Effect of air-splint application on soleus muscle motoneuron reflex excitability in nondisabled subjects and subjects with cerebrovascular accidents.

Key Words: Alpha motoneuron reflex excitability, Cerebrovascular accident, H-reflex, Physical therapy, Pressure, Rehabilitation.

Increased motoneuron excitability has been postulated to be a contributing factor in causing spasticity defined as a velocity-dependent increased resistance of the stretch reflex) in persons with central nervous system lesions.(1,2) Although spasticity may not be the primary cause of movement dysfunction in these patients, increased motoneuron excitability may lead to excessive activity in muscle groups such as the elbow flexors and ankle plantar flexors, which, because that activity is unopposed by antagonists, may lead to contracture.(1) Permanent muscle shortening from loss of sarcomeres has been shown to occur very rapidly when unopposed muscle contractions are induced experimentally.(3) Therapeutic techniques to reduce motoneuron excitability, therefore, may have potential for maintaining muscle length and preventing contractures in those muscles that are most susceptible to length changes in the patient with neurological disease. Clinicians and researchers have attempted to alter motoneuron excitability through a variety of measures including cooling, vibration, and pressure.(1,4-7) TABULAR DATA OMITTED

Numerous investigators(8-14) have studied the effects of pressure on the amplitude of the H-reflex. Kukulka and colleagues(8) studied the application of continuous pressure over the Achilles tendon. A decrease in the soleus muscle H-reflex amplitude was demonstrated, but this decrease was short lasting and independent of the amount of pressure applied.(8) The duration of H-reflex reduction by tendon pressure, however, has been correlated with the type of pressure applied, with intermittent pressure providing longer-lasting decreases than continuous pressure.(9) These results have been reported for both subjects with no history of neurological disease and subjects with cerebrovascular accidents (CVAs).(6,9) The effects of pressure applied to muscle bellies are less consistent than the effects of tendon pressure on changing the amplitude of the H-reflex. Muscle tapping has been shown to result in both decreases(10) and increases(11) of the H-reflex response. An increase in the H-reflex amplitude was noted when continuous pressure was applied over the soleus muscle belly in neurologically normal subjects; however, there were limitations in the results of this study.(12) In addition, Morelli and colleagues(13,14) have demonstrated that massage over the belly of the triceps surae muscle produced a decrease in the H-reflex. None of these studies,(6,8-10,13,14) however, reported long-lasting effects.

The component of muscle tone that results from reflex contraction is hard to quantify,(2) and the effectiveness of various treatments is difficult to assess. An indirect measurement of muscle tone is the measurement of motoneuron reflex excitability.(6,8,15) Soleus muscle motoneuron reflex excitability can be assessed by evaluating changes in the Hoffman reflex (H-reflex).(8,16-18) The H-reflex is an electrically stimulated monosynaptic reflex that excites the muscle spindle's Ia afferents. TABULAR DATA OMITTED

Action potentials are transmitted to the spinal cord where monosynaptic connections cause motoneurons to reach threshold, thereby causing the extrafusal muscle fibers to contract.(16,17) Changes in this reflex excitability can be evaluated by measuring amplitude changes of the H-reflex.(12,19) A finding of decreased motoneuron reflex excitability after use of a procedure would suggest a condition that may be conducive to reducing muscle tone.(6)

An air-splint is a pneumatic sleeve that is applied around an extremity and inflated to various pressures. It provides circumferential pressure to peripheral receptors and to agonist and antagonist muscles. Therapists have postulated that air-splints can decrease muscle tone(5); however, this postulate has never been systematically evaluated. The purpose of this study was to investigate the effect of circumferential pressure provided by an air-splint on the soleus muscle motoneuron reflex excitability in nondisabled subjects with no history of neurological disease and in subjects with CVAs.

Method

Subjects

Eighteen nondisabled, neurologically normal subjects (6 men, 12 women) and 8 subjects with CVAs (4 men, 4 women) participated in the study. The nondisabled subjects had no history of neurological disease or low-erextremity muscular disorders and ranged in age from 20 to 54 years ((-)X=29.4, SD=8.7). The subjects with CVAs had had strokes at least 3 months prior to the study ((-)X-=16.25 months, SD = 19.48 months), demonstrated increased tone in the involved leg (Ashworth Scale measurement of [equal to or greater than] 1),(20) had no history of low-erextremity muscular disorders, and ranged in age from 26 to 76 years (-)X= 54.0, SD= 19.09) (Tab. 1). All subjects were asked to refrain from the ingestion of caffeine and alcohol for 12 hours prior to the study because these substances can alter motoneuron excitability.(21) All subjects gave informed consent before participating in the study.

Instrumentation

A Nicolet Viking II electromyograph(*) was used for all nerve stimulation and reflex recording. Monopolar constant-current stimulation with 1-millisecond square waves was applied to the skin overlying the tibial nerve at 5-second

(*) Nicolet Biomedial Instruments, 5225-4 Verona Rd. PO Box 4287, Madison, WI 53711-0287. intervals. The electrical activity associated with the reflexes was monitored on an oscilloscope, and the data were stored on a computer disk for further analysis. H-reflex amplitudes (peak-to-peak measurement) were measured on a Nicolet Viking II digital oscilloscope,(*) which has a resolution to 10 [micro]V.(22) Pressure within the air-splint was monitored by a pressure meter that measured the backflow of pressure (to 0.05 mm Hg) from the splint. Atmospheric pressure was measured by this meter prior to inflation of the air-splint. This value was subtracted from the total value displayed by the pressure meter.

Procedure

Subjects were positioned prone with a pillow placed under the abdomen. The heads of the subjects with CVAs were turned toward the side of the air-splint application. The side was randomly chosen for the nondisabled subjects. The air-splint was applied to the hemiplegic leg of the subjects with CVAs.(23) On the selected leg, the hip was placed in approximately 0 degrees of extension and abduction, the knee was placed in 20 degrees of flexion, and the ankle joint was freely positioned in plantar flexion. Bipolar surface recording electrodes(*) were placed approximately 3 to 5 cm apart over the dorsal medial surface of the posterior calf, inferior to the belly of the gastrocnemius muscle. The reference electrode was placed midway between the stimulating and recording electrodes over the lateral calf.(24) A 33-cm-long (13-in-long) air-splint was then applied over the entire lower leg, with the distal end at the level of the medial malleolus (Fig. 1). In the popliteal fossa, a 1-millisecond stimulation was applied to the skin over the tibial nerve, and proper cathode positioning was determined when (1) the direct motor reflex (M-wave) and H-reflex (H-wave) displayed similar wave configurations, (2) the H-wave was evoked before the M-wave, and (3) the least amount of current was required to elicit an H-reflex.(25) The stimulating intensity was increased until a maximal H-reflex was observed, after which the on-line average of 10 H-reflexes was recorded. While observing the on-line average of the maximal H-reflex, the intensity was decreased until 50% of the maximal H-reflex was obtained. At this stimulating intensity, a subject's baseline H-reflex was established by averaging 10 stimulations of the tibial nerve.(25) With continued tibial nerve stimulation at 5-second intervals, the air-splint was manually inflated with an air pump and a hand-held bulb and maintained within a range of 36.7 to 40.8 mm Hg for 5 minutes. The air-splint was then deflated. H-reflex recordings were made for an additional 5 minutes. During the experiment, the M-wave from each stimulus was monitored to ensure stimulating and recording electrodes were not displaced. If the M-wave amplitude or shape changed, the data were not used in the analysis. Ten H-reflexes were recorded and averaged for each subject before inflation of the air-splint to obtain a baseline value (test 1). H-reflexes were also recorded at 1, 3, and 5 minutes after inflation of the air-splint tests 2-4) and at 1, 3, and 5 minutes after deflation of the air-splint (tests 5-7). The first two pressure measurements were taken during air-splint inflation and pressure stabilization. The third pressure measurement was recorded after the pressure had stabilized. If the air-splint pressure had not stabilized by the fourth minute, the data from that subject were not used in the analysis.

Data Analysis

A Statview II statistical program was used for all data analyses.(26) Ten H-reflex amplitudes (peak-to-peak measurement) were averaged for the baseline condition and for each of the six test conditions. Separate one-way analyses of variance (ANOVAs) for repeated measures were used to evaluate changes in the H-reflex amplitude across test conditions for each group. A two-way ANOVA was used to make comparisons between the two groups of subjects and across the test conditions. Post hoc t tests (with Bonferroni's correction for multiple comparisons) were used when significant F values were demonstrated. All post hoc tests' level of significance was designated at .008.

Results

Significant differences in H-reflex amplitude were demonstrated between the nondisabled subjects and the subjects with CVAs (Tabs. 2, 3). Post hoc tests revealed a significant (P[is less than or equal to].008) decrease in the nondisabled subjects' H-reflex amplitudes at 1, 3, and 5 minutes of pressure application when the measurements were compared with the baseline value. The H-reflex amplitude was decreased by 55% at minute 1, 52% at minute 3, and 40% at minute 5 of pressure application when compared with the baseline value. The first two postpressure measurements were increased by 24% and 26%, respectively (P[is less than or equal to].008) (Figs. 2, 3). By the fifth minute postpressure, the H-reflex was not significantly different from the baseline value.

The subjects with CVAs demonstrated a significant decrease in the amplitude of the H-reflex for the 1-, 3-, and 5-minute pressure measurements. During pressure application, the H-reflex was decreased by 41% at minute 1, 48% at minute 3, and 52% at minute 5 (P[is less than or equal to].008) Figs. 4, 5). Post-pressure measurements at 1, 3, and 5 minutes were not significantly different from the baseline value.

Comparisons of H-reflex amplitudes between the nondisabled subjects and the subjects with CVAs revealed a significant groupXtest interaction (Tab. 4, Fig. 6). An independent t test revealed a significant difference between the groups at the 1-minute postpressure measurement.

Discussion

This study showed that circumferential pressure applied by an air-splint around the lower leg reduced soleus muscle motoneuron reflex excitability in both neurologically normal subjects and subjects with CVAs. This reduction in reflex excitability lasted throughout the 5 minutes of pressure application. These findings differed from those of previous pressure studies(8,10,13,14) in that the H-reflex amplitudes demonstrated by our subjects remained depressed for a longer time. A possible explanation for the increase in duration of inhibition may be the method of pressure application. In the previous studies,(6,8-10,13,14) the investigators either massaged the muscle or applied pressure by slowly pressing a small, blunt object into a tendon or muscle belly. Pressure applied in this way slowly stretches the muscle with minimal cutaneous stimulation, Mark and colleagues(27) showed that tonic stretching of calf extensor muscles briefly inhibits the H-reflex through a postsynaptic inhibitory mechanism mediated by group II spindle afferents.

In this study, we applied pressure by inflating an air-splint circumferentially around the limb. Circumferential pressure compresses the limb with minimal muscle stretching. We believe the effect on motoneuron excitability from muscle stretch receptors would therefore be negligible. Assuming this to be true, we believe the H-reflex inhibition observed in this study is more likely related to the cutaneous effects that occur when an air-splint is inflated around the skin. This hypothesis also would explain the sustained inhibition that resulted after air-splint inflation. Cutaneous stimulation has been demonstrated to have long-lasting effects on motoneuron reflex excitability.(28,29) The cutaneous origin of the observed inhibition, however, remains speculative and requires further investigation.

The increase in the H-reflex amplitude shown by both groups with pressure release may be a response of thermoreceptors. Air leaving the splint may cause a cooling effect, which would increase the H-reflex amplitude.(4) Additionally, pressure release could facilitate the cutaneous mechanoreceptors. These mechanisms, therefore, could further increase soleus muscle motoneuron reflex excitability. Although both groups showed increases in H-reflex amplitude, the nondisabled subjects demonstrated significant increases above the baseline measurement for the 1- and 3-minute postpressure measurements. Only two of the subjects with CVAs demonstrated similar increases in H-reflex amplitudes with pressure release (Fig. 7).

The apparent difference in the degree of facilitation with the release of pressure for the subjects with CVAs may be explained by the presence of increased tone. These subjects may initially have had a higher level of motoneuron reflex excitability than that of the subjects with no neurological deficits; thus, increases of the H-reflex above baseline may not have been as apparent.

Clinical implications

These results support the clinical use of air-splint pressure in reducing motoneuron reflex excitability in patients with CVAs. This decrease in motoneuron reflex excitability may suggest a condition that may be conducive to reducing muscle tone.(6) Clinicians who use air-splints to promote joint stability should be aware that they may actually be inhibiting the activity of muscles encompassed by the air-splint.

Conclusion

Circumferential pressure applied by an air-splint around the lower leg reduced soleus muscle motoneuron reflex excitability in neurologically normal subjects and subjects with CVAs in this study. This reduction lasted throughout 5 minutes of pressure application. Further research on varied patient populations is needed to understand the clinical and physiological effects of circumferential pressure by air-splint application on the central nervous system.

Acknowledgments

We thank Bobby R Ellis of Innovative Tool Design, Shreveport, La, for his help in designing the air-splint pressure meter. We also thank Dr Martha Clendenin and Dr Carl Kukulka for their editorial comments.

References

1 Young RR, Wiegner AW. Spasticity. Clin Orthop. 1987;219:50-62.

2 Katz RT, Zev Rymer W. Spastic hypertonia: mechanisms and measurement. Arch Phys Med Rebabil. 1989;70:144-155.

3 Huet De La Tour E, Tardieu C, Tabary JC, et al. Decrease of muscle extensibility and reduction of sarcomere number in soleus muscle following a local injection of tetanus toxin. J Neurol Sci. 1979;40:123-131.

4 Urbscheit N, Bishop B. Effects of cooling on the ankle jerk and H-response. Phys Ther. 1970;50:1041-1049.

5 johnston M. Current advances in the use of pressure splints in the management of adult hemiplegia. Physiotherapy. 1989;75:381-384. 6 Leone JA, Kukulka CG. Effects of tendon pressure on alpha motoneuron excitability in patients with stroke. Phys Ther. 1988;68: 475-480.

7 Umphred DA, McCormack GL. Classification of common facilitory and inhibitory techniques. In: Umphred DA, ed. Neurological Rehabilitation. St Louis, Mo: CV Mosby Co; 1985: 72-117.

8 Kukulka CG, Fellows WA, Oehlertz JE, Vanderwilt SG. Effect of tendon pressure on alpha motoneuron excitability. Phys Ther. 1985;65:595-600.

9 Kukulka CG, Beckman SM, Holte JB, Hoppenworth PK. Effects of intermittent tendon pressure on alpha motoneuron excitability. Phys Ther. 1986;66:1091-1094.

10 Belanger AY, Morin S, Pepin P, et al. Manual muscle tapping decreases soleus H-reflex amplitude in control subjects. Physiotherapy Canada. 1989;41:192-195.

11 Buller NP, Garnett R, Stephens JA. The reflex responses of single motor units in human hand muscles following muscle afferent stimulation. J Physiol (Lond). 1980;303:337-349.

12 Kukulka CG, Haberichter PA, Mueksch AE, Rohrberg MG. Muscle pressure effects on motoneuron excitability: a special communication. Phys Ther. 1987;67:1720-1722.

13 Morelli M, Seabome DE, Suilivan SJ. Changes in H-reflex amplitude during massage of triceps surae in healthy subjects. Journal of Orthopaedic and Sports physical Therapy. 1990;12(2):55-59.

14 Sullivan SJ, Williams LRT, Seaborne DE, Morelli M. Effects of massage on alpha motoneuron excitability. Phys Ther. 1991;71: 555-560.

15 Kots IM. the Organization of Voluntary Movement. Neurophysiological Mechanisms. New York, NY.. Plenum Press; 1977:49-50.

16 Schieppati M. The Hoffman reflex: a means of assessing spinal reflex excitability and its descending control in man. Prog Neurobiol. 1987;28:335-366.

17 Honore J, Demaire C, Coquery JM. Effects of spatially oriented attention on the facilitation of the H-reflex by a cutaneous stimulus. Electroencephalogy Clin Neurophysiol. 1983;55:156-161.

18 Angel RW, Hoffman WW. The H-reflex in normal, spastic and rigid subjects. J Neurol. 1963;65:21-26.

19 Crayton JW, King S. Inter-individual variability of the H-reflex in normal subjects. Electromyogr Clin NeuropPhysiol. 1981;21:183-199.

20 Ashworth B. Preliminary trial of carisoprodol in multiple sclerosis. Practitioner. 1964; 192:540-542.

21 Eke-Okoro ST. The H-reflex studied in the presence of alcohol, aspirin, caffeine, force and fatigue. Electromyogr Clin Neurophysiol. 1982;22:579-589.

22 Nicolet Viking User's Guide for Use with Version 2.0 Software. Madison, Wis: Nicolet instruments Corp; 1989.

23 Hayes KC, Sullivan J. Tonic neck reflex influence on tendon and Howman reflexes in man. Electromyogr Clin Neurophysiol. 1976; 16:251-261.

24 Maryniak O, Yaworski R. H-reflex: optimum location of recording electrodes. Arch PhysMedRebabil. 1987;68:798-801.

25 Hugon M. Methodology of the Hoffman reflex in man. In: Desmedt JE, ed. New Developments in Electromyography and Clinical Neurophysiology. New York, NY: S Karger Publishers Inc; 1973:277-293.

26 Statview II. Berkeley, Calif Abascus Concepts Inc; 1986.

27 Mark RF, Coquery JM, Paillard J. Autogenetic reflex effects of slow or steady stretch of the calf muscles in man. Exp Brain Res. 1968; 6:130-145.

28 Agostinucci J. Spinal Reflexes Following Topical Desensitization of the Skin. Boston, Mass: Boston University; 1988. Doctoral dissertation. 29 Agostinucci J. Excitability modulation after desensitization of the skin by iontophoresis of lidocaine hydrochloride. Arch Phys Med Rebabil. In press.

JA Robichaud, PT, completed this study in partial fulfillment of the requirements for her advanced physical therapy master's degree in health science at the University of Florida. She is currently Visiting Instructor, Physical Therapy Department, College of Health Related Professions, University of Florida, Box 100-154, Gainesville, FL 32610 (USA). Address all correspondence to Ms Robichaud. J Agostinucci, ScD, OT, is Assistant Professor, Department of Occupational Therapy, College of Health Related Professions, University of Florida. DW Vander Linden, PhD, PT, is Assistant Professor, Department of Physical Therapy, College of Health Related Professions, University of Florida.

This research project was partially supported by a Paralyzed Veteran's Society Grant.

This study was approved by the University of Florida Health Science Center Institutional Review Board. This article was submitted April 18, 1991, and was accepted October 4, 1991.

Commentary

Spasticity is a highly overrated symptom of upper motor neuron syndrome that has occupied the center of attention and efforts of neurological physical therapists and occupational therapists since the 1950s.(1) Despite reports in the literature that spasticity does not cause the primary movement dysfunctions that occur following central nervous system damage,(2,3) therapists are still linking abnormal movement patterns and spasticity and proclaiming that we must provide the patient with inhibition of abnormal patterns and tone in order to restore normal, voluntary movement.(4) It is refreshing to see in this article that the authors have been precise in their definition of spasticity and thus realistic in the clinical implications of their results.

Spasticity is an increase in resistance to passive stretch that is proportional to the velocity of the stretch.(5,6) It is no longer thought to be due to hyperactivity of gamma motoneurons resulting from loss of inhibition from higher centers, but rather to a disturbance of reflex circuits within the spinal cord that is manifested by an increased excitability of alpha motoneurons.(5,7) The authors of this article have measured alpha motoneuron excitability, by using the Hoffman reflex (Hf-reflex), in order to evaluate the effects of the application of airsplints in nondisabled individuals and individuals who have had a cerebrovascular accident (CVA). They infer from the literature that by reducing motoneuron excitability, contractures may be prevented. Although contractures that develop following neurological damage are probably due mainly to lack of active muscle contraction and to lack of joint motion and muscle stretching, the hyperexcitability of the stretch reflex may indeed contribute somewhat to the immobilization in the shortened range of motion, which results in loss of sarcomeres as well as significant changes in connective tissue and the joint capsule.(8,9) Therefore, if the excitability of motoneurons can be decreased, it may be possible to apply passive range of motion PROM) to attempt to prevent some of the muscle and joint capsule changes.

I have two methodological concerns regarding the way the data were analyzed and presented. First, the "Data Analysis" section states that the averages of 10 H-reflex amplitudes for each time (baseline and six test conditions) were the dependent variables for the analyses of variance (ANOVAs). The results, however, were reported both in the text and in the figures as percentages of change from baseline. judging by the degrees of freedom in the two one-way ANOVAs, average amplitudes were used. It is unclear whether average amplitudes were used in the two-way ANOVA, because the baseline was dropped from the analysis. This brings me to my second concern. Why were the two one-way ANOVAs carried out, analyzing each group separately? By using a two-way ANOVA, including baseline values, all of the post hoc within-group and between-group comparisons could have been carried out, given significant interaction and simple main effects. It is unusual, and usually undesirable, to perform multiple statistical tests on the same data, as multiple tests increase experimentwise error. Although the authors have chosen a rather stringent alpha level that would counteract the effects of multiple tests, I am unclear why the authors chose to do it this way. In addition, I am unclear why the authors did not include the baseline values in the two-way ANOVA. In their discussion, they attempt to explain the difference in response of the two groups after the pressure is released by the presence of increased tone, and yet they have not performed the appropriate test to show whether the two groups indeed demonstrated a difference in alpha motoneuron excitability during the baseline condition, prior to the application of treatment. As the premise is that individuals with spasticity demonstrate hyperexcitability of alpha motoneurons, it would be important to demonstrate this phenomenon in the subjects who participated in this study. Without the baseline values, it is hard to explain why the only difference between the groups occurs at 1 minute after release of pressure. The clinical importance of the findings in this study is interesting to consider. In the individuals with spasticity (as determined by the Ashworth Scale), the reduction of motoneuron excitability lasted only during the application of the air-splints. As mentioned earlier, PROM could be applied perhaps more effectively during this time, therefore preventing some of the changes in muscle and in the joint capsule. It was also interesting to note that the excitability across the 5 minutes of pressure application in the subjects with CVAs was continuing to decrease. Therefore, although there was a rebound toward baseline levels after release of pressure, it was not reached for 5 minutes (although the difference was not statistically significant). It would be interesting to know whether this trend would continue during longer application or stabilize. If greater reduction of excitability was obtained during application, then there might be some additional carryover after removal of the splint. Would there be any benefit to asking the patient to perform voluntary, functional tasks while wearing the splint? It is likely that the decrease in motoneuron excitability is occurring in the synergists and antagonists of the soleus muscle as well. it is also known that one of the major problems for individuals with central nervous system damage is the diminished (as well as disordered) recruitment of motor units. In addition, there is a disruption of the normal reciprocal inhibition that occurs during voluntary movement.(5) Therefore, a reduction in motoneuron excitability might actually be detrimental for voluntary movement and, at the least, would have no benefit. The authors have carried out a well-designed, careful study, and they have interpreted the clinical implications of their results equally as carefully, presuming that clarifications on the statistical analysis support the reported findings. As they point out, follow-up studies are needed to examine the effects of circumferential pressure from air-splint application in other populations, as well as to evaluate the effectiveness of this treatment, in conjunction with other physical therapy techniques, in preventing contractures in individuals with neurological damage. in addition, further under-standing of the mechanisms involved in the reduction of motoneuron excitability may lead to more beneficial treatment applications.

Jean M Held, EdD, PT Associate Professor of physical Therapy University of Vermont 305 Rowell Bldg Burlington, VT 05405

References

1 Giuliani CA. Should we measure spasticity, tone and other ugly terms? In: Proceedings of the Forum on Neurological physical Therapy Assessment. Alexandria, Va: Neurology Section, American Physical Therapy Association; 1990: 25-27.

2 Sahrmann SA, Norton BJ. The relationship of voluntary movement to spasticity in the upper motor neuron syndrome. Ann Neurol. 1977;2:460-465.

3 Knutsson E, Martensson A. Dynamic motor capacity in spastic paresis and its relationship to prime motor dysfunction, spastic reflexes and antagonistic coactivation. Scand J Rebabil Med. 1980;12:93-106.

4 johnston M. Current advances in the use of pressure splints in the management of adult hemiplegia. Physiotherapy, 1989;75:381-384.

5 Burke D. Spasticity as an adaptation to pyramidal tract injury. In: Waxman SG, ed. Advances in Neurology: Functional Recovery in Neurological Disease New York, NY- Raven Press; 1988;47:401-423.

6 Katz RT, Rymer WZ. Spastic hypertonia: mechanisms and measurement. Arch Phys Med Rebabil. 1989;70:144-155.

7 Young RR, Wiegner AW. Spasticity. Clin Orthop. 1987;219:50-62.

8 Goldspink G, Williams P. Muscle fibre and connective tissue changes associated with use and disuse. In: Ada L, Canning C, eds. Key Issues in Neurological Physiotherapy London, England: Butterworth/Heinemann Ltd; 1990:197-218.

9 Ada L, Canning C. Anticipating and avoiding muscle shortening. In: Ada L, Canning C, eds. Key Issues in Neurological Physiotherapy. London, England: Butterworth/Heinemann Ltd; 1990:219-236.

Author Response

We appreciate Dr Held's thoughtful commentary on our article. Spasticity is indeed an overrated symptom of upper motor neuron syndrome that has received much attention in the professional literature. We concur that clinical techniques to reduce spasticity may continue to be most useful when trying to maintain passive range of motion. Additionally, we agree that further studies are indicated to determine the clinical importance of air-splint pressure in other patient populations and during voluntary movement. The choice of statistical analysis can be debated. Our data clearly demonstrated lowered alpha motoneuron reflex excitability during pressure application in both the nondisabled subjects and the subjects with cerebrovascular accidents. Therefore, we believe clinical implications were appropriately drawn from our results.

Julie A Robicbaud, PT James Agostinucci, ScD, OT Darl W Vander Linden, PhD, PT