati ve measurements as a basis for assessing effectiveness of therapeutic intervention. Arch Phys Med Rehabil 1989;70:6-15.

18. Benton LA, Baker LL, Bowman BR, Waters RL. Functional electrical stimulation-a practical guide. Rancho Los Amigos Rehabilitation Engineering Center, 1981.

19. Packman R. Respond II-Gait Training Protocol. Moss Rehabilitation Hospital, 1984.

20. Cranston B, Larrson L, Prevec T. Improvement of gait following functional electrical stimulation: investigations on changes in voluntary strength and proprioceptive reflexes. Scand J Rehabil Med 1977;57:7- 13.

21. Lee K, Johnston R. Electrically induced flexion reflex in gait training of hemiplegic patients; induction of the reflex. Arch Phys Med Rehabil 1976;57:311-14.

22. Takebe K, Basmajian J. Gait analysis in stroke patients to assess treatment of foot drop. Arch Phys Med Rehabil 1976;57:305-10.

23. Noth J, Mathews HR, Friedmann H-H. Long latency reflex force in response to imposed sinusoidal movements. Exp Brain Res 1984;55:317-24.

24. Halstead LS, Seager SW. The effects of rectal probe stimulation in spinal cord injured spasticity. Paraplegia 1991;29:43-7.

25. Bajd T, Gregoric M, Vodovnik L, Benko H. Electrical stimulation in treating spasticity resulting from spinal cord injury. Arch Phys Med Rehabil 1985;66:515-17.

26. Ashworth B. Preliminary trial of corisoprodol in multiple sclerosis.

Practicioner 1964; 192:540-52.

27. Wartenberg R. Pendulousness of the legs as a diagnostic test. Neurology 1951; 1:18-24.

28. Bajd T, Vodovnik L. Pendulum testing of spasticity. I Biomed Eng 1984; 6:9-16.

29. Sahrmann S, Norton B, Bomze H, Eliasson S. Influence of the site of the lesion and muscle length on spasticity in man. Phys Ther 1974;54: 1290-96.

30. Wyke B. Neuromechanisms in spasticity: brief review of some current concepts. Physiotherapy 1976; 62:316-19.

Suppliers

a. Respond II Stimulator, Medtronic Nortech Division, 10237 Flanders Court, San Diego, CA 92121.

b. NeuroAid electrodes, Medtronic Nortech Division, 10237 Flanders Court, San Diego, CA 92121.

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