Brain Research, 99 (1975) 387-392 © Elsevier Scientific Publishing Company, Amsterdam - Printed in The Netherlands
387
Electromyographic patterns during ballistic movement of normal and spastic limbs
RONALD W. ANGEL Department of Neurology, Veterans Administration Hospital, Palo Alto, Calif. 94304, and Department of Neurology, Stanford University School of Medicine, Stanford, Calif. (U.S.A.)
(Accepted August 4th, 1975)
During a ballistic movement of the upper limb, the agonist muscle shows a distinctive pattern of E M G activity. The first event is a burst of muscle action potentials related to acceleration of the limb. This is followed by an electrical 'silent period' at about the time of maximal velocity. Finally, a second burst of E M G activity occurs while the limb is decelerating. This E M G pattern was originally found in human subjects~,6,8,16,17 but it has recently been demonstrated in squirrel monkeys, opening the way to a more direct study of the related central processes. Terzuolo et al. have shown that the pattern is remarkably similar in the two species, not only in general structure but also in the time relations between muscular activity and the physical parameters of movement 14. As they have pointed out, these time relations satisfy the conditions for relating central activity with the movement under study. Since the mechanical and E M G patterns obtained during movement are a reflection of central activity, one might expect to find deviations from the normal in patients with disease of the m o t o r system. For example, the effects of unilateral brain damage might be studied by comparing the patterns obtained from the right and left arms of a patient with hemiparesis. The goals of this communication are (1) to describe a method for quantitative comparison of motor behavior on two sides of a patient with spastic hemiparesis, (2) to illustrate the use of this method in a specific case, and (3) to interpret the results in terms of neuronal mechanisms known from animal experiments. The apparatus used to record position and velocity of the limb has been described elsewhere a. For each test, the subject is seated with one arm extended toward the recording handle and the forearm supported by an aluminum half-shell which is linked to the chair through rods and ball-bearing joints. The arm support allows free movement in the horizontal plane but prevents the arm from falling. Hence, one can study the movement of a limb that may be too weak for the patient to raise without assistance. Just beyond the recording handle is an oscilloscope on which two vertical
388 lines are displayed. One of these, the target line, remains centered until the experimenter pushes a button, causing it to j u m p to the right or left. The other line move~ in response to right-left movement of the recording handle. The apparatus is calibrated so that a hand movement of 10 cm to the right or left will superimpose the two lines after a target j u m p in the same direction. Muscle action potentials are recorded by means of Beckman skin electrodes, used with Beckman electrode paste and adhesive collars. Two electrodes are fastened over the posterior fibers of the deltoid muscle, one about 2 cm below the acromion and one about 4 cm medially. This portion of the muscle functions as an agonist during abduction of the humerus. In order to permit objective measurement of the E M G responses, the muscle action potentials are rectified and smoothed by means of a state-variable averaging filter 7. On the filtered E M G record, all deflections are upward, and each point represents the sum of all E M G activity in the preceding 44 msec. Points of maximal and minimal activity are defined more clearly than on the 'raw' EMG. Despite the timelag introduced by the filter, it is legitimate to compare records taken from the right and left deltoids, because the same averaging window is used on all trials. At the start of each test, both the target line and the cursor are located at the center of the oscilloscope. The signal consists of a step-function displacement of the target to the right or left, depending on which arm is used. In response to the signal, the subject moves the handle as rapidly as possible so as to re-align the cursor on the target. This requires abduction of the arm, moving the hand l0 cm in the direction of target movement. When the movement has been completed, the target is recentered, and the process is repeated at least 20 times to obtain sufficient data for analysis. During each trial, a Grass model 7 polygraph is used to record: (a) position of the target line, (b) position of the hand, (c) velocity of the hand, (d) E M G from the deltoid muscle, and (e) the filtered EMG. F r o m the record of each response, 10 measurements are taken as illustrated in Fig. 1 : (1) the time interval between the target step and the first upswing of the velocity curve; (2) the maximal velocity, i.e., the highest displacement of the velocity curve above the base line (Vmax); (3) the interval between the onset of movement and the time of maximal velocity (TVmax); (4) the interval between the target step and the first clear deflection on the unfiltered E M G record. The remaining 5 measurements are taken from the filtered E M G record: (5) the height of the initial peak, measured in millimeters above the base line (P1); (6) the lowest point on the record at any time during movement (Min); (7) the higest deflection following the minimum (P~); (8) the time interval between the onset of activity and the first peak (TP1); (9) the interval between the onset of E M G activity and the minimum (Train). The timing of the second peak could not be measured reliably, because it was often almost equal in size to other nearby potentials The method is illustrated by the results of testing a patient with spastic hemiparesis. This patient was a 23-year-old veteran whose left cerebral hemisphere had been damaged by shell fragments. At the time of testing, muscles of the right shoulder girdle and upper arm were graded 4 out of 5 in strength. Forearm muscles were graded
389 TABLE 1 BALLISTIC ABDUCTION OF THE NORMAL AND PARETIC ARM*
Time to onset of movement Maximalvelocity (cm/sec) Time of maximal velocity Time to onset of EMG Height of first EMG peak (P1) Minimum of EMG (Min) Height of second peak (PD Time to first peak of EMG (TP1) Time to minimum of EMG (Tmn~)
Normal arm ( h f t )
Paretic arm (right)
Mean
Mean
S.D.
t
P
315 84 232 200
64 18 44 78
3.9 3.8 9.1 3.0
~. 0.01 • 0.01 ~: 0.0l < 0.01
0.7 4.6 2.4
N.S. < 0.01 < 0.05
247 66 127 144 26.6 1.2 16.7
S.D.
54 14 34 45 7.4 1.2 6.2
25.2 3.1 12.9
5.7 1.6 3.9
89
34
188
36
9.5
-< 0.0l
300
107
409
70
3.8
< 0.01
* Times are in msec. EMG amplitudes are in mm.
3-4. The p a t i e n t was able to curl the fingers a r o u n d the r e c o r d i n g handle, b u t they could n o t be m o v e d independently. Muscle stretch reflexes were all m o r e active on the right side t h a n on the left, a n d the p l a n t a r response was extensor. There was no facial paresis or visual field defect. The p a t i e n t could speak and c o m p r e h e n d instructions. All m o t o r functions, including reflexes, were n o r m a l on the left side. M o v e m e n t s o f b o t h arms were tested a c c o r d i n g to the m e t h o d described above, a n d the resulting d a t a showed a n u m b e r o f differences between the two sides (Table I). The visual r e a c t i o n time, m e a s u r e d f r o m the signal to the b e g i n n i n g o f E M G activity or to the onset o f m o v e m e n t , was significantly longer on the affected side. H o w e v e r , the m a x i m a l speed o f h a n d m o v e m e n t was greater on the affected side, resulting in a variable degree o f o v e r s h o o t , as illustrated in Fig. 1. The mean time between the onset o f m o v e m e n t a n d the a t t a i n m e n t o f m a x i m a l h a n d velocity was greater for the right a r m t h a n for the left. This implies that, a l t h o u g h the right h a n d a t t a i n e d higher velocities, its m e a n acceleration was less t h a n n o r m a l (362 cm/sec ~, right; 520 cm/sec 2, left). O n the filtered E M G record, the absolute size o f P1 has no significance, since it d e p e n d s on electrode placement, the a m o u n t o f amplification a n d o t h e r external factors. Therefore, the gains were a d j u s t e d d e l i b e r a t e l y so as to m a k e P1 a b o u t the same o n the two arms. (The table shows t h a t the values were n o t significantly different.) Hence, one m a y c o m p a r e the relative a m p l i t u d e s as well as the t i m i n g o f Min and P2 on the two sides. The time f r o m onset o f filtered E M G to the first p e a k (TP1) was m o r e than twice as long on the spastic side. Similarly the time when E M G activity d r o p p e d to a m i n i m u m (Train) was m o r e t h a n 100 msec later on that side. The a m o u n t o f activity
390 I
SIGNAL
HAND POSITION
/
//
(
ill I
/ FILTERED EMG
!
,.
(
~:e,
t:
e
I
P1 /
\r, I
P2 Min
.-.~___ -L_ ~ _ l . . . . . '~ TP1 Train
\/~\/~./~..
,,
_~. . . . . . . . . . . . . TP2 L
,
250
rnsec
Fig. 1. Abduction of the spastic limb. At the time 0, the signal line jumps to right, The EMG response begins at time 1. Hand movement begins at time 2 and reaches maximal speedat 3. On filtered EMG, the first and second peaks are labeled P1 and P2. Minimal activity is at Min. The times of P1 and Min are measured from point indicated by broad arrow.
during the 'silent period' was greater and the height of the second peak was lower in the spastic muscle. The differences between the normal and spastic limbs suggest a number of tentative conclusions. The reaction time to a visual signal was clearly longer on the affected side, suggesting that there is a delay in the transmission of m o t o r commands from the damaged hemisphere. In the presence of damage to the corticospinal tract, it would be impossible to recruit the usual number of fibers, but temporal s u m m a t i o n could still occur through repetitive discharge of the remaining fibers. Consequently, a longer time would be necessary to excite the required amount o f motoneuron activity. The increased duration of the initial E M G volley resembles that which occurs
391 when a normal limb moves against an inertial load '). One mechanism that could account for this finding is the unloading reflex 3. Vallbo has shown that voluntary innervation of a skeletal muscle is accompanied by an increased rate of spindle afferent discharge 1.5. It is reasonable to infer that this Ia activity contributes to the excitation of motoneurons causing a ballistic movement. If one assumes that the spindles are unloaded during rapid movement, then the termination of the initial volley may be due in part to a decrease of facilitation by way of the la afferents. In the paretic limb, movement is slower, and one might infer that the spindles are not unloaded so rapidly or so completely. Hence, the Ia discharge would be continued longer than normal, exciting the motoneurons to prolonged activity. Another spinal mechanism that might affect the duration of the initial motor volley is inhibition, due to excitation of the Golgi tendon organs. Since the most effective stimulus to these receptors is the force caused by muscular contraction, they would be expected to fire during acceleration, and the resulting discharge of lb fibers would tend to inhibit the motoneurons reflexly. In the paretic limb, the force on the tendon would be less than normal, and the motoneurons would thus receive fewer inhibitory impulses. The result would be a delayed and less complete silent period. The Renshaw cells provide a third mechanism that might affect the duration of the initial volley. These cells, which are excited by recurrent collaterals of the alpha motor neurons, are believed to inhibit the alphas 11. Because of the reduced motor activity on the paretic side, the Renshaw cells would receive fewer impulses during the initial volley, and the motoneurons would be subjected to less inhibition. In speculating about the results of this pilot study, it must be recognized that muscle afferents project to the cerebral cortex, as well as to the spinal cord 1°, and several experiments point to the existence of cortical mechanisms that may have a role in voluntary movementSAL In the monkey, for example, neurons of cortical area 3a have been shown to reflect the length of a forearm muscle during maintenance of steady postures la, and the precentral neurons respond very rapid when the moving limb encounters an unexpected change of load 4. When the corticospinal system is damaged by disease, a maximal discharge of the upper motor neurons will sometimes fail to elicit the desired acceleration. Information from the slowly moving limb could then excite cortical 'reflexes' to adjust the motor discharge appropriately. Another finding in the present case was the relative smallness of the second E M G volley on the affected side. This is analogous to another finding reported in patients with hemiparesis 1. When a muscle is unloaded during voluntary contraction, the E M G normally shows a brief silent period followed by a volley of renewed activity. This volley has been found to be smaller on the affected side of patients with hemiparesis. As Landau has suggested, powerful excitatory connections of the upper motor neuron pathway may be necessary for the rapid return of activity after the transient removal of segmental afferent tone by the unloading procedure 9. The patient with unilateral brain disease provides a useful model for the study of pathophysiology. Although one cannot use microelectrodes, as in primate experiments, the patient is able to provide a great variety of voluntary movements on
392 request, an d the n o r m a l side offers a m a t c h e d c o n t r o l for the affected limb. T h e t e c h n i q u e described here is one a p p r o a c h to the q u a n t i t a t i v e study o f such patients.
1 ANGEL,R. W., Unloading reflex in patients with hemiparesis, Neurology (Minneap.), 18 (1968) 497-503. 2 ANGEL, R. W., Electromyography during voluntary movement: the two-burst pattern, Eh, ctroenceph, elin. Neurophysiol., 36 (1974)493-498. 3 ANGEL, R. W., EPPLER, W., AND IANNONE,A., Silent period produced by unloading of muscle during voluntary contraction, J. Physiol. (Lond.), 180 (1965) 864-870. 4 CONRAD, B., MATSUNAMI, K., MEYER-LOHMANN,J., WIESENDANGER,M., AND BROOKS, V. B., Cortical load compensation during voluntary elbow movements, Brain Research, 7t (1974) 504514. 5 EVARTS, E. V., Motor cortex reflexes associated with learned movement, Science, 179 (1973) 501-503. 6 GARLAND,H., AND ANGEL, R. W., Spinal and supraspinal factors in voluntary movement, Exp. Neurol., 33 (1971) 343-350. 7 GARLAND,H., ANGEL, R. W., AND MELEN,R. D., A state variable averaging filter for electromyogram processing, Med. Biol. Engng, l0 (I972) 559-560. 8 HALLET, M., SHAHANI,B. T., AND YOUNG, E. R., EMG patterns during stereotyped voluntary movements in the human. In B. T. SHAHANI(Ed.), Proc. int. Union Physiol. Sci., New Delhi, 1974, Elsevier, Amsterdam, 1975, in press. 9 LANDAU,W. M., Spasticity and rigidity. In E. PLUM(Ed.), Recent Advances ht Neurology, Davis, Philadelphia, Pa., 1969, p. 6. 10 OSCARSSON,O., AND ROSI~N, I., Short-latency projections to the cat's cerebral cortex from skin and muscle afferents in the contralateral forelimb, J. Physiol. (Lond.), 182 (1966) 164-184. 11 PIERROT-DESEILLIGNY,E., AND BUSSELL,B., Evidence for recurrent inhibition by motoneurons in human subjects, Brain Research, 88 (1975) 105-108. 12 PHILLIPS,C. G., Motor apparatus of the baboon's hand, Proc. roy. Soc. B, 173 (1969) 141-174. 13 TANJI,J., Activity of neurons in cortical area 3a during maintenance of steady postures by the monkey, Brain Research, 88 (1975) 549-553. 14 TERZUOLO,C. A., SOECHTING,J. F.. AND PALMINTERI,R., Studies on the control of some simple motor tasks. III. Comparison of the EMG pattern during ballistically initiated movements in man and squirrel monkey, Brain Research. 62 (1973) 242-246. 15 VALLBO,ilk. B., Discharge patterns in human muscle spindle afferents during isometric voluntary contractions, Acta physiol, scand., 80 (1970) 552-566. 16 WACHHOLDER, K.. Willkiirliche Haltung und Bewegung insbesondere ira Lichte electrophysiologischer Untersuchungen, Ergebn. Physiol., 26 0928) 568-775. 17 WACHHOLDER,K., UND ALTENBURGER,H., Beitr~igezur Physiologie der willktidichen Bewegung. IX. Mitteilung. Fortlaufende Hin- und Herbewegungen. Pfliigers Arch. ges. Physiol., 214 (1926) 625 641.
387
Electromyographic patterns during ballistic movement of normal and spastic limbs
RONALD W. ANGEL Department of Neurology, Veterans Administration Hospital, Palo Alto, Calif. 94304, and Department of Neurology, Stanford University School of Medicine, Stanford, Calif. (U.S.A.)
(Accepted August 4th, 1975)
During a ballistic movement of the upper limb, the agonist muscle shows a distinctive pattern of E M G activity. The first event is a burst of muscle action potentials related to acceleration of the limb. This is followed by an electrical 'silent period' at about the time of maximal velocity. Finally, a second burst of E M G activity occurs while the limb is decelerating. This E M G pattern was originally found in human subjects~,6,8,16,17 but it has recently been demonstrated in squirrel monkeys, opening the way to a more direct study of the related central processes. Terzuolo et al. have shown that the pattern is remarkably similar in the two species, not only in general structure but also in the time relations between muscular activity and the physical parameters of movement 14. As they have pointed out, these time relations satisfy the conditions for relating central activity with the movement under study. Since the mechanical and E M G patterns obtained during movement are a reflection of central activity, one might expect to find deviations from the normal in patients with disease of the m o t o r system. For example, the effects of unilateral brain damage might be studied by comparing the patterns obtained from the right and left arms of a patient with hemiparesis. The goals of this communication are (1) to describe a method for quantitative comparison of motor behavior on two sides of a patient with spastic hemiparesis, (2) to illustrate the use of this method in a specific case, and (3) to interpret the results in terms of neuronal mechanisms known from animal experiments. The apparatus used to record position and velocity of the limb has been described elsewhere a. For each test, the subject is seated with one arm extended toward the recording handle and the forearm supported by an aluminum half-shell which is linked to the chair through rods and ball-bearing joints. The arm support allows free movement in the horizontal plane but prevents the arm from falling. Hence, one can study the movement of a limb that may be too weak for the patient to raise without assistance. Just beyond the recording handle is an oscilloscope on which two vertical
388 lines are displayed. One of these, the target line, remains centered until the experimenter pushes a button, causing it to j u m p to the right or left. The other line move~ in response to right-left movement of the recording handle. The apparatus is calibrated so that a hand movement of 10 cm to the right or left will superimpose the two lines after a target j u m p in the same direction. Muscle action potentials are recorded by means of Beckman skin electrodes, used with Beckman electrode paste and adhesive collars. Two electrodes are fastened over the posterior fibers of the deltoid muscle, one about 2 cm below the acromion and one about 4 cm medially. This portion of the muscle functions as an agonist during abduction of the humerus. In order to permit objective measurement of the E M G responses, the muscle action potentials are rectified and smoothed by means of a state-variable averaging filter 7. On the filtered E M G record, all deflections are upward, and each point represents the sum of all E M G activity in the preceding 44 msec. Points of maximal and minimal activity are defined more clearly than on the 'raw' EMG. Despite the timelag introduced by the filter, it is legitimate to compare records taken from the right and left deltoids, because the same averaging window is used on all trials. At the start of each test, both the target line and the cursor are located at the center of the oscilloscope. The signal consists of a step-function displacement of the target to the right or left, depending on which arm is used. In response to the signal, the subject moves the handle as rapidly as possible so as to re-align the cursor on the target. This requires abduction of the arm, moving the hand l0 cm in the direction of target movement. When the movement has been completed, the target is recentered, and the process is repeated at least 20 times to obtain sufficient data for analysis. During each trial, a Grass model 7 polygraph is used to record: (a) position of the target line, (b) position of the hand, (c) velocity of the hand, (d) E M G from the deltoid muscle, and (e) the filtered EMG. F r o m the record of each response, 10 measurements are taken as illustrated in Fig. 1 : (1) the time interval between the target step and the first upswing of the velocity curve; (2) the maximal velocity, i.e., the highest displacement of the velocity curve above the base line (Vmax); (3) the interval between the onset of movement and the time of maximal velocity (TVmax); (4) the interval between the target step and the first clear deflection on the unfiltered E M G record. The remaining 5 measurements are taken from the filtered E M G record: (5) the height of the initial peak, measured in millimeters above the base line (P1); (6) the lowest point on the record at any time during movement (Min); (7) the higest deflection following the minimum (P~); (8) the time interval between the onset of activity and the first peak (TP1); (9) the interval between the onset of E M G activity and the minimum (Train). The timing of the second peak could not be measured reliably, because it was often almost equal in size to other nearby potentials The method is illustrated by the results of testing a patient with spastic hemiparesis. This patient was a 23-year-old veteran whose left cerebral hemisphere had been damaged by shell fragments. At the time of testing, muscles of the right shoulder girdle and upper arm were graded 4 out of 5 in strength. Forearm muscles were graded
389 TABLE 1 BALLISTIC ABDUCTION OF THE NORMAL AND PARETIC ARM*
Time to onset of movement Maximalvelocity (cm/sec) Time of maximal velocity Time to onset of EMG Height of first EMG peak (P1) Minimum of EMG (Min) Height of second peak (PD Time to first peak of EMG (TP1) Time to minimum of EMG (Tmn~)
Normal arm ( h f t )
Paretic arm (right)
Mean
Mean
S.D.
t
P
315 84 232 200
64 18 44 78
3.9 3.8 9.1 3.0
~. 0.01 • 0.01 ~: 0.0l < 0.01
0.7 4.6 2.4
N.S. < 0.01 < 0.05
247 66 127 144 26.6 1.2 16.7
S.D.
54 14 34 45 7.4 1.2 6.2
25.2 3.1 12.9
5.7 1.6 3.9
89
34
188
36
9.5
-< 0.0l
300
107
409
70
3.8
< 0.01
* Times are in msec. EMG amplitudes are in mm.
3-4. The p a t i e n t was able to curl the fingers a r o u n d the r e c o r d i n g handle, b u t they could n o t be m o v e d independently. Muscle stretch reflexes were all m o r e active on the right side t h a n on the left, a n d the p l a n t a r response was extensor. There was no facial paresis or visual field defect. The p a t i e n t could speak and c o m p r e h e n d instructions. All m o t o r functions, including reflexes, were n o r m a l on the left side. M o v e m e n t s o f b o t h arms were tested a c c o r d i n g to the m e t h o d described above, a n d the resulting d a t a showed a n u m b e r o f differences between the two sides (Table I). The visual r e a c t i o n time, m e a s u r e d f r o m the signal to the b e g i n n i n g o f E M G activity or to the onset o f m o v e m e n t , was significantly longer on the affected side. H o w e v e r , the m a x i m a l speed o f h a n d m o v e m e n t was greater on the affected side, resulting in a variable degree o f o v e r s h o o t , as illustrated in Fig. 1. The mean time between the onset o f m o v e m e n t a n d the a t t a i n m e n t o f m a x i m a l h a n d velocity was greater for the right a r m t h a n for the left. This implies that, a l t h o u g h the right h a n d a t t a i n e d higher velocities, its m e a n acceleration was less t h a n n o r m a l (362 cm/sec ~, right; 520 cm/sec 2, left). O n the filtered E M G record, the absolute size o f P1 has no significance, since it d e p e n d s on electrode placement, the a m o u n t o f amplification a n d o t h e r external factors. Therefore, the gains were a d j u s t e d d e l i b e r a t e l y so as to m a k e P1 a b o u t the same o n the two arms. (The table shows t h a t the values were n o t significantly different.) Hence, one m a y c o m p a r e the relative a m p l i t u d e s as well as the t i m i n g o f Min and P2 on the two sides. The time f r o m onset o f filtered E M G to the first p e a k (TP1) was m o r e than twice as long on the spastic side. Similarly the time when E M G activity d r o p p e d to a m i n i m u m (Train) was m o r e t h a n 100 msec later on that side. The a m o u n t o f activity
390 I
SIGNAL
HAND POSITION
/
//
(
ill I
/ FILTERED EMG
!
,.
(
~:e,
t:
e
I
P1 /
\r, I
P2 Min
.-.~___ -L_ ~ _ l . . . . . '~ TP1 Train
\/~\/~./~..
,,
_~. . . . . . . . . . . . . TP2 L
,
250
rnsec
Fig. 1. Abduction of the spastic limb. At the time 0, the signal line jumps to right, The EMG response begins at time 1. Hand movement begins at time 2 and reaches maximal speedat 3. On filtered EMG, the first and second peaks are labeled P1 and P2. Minimal activity is at Min. The times of P1 and Min are measured from point indicated by broad arrow.
during the 'silent period' was greater and the height of the second peak was lower in the spastic muscle. The differences between the normal and spastic limbs suggest a number of tentative conclusions. The reaction time to a visual signal was clearly longer on the affected side, suggesting that there is a delay in the transmission of m o t o r commands from the damaged hemisphere. In the presence of damage to the corticospinal tract, it would be impossible to recruit the usual number of fibers, but temporal s u m m a t i o n could still occur through repetitive discharge of the remaining fibers. Consequently, a longer time would be necessary to excite the required amount o f motoneuron activity. The increased duration of the initial E M G volley resembles that which occurs
391 when a normal limb moves against an inertial load '). One mechanism that could account for this finding is the unloading reflex 3. Vallbo has shown that voluntary innervation of a skeletal muscle is accompanied by an increased rate of spindle afferent discharge 1.5. It is reasonable to infer that this Ia activity contributes to the excitation of motoneurons causing a ballistic movement. If one assumes that the spindles are unloaded during rapid movement, then the termination of the initial volley may be due in part to a decrease of facilitation by way of the la afferents. In the paretic limb, movement is slower, and one might infer that the spindles are not unloaded so rapidly or so completely. Hence, the Ia discharge would be continued longer than normal, exciting the motoneurons to prolonged activity. Another spinal mechanism that might affect the duration of the initial motor volley is inhibition, due to excitation of the Golgi tendon organs. Since the most effective stimulus to these receptors is the force caused by muscular contraction, they would be expected to fire during acceleration, and the resulting discharge of lb fibers would tend to inhibit the motoneurons reflexly. In the paretic limb, the force on the tendon would be less than normal, and the motoneurons would thus receive fewer inhibitory impulses. The result would be a delayed and less complete silent period. The Renshaw cells provide a third mechanism that might affect the duration of the initial volley. These cells, which are excited by recurrent collaterals of the alpha motor neurons, are believed to inhibit the alphas 11. Because of the reduced motor activity on the paretic side, the Renshaw cells would receive fewer impulses during the initial volley, and the motoneurons would be subjected to less inhibition. In speculating about the results of this pilot study, it must be recognized that muscle afferents project to the cerebral cortex, as well as to the spinal cord 1°, and several experiments point to the existence of cortical mechanisms that may have a role in voluntary movementSAL In the monkey, for example, neurons of cortical area 3a have been shown to reflect the length of a forearm muscle during maintenance of steady postures la, and the precentral neurons respond very rapid when the moving limb encounters an unexpected change of load 4. When the corticospinal system is damaged by disease, a maximal discharge of the upper motor neurons will sometimes fail to elicit the desired acceleration. Information from the slowly moving limb could then excite cortical 'reflexes' to adjust the motor discharge appropriately. Another finding in the present case was the relative smallness of the second E M G volley on the affected side. This is analogous to another finding reported in patients with hemiparesis 1. When a muscle is unloaded during voluntary contraction, the E M G normally shows a brief silent period followed by a volley of renewed activity. This volley has been found to be smaller on the affected side of patients with hemiparesis. As Landau has suggested, powerful excitatory connections of the upper motor neuron pathway may be necessary for the rapid return of activity after the transient removal of segmental afferent tone by the unloading procedure 9. The patient with unilateral brain disease provides a useful model for the study of pathophysiology. Although one cannot use microelectrodes, as in primate experiments, the patient is able to provide a great variety of voluntary movements on
392 request, an d the n o r m a l side offers a m a t c h e d c o n t r o l for the affected limb. T h e t e c h n i q u e described here is one a p p r o a c h to the q u a n t i t a t i v e study o f such patients.
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