Abstract - Semantic Scholar

Is the Measurement of Muscle Strength Appropriate in Patients with Brain Lesions? A Special Communication

Controversy exists as to whether muscle strength is a variable that should be measured inpatients with brain lesions. The purpose of this special communication is to provide evidence for the inclusion of muscle strength testing in the assessment of these patients. This evidence consists of information that 1) is relevant to weakness following brain lesions and concerns about its measurement, 2) provides a precedent and support for muscle strength testing and 3) relates muscle strength to patient capacity and outcome I believe that this information justifies the inclusion of muscle strength in the assessment ofpatients with brain lesions, but not to the exclusion of other behavioral functional variables. [Bohannon RW: Is the measurement of muscle strength appropriate in patients with brain lesions? A special communication. Phys Ther 69:225-236, 1989.]

Richard W Bohannon

Key Words: Cerebrovascular disorders; Hemiplegia, gait; Muscle performance, measurement; Paresis.

The most obvious, although by no means ubiquitous or sole, consequence of cerebrovascular accidents (stroke) is a predominantly unilateral muscle weakness.1 Nevertheless, some educators and authors have been suggesting for years that the measurement of muscle strength is inappropriate (ie, invalid) in patients with stroke. During the same time, many researchers have used a variety of methods to measure the strength of patients with hemiparesis. In addition to providing a well-founded precedent for such measurements, the researchers have demonstrated a relationship between muscle strength and functional capacity and outcome. The purposes of this special communication are to 1) discuss the issue of weakness

following brain lesions, 2) address a few of the specific concerns that have been voiced by opponents to the strength testing of patients with brain lesions, 3) provide an indication of the magnitude of the support and precedent that exists for muscle strength testing of these patients, and 4) present information that relates muscle strength to functional capacity and outcome.

Muscle Weakness Following Brain Lesions and Concerns About Its Measurement Given the demonstrated relationship between cortical and pyramidal tract activity and muscle force production in primates,2-6 muscle weakness should

R Bohannon, EdD, PT, is Associate Professor, Program in Physical Therapy, School of Allied Health Professions, University of Connecticut, PO Box U-101, 358 Mansfield Rd, Storrs, CT 06268 (USA). This article was submitted August 4, 1988, and was accepted October 19, 1988.

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be an expected result of lesions affecting corticomotoneuron cells, their projections, and their targets. Paresis from brain lesions can be classified as resulting primarily from reduced agonist output or from antagonist subtraction.7 Reduced-output paresis is a result of a decreased ability of the motoneuron pool to drive the motor units of a target agonist muscle.7 This reduced output has been documented in stroke patients during specified muscular efforts8-10 and during activities requiring patterns of muscular recruitment.11,12 Reduced output apparently affects the number and type of motor units recruited and the frequency of motor unit recruitment.8,9,13-15 Subtraction paresis results from resistive antagonist forces.7 In acknowledging the reality of subtraction paresis, it is important to note that 1) antagonist restraint can occur when the antagonist is electrically inactive (because of the passive stiffness of the antago-

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nist)12,16-18; 2) active antagonist resistance is unusual during static or slow-speed force measurements8,19,20; 3) active antagonist restraint is more likely during rapid and possibly reciprocal muscle contraction20,21; and 4) coactivation of antagonists can be, but is not always, a problem during functional activities.11,20-22 The presence of subtraction paresis is probably one of the greatest concerns of those who recommend against strength testing hemiparetic patients. Bobath states that muscle weakness is not real but relative to opposition by spastic antagonists.23 The literature outlined in the paragraph above, however, does not indicate that antagonist restraint should be a major problem during static strength testing. Other concerns about strength testing patients with brain damage include issues relevant to the position of testing23,24 and issues relevant to muscular function during strength testing as compared with during other activities. In regard to position, the relative capacity of brain-damaged patients to activate their muscles in different positions may not be affected in the manner that therapists have come to believe.25,26 For example, Sjöström et al concluded that "placement of the legs within patterns believed to facilitate (0° knee position) or inhibit (90° knee position) extensor motoneurons did not give rise to systematic strength variations different from those of the control subjects."25(p58) Bohannon similarly showed that patients with hemiparesis had comparable gravity-eliminated sitting-supine knee flexion torque ratios on the paretic and nonparetic sides.26 Muscles no doubt function differently depending on the circumstances of their activation. For example, the quadriceps femoris muscles of a patient with hemiparesis may act quite differently when used to extend the knee of a seated subject than when used during a sit-to-stand maneuver. This fact notwithstanding, strength testing may still provide an indication of brain-damaged patients' capacity to activate a muscle group under a known set of circumstances.

Support and Precedent for Muscle Strength Testing Despite the opposition that some have voiced for muscle strength testing in patients with intracranial lesions,23-24 some clinical scientists hold paresis as a major problem27-29 and as a problem worthy of measurement. Many investigators, some of considerable eminence, have measured muscle group strength in patients with hemiparesis. Muscle group strength has been measured with ordinal scales (eg, manual muscle testing) of 3 to 10 categories,30-50 weights,35 handgrip dynamometers,51-53 hand-held dynamometers,49,54-67 fixed dynamometers,8,9,19,68-73 and dynamic dynamometers (sometimes used in isometric mode).20,26,41,74-81 These investigations demonstrate that the clinical measurement of muscle strength in patients with hemiparesis has spanned nearly 80 years, has involved a host of investigators and institutions, and has included a variety of muscle groups and test conditions. Although such precedence alone does not justify the measurement of strength, it does demonstrate alternatives to the opinions of such clinicians as Bobath23 and Davies.24 Some of these investigators have made statements that provide support for the testing of muscle strength. Others have noted limitations of strength testing. Barer et al stated that overall neurological scores are of "dubious validity" if the progress of patients with different patterns of disability are to be compared.47 Instead, they recommended the monitoring of individual neurological signs, among them motor function (using an ordinal strength scale). Sjöström et al suggested that "structural and strengthwise changes may be parallel signs of brain injury per se."25(p58) Demeurisse et al claimed that their "motricity index," which is based on ordinal strength scores, gives a rapid indication of patient progress in motor recovery and allows interpatient comparisons and the "establishment of correlations with other clinical data."36(p382) In a personal communication in 1988, Demeurisse stated, "The measurement of muscle

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strength is essential for monitoring a rehabilitation program and for establishing an early prognosis." Wade voiced a similar stand in a personal communication (DT Wade, personal communication, 1988). He said, "I have always suspected that strength weakness is a dominant factor in determining function after stroke." After comparing handgrip strength with three other measures of upper extremity function, Heller et al concluded that "recovery of recordable (30 mm Hg) grip strength nearly always preceded other measurements of arm function during recovery and suggests that it is the most sensitive test of initial recovery. " 52( P 717) Watkins et al stated that the "Cybex II system can provide useful and objective information about altered motor behavior of patients with hemiparesis."41(p189) Kozlowski concluded, following a study of the reliability of isokinetic testing of patients with hemiparesis, that "it may be erroneous to assume that measures of strength in hemiplegic subjects are not reliable secondary to the influence of spasticity or abnormal postural reflexes."75 I have demonstrated in two additional unpublished studies that knee extensor muscle strength can be measured reliably (ICC > .90) in patients with stroke. Knutsson provided similar, but qualified, support for testing muscle force in patients with spastic hemiparesis. He stated: "With correction for gravitation and control of acceleration, isokinetic movements can be used for precise measurements of muscle force produced within a large range of movement speeds. " 81( P 205) He also indicated, however, that assessments of motor capacity should preferably include estimates of such components as exaggerated stretch reflexes, contractures, and excessive coactivation. He recommended the incorporation of electromyography for this purpose. Concerns similar to those of Knutsson probably underlie the comment of Hammond et al that muscle strength measurements "do not provide an understanding of the neurophysiologic basis of functional impairment."82(p106) Winter has expressed similar concerns regarding gait analysis.83 Accepting these concerns 226/57

as legitimate, I would note that measures such as pulse rate, blood pressure, body temperature, and body weight are of value despite their failure to explain underlying mechanisms. I find little cause either for rejecting a measure simply because it does not indicate underlying mechanisms or for complacently accepting a measurement as indicative of all that I want to know if it does not indicate such mechanisms.

Relationship Between Muscle Strength and Patient Capacity and Outcome Beyond the precedent presented above, additional support exists for the measurement of muscle force-torque production (strength) in patients with intracranial lesions. This support is founded on the relationships demonstrated, in numerous studies, between strength and patient (present) capacity and (future) outcome. The purpose of this section is to present evidence that force measurements can be used to explain a portion of the variance in present and future status. I believe, as does Perry,84 that connective tissueflexibility,muscle strength, and selective neural control are all important to function. Perhaps the most fundamental of findings related to muscle strength in brain-damaged patients is that measurements obtained at one point in time correlate with measurements obtained at a later time and with other motor indexes. This finding can be important when patients have questions such as, "Will I get my strength back?" Logigian et al found thatfinalMMT scores were significantly correlated (r = .78, p < .01) with initial MMT scores in 42 patients undergoing rehabilitation.45 Bohannon showed significant correlations (r = .56-.83) between initial and final force measurements obtained by hand-held dynamometry from 16 muscle groups of 38 hemiparetic patients.55 Bohannon and Smith found similar relationships when upper extremity muscle strength deficits were compared between initial and final assessment in 58 stroke 58/227

patients undergoing rehabilitation (r=.73-.85).58 Smedley et al, who measured upper extremity muscle strength using an ordinal scale, found it to be correlated (p < .05) with both fine and gross motor coordination in 50 hemiparetic patients.37 Dohrmann and Nowack also found a significant relationship (p < .005) between upper extremity weakness and decreased skill.34 They concluded that the relationship was logical "because a weak upper extremity cannot accomplish skilled movements."34(p376) Sjöström et al reported the maximal plantar-flexion torque of the affected lower extremity to be significantly correlated with the extremity's Fugl-Meyer motor score (rs = .66, p < .05) in 19 subjects with hemiparesis.25 Bohannon found a correlation (r) of .631 between knee flexion force and movement speed in the lower extremity of stroke patients.67 The variance in movement speed explained by the strength of four lower extremity muscle groups was 49.5%. Sheikh et al used a very gross four-level scale to document limb muscle function.43 They reported significant correlations (p < .001) between activities-of-daily-living scores and upper limb function (-.487) and lower limb function (—.544). Logigian et al reported significant correlations (r = .34) between MMT grades and scores on the Barthel Index (an ordinal scale rating 10 self-care and mobility activities).45 The MMT-Barthel Index correlations were significant on admission, on discharge, and across time. Wade and Hewer obtained similar findings.44 Their ordinal strength measurement scores for hemiparetic patients were correlated with the Barthel Index scores initially (.749), at three weeks postinjury (.774), and at six months postinjury (.610). Feigenson et al described weakness in stroke patients as "mild," "moderate," or "severe."31 They found such weakness to be one of the strongest predictors of patient placement upon discharge; dressing, feeding, and hygiene performance; and bowel and bladder control.

Weakness was also related to length of hospital stay. Hamrin et al reported positive and sometimes significant (8 of 24) correlations between elbow flexion-extension torques and the performance of hygiene, dressing, and household activities.77 Fullerton et al studied the relationship between a host of predictor variables and mortality and functional outcome.50 "Arm power" and "leg power," which were measured on afive-levelordinal scale, were among the significant predictors of functional outcome (p < .0001). The performance of activities addressed directly by physical therapists has been correlated with measures of muscle strength. Primary among those activities is gait. Wade and Hewer found walking independence (ie, alone, with another person, unable) to be significantly correlated with ordinal measures of leg muscle strength (y = -.860).44 Feigenson et al reported weakness to be a strong predictor of ambulation.31 In addition to a study by Bohannon,62 at least four other studies have documented a relationship between quantitative measurements of muscle strength and gait performance. Hamrin et al reported that isokinetic torques of the paretic and nonparetic knees were correlated with locomotion.77 The correlations were higher on the paretic side (rs = .71-90) than on the nonparetic side (rs = .38-.67). Hamrin et al claimed that the highly significant correlations support the validity of the isokinetic strength test in the patients. In a more recent study, Bohannon found significant (p < .01) correlations between individual lower extremity paretic muscle group strength measurements and gait independence, distance, speed, and cadence (rs = .556-.840). The correlations were significant on initial assessment, final assessment, and across time.85 In an earlier study, Bohannon investigated nine variables as potential explanations for four gait performance variables.56 Although motor control and balance offered the best explanation of ambulatory capacity, normalized muscle strength of the paretic lower extremity was significantly correlated with gait velocity, cadence, appearance,

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and independence (r = .369—.511)- In 11 hemiparetic patients, Nakamura et al found knee extension torque (isokinetic torque at 30°, 90°, and 180°/ sec and isometric torque at 90° and 60° of flexion) to be significantly correlated with walking speed (r = .595-.847) and cadence (r = .609-.853).79 They used stepwise regression to further analyze their data and found that isokinetic torque at 90°/sec explained 75.6% of the variance in gait speed and that isokinetic torque at 180°/sec explained 72.7% of the variance in gait cadence. In another study on patients with stroke, Nakamura found that "strength of the affected side was the primary determinant of walking speed and that the variance explained by it gradually increased with a period of training."80(p111) Variance explained by strength of the affected side ranged from 25% at the initiation of gait training to 50% eight weeks later. Among the other factors of specific interest to physical therapists and to which muscle strength measures are related are transfer performance, standing performance, rolling independence, and shoulder pain and shoulder-hand syndrome. In a study by Bohannon, the relationships between various paretic muscle group strengths and transfer independence were all significant on initial assessment (rs = .468-.643).64 The correlations on final assessment and across time, although positive, were rarely significant (rs = .304-.477). The standing performance of 81 stroke patients was found by Bohannon to correlate significantly with the strength of six of seven muscle groups on both the paretic and nonparetic sides (rs = .255-.464). In an unpublished follow-up study, Bohannon confirmed the existence of significant correlations on initial assessment, final assessment, and across time. Although Bohannon, in a different study, did not find that muscle strength of the paretic side consistently explained rolling independence, he did find that the muscle strength of the nonparetic side explained rolling independence (r = .51-.75).66 Chalsen et al concluded, from a study in which various potential causes of

shoulder-hand syndrome were examined, that "weakness is a necessary but not sufficient cause for the development of shoulder-hand syndrome poststroke."42(p137) Bohannon found shoulder abduction and lateral (external) rotation force production to be negatively and significantly correlated with shoulder pain in hemiparetic patients on initial assessment, on final assessment, and across assessment times (rs = -.375 to -.583).65 He concluded that "patients with greater weakness may be prone to the development of pain because their muscles lack adequate strength to move the joint and prevent adhesive capsulitis."65(p111)

Conclusion Muscle strength is by no means a variable of such great importance that it can be justified as a sole indicator of status, change, capacity, or outcome in patients with brain lesions. Substantial precedents and evidence exist, nevertheless, to support the appropriateness of muscle strength testing in these patients. Before accepting the direction of those opposed to such testing, the clinician should consider the information presented in this communication. Because considerable variance in patient performance remains unexplained by muscle strength, the search should continue for even better targets of measurement and treatment.

References 1 Wade DT, Hewer RL, Skilbeck CE, et al: Stroke: A Critical Approach to Diagnosis, Treatment, and Management. Chicago IL, Year Book Medical Publishers Inc, 1985, p 23 2 Evarts EV: Relation of pyramidal tract activity to force exerted during voluntary movement. J Neurophysiol 31:15-28, 1968 3 Thatch WT: Correlation of neural discharge with pattern and force of muscular activity, joint position, and direction of intended next movement in motor cortex and cerebellum. J Neurophysiol 41:654-676, 1978 4 Hepp-Reymond MC, Wyss UR, Anner R: Neuronal coding of static force in the primate motor cortex. J Physiol (Paris) 74:287-291, 1978 5 Cheney PD, Fetz EE: Functional classes of primate corticomotoneuronal cells and their relation to active force. J Neurophysiol 44:773791, 1980

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6 Evarts EV, Fromm C, Kroller J, et al: Motor cortex control of finely graded forces. J Neurophysiol 49:1199-1215, 1983 7 Freund HJ: The pathophysiology of central paresis. In Struppler A, Weindl A (eds): Electromyography and Evoked Potentials. Berlin, Federal Republic of Germany, Springer-Verlag, 1985, pp 19-20 8 Tang A, Rymer WZ: Abnormal force-EMG relations in paretic limbs of hemiparetic human subjects. J Neurol Neurosurg Psychiatry 44:690698, 1981 9 Rosenfalck A, Andreassen S: Impaired regulation of force and firing pattern of single motor units in patients with spasticity. J Neurol Neurosurg Psychiatry 43:907-916, 1980 10 Sahrmann SA, Norton BJ: The relationship of voluntary movement to spasticity in the upper motor neuron syndrome. Ann Neurol 2:460-465, 1977 11 Knutsson E, Richards C: Different types of disturbed motor control in gait in hemiparetic patients. Brain 102:405-430, 1979 12 Dietz V, Berger W: Interlimb coordination of posture in patients with spastic paresis. Brain 107:965-978, 1984 13 Edstrom L: Relation between spasticity and muscle atrophy pattern in upper motor neuron lesions. Scand J Rehabil Med 5:170-171, 1973 14 McComas AJ, Sica REP, Upton ARM, et al: Functional changes in motoneurons of hemiparetic patients. J Neurol Neurosurg Psychiatry 36:183-193, 1973 15 Chokroverty S, Reyes MG, Rubino FA, et al: Hemiplegic amyotrophy: Muscle and motor point biopsy study. Arch Neurol 33:104-110, 1976 16 Hufschmidt A, Mauritz KH: Chronic transformation of muscle in spasticity: A peripheral contribution to increased tone. J Neurol Neurosurg Psychiatry 48:676-685, 1985 17 Lee WA, Boughton A, Rymer WZ: Absence of stretch reflex gain enhancement in voluntarily activated spastic muscle. Exp Neurol 98:317-335, 1987 18 Bohannon RW, Larkin PA: Resistance to ankle dorsiflexions in hemiparetic stroke patients. Clinical Rehabilitation 1:175-180, 1987 19 Colebatch JG, Gandevia SC, Spira PJ: Voluntary muscle strength in hemiparesis: Distribution of weakness at the elbow. J Neurol Neurosurg Psychiatry 49:1019-1024, 1986 20 Knutsson E, Martensson A: Dynamic motor capacity in spastic paresis and its relation to prime mover dysfunction, spastic reflexes and antagonist co-activation. Scand J Rehabil Med 12: 93-106, 1980 21 Mizrahi EM, Angel RW: Impairment of voluntary movement by spasticity. Ann Neurol 5: 594-595, 1979 22 Freund HJ, Hummelsheim H: Lesions of the premotor cortex in man. Brain 108:697-733, 1985 23 Bobath B: Adult Hemiplegia: Evaluation and Treatment, rev ed 2. London, England, William Heinemann Medical Books Ltd, 1978, pp 18-19 24 Davies PM: Steps to Follow: A Guide to the Treatment of Adult Hemiplegia. New York, NY, Springer-Verlag, New York Inc, 1985, pp 48-49 25 Sjostrom M, Fugl-Meyer AR, Nordin G, et al: Post-stroke hemiplegia: Crural muscle strength and structure. Scand J Rehabil Med [Suppl] 7: 53-61, 1981

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26 Bohannon RW: Decreased isometric knee flexion torque with hip extension in hemiparetic patients. Phys Ther 66:521-523, 1986 27 Brodol A: Self-observations and neuroanatomical considerations after stroke. Brain 96:675-694, 1973 28 Landau WM: Spasticity: The fable of a neurological demon and the emperor's new therapy. Arch Neurol 31:217-219, 1974 29 Duncan PW, Badke MB: Determinants of abnormal motor control. In Duncan PW, Badke MB (eds): Stroke Rehabilitation: The Recovery of Motor Control. Chicago, IL, Year Book Medical Publishers Inc, 1987, pp 141, 144 30 Andrews K, Brocklehurst JC, Richards B, et al: The prognostic value of picture drawings by stroke patients. Rheumatol Rehabil 19:180-188, 1980 31 Feigenson JS, McDowell FH, Meese P, et al: Factors influencing outcome and length of stay in a stroke rehabilitation unit: Part 1. Analysis of 248 unscreened patients—medical and functional prognostic indicators. Stroke 8:651656, 1977 32 Feigenson JS, McCarthy ML, Greenberg SD, et al: Factors influencing outcome and length of stay in a stroke rehabilitation unit: Part 2. Comparison of 318 screened and 248 unscreened patients. Stroke 8:657-662, 1977 33 Adams RJ, Meador KJ, Sethi K, et al: Graded neurologic scale for use in acute hemispheric stroke treatment protocols. Stroke 18:665-669, 1987 34 Dohrmann GJ, Nowack WJ: Relationship between various clinical signs in lesions of the descending motor system. Diseases of the Nervous System 35:375-377, 1974 35 Inaba M, Edberg E, Montgomery J, et al: Effectiveness of functional training, active exercise, and resistive exercise for patients with hemiplegia. Phys Ther 53:28-35, 1973 36 Demeurisse G, Demol O, Robaye E: Motor evaluation in vascular hemiplegia. Eur Neurol 19:381-389, 1980 37 Smedley RR, Fiorino AJ, Soucar E, et al: Slot machines: Their use in rehabilitation after stroke. Arch Phys Med Rehabil 67:546-549, 1986 38 Andrews K, Brocklehurst JC, Richards B, et al: The rate of recovery from stroke and its measurements. Int Rehabil Med 3:155-161, 1981 39 Andrews K, Brocklehurst JC, Richards B, et al: The recovery of the severely disabled stroke patient. Rheumatol Rehabil 21:225-230, 1982 40 Verhas M, Schoutens A, Demol O, et al: Study in cerebrovascular disease: Brain scanning with technetium 99m pertechnetate: Clinical correlations. Neurology 25:553-558, 1975 41 Watkins MP, Harris BA, Kozlowski BA: Isokinetic testing in patients with hemiparesis: A pilot study. Phys Ther 64:184-189, 1984 42 Chalsen GG, Fitzpatrick KA, Navia RA, et al: Prevalence of the shoulder-hand pain syndrome in an inpatient stroke rehabilitation population: A quantitative cross-sectional study. Journal of Neurologic Rehabilitation 1:137-141, 1987 43 Sheikh K, Smith DS, Meade TW, et al: Assessment of motor function in studies of chronic disability. Rheumatol Rehabil 19:83-90, 1980 44 Wade DT, Hewer RL: Motor loss and swallowing difficulty after stroke: Frequency, recovery, and prognosis. Acta Neurol Scand 76: 50-54, 1987

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45 Logigian MK, Samuels MA, Falconer J, et al: Clinical exercise trial for stroke patients. Arch Phys Med Rehabil 64:364-367, 1983 46 Merletti R, Acimovic R, Grobelnik S, et al: Electrophysiological orthosis for the upper extremity in hemiplegia: Feasibility study. Arch Phys Med Rehabil 56:507-513, 1975 47 Barer DH, Ebrahim SB, Mitchell JRA: The pragmatic approach to stroke trial design: Stroke register, pilot trial, assessment of neurological then function outcome. Neuroepidemiology 7:1-12, 1988 48 Demeurisse G, Demol O, Robarge E: Le bilan fonctionnel dans l'hemiplegie vasculaire. Bruxelles Medical 59:95-100, 1979 (French) 49 Dickstein R, Hockerman S, Pillar T, et al: Stroke rehabilitation: Three exercise therapy approaches. Phys Ther 66:1233-1238, 1986 50 Fullerton KJ, Mackenzie G, Stout RW: Prognostic indices of stroke. Q J Med 66:147162, 1988 51 Nakamura R, Taniguchi R: Reaction time in patients with cerebral hemiparesis. Neuropsychologia 15:845-848, 1977 52 Heller A, Wade DT, Wood VA, et al: Arm function after stroke: Measurement and recovery over the first three months. J Neurol Neurosurg Psychiatry 50:714-719, 1987 53 Wade DT, Hewer RL, Wood VA, et al: The hemiplegic arm after stroke: Measurement and recovery. J Neurol Neurosurg Psychiatry 46:521524, 1983 54 Bohannon RW: The relationship between static standing capacity and lower limb static strength in hemiparetic stroke patients. Clinical Rehabilitation 1:287-291, 1987 55 Bohannon RW: Relationship between static strength and various other measures in hemiparetic stroke patients. Int Rehabil Med 8: 125-128, 1987 56 Bohannon RW: Gait performance in hemiparetic stroke patients: Selected variables. Arch Phys Med Rehabil 68:777-781, 1987 57 Bohannon RW, Smith MB: Assessment of strength deficits in eight paretic upper extremity muscle groups of stroke patients with hemiplegia. Phys Ther 67:522-525, 1987 58 Bohannon RW, Smith MB: Upper extremity strength deficits in hemiplegic stroke patients: Relationship between admission and discharge assessment and time since onset. Arch Phys Med Rehabil 68:155-157, 1987 59 Beevor CE: Remarks on paralysis of movement of the trunk in hemiplegia. Br Med J 1:881-885, 1909 60 Mastaglia FL, Knezevic W, Thompson PD: Weakness of head turning hemiplegia: A quantitative study. J Neurol Neurosurg Psychiatry 49:195-197, 1986 61 Bohannon RW, Larkin PA, Smith MB, et al: Relationship between static muscle strength deficits and spasticity in stroke patients with hemiparesis. Phys Ther 76:1068-1071, 1987 62 Bohannon RW: Strength of lower limb related to gait velocity and cadence in stroke patients. Physiotherapy Canada 38:204-206, 1986 63 Bohannon RW, Andrews AW: Relative strength of seven upper extremity muscle groups in hemiparetic stroke patients. Journal of Neurologic Rehabilitation 1:161-165, 1987 64 Bohannon RW: Determinants of transfer capacity in patients with hemiparesis. Physiotherapy Canada 40:236-239, 1988

65 Bohannon RW: Relationship between shoulder pain and selected variables in patients with hemiplegia. Clinical Rehabilitation 2:111— 117, 1988 66 Bohannon RW: Rolling to the nonplegic side: Influence of teaching and limb strength in hemiplegic stroke patients. Clinical Rehabilitation 2:215-218, 1988 67 Bohannon RW: Relationship between strength and movement in the plegic lower limb following cerebrovascular accidents. Int J Rehabil Research 10:420-422, 1987 68 Saltin B, Landin S: Work capacity, muscle strength and SDH activity in both legs of hemiparetic patients and patients with Parkinson's disease. Scand J Clin Lab Invest 35: 531-538, 1975 69 Merletti R, Zelaschi F, Latella D, et al: A control study of muscle force recovery in hemiparetic patients during treatment with functional electrical stimulation. Scand J Rehabil Med 10:147-154, 1978 70 Winchester P, Montgomery J, Bowman B, et al: Effects of feedback stimulation training and cyclical electrical stimulation on knee extension in hemiparetic patients. Phys Ther 63:1096-1103, 1983 71 Baker LL, Yeh C, Wilson D, et al: Electrical stimulation of wrist and fingers for hemiplegic patients. Phys Ther 59:1495-1499, 1979 72 Basmajian JV, Kukulka, LG, Narayan MG, et al: Biofeedback treatment of footdrop after stroke compared with standard rehabilitation technique: Effects of voluntary control and strength. Arch Phys Med Rehabil 56:231-236, 1975 73 Stephanovska A, Gros N, Vodovaik L, et al: Chronic electrical stimulation for the modification of spasticity in hemiplegic patients. Scand J Rehabil Med [Suppl] 11:115-121, 1988 74 Bohannon RW: Relative decreases in knee extension torque with increased knee extension velocities in stroke patients with hemiparesis. Phys Ther 67:1218-1220, 1987 75 Kozlowski BA: Reliability of isokinetic torque generation in chronic hemiplegic subjects. Abstract. Phys Ther 64:714, 1984 76 Stern PH, McDowell F, Miller JM, et al: Factors influencing stroke rehabilitation. Stroke 2:213-218, 1971 77 Hamrin E, Eklund G, Hillgren AK, et al: Muscle strength and balance in post-stroke patients. Ups J Med Sci 87:11-26, 1982 78 Stern PH, McDowell F, Miller JM, et al: Effects of facilitation-exercise techniques in stroke rehabilitation. Arch Phys Med Rehabil 51: 526-531, 1970 79 Nakamura R, Hosokawa T, Tsuji I: Relationship of muscle strength for knee extension to walking capacity in patients with spastic hemiparesis. TohokuJ Exp Med 145:335340, 1985 80 Nakamura R, Watanabe S, Handa T, et al: The relationship between walking speed and muscle strength for knee extension in hemiparetic stroke patients: A follow-up study. Tohoku J Exp Med 154:111-113, 1988 81 Knutsson E: Assessment of motor function in spastic paresis and its dependence on paresis and different types of restraint. In Eccles J, Dimitrijevic MR (eds): Recent Achievements in Restorative Neurology: 1. Upper Motor Neuron Functions and Dysfunctions. Basel, Switzerland,

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S Karger AG, Medical and Scientific Publishers, 1985, pp 199-209 82 Hammond MC, Kraft GH, Fitts SS: Recruitment and termination of electromyographic activity in the hemiparetic forearm. Arch Phys Med Rehabil 69:106-110, 1988

83 Winter DA: Concerning the scientific basis for the diagnosis of pathological gait and for rehabilitation protocols. Physiotherapy Canada 37:245-252, 1985 84 Perry J: Integrated function of the lower extremity including gait analysis. In Cruess RL, Rennie WRJ (eds): Adult Orthopaedics. New

York, NY, Churchill Livingstone Inc, 1984, p 1161 85 Bohannon RW: Selected determinants of ambulatory capacity in patients with hemiplegia. Clinical Rehabilitation, to be published

muscle performance tests appear to be highly reliable for some types of patients with CNS lesions.

literature. We will discuss only those studies that were cited as providing research evidence for the use of muscle testing in patients with CNS lesions.

Commentary

Many therapists are taught during their schooling that it is inappropriate to use standard types of muscle testing during the evaluation of patients with central nervous system (CNS) lesions. One of the classic texts of manual muscle testing by Daniels and Worthingham even includes a warning about testing patients with CNS lesions.1 There appears to have been widespread agreement that, because of the nature of CNS lesions, standard approaches to muscle testing may yield measurements that are unreliable or invalid. Unfortunately, what many of us were taught appears to have been based more on opinions than on documented observations or research reports. The time to question dogmatic approaches to the use of muscle testing of patients with CNS lesions is at hand. The works of Bohannon and our own research have now indicated that some forms of muscle testing of patients with CNS lesions yield relatively reliable measurements (see article by Riddle et al and commentary by Bohannon in this issue). Past arguments about the reliability of measurements obtained from these patients2 need to be reconsidered. Perhaps one important lesson to be learned from the biases of the past is the need to test widely held beliefs and to obtain data. Often it is easy to make an argument as to why a measurement may not be reliable, but only through research can we determine the real degree of reliability. Some forms of

We must, however, be cautious and not replace old biases against testing with unfounded enthusiasm in favor of testing. Reliability is only one of two major requirements for meaningful measurements. Measurements must also be useful for something. Measurements must be valid and have inferential uses if they are to be clinically meaningful.2 Bohannon rightly notes that some persons are opposed to muscle performance testing of patients with CNS lesions. We do not, however, consider ourselves in that category. We believe that what is needed is not a discussion of adversaries, but rather a critical examination of the theoretical and practical issues relating to muscle testing. Most importantly, we believe that the data justifying the usefulness of these measurements must be analyzed. The numerous citations put forth by Bohannon provide a good starting point for a meaningful discussion. Bohannon argues in the bulk of his special communication that muscle force measurements can be used to make inferences relating to function. These arguments are put forward under the heading "Relationship Between Muscle Strength and Patient Capacity and Outcome." To make our discussion easier to follow and to relate more directly to Bohannon's, we will follow his sequence in discussing the

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According to Bohannon, muscle performance measurements in brain-lesioned patients appear to correlate with measurements of functional capacity. The logic is clear: If the muscle performance measurement is related to function, then that measurement can be used to predict function. We have no argument with the logic, but we have questions about the literature cited. Correlation of muscle performance measurements with functional measurements can be made along a vast continuum. Clinical usefulness of measurements is dependent not on the existence of a relationship, but on the strength of the relationship. Linton and Gallo put it eloquently when they stated, "The delightful glow that researchers feel when their data turn out to be 'significant' often seems to impair their judgment on the meaning of their findings. When a statistical test indicates that the relationship between two variables is significant, it tells us only that, at a specified probability level, the relationship exists to some extent in the population from which the subjects have been randomly drawn and that it is not due to the operation of chance sampling factors. It cannot be stressed too strongly that a statistical test tells us no more. A relationship may be very weak and still quite real."3(p329) 230/61