QUANTITATIVE CLINICAL MEASUREMENT OF SPASTICITY by ALFRED CHAO S.B., Massachusetts Institute of Technology (1973) SUBMITTED OF THE IN PARTIAL FULFILLMENT REQUIREMENTS DEGREE OF MASTER FOR THE OF SCIENCE at the MASSACHUSETTS INSTITUTE OF TECHNOLOGY February, 1976 Signature of Author DepartiTnintf to ronaut i,'s annd-As trIonautcs January 28, 1976 Certified by Thesis Supervisor Accepted by Chairman, Dc'-artme0nta1 Graduatu Committee Room 14-0551 MITL-Ibrries Document Services 77 Massachusetts Avenue Cambridge, MA 02139 Ph: 617.253.2800 Email: docs@mit.edu http://Iibraries.mit.edu/docs DISCLAIMER OF QUALITY Due to the condition of the original material, there are unavoidable flaws in this reproduction. We have made every effort possible to provide you with the best copy available. If you are dissatisfied with this product and find it unusable, please contact Document Services as soon as possible. Thank you. The images contained in this document are of the best quality available. 2 QUANTITATIVE CLINICAL MEASUREMENT OF SPASTICITY .by Alfred Chao Submitted to the Department of Aeronautics and fulfillment Astronautics on January 28, 1976, in partial of the requirements for the degree of Master of Science. ABSTRACT Present clinical methods of evaluating spasticity is based mostly on subjective assessment. An existing arm manipulator was modified into a device for applying controlled rotation of the forearm- and strain gauges and surface EMG electrodes were used for obtaining quantitative and objective measurements of muscular activities. device, studies were made of th.e abnormal Using this muscular reactions of spastic patients. Stretch reflex in normal subjects, induced by isometric contraction was also studied. These results were compared with data from the spastic patient. Thesis Supervisor: Laurence R. Young Title: Professor of Aeronautics and Astronautics 3 ACKNOWLEDGEMENT I wish to express my sincere appreciation for the patient guidance of Professor Laurence R.. Young throughout this research, and for his suggestions encouragements.. and I am particularly grateful to Mr. Bill Morrison for his invaluable technical expertise and constant assistance. This project was supported in part by a grant from the Rehabilitation Services Administration, HEW 23-P-55854/l. -4- TABLE OF CONTENTS Chapter 1 Page No. INTRODUCTION 5 1.1 Scope and Objective of Research ' 1.2 Review of the Neuromuscular Control System 8 1.3 2 3 4 11 EXPERIMENTAL DESIGN 13 2.1 General Description 13 2.2 Motor Servocontrol 14 2.3 Measurement Devices 16 2.4 Safety Precautions 17 EXPERIMENTS ON NORMAL SUBJECTS 31 3.1 Experimental Protocol 31 3.2 Experimental Results 33 3.3 Summary 35 EXPERIMENTS ON SPASTIC PATIENTS 51 4.1 Experimental Protocol 51 4.2 Experimental Results on Passive Stretch 52 Experiments with Pre-stretch Isometric Contraction 55 Summary 56 4.3 4.4 REFERENCES Related Research 80 -5- CHAPTER 1 INTRODUCTION 1.1 and Objective of Research .Scope Spasticity is a neuromuscular disorder due to upper motor unit damage and afflicts victims of spinal cord trauma, stroke, and a number of congenital cerebrovascular diseases affecting the motor cortex, frontal lobe region, the internal capsule, or other extrapyramidal projections at the These patients present a clinical picture commonly basal ganglia level. attributable to a state of greatly increased activity in the motoneurones, leading to the condition of muscular hypertonia and hyperreflexia. these signs include: Some of uncontrolled spasms as in chronic paraplegia, uncon- trolled continuous contraction as in Athetoid Dystonia, excessive sensitivity and reaction to noxious or tactile stimuli, and widely spreading reactions which tend to overwhelm local reflex signs. As in decerebrate rigidity, spastic patients exhibit hypertonia in antigravity muscles. stiffly extended and resists flexion. The leg is The arm is held flexed and pronated and resists extension. A particularly crippling factor affecting coordinated movement is exaggerated and often spreading contraction in response to passive stretch of a muscle. It interferes with reciprocal innervation and hence diminishes the patient's strength and interferes with his volitional movements. A considerable amount of effort is expended in the treatment of spasticity. Highly touted drugs, such as the widely used central nervous system depressent -6- Valium, and the special neuromuscular blocking agent dentrolene sodium, surface perennially, generating much hope. New physical therapy programs, which can be very strenuous and exhausting to the patient, are continuously being proposed and applied. In view of all this, the present method for evaluating patient progress and effectiveness of therapy is very ill-defined. Usual clinical assessments, as in the case of cerebral palsied patients, consist of observing the patient's gait and strength and degree of self-interference in volitional movements as in hand slapping motions. Evaluation of the exaggerated stretch reflex is accomplished by the physician holding the patients limb and stretching a stiff muscle slowly. tive and highly variable. This type of method is necessarily subjec- To the extent that the physician probably prescribed the drug or physical therapy, and hence has a vested interest in obtaining improvements, his observation and assessment is prone to be self-fulfilling or at least tainted with the "placebo" effect. Considering the energy involved, both physical and mental, a more reliable and objective means of clinical evaluation is needed. This research attempts to study the feasibility of an objective and meaningful method of measuring spasticity. An existing arm movement device has been modified and the necessary instrumentation built so that accurate and controlled muscle stretches could be applied to patients and quantitative measurement data could be obtained for assessment. Repeatability and con- sistency of the test protocol must first be established. Emphasis will then be on the identification and definition of meaningful measurement parameters. An initial set of experiments was run on normal subjects to provide a data base for comparison with spastic patients. Thus the main objectives of the study are: 1. The construction of the experimental device. -7- 2. The evaluation of the device on normal subjects to provide comparative data. 3. The evaluation of the device on patients in order to establish a consistent and useful test protocol for clinical application. The actual clinical testing of patients is not included in this study and shall be left to further research by physicians in a clinical environment. The patients selected for the study were from a pool of cerebral palsied patients at the Children's Hospital Medical Center, Harvard Medical School, Boston. plegics. The group was primarily adolescents, and had been diagnosed as hemiThe reason for choosing hemiplegics lies in the availability of the unaffected side for comparative study. The muscle group selected for study are those involved in the rotation of the forearm, namely the pronator teres and pronator quadratus for pronation, and the supinator and biceps brachii for supination. These muscles were picked since they are easily accessible, being used frequently by physicians in subjective tests, and because they are less commonly altered through the need for corrective surgery than is the case for the ankle joint where bone fusion is often administered to compensate for spasticity in the antigravity muscles. 1.2 Review of the Neuromuscular System Most muscles are composed of three types of extrafusal fibres. The large pale A fibres have few mitochondria ATPase and receive few blood vessels. The small C fibres are loaded with mitochondria and have the richest blood supply, hence the dark color. B fibres are intermediate in structure. Most pale muscles contain varying ratios of the three types of fibres, hence the pale color. Red muscles such as the cat's soleus muscle consist solely of type B fibres and appear homogeneous under the microscope. -8- A functional motor unit is defined as being composed of an a-motoneurone and the muscle fibres innervated by its many axon collaterals. Evidence sug- gests that a-motoneurones innervate only a single type of muscle fibre, so that there are essentially three types of motor units. Large type A units have more fibres per unit than type B and C units and are innervated by larger and faster conducting neurones. tracting and develop higher maximal tension. There are more slower and smaller units since the number of fibres per unit is less. tension and allow for finer control. due to their abundant blood supply. They are fast con- Hence they develop less They are also less susceptible to fatigue The order of recruitment is organized and determined at the spinal level by the size of the motoneurone. Smaller moto- neurones and hence smaller units are easily excitable and provide fine control at low tension levels, and since they are activated more often, need to be relatively unaffected by fatigue. As tension increases, larger units are recruited, providing larger increments of force. There are two types of stretch receptors. Muscle spindles are composed of connective tissues containing two kinds of intrafusal fibres. Nuclear bags are larger and contain large nuclei in the central expanded region.- The smaller nuclear chains are attached at the two ends to nuclear bag fibres. Motor inner- vation of these fibres are provided by two types of small y-motoneurones. y1 fibres terminate in discrete motor end plates and appear identical except in size to extrafusal fibres. y2 fibres end in complex ramifications. mental evidence suggests a distinct scheme of innervation, and Some experi- Y on nuclear bags, y2 on nuclear chains. Spindle afferents consist usually of one Group Ia fibre supplying primary annulospiral endings on both bag and chain fibres, and several group II fibres supplying secondary endings primarily on chain fibres. With gamma support, the -9- primary endings respond to both velocity of stretch and static stretch, whereas secondary endings are essentially tonic length sensitive devices. Recent experimental evidence (Bergman and Grillner, 1969) suggests differential control of the two gamma cells. Thus the phasic (velocity) sensitivity of the Ia affer- ents derives from primary endings on the nuclear bags and hence is controlled by Y1 fibres, while their static sensitivity originates in the primary endings on nuclear chains and is adjusted via Y2 fibres. Ia afferents are excitatory to their own motoneuronal pool and inhibitory to y-motoneurones of the antagonist muscle; whereas Group II afferents are excitatory for flexors and inhibitory for extensors. The mechanism of the so-called stretch reflex, and the role of the spindle afferent loop, as elucidated by Sherrington, is reviewed below because of its significance in the pathophysiology of spasticity. Merton (1951) proposed the follow-up servo model, which features the spindle afferent reflex loop as the principle mechanism for voluntary muscle contraction. According to this theory, movements are initiated via y-motoneurones. Efferent volleys in the gamma fibres cause the intrafusal fibres to contract and thereby elicit afferent discharge in Ia and II afferents. the This activity reflexly excites ot-motoneuronal pool, causing the extrafusal fibres to contract, unloading the spindles until a new steady state length is reached. Eldred, Granit and Merton (1953) showed that reflexly evoked contraction of the soleus muscle of the decerebrate cat, as by neck flexion, was accompanied by accelerated spindle discharge, indicating fusimotor stimulation to compensate for spindle unloading. If the servo loop was opened by dorsal root section, no contraction was observed, but increased spindle activity was again reported, pointing to gamma activity. However, voluntary movement can occur even in a totally de-afferented limb (Eldred, 1960). It is generally accepted that in -10- most centrally initiated movements, alpha and gamma coactivation is involved. Alpha activity directly commands extrafusal contraction, while gamma firing maintains the spindles in their sensitive region and hence in a position to correct for load disturbances. Wilson's (1964) elegant analysis of the locust flight control system, which consists of fewer than twenty motoneurones for each wing, showed that the removal of the two sources of proprioceptive input, namely stretch and lift transducers in the wings, caused no qualitative alteration in the motor pattern. There was only a reduction in the wing beat frequency. Thus the phasic affer- ent information appears to provide no more than a tonic reinforcement to a centrally patterned motor output. Recent studies by Engberg and Lundberg (1969), correlating EMG activities of the flexors and extensors of the cat's hindlimb in normal walking, found that the onset of extensor activity during placement of the paw actually precedes contact with the floor. Hence it could not have been produced by proprioceptive feedback from spindle afferents. trally programmed. It was concluded that stepping motion is cen- Peripheral feedback may augment and modify this activity, but does not initiate or maintain it. In contrast to the apparently supplementary and compensatory role it serves in normal volitional movements, the afferent feedback loop appears to exert a heavy influence upon the a-motoneuronal pool in a spastic muscle. The hyperactive tonic stretch reflex reflects an abnormally heavy inflow in the gamma system, leading to the high reflex gain. It is also plausible that it is the loss of descending presynaptic inhibitory influence, or a release of descending, supraspinal, facilitory lines converging on the afferent pathways, together with some degree of gamma support, that is responsible for the spastic reaction to passive stretch. -11- This is plausible in the light of considerable experimental evidence (Lundberg, 1962; 1967) which suggests that most segmental pathways between primary afferents and motoneurones receive convergent inputs from descending systems. Thus, for instance, the interneurones that mediate Group Ia inhibi- tory influence on an antagonist flexor muscle were shown to receive, monosynaptically, axons originating from the Deiter's nucleus and descending in the vestibulospinal tract. And Group Ia inhibitory interneurones projecting to both flexor and extensor muscles are excited by fibres in the rubrospinal tract (Hongo, 1969), and, in fact, with longer latency, by axons of the corticospinal tract (Lundberg, 1962). According to these observations, the inter- ruption of this type of descending supraspinal projections, as in spasticity, would lead to a state of hyper-reflexia. At the same time, it would explain the concommitant deficiency in reciprocal inhibition in antagonist muscles. 1.3 Related Research Bomze (1973) developed an elaborate hydraulic system for studying spasticity in the biceps. His data, as well as Leavitt and Beasley's (1964) suggests that patient data are highly variable, and depend on mood, cigarettes, and inadvertent tactile stimulation during testing. Measurements of resistance in spasticity were complicated by voluntary non-reflex components of tension in studies by Herman (1970), while tests utilizing EMG such as reported by Burke et al (1971) with sinusoidal stretches of the hamstring and quadriceps yielded valuable phase relationships, pointing to the dynamic and tonic components of the stretch reflex, but little quantitative force measurements. Dmitrijevic and Nathan (1967) did extensive clinical observations of spastic patients with spinal cord injury. However, and only phasic tendon jerk stimuli were given. ponses that spread to other muscles. again only EMG were recorded They reported exaggerated res- -12- Neilson (1972) worked with athetoid-spastic patients and used elaborate statistical methods for data reduction. Frequency response characteristics of the tonic stretch reflex in both normal and spastic subjects were obtained with the subjects sustaining various levels of voluntary contraction of the biceps brachii. Correlation techniques were used to get rid of the voluntary components of reaction and the results indicated the gain of the tonic stretch reflex increased with the level of voluntary contraction in normal subjects, but remained at a high constant level in spastic patients. Also the gain versus frequency curves for normal subjects contained sharply tuned resonant peaks, pointing to rather complex long loop pathways in the reflex. Patient data did not show such peaks, suggesting the loss of complex supraspinal loops as well as descending spinal influence in spastic patients. Study of tonic vibration reflex by Hagbarth and Eklund (1968) and Burke and Ashby (1971) also point to similar conclusions. Vibrations were found to suppress the monsynaptic reflex and the H reflex in normal subjects, whereas the suppression is less in spastic patients, indicating a loss of spinal presynaptic inhibitory mechanism. Hyperactivity in the gamma system appears to be a necessary condition for the exaggerated stretch reflex in spasticity. Rushworth (1969) showed that in the decerebrate cat, selective block of gamma fibres abolished the rigidity and stretch reflex. In man, he reported that 1% procaine applied around the major nerve trunk abolished hyperactive stretch reflexes without affecting voluntary motor power. -13- CHAPTER 2 EXPERIMENTAL DESIGN General Description 2.1 The particular muscles selected for clinical evaluation were the pronators of the forearm, the pronator teres and the pronator quadratus. The choice was based on the fact that rotation of the forearm can be easily performed and is often used by physicians in qualitative assessments of spastic patients. The forearm is also less often interfered with by prior corrective surgery as is often the case with the ankle joint. An existing arm movement (humeral rotation) device was modified into a servo-controlled manipulator of the forearm. A high torque motor is mounted vertically in an aluminum block which also houses a 6:1 step down gear train. The stall torque at the output handle is approximately 350 lb-in (Allum, 1974). A spade type handle (Figure 2.1) is attached to the output shaft. Strain gauges on the integral torsion tube of the handle register the subject 's muscular reaction. Separate feedback and measurement potentiometers are attached using anti-backlash gears. A separate measurement potentiometer was used to reduce the effect of slack present in the gear train between the motor output and the final geared down output shaft. -14- The motor is servo-controlled with the control circuits on an analog computer (GPS 290T) and is driven by a pulse-width modulated power supply. Microposition switches cut off the power to the motor in case the handle exceeds about 800 of rotation in either the pronation or supination direction. Mechanical stops also prevent such excessive excursions should the electric stops fail. This entire structure with the motor, gears, handle, strain gauge electronics and two 60 Hz filters for the input and feedback signals is mounted on a heavy metal stand. A horizontal beam attached to the stand has on its distal end a movable elbow cup which serves to support the subject's elbow as well as align his ulna with the axis of rotation. A modified dental chair is used which allows for the proper positioning and posturing of the subject. Shoulder harnesses are employed to provide a certain amount of restraint and support for the subject and are especially useful for some of the patients. The surface electrodes used were buffer-amplified types (Jacobssen). Grass P5-AC preamplifiers were used. EMG signals were recorded from the pronator teres, the powerful pronator of the forearm, and the biceps brachii, which is employed in supination. EMG signals were full-wave rectified and filtered on the analog computer. Arm angle, torque and two channels of EMG were recorded on a four channel strip chart recorder (Brush) and the torque was plotted against arm angle on an X-Y plotter (Moseley Model 135). Figure 2.2 shows some of the experimental set up and equipment. 2.2 Motor Servocontrol The motor servomechanism consists of a positional feedback and a pulse width modulated power supply (Figure 2.3). If a simple unity feedback gain -15- is used without any series compensation, the system dynamics is very sluggish and the output impedance is too high for any reasonably heavy load. Thus lead compensators were used in both the forward and feedback paths and a high feedback gain is used so that the system now has a response time of about 450 milliseconds. It has negligible overshoot and is fairly unFigure 2.4 shows the uncompensated affected by disturbance in the output. and compensated time responses. Note that the dynamics are very accurate for step and ramp inputs (Figure 2.5). The reduced third order model for the motor system has the transfer function: E)(s) = I )2 ( n K -(S+ -S ( + a) S2 + 2Cw +W n where w n = = 25 rad/sec a = 0.7 2 fl 137 rad/sec = 56.6 rad/sec The motor control and compensation circuits are shown in Figure 2.6. The detailed derivation can be found in Allum's thesis (1974). The error (control) signal modulates nominal frequency of 1 kHz. a ± 35 volt square wave with a Since there is an inherent instability in the flipflop stage of the modulator preamplifier which causes the square wave to saturate to a constant 35 V level of the opposite sign, the input has to be limited so that saturation never occurs. This does not happen in any case except at the edge of a step which has been lead compensated. Both the control and feedback signals are filtered (first order filtered, break frequency 40 Hz) to reduce the effect of 60 Hz noise. -16- Measurement Devices 2.3 The method for measuring the subject's muscular force was to use the torsion in the tube part of the spade handle. The design of a torsion tube requires that it have sufficient sensitivity to torsional stress. A hollow tube of a high enough sensitivity would have a wall so thin that it would be very susceptible to the bending mode. Instead a slit tube of one inch outer diameter and 1/32 inch thickness was bored into the integral part of the handle that fits over the motor shaft. The slit effectively interrupts the shear flow and drastically reduces its torsional stiffness. The derivation of the stress-strain characteristics of the tube is quite involved due to the complex boundary conditions. Figure 2.7 shows the bridge and amplifier circuits. Four BLH film gauges are attached to the center portion of the tube and are arranged in a push-pull bridge configuration. is 5 volts. Thus V gauge where R Factor = = 120 ohm, 2. The bridge input voltage = V. AR/R i V. = 5 volts, AR/R = (Gauge Factor) x 6, and Gauge Thus Vgauge = 10s, where e is the strain carried by the gauges. The bridge output is amplified 104 times and the calibration curve (Figure 2.8) shows a slope of 0.21 V/lb-in with good linearity. hanging weights. 5 Therefore, V output = 10 5, Calibration was done with and the actual strain per lb-in is 2.1 x 10-6 which is approximately the theoretical value calculated. Since the maximum torque is not expected to be over 50 lb-in, the maximum strain will be less than aluminum. 10 4, which is within the elastic strain limit of 10 3 for -17- The measurement potentiometer is a Helipot (3 turn, 20K). The calib- ration curve is shown in Figure 2.9 and has a slope of 90 mV/deg. The Jacobssen electrodes require a ± 5 volt supply and have a mid-frequency gain of 350. They have a built-in low frequency roll off (20 dB/decade) with break frequency at 50 Hz and a high frequency first order roll-off breaking at 5 kHz. The integral FET buffer amplifier produces a better signal to noise ratio. The Grass P5-AC preamplifiers have gain of about 20 and have first order roll-offs at 35 Hz and 2 kHz. Raw EMG signals are full-wave rectified and first order filtered to The processor circuit is shown in Figure 2.10. simulate peak-followers. Figure 2.11 shows some typical raw and filtered EMG. The filter time con- stant was about 100 msec. The pronator quadratus and the supinator are the primary muscles involved in the rotation of the forearm, however they are imbedded among other forearm muscles. Thus the pronator teres and the biceps brachii are used. 2.4 Safety Precautions The safety shutoff mechanism consists of a relay box and a bell which is excited when the motor power is cut off. This is important since the motor has more than enough torque to overpower the forearm. Four switches can trip the relay: the two microposition switches on the motor chassis, a switch on the analog computer, and a hand-held panic button. The microswitches are mounted on aluminum brackets and a one-inch steel rod attached radially to the handle shaft will contact the switches should the -18- rotation exceed approximately 800 from the vertical in either direction. In the unlikely case that these switches fail, the steel rod will hit the brackets and the handle will be stopped mechanically. A further safety device is used on patients who exhibit a continuously contracted fist. Since these patients may not be able to let go of the handle in case the movement is in fact causing pain, an electronic circuit on the analog computer is used to monitor force level. This will switch off the power should the force exceed a certain preset level. The torque output from the gauges is summed with the reference level and feeds a comparator. When the torque becomes larger than the reference, the comparator output becomes 0 V so that the Set input of the SR flipflop is grounded, setting the ONE output to -3 V. The output converter converts the -3 V to 6 V which feeds an electronic switch and open-circuits the 10 V power supply voltage to the relay, thereby cutting the power to the motor. The flipflop output will remain at -3 V and the power remain cutoff until the reset input is grounded via a Clear switch. With the flipflop in the low state, as long as the torque is less than the safety level, the comparator output will be at 6 V and the Set input of the flipflop will be at -3 V. The flipflop output will thus be at 0 V so that the electronic switch will remain closed and power will be delivered to the motor. in Figure 2.12. The circuit is shown -19- steel r od for triggering s afety switch L5 V94V~e FIG.2.1,- Diagram showing. dimensions for the instrumented spade handle and strain-gauge bridge circuit. -20- -' F'PL.Ar waTR W - - -- A'MAkf 4ALE - POT #40OR+ mo EM TAA4N- M&T R LZJ F* 7A.b ;; D8ACK 7 ~4A&AU6ES - Pay LW C' I Aurnrur MAW~ &.,I ~ CEMr AMP3 TR/AK 1t VEY O Co 6W(R - BM UFFER XY e07 T, S &AL1/ f &QAI(Yr MS b~I SAFFTY Cv-rOFF act/Cv,7 r=-ffuw FIGURE 2.2- Pictures showing experimental cquipment. Compens ator Motor INPUT Error-signal Limiter Pulse-width Modulated Power-Supply Safety Cutoff Feedback FIGURE 2.3 - Block Diagram of Servo-controlled Manipulator Drive System. motor angle -22- ' j ''I t-4 ~' j I ii. l -- f j - - - -~ - - - . - - - f f ____ _ I f I --I---I--I----I------I---I------+------I---I---I-----1---I---.I. I I I I -I-I-i-V-I III IIej~ I -~ -i-I-i.-..-- I J~ I 1~. -. 2 -~ JRATION Iii S -li--i I I t t I ESUFr AL o N~w I I - -I-.-..' - I 1111111 I- I I -- - - I I I I I I I I ~ I I LLLJ41. I w~ I ____ - .1.2 P~i7i 7.Lr' ~4 j LL 'I * I ~1SEC..J. I *1 FIGURE 2.4 - ' I ~--b-' I --~ I *i I I I 11 -. j 4............4.......1...... 1 II I *I t tl:1f1 1 ll.K~ I II I L I . I.., -± _________ [ ~ '~ 'I' - .1 12 1 1 ' .. i~ -. - I-.-.-.1 I ~1~~~ - 'A- t - 1* I Ii -- - ~ System time response. Top traces with unity feedback and no compensation. Lower traces with input and feedback compensators. . i -I ..I I -23- LilI- I I I ! I !I !:T I- -- - I V I _ _.f -4 ~ - - - ~. ~ -J I-1-****- - -'-4.-; II "f'I' t~f~t~ It Ii 1:1{7;i f--i I I I I I -I ---I-----I-+----*I---1-----+--- I --- I _ A1--- I I - f I ? {--f ---z1'K K 1I - 20' - I- - -I - -I- pron I I 'I -- 1 I -- ----I-- -100 msec I L- - -- I.--A --- I -- -I-- I i I I I I- * I E ----1- -I--LIT I -I I- 1 -1 I I I I S.I-----I -- I I I I I _ I 7VV7 TI -FP-7412 --I----I* III:- ~~~~1~~~~ !~..... - --- i 1~~ / ~ -- isec - - 1~ "I - ---- -- - I---I-I -i--- i-ti-i--if-I~I1iIii~i~ I I I I I I- - -i --1- f-----4-I--I 71 7? ~4 __-K1----~ - 71 __ // .0 I / C6' VI,,P K1irLLj~~ FIG. 2.5 - Compensated systens dynamics. I ~ ___ Top traces show step response; bottom traces response to triangular wave. Bias -10.0 Input Waveform 1/s1 1To B Las Error Limiter 1.0 ~11 An Fe Edback 137 FIGURE 2.6 - Circuit Diagram for Input (Top) and Feedback (Bottom) Compensatorso Battery switch 1M Strain gauge 56K 50K -15 Wheatstone bridge Gauge switch V. 6 v0 5. 11K 56K 25K LO CN ' 3 R vR 2 2 4 . -- K Output -103 (v 2 50K Bridge Excitation adjustment Trimpot balance S+15 v 1K FIG. 2.7 - Circuit for strain gauge bridge and amplifier. - rrrP Volts ------- -- -- - ....... _ _---_ -6-.. S--. I - 5 4. - . . .~ - I ____ ____ tI ____ 1 20 1 4_____ .4 I_15 -IL .... .. . . --- I S4 41 10 Lope I 0, -21--Yol 1 s/lb UPinat ion ~~~~1~*~~ f 1: 51 2025 L I II -3 .1 .4 1 3~0 -j-orq e- (l-in- -2 I I 15 4:1 - 25 -I I jI __ 1 Pronation .1. II.:;.. I -__ _____ - .*i*<y.KIY~<.I11 K: I..fjl .1 .1 _ ____ -~- I __ .... I' :1:: '7- :. TiI -7 :_-7 -7 -. * IG, 2. 8 - Calibration Curve --f'or-S train. Gauge -Amplifier Output----- I ____ I T~4- 1 iI.....i I - ... ._._.... _ .. . sOJ ts/degrel ------------_ _ _ _ _ _ _ _77- __ I __ __ __ __ K***i ----------- -L 75 -- 7 dl~e is1,5 0. i 7;~- 7~7i7IiI 0 -300 77-i _ 7_11A1Mr ___ -4I i t 1 4- 7-747 1 14 FIG 2 9 ---- Clbaoncurve---for -the -Arm-angle: me asurem enL -potenti.oieter K-v-4 t -. 7 --1ComparRaw nc Fator no E MG 10/s Electronic Switch 00 0.1 Full-Wave Rectifier FIG. 2.10 - Filter Circuit for EMG Processor with Full-wave Rectification and First-order Filter. -- -29- W71. 111 I I I I iji jIA 1 fr~ L -1 11.. I -+-------1----I--I -I-f-I I I I 111 I ~I ___ I ___ ~ I_ , [-I 1 1 *. ba ,ws -1-----I--f-'I-- I I I Th~ - I -. Fill- -F-i-_ 44-{ 4+ - - - .- I I I 'liii 2V- .A. 1 E G 11 2. I - Raw EMG and filtered EMG. Top two traces from Pronator from traces two Biceps Brachii. Lower Terres. Records taken together to show action of reciprocal innervation. RELAY POWER - MOTOR nc >O +10V>c Motor Power no Switch Electronic Switch FlipFlop TorqueSR Comparator Re -- Input Convert,---6V->;o - 3V 1 S R 0 Output Convert.-3V -+ 6V . Reset Switch FIG. 2.12 - Circuit diagram for force-level safety monitor and motor cutoff - ---1lr't 11' , I 1 -1 _f, -31- CHAPTER 3 EXPERIMENTS ON NORMAL SUBJECTS 3.1 Experimental Protocol The following experiments were designed to study the tonic stretch reflex in the forearm of normal subjects. These results shall thus pro- vide a valuable basis for comparison with those of spastically afflicted patients. The tonic stretch reflex, which is hyperactive in spasticitiy and more easily demonstrable in decerebrate animal preparations, is usually absent or very small in the relaxed muscle of normals. Monosynaptic reflexes to highly phasic stimuli such as tendon tap may be elicitable in the normal relaxed muscle, but reflexes with longer and more complex pathways appear to be under conscious control and can be voluntarily modified and suppressed. Thus it is difficult to patients. obtain results comparable to that from spastic Even with methods that produce muscular responses resembling stretch reflexes, it is still difficult to evaluate and interpret the experimental results. They do however provide a qualitative basis for comparison. The experiments involved the controlled pronation or the supination of the forearm. Movement waveforms included steps and terminated ramps. sions were usually 45 degrees from the vertical. Excur- The subject was asked to -32- maintain prestretch isometric contraction in the muscles to be tested, that is, the pronators or supinators. The timing of the movement cycles was randomized to minimize prediction on the part of the subject. The subject was seated upright on the adjustable dental chair, with the humerus abducted about 150 from the vertical. The movable elbow cup aligned his ulna with the axis of rotation and the height of the chair was adjusted so that his elbow joint roughly subtended an angle of 1100. EMG electrodes were attached to the biceps brachii or the pronator teres and the subject was told to hold the spade handle. The experimental variables included: 1. Velocity of stretch which varied from about 850 /sec (the approximately linear response to a step input) to terminated ramps of approximately 450 /sec and 200 /sec. 2. Initial prestretch condition. Subjects were required to maintain different levels of isometric contraction before stretch of 5, 10, 15 and 20 lb-in of torque. The torque was displayed to the subject on a small calibrated meter. A few experiments were performed where the prestretch bias force was maintained, but with the forearm undergoing a slow movement in the direction of the bias force, before the forearm was stretched in the opposite direction. Results do not indicate any significant differences. angles were also tried. Different initial arm The effects, if any, were small. The recorded measurements were: 1. Arm angle 2. Torque supplied by the forearm 3. Raw EMG from the biceps brachii (a supinator) and pronator teres 4. Filtered EMG signals -33- These were displayed on a four-channel strip chart and force versus arm angle diagrams were obtained on an X-Y plotter. 3.2 Experimental Results The activated muscle Precise instructions to the subject were difficult. with increased alpha and gamma activity is known to facilitate the stretch reflex in normals. This can be achieved by isometric contraction. The muscu- lar response, however, is still dependent on the instructions given to the subject so that some reflex components are not consistently present and are not readily distinguishable from voluntary contraction. Initially, experiments were run with the subject being told to-relax the forearm, but not let go of the handle, as fast as possible after the stretch was administered. In this way, the voluntary component of resistance was thought to be minimized or eliminated. Figures 3.1 and 3.2 show the typical time history of response. stretch EMG activity was due to isometric contraction. As can be seen, a short latency EMG burst of about 40 msec is usually present. to a monosynaptic reflex pathway. The pre- This may be due EMG activity decreases after about 70 msec, indicating relaxation in accordance with the instructions. A burst of renewed ENG activity often occurs at about 120 msec, concomittant with or slightly trailing the peak of the reaction force. The force increases instantaneously with the start of the stretch, before any change in the EMG. to the visco-elastic property of the activated muscle. This must be due The reaction force is very smooth and does not shown any "humps" in response to the EMG bursts. Figures 3.3, 3.4 and 3.5 show typical force angle hysteresis loops for these experiments. The smooth linear rise in force is due to the elastic -34- property of the contracted muscle. These plots were obtained real-time, where usually the second applied stretch was recorded, and thereafter, alternate cycles were selected for display. Invariably, the first cycle shows a longer relaxation time and hence reached a higher force level. The spring constant for the activated muscle, as reflected in the slope of the force-angle diagrams, increases with the level of isometric contraction. Figures 3.3 and 3.4 show the hysteresis loops for two stretch speeds for the same subject. dependent on stretch speed. As expected, the spring constants are not Figure 3.6 shows the spring constant as a func- tion of isometric pre-stretch force level for three subjects. The stretch in these cases was &510/sec ramps in response to. step inputs. Control experiments were performed with the subject's forearm relaxed and the subject instructed to resist the movement as fast as possible. Figure 3.7 shows two representative time courses of response. Response time, as indicated by the onset of EMG activity is about 120 msec with very small variance from subject to subject. This figure is substantially smaller than Allum's (1974) results with humeral rotation where voluntary response was interpreted to have a latency of about 225 msec. Evarts (personal communica- tion) however found a voluntary component in pronation and supination as fast as 70 msec. As reported in the first set of experiments, there is usually a 120 msec EMG burst which appears to be involuntary and comes after EMG activity has in fact decreased to a very low level. Thus this 120 msec latency response may in fact represent a long supra-spinal reflex loop which is biased on during the voluntary resistance task and which is also activated by pre-stretch isometric contraction. In the latter case, its reflex action to stretch appar- ently occurs even after conscious relaxation of the muscle. -35- Two other experimental conditions were tried. contraction was again required of the subject. Pre-stretch isometric Post-stretch instructions were changed in one case to voluntary resistance to stretch. shows some typical results. Figure 3.8 The fastest component of response is again about 40 msec which is probably monsynaptic, and a long latency component at approximately 120 msec. In a few cases, an intermediate latency response (about 80 msec) can be discerned. The peak force reached was much higher. However, the force increase was again very smooth in most cases. Another set of experiments was run where the instruction was not to relax, but also not to consciously resist movement. The instruction is somewhat ambiguous, but results again revealed a 40 msec reflex and a 120 msec main burst. The peak force is lower than in the case of voluntary resistance, but is sustained longer than in the case of conscious relaxation. Figures 3.9, 3.10, and 3.11 contain typical time history and force-displacement loops for this test condition. Figures 3.12, 3.13, and 3.14 contain force displacement hysteresis loop diagrams from three different subjects comparing the response to the three test instructions. As expected, the spring constants, which are the initial slopes of the loops, are essentially identical in the three cases. The reaction force is higher in the case of conscious resistance, however the force increase in all cases was smooth. 3.3 Summary Results on the tonic stretch reflex in normals were obtained. Precise instructions were difficult and the subject's response varies accordingly. -36- In all three cases, pre-stretch isometric contraction was needed to elicit a stretch reflex. With higher velocities of stretch, namely 850 /sec and 45 /sec, there is present in most cases a 40 msec monosynaptic reflex and a 120 msec delayed main component of EMG activity. This is true under all three test instructions, although in the case of conscious relaxation, the 120 msec burst occurs after EMG activity has actually declined in accordance with the instruction to relax. Thus it appears that the 120 msec EMG activity is probably reflex in nature and is biased on even in the case of voluntary resistance without prestretch isometric contraction. It is unlikely that this burst represents a conscious maneuver, say to regain grip on the handle, since if that were the case, the burst will have a minimum delay of 120 msec after relaxation began. The spring constant of the activated muscle is not dependent on velocity of stretch or instructions to the subject. It increases however with the level of prestretch isometric contraction. The force-angle hysteresis loop diagrams are of different shape according to test instructions. However, they all exhibit smooth and even slopes. They do not contain segments of noticeably different slopes in the region of increasing force. This feature is not expected to be found in measurements of spastic patients. -37- i-1t~Fii1I'~H'~ _I _______ '1 7~I~7'F -~ - --- - -1 - _- 1O-Ilb-inn - -- I I I~I I ~ - - - - - - - - I~LILLi - ~1~ I -h+-' FE -I-i~tiIijij - Li2__(1)(Z) ~4 (13Y I I - t I I---- I S ms1~ 1 1T1.I 11 - j j.- If Pronator Teres -T-1 -4L FIG. I111I I I I T~1~~~f.Ti _J1 !...... 0 0 -ms - - iII7 711 -1 - -- 3.1 - Response to 85 /sec stretch with instruction to relax as fast as possible. Trace 1, angle; trace 2, torque; trace 3, raw EMG; trace 4, integrated EMG. Arrow l indicate timing of start of stretch, indicates short latency burst (2) and (3) shows long latency (120mscc) burst. Irregularity in angle trace is due to pot noise. -38- YORK :1 II I I iii: 'FFF ZJIlIiIIIII1IiTVPTh 1 1 1 1~ 1' _ _ I I 1 I hi PHi fi 114 I I ZiI'I~K - - - . - 71]itIT -~ 5...sUp~. I Iii' I -I----I--I-----I-----1---]-I-- -I.--- I--- -I I -- I---I----4--I----t--- ---I -4----] - ___ - i 4b .7 - I~ ~ - r 1}iiLj iyhih ___________j 1' 1 3Fd~.L~ - - 11 - - zHizi.L1 .Jzz1 __ -----I--]-----I--I- - ms 0-0Teres FIG.3.2 - Pronator - - - Response to 85 0 /sec stretch with instruction to relax as fast as possible. 4 ,p. i :. _ _ p_ I 20 Im t: 7 -7 7T 77____ -. '-' 7~"i -4 nhaedretoo ws t aspossbl0 relx a soo Instucton /sec.~ stec.Arw ~~ 1 .1 rvlo op - ... 7 ....... -f 7 7- I. I + 1; I- - 7 -7:',- - - ; - -- - - I _ - -- - - -7 - - 10- 1' ; - in 0FIG. 3.4 Response to 20 /sec. stretch. Instruction was to relax consciously. as fast as possible after stretch. . ......... .......... .......... 77 ..... .. ............ ... ... .... ... ..... .. ... ... - -Arm rl Ow V rt %A\- 7N .......... ...... .. . ... ... ............. LAI XX WR - .... ... V: Al V Lo 4J - --------- -4J 4-) Ln 4J o 444 Ln ........0 1 H Ln' ........... K -- sprin'g-constatt: in/deg __ *' .i**... -- ----- ------ -----__-lb _ H ___ ~ I- 7.I.'7-I7 ~~IiI~ . ~ I. -----. I...... .1 __ _ ___ _-7 -:0-1-__2- 7K -- -- *1 ---_- - -- - --- - ---- -- 45 --- _______ __ ___ -1 ___i7tT~ 1 _--__1 I _5_-- I -4 '' Lw- , L -1 * -1 _2d F ismetrc cotracionievei lbin, 7 Muscle spring constant~ as a 0uc b fpre-seretch :. I.. i i I .1 t ~ it! mti '--contraction .. level .?-oints ~&averages: of....atlea-st__ foturyc.1e.4 - --Data f or th ree subj cts, . 1 VHfl7i7~ i FG:3.6 ,. * j.777 and' stretch' speed wa5 85 /se6, I ? -43- FT 7 45profl'p_ -f -~ *1II *j} ~.41II. jiff I -~-1 ~[ 1 1 1 1 I 1 I 1 1 ~II I --1---1-[-f---I----4-----I------I I I I I 5- - h{- -~y± I - I -I---I----4--I-----f----1----f---I----I ~rach"i-7 ---1- 00 - I - 1I I [JfI -- ~ I I -1L4 ___ -I---I----f----f - -- I -[ I I I II t -- -.-. - Ill- - 3 FIG. 3.7 ~~1~~ I----1---i---1-I---I.-.-I --I -- - I ~iI II 'I I II - b n t* -4. I 'I'l-~ -i-~i-i7I--1--I-~ I I Fv-i-I-i-K 0 I . l~ - Response to 85 0 /sec stretch, voluntary resistance to stretch with no prestretch isometric activity. -44- F 11111 JZLLLLLL 11 ~II17~~ 7 F I ~ I 'I I -7 Ff -P1 30 ------ 5. n...I ---- - -------- I--- ----- --ps- I - ----- i -I--I ---- LJJ~~~] ~TT7. L1~ ET ;I-L Hi-,, ~ __________________-I (x) -- i---' H a) Ci)t~.) I 1 ~ I * 3.8 - Response to 85 0 /sec. I- 11.11 ~ -*--. I FIG. I --I------I- I- - V.F- 1 I I'i 'j ~ ____________ Cl)2) '- I -I-I I I I stretch; instruction was to resist consciously. 5 lb-in prestretch isometric contraction. Arrows (1) for start of for short latency ; (3) for long latency bursts. (x) indicates intermediate burst. stretch; (2) -45- I~ i~~ILrr -- o.p - -- -.- 1 -4 F- --- lbV-in mI*I--[--{-*-*---II-- I -- I- Me,1-- I F I i00ms- rr Biceps I Brachii -4.0 li-I I +3142 i 4 FIG. 3.9 I I I I I I I ~'T'"T Response to 85 /sec. stretch. Instruction to not relax or resist consciously. Arrows 1 show start of stretch, 2 show short latency burst, 3 indicate long lantency burst. -f-77-- . ..... ..... .......... --J . ..... .... T A ..... . .... .... ... 7T .. .... ... ... .. . . .. . .. . . . . . a ...... .... ..I . .... .... TI.... .. ........ ..... .... .... ... .. .... . .... .... .. . .... .... ...I .... ... .... ......... .. .... .... ............ 1-7 ;iZ .... .. . .... . .... .... .... '77 . .. ... .... ... .... .... .... .... .... .. .... .... I a . .... .... ... T PI/, L------ 7: - 7 . . ... .... .... .... .. ... ...... ... .... .... .... . ... .... .... ... ... --------77 45 sup 'r0 m%4- 1% T 17 k" e-. 4-! 4-rk v-k% ----- [777 7- .... %F in V, 0 rga a t- TI eq.A e% a T . . t ir -7 7 ~- L 1 T. .. 7_ S7P 145 FI 4FI.374 -7---77- i 3 s u dc teeSbetwa 0t -0- - odntt ea rrss - -- - - -- -- - .... .. ... 4 .......... . . . .. . . . 1 ....... ~ ..... I ----------- Co __ __71{i7 -.- . 7.... .~.. . - I . . .. . . . . . . . . .. . 0 FIG. 3.12- 45 /sec. stretch. Top three traces voluntary resistanceA-middle two, traces not consciously resisting or relaxing; lower traces relaxation, . * ~. .. . . ..... 1 ....... 7 7- 7. ..... -------- -- 7-7- 7 .. . 7- J - II 45. s. 0 F'IG. 3. 13 8 5 /sec. stretch.I I 7 7- .~ .. ... 0 . . . .. ......... - ------------ ....... .... ... . .. . . . . -7 . . . .. . . . . . .. . . - -- - - - - - - - . .. . . . 7 . . . .. . . . . . . .. . . . . . . . It -- - - - - -- -- - . ....... .. A m :A ... ... .. 7 w. 7 .... . ....... ....... .. ... 7. .7 .. ...... --------- a I :7-7-T---7- t-n 0 I -7 7- r L 1-4 -r'i RES IS,T 01 ,E/A)( 7 .77 I r '00;. -7 .. .... ... .... -PEtAX A: --- f7-7 .177-7 -7 ... ... 77 '77 ------------ .... .... 16 ...... Aa".41 - .450 FIG. 3 14 0 -85:,./sec.-.stre ch%--- FJA -51- CHAPTER 4 EXPERIMENTS ON SPASTIC PATIENTS Experimental Protocol 4.1 Special precautions were observed in experiments with patients. It was observed that patients will often shift the position of their torso to accomodate the stretching of the forearm. Thus shoulder harnesses were used to somewhat restrain this motion, but without causing undue discomfort. Also, the force level monitor and cutoff switch (Chapter 2) was used to prevent excessive force from developing. Trapezoidal stretches with speeds of approximately 20, 45, 90, and 135 degrees/second were given. The range of motion was determined before the actual experiments by manually controlling the voltage from a motor position bias potentiometer. In this way, a slow and smooth rotation of the forearm can be achieved; and the patient was asked to report any excessive stiffness or pain that was induced. obtained. An initial estimate of motion range was thus Faster movements were then given to make sure that the range was not excessive for higher speeds. The measurements taken were again arm angle, reaction torque, EMG from the pronator teres, and EMG from the biceps brachii. recorded on tape as well as on a strip-chart. Measurements were Torque versus angle hsyter- esis loops were again obtained on an XY-plotter. -52- the patient was told to relax as much as possible and allow his forearm to be passively rotated. speeds. About 12 to 15 cycles were used for each of the four Stretches were given first in order of increasing speeds, with a About 5 cycles per rest period of about 5 minutes in between these groups. group were then applied in reverse order of speed in order to observe any correlated or adaptation effects. Experimental Results on Passive Stretch 4.2 Patient J.K., male, age 33, had been diagnosed as left hemiplegic. The results showed spasticity of the supinator muscles, and to a milder degree, of the pronators. The preoators, in particular, showed spastic reactions that were more pronounced when stretched at higher speeds. For both pronators and supinators, muscular responses were highly variable from cycle to cycle, but did not show any trend toward adaptation. EMGs were taken from the pronator teres, which is more superficial, even though the pronator quadratus is usually more active. However, the signal suffers- from contaminating discharges from other flexor muscles of the hand. This is particularly a problem in spastic patients whose reactions more often than not, involve several muscles at the same time. Figure 4.1 defines some of the quantities and variables that appear in subsequent time records. Figures 4.2 through 4.5 show typical responses for stretches of 20 deg/sec. At this speed, stiffness. the pronators exhibit very little With the forearm in the maximally pronated position, there is usually a rapid decline in the biceps EMG, along with a similar drop in force, indicating relaxation of the biceps immediately following stretch. With the start of linear stretch in the supination direction (Phase 1, Figure 4.1), the force records invariably show a small reaction force with no increase in pronator EMG (Figures 4a, 5a, these designations refer to events marked in the -53- respective figures). This probably represents a combination of the static weight of the forearm and the stiffness in the flexor muscles of the hand. The force reduces to zero as the arm appraoches the vertical position (see Figure 4b, 5b). The pronator EMG, meanwhile, remains at the same level, or in the region about the in some cycles actually decreases to a lower level, vertical. The EMG starts to increaseas, or shortly after (Figures 2a, 3a, 4c and 5c) the arm goes into supination (Phase 2). around maximum supination (Figure 4d). It peaks with the force The pronator EMG and force drop only slightly during static extension. The pronator EMG (Figures 2b, 3b) continues to decay as the arm moves toward pronation (Phase 3), but does not reach a low level until the arm is nearly vertical (Figures 2c, 4e). Biceps EMG and supinator force usually show no immediate rise (Figures 3c, 4f) as the arm moves from the maximal supinated position (Phase 3). They then undergo a big increase (Figures 2d, 4g) as the arm goes through the vertical into pronation (Phase 4). This in- crease is usually accompanied by either a rise in the slope of the torque record, or in some cases, by almost a step change in the supinator force. The biceps EMG peaks, with the resultant force, slightly before maximum pronation and decays rapidly in the stationary flexed position. The pronator EMG activity decreases as the forearm was moved from the maximum pronated toward the vertical position (Phase 1). This occurred even though the pronators are being stretched during this phase. As the arm goes into supination (Phase 2), the pronators begin to resist and the resistance is maintained during the period of static-extension. In fact, it continues even when the supinated arm begins to pronate towards the vertical position. This happens despite the fact that the pronators are now in fact in the shortening phase. Thus the pronators appear to be activated when the forearm is in any supinated position. -54- EMG The biceps, on the other hand, appears to behave quite differently. activity and supination force rise as soon as the arm moves in the direction This is true even when the arm is in a supinated position as of pronation. during Phase 3. The EMG and force shows an increase as the forearm goes into pronation (Phase 4). They then decay rapidly during static pronation, and remain at a low level as the arm rotates towards supination (Phase 1). During this phase, the biceps is shortening even though it is still in stretch. Hence, it appears to be primarily sensitive to velocity of stretch; and when that condition is met, as during Phase 4, it receives reinforcement from a static stretch sensitive component of resistance. Thus, at this slow speed, at least, the pronators appear to be sensitive to position of stretch and hence their EMG are in phase with the angle record. The supinators, or at least the biceps, appear to be most sensitive if stretched in the pronated region. Thus their EMG usually leads the arm angle by 900. Figures 4.6 through 4.10 show typical records of response for higher stretch velocities. tests. Both the pronators and the supinators become more spastic in these This is revealed in the average level of reaction force, although the stiffness still varied significantly from cycle to cycle. The phase relationships described above still obtain for the biceps. is shown inFigures 6a, 7a, 8a, 10a, and 10b. This In several cycles, the biceps develop some level of excitation during rotation towards supination (Phase 2), as seen in Figures 6d and 8c. This is however almost certainly due to coacti- vation with the large pronator activity at those instants. The pure positional dependence of the pronator EMG, however, is observed only at Figures 6b and 6c. At Figures 8b, 9a and 10c for instance, the pronator exhibited velocity sensitivity similar to that observed in the -55- biceps: EMG activity increases simultaneously with the start of movement towards supination (Phase 1), and undergoes another increase as the arm is led into supination (Phase 2). In Fig. 8[b], the early EMG signals (during Phase 1) may be attributable to the activity in the biceps. However, this is not the case in Fig. 9[a] or 10[c], where biceps activity was in fact constant and low. Thus a velocity sensitive component is present in the pronator reaction to fast stretches. Fig. 4.11 shows a stretch cycle at 135*/sec. with an expanded time scale. In this cycle at least, the pattern of the pronator's positional and the biceps' velocity sensitivity appears to be similar to that observed under slower stretches. Fig. 4.12-18 are typical torque-arm angle hysteresis loops obtained from the patient. The four stretch phases (ref. Fig. 4.1) are marked on Fig. 4.12. The pronator force is very small during Phase 1 of the cycle. In some of these loops, an almost linear rise in pronator torque is observed, starting early in Phase 2 when the arm goes into supination. 13[a), 14[a] and 17[a]). (Fig. 12[a], The higher supinator force increases quite linearly from the maximal supinated position, especially in faster stretches. In some cases (Fig. 13[b] and 15[a]), an increase in slope can be seen as the stretch enters into the pronated region. biceps EMG activity described earlier. This reflects the increase in Except for Fig. 4.18, all these superimposed hysteresis loops indicated considerable variation in the patient's response between cycles. 4.3 Experiments with Pre-Stretch Isometric Contraction Experimental conditions similar to that used for testing normal subjects were also tried on patient J.K. -56- Tests involved the supination of the spastic arm. As reported before, the pronators of this patient were mildly spastic, and pre-stretch isometric contraction was easily achieved. on a meter for the subject. The level of contraction was again displayed Stretches were 45* supination from the vertical; and the instructions were, as before, to relax or resist as fast as possible. Selected results from both test conditions are shown in Fig. 4.19 and 4.20. They reveal results quite similar to those from normals. There is a monosynaptic burst with about 40 msec. delay, and a bigger, longer burst at 120 msgc. The patient takes much longer to relax, and his biceps EMG shows some coactivation. Fig. 4.21, which shows the hysteresis loops for the relaxation condition, in fact bears a strong resemblance to those obtained from normals with the instruction to not consciously resist or relax. Fig. 4.22, showing the plots for voluntary resistance, are similar to those from normals. Summary 4.4 The results obtained agree with reports from other researchers (Bomze, 1973) and (Leavitt, 1964), namely, that spastic reactions are highly variable even for the same patient. Muscular reactions can vary considerably from cycle to cycle, but they do appear to increase with speed of stretch. The phase characteristics for the biceps and the pronators are quite distinct at slow speeds. The biceps is primarily sensitive to velocity of stretch, while the pronators react mostly according to the position of stretch. At higher stretch velocities, a velocity sensitive component of pronator activity can sometimes be discerned. The patient's pronators are capable of quite powerful voluntary contractions. With prestretch isometric contraction, the instructions to either relax or resist supination, it was found that the mildly spastic pronator appears to have the same reflex activity as a normal muscle. The EMG bursts do not appear to be stronger. However, in the patient, conscious relaxation takes considerably longer, and the muscle remains active when in the case of normals, such acitivity would have been suppressed. -58- . Ii7j N der - -~I I - -- I I - r -N % I I i I iii' -1- ---1 v-u -A---... __ H L.4 L'L'~L L -±-~r 1 I PIZ * I I I I I i FIG. 4.1 - Typical results to illustrate and define parameters and variables. Top trace: arm angle is divided into 4 phases, numbered accordingly. -59- GRAPHIC CON 7q .1 Sr-I 1~ I ----- -- --P rf--I -I -- I--f iI------I-I-I---I-j--f--------- ---- - f - I - tTI. IA i LI ~ I-~--i- -I-*- -I * i ---I - - I N' I --I---I -- I-- I--t------~ I j di 4--i iit iii FIG, 4.2 - Typical patient results. Stretch speed : 20 /sec. Arrows and letters mark events referred to in the text. -60- PRINTED .0 # N U.S.A. I 114I I I I - - -4 4-- 71.. _FLhT9 I---- I---II -I--~I f--- V- -I-- T I- ------- I-4---I--f-f---F--I--- 00 FIG 4.1 ain' aaSrthsed2 sc -61- Pq8NT EO SN U.S.A. -- 11n K ~1~~* -+ + --- -- I77- - --- - ---- -- pro0 - 4-H -~--4i- ilk - - - -~ -I L- -I+- - - - - I 1-- -- -- 71 FGL. FIG. 4- 4.4 LI -Patient ti d data. Ltre t spe-d: K LL.1 2 L Stretch speed: / s1" 20 0/sec. 7 -62- Il I 1 1; t4L FIG. 4.5 - P Patient data. -T -4 - i iec. 2 Stretch speed: O /sec. -63- paINTED IN U-S.A 6T li -4 FIG. 4.6 - 4 -417 Patient data. Stretch speed:45 /seCo I :,I -64- GRAPHIC CONTROLS I j tij ~ p CORPORATION * p p BUFFALO. N(-W p i p i -11I 11111 ~izfzzz71zzzz7 I I t I ' ii 1 '' - -~ F. L I,-,--, _____ 1- I -4-- I -I -- F --I ----- --I- --- I ---- -4---I-----I----~ LI 1I [ -~- -I ct '6~ ~ I IIF. L FIG. L if LL Spikes sped:45 /sec. data Stretch 4.7 -Patient in EMG records arc from electromagnetic stray fields; source unknown and had not been a problem prior tthis set of experiments ~EORDING BUFFALI --- a .- 7i. -4- 7 A! I - CORPORATION GRAPHIC CONTROLS .............................................. CNARiT] 1- L U I' I ~- i-I I -HI I I I- -I-- I1-1LI..1 I I~~I1I-1-1- I I zj~i eiig Ii-i~~1 I~~IL-f-I- II ___ I v I 1. i-.i~-~i-I--.1-.--I.---I.-------i------+---I------I-----I----1--f-----' -I --+------I---i-----I----I-~ I - --- 9 III'' - '4 ~-,-------t - lierrsecv-{- ---1 ron ~ - itr±iiizIZELI~i-----L- 09 il 1 IL 1..7-1.;;1~ i -I1ec-1 7I - ~~~99~~ FIG. 4.8 - I1 - 11t i- . - I -- ------ [I -- I-- I ui.--- t - I- - l i i i Patient's response time history. Stretch speed is 90 0 /sec. -66- t~fNT [-,S OFIPORATION -- BUFFALO. NEW YORK 75SI A I -------- - T-- 7 - )d!- -- - N L - -- - - - j, sec-", i--I I FIG. - 4.9 I I -I--I--I Patient I -- I response. -- I-- 1--I--A --- Srthsed9 H -- II- - - - I - sc -67- 1~ I 1'/l Ifk i V I/I I, 1--\ 'I I I i !1 I ' I I I I I J-! I /l i k, I II I I I* 1- ---4 -1I I 1 1 1 I L-- I 4----I 7-- LE I ThTT eL ~~ - -- I ~ ~~ f ' F - - -I FIG. .10 atien iifL -4 ~~ f--- -- I--I----I------ AA LLI *-1-I-- Resonse Ij ~ -I ---- {---I--- 1- * -- - A 1 - 147f11V[I -T-vn-I 0 Stec sI...j]1 1 /sec i-I. I t-~. I I _____ ____ II I I -ILl--i--li I I - ___ I 177V7 1,111 34~~!.s I I I: - ~.J I F -I II I -'-s VtK1 I- -~ 1 I I I I I I - i I I I 1 I -- n- I I *----~-------±__ -- -I- 1*1 I r _17 '#. J .. I . I F 1 ~~' I see ---- t--i i 0/se7 L- 00 - I I I 'F''ITVV' I I I I TF I I_ 0 - I -i7- I .7. FIG. 4.11 I IiT 11 1"V' FIV 01_ _ - I t L I -T 1II i-& - L4 .1L2 44.1 I 1 4 II' II I -i7-F I :ji]'4 -- 11 I--F--I'i--IIiIil T77P~L ~~~4~- I i - I Ii ~-i Li~~'L I I I __L j ~-. I I .-...' I I -I t I I I I I I I I 4 I I I I -4 H F--i- --- 0- ~2A I- I - - -4-, a I I I I K~1KN% ... i.....111 i..***.***~lj***~.*j** I I I I I ,~o; 1 ~ f I II 'Till 4>. Ii ____ * ___ ___ 1 I I-I '1 I ~ ________ -- _ Patient response to 135 /sec. stretch. Expanded time-scale. Ripple on torque traceis 60Hz. noise. >4 ... Surination C)0:... a.........2i .......t .... Arm Ang1e OK!0i O0 T ---- j 45 Pronation iis- 7 TOrque .15 -/NCASfA.' -i 7~ PHA -57-RETCH - rI..:: 7.- 7 - 10 -7'C17--1 - n --- -- 1 -- --- -- ''20-T AA5 -- 4 FIG 4.12 Torque-Arm angle hysteresis loops. Arrow indicates progression of stretch cycle. Stretch: 20 0 /sec, 3Q 0 5 ___ A UO I__ Ih" ~~ ____ , t1 I tion0 __ I ti I -tPro. lb~. I .. ........ ..... FIG.'4.13 Torque-angle hysteresis loops. Stretch speed: 20 /sec. _ _ 2 0 ... 1 Su~riaio i10__ -- -f ... . ....... .- ronation __ PAr.1Angl1e -15- 7T 0 I -- - ---- --- ---- 7 .. lb- in: H ... J.: .. t 41 S2 .-7 FIG ...... .... I . 4 4 5 Strtchts. ec....3 .... .. I.... 7... 7 Supination_______ I Armr Anrile I Pronataion Trui '~15t 1_1 lb-in - - - - - - -- .. .. I FIG. 4.15, Stretch ed45 /sec. . :1 ... I f ...... ......... 0 Sunination, 45 -7 717 4 591 Pronatio -7-1 7 ... ..... ........ 71 P ron. t 1 b - I'n Sup 7.. . . . .. . . . 7-- r ------- ---- ......... .... . .... ... 7- 1.... ....... . -77'-:j:*: .... ... :1 ... ... ... ........ .......... ---------------- -.7--17= ... .... t a: : : 7 2 ......... . ... ... . ..... IG.- 41.16 St!ret!h.s!eed' 90, /sec..; 30 *. ... - 1. .1.......... .... ::T : o:: u i a r -7450 -.:._.._.. 175. .................. F7 .............. ___ ............ Arrrn' Aanale 1 1 q m. . 1, 7 I K 7- I I.7' I I7 ii __ -7T rqiuq ..... . ....... ~ + 1\I j.t.. lb- ih 1 ?1 I w a ..20. . . 7 1 w0 FIG. 4.17 1-Stretch spe~ e 90 /sec., I ._ . ... r QT0 . 'IF 0: 77': SuT)i n ai .'.'.7 ......1.0 ... ........ on Ar miAngle- I 7 f'=' :.d 7- ... .... .... ... . 77 . ... ...... .............. .... on :t 15 :,A s .... ...... ... . .. ..... . w. ... + .... .... ... N, .1 O_ .. .. ... .. .... q ... .... ...... ... . 7 :7 7 .... ... . ... ......... .... .. . .... .. ...... . ....... .. ...L ...... ........ .... .... IL-4--d -7'-7 a. :j .... ... A:::, = ... ... T7 Pron*v- . . .... .... .... ..... . .0 : . .. .... .. . ... ... ... .777 -A -7 w ... ... ..... .... . . ..... "-7 ------*- __4 --------- _7 . 1:A . ... .. :T . . .... .... .... .... 7, 77:. 7: .... .... .... :7. .......... ... .... ..... -7 - 77 .... .... ... ... .... .... .... .... w :::;I:::: 1-77-7-1 .......... ... 7 - ------ i' 7 7 -7 V w 1-77-7- 77-1--7-7-17 Ii lun I ..... . .. .... . .7 ........ ... .... . .. .... rr ...... 7: 777. 17 .... .. ............. 777 . a . . w. -2 -7T-7-177 J .. .... 77 .... ... .... ... .. .......... .1 . .. .. . .. .... A .- 77 F 4 18 _.Strett-.h'speed:l:-135' sec-..---j- m 4. -4-30 -7---s .. . ....... -763. NEW YOPK ts ILYIT iij~.f~jiij liii H~HI-& ri-I FiEI~i~ I{L f1H"Iit F-F--- - 1 44 11 K ----I *-J- I-~*--~I - I I I JMccp 1 $ I -. I FIG. 4.19 - I 1( I 1-. I - I1i LL u~Li ~- I 4 r £ BUFFALO. NEW YORK cnRlPORAl ION I I - Response with isometric contraction and instruction to relax as fast as possible after stretch starts. Arrows (l)- onset of stretch; (2)-first EMG burst; (3)-Second EMG burst. ~L L.L..L.......L...L........L.....~A .......... i I I I 4 I I I -77- I -- Kt-+ 0 -- +--+---I--+-_- - - ---- 11 -1 - - - - IT - - I FJF FIG.220 - ana Response with isometric contraction possible. as 0instruction to resist as fast (2)- first EMG Arrows (1)-start of stretch; burst; (3)-second EMG burst. 12 -7 . ..l .. ... .. ... ... 7 . .t. I . . 1;2 i /.. ... . .! f oe .U 20 VK N4 - ...i _____________7 ~ 4~ qi FIG 4.1 IoerccnrcinIstuto L /6 ,0 1 Oki o lh i at- AII .......... -- FIG. .4.22 T relsist stretch. 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