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The scaling of muscle activation and movement amplitude in Parkinson's disease
$218 segmental effects. The phenomenon may be a powerful model for studying neuronal and synaptic bases of primate memory, and may provide a new therapeutic technique for alleviating abnormal segmental reflex activity prominent in many chronic neurologic disorders, including cerebral palsy, multiple sclerosis, spinal cord trauma, and stroke.
supraspinal pathway which was tested by tibial nerve stimulation. The leg muscle E M G responses induced by gait perturbations are suggested to be evoked by group II afferents and mediated by a spinal pathway. The CP evoked during gait most probably reflect the processing of these supraspinal motor centres for the coordination of widespread arm and trunk muscle activation, needed when body equilibrium becomes unstable.
P42.02 C O N T I N U O U S E X A M I N A T I O N O F T H E HEAD R I G H T I N G REACTION. M. Horie, T. Koike, H. Suzuki and A. Katada
P42.04 E L E C T R O M Y O G R A P H I C C O R R E L A T E S O F ACCURACY D U R I N G T H E P E R F O R M A N C E O F A BALLISTIC P R E C I S I O N GRIP SKILL.
(Saitama, Japan) J.M.M. Brown and R. Bronks
In order to investigate quantitatively the righting reaction of the head to tilting of the body in infants we used a special apparatus that was designed to give continuous angle changes of the tilting trunk axis and the displacement of the head position. The baby was seated on a stool of this device and supported by the examiner's hands so that both baby and stool were inclined manually. Surface E M G from neck muscles was also recorded. Four states of head righting were distinguishable; (1) welldeveloped head righting in which the head was maintained almost in the upright position, (2) with head raised more vertically than the tilting angle, but not enough to reach the vertical axis, (3) the head being lifted up at least along the trunk axis but unstably, and (4) the head being dropped down under gravity. A m o n g the subjects who showed weak or unclear reaction, however, instantaneous head lifting was observed temporarily through differentials of the head displacement, and the effort to lift the head was further confirmed from the neck muscular activity even in the fourth stage. The method was effective in the detailed examination of the suspected motor-retarded infant.
P42.03 A F F E R E N T C O N T R O L O F P O S T U R E AND GAIT.
(Brisbane, Australia) Changes in the electromyographic patterns of intrinsic and extrinsic hand muscles were evaluated during the performance of a ballistic isometric precision-grip skill. Ten subjects, aged 17 to 28 yrs, attempted to attain 50% of a predetermined criterion value over 100 trials. Feedback was provided by a visual percentage error display. Responses were placed in three groups; (1) accurate+ 5%, (2) overshoot 20% + , and (3) undershoot - 2 0 % or less. E M G potentials were obtained by 4 m m bipolar surface electrodes from 1st Dorsal lnterosseus (DI), Adductor Pollicius (AP), Abductor Pollicis (AbP), Long Flexors (LF) and Extensor Digitorum (ED) and amplified through Medelec AA6 amplifiers (band-pass 3.2Hz to 1.6kHz) and stored on a PDP 11/23 computer. During accurate trials, D1 and AP initiated the contraction and ceased activity after m a x i m u m force was reached (p < 0.05). However, in both over shoot and undershoot trials, their activity ceased at the same time as m a x i m u m force. ED ceased activity before DI and AP during accurate trials (p < 0.02) although this relationship was not evident in either overshoot or undershoot performance. The proportional contribution of the E M G of DI, AP and LF to the production of force did not change with accuracy, although there were some differences in the timing of muscle activity.
V. Dietz, W Berger and J Quintern
(Freiburg, W. Germany) The cerebral potentials (CP) evoked by electrical stimulation of the tibial nerve during stance and different phases of gait were compared with the CP and leg muscle E M G responses evoked by perturbation. During gait the CP evoked by an electrical stimulus appeared with a longer latency (first positive peak: mean 63 msec as against 43 msec) and a smaller amplitude compared to the stance condition. When the electrical stimulus was applied during stance under ischemia, the CP became similar to those evoked during gait. The CP evoked by perturbations were larger in amplitude but similar in latency and configuration. It is concluded that during gait the signals of group I afferents are blocked in their segmental as well as their
P42.05 T H E SCALING OF M U S C L E ACTIVATION AND M O V E M E N T A M P L I T U D E IN P A R K I N S O N ' S DISEASE. J.C. Rothwell, A. Berardelli, B.L. Day, J.P.R. Dick and C.D. Marsden
(London, U K ) Patients with Parkinson's disease cannot make arm movements as rapidly as normal subjects because the first burst of EMG activity in the agonist muscle is too small. The reason for the reduction in the agonist burst size is not clear. It could be due to saturation into the mechanism which produces the burst. To test this we asked patients with Parkinson's disease to perform movements of different amplitude, or against different loads,
$219 which are accomplinied in normal individuals by considerable changes in size of the agonist E M G burst. Wrist flexion movements of 150 or 600 were made with or without a large opposing load (2.2Nm). As in normal subjects, the size and duration of the agonist E M G burst increased with large or loaded movements, but always was smaller than normal. Thus the size of the agonist E M G burst was not saturated, at least for 150 unloaded movements. Nevertheless the movements still were slow. We suggest that the size of the agonist E M G burst in Parkinson's disease is scaled inappropriately to the size and load of the movements.
P42.06 V O L U N T A R Y M O T O R C O N T R O L IN PARKINSONISM.
S. Fujirnoto, N. Yanagisawa and R. Tanaka (Matsumoto, Japan) Quick-step mode tracking by pretibial muscles was studied in 17 Parkinsonism patients and 13 normal subjects to analyse rapid voluntary movement. Horizontal markers were presented on an oscilloscope, one with a 10mm width zone (T) as target and the other (F) as control cursor driven by a torque force obtained by isometric dorsiflexion around the ankle. T was moved quickly upwards from the centre. The subject was requested to move F into the range of T as quickly and accurately as possible. This task was performed in 4 torque conditions. In Parkinsonism, the torque obtained by maximal dorsiflection at the ankle decreased significantly in comparison with normal subjects (p < 0.01). Initial peak torque of ballistic catch-up movement (IPT) was smaller than in normal subjects; catch-up time (CT) from onset of movement until reaching the shifted target zone was prolonged significantly in Parkinsonism with weak contraction (p < 0.0l). As the required strength increased IPT was constant, but CT increased further in 11 cases with marked disabilities. In contrast, normal subjects accomplished each of the different required strengths in the same CT period: larger required strengths were made with larger IPTs. These disabilities in voluntary movement in Parkinsonism were clearly correlated with the grade of the clinical disabilities.
P42.07 CLINICAL, E L E C T R O P H Y S I O L O G I C A L A N D P H A R M A C O L O G I C A L I N V E S T I G A T I O N O F ASTERIXIS A N D NEGATIVE M Y O C L O N U S .
M. Osawa, I. Kobayashi and S. M a r u y a m a (London, U K and Tokyo, Japan) Asterixis is characterized by synchronous brief pauses in ongoing voluntary E M G activity. Apparently similar E M G pauses are called negative myoclonus when they are associated with a positive myoclonic jerk.
The purpose of this study is to compare negative myoclonus with asterixis occurring without any myoclonus clinically, electrophysiologically and pharmacologically. In 48 patients with asterixis startle reaction was not present, but disturbance of consciousness was seen: EEG background activity was slow or normal, somatosensory evoked potentials (SEPs) to median nerve stimulation were not enhanced, while C-responses were never induced at rest. Thyrotropin releasing hormone (TRH) suppressed asterixis, but clonazepam was not effective. Startle reaction was seen in one of the 8 patients with negative myoclonus: paroxysmal high voltage slow wave discharges with or without accompanying spikes a n d / o r photomyoclonic responses were recognized in the EEG of three patients: SEPs were enhanced in three patients, and in two patients C-responses were induced at rest. Clonazepam suppressed negative myoclonus, but T R H was not effective. Possible mechanisms of asterixis and negative myoclonus are discussed. It is speculated that the basic disturbance in asterixis is primary dysfacilitation probably in brain-stem reticular formation, while in negative myoclonus the basic disturbance is primary or secondary transient inhibition in excitatory cerebral cortex or disinhibited brain-stem reticular formation.
P42.08 E M G ANALYSIS O F GAIT IN H E M I P A R E T I C S A N D ITS I M P R O V E M E N T BY SPINAL C O R D S T I M U L A TION.
Beatrice Cioni, M. Meglio, R. Sgaramella and A. Zamponi (Rome, Italy) The gait patterns of 10 hemiparetic ambulatory patients have been studied and compared to those of 5 normal adults. Changes induced by spinal cord stimulation applied at cervical level through percutaneously inserted epidural electrodes were also analysed. E M G activity during standing and gait was recorded by surface electrodes placed over the bellies of quadriceps, adductors, hamstrings, tibialis anterior and triceps surae muscles on the hemiparetic side. A midfoot switch was employed to mark the phases of gait. 4 patients walked considerably slower than the controls and their stance phase was 5 to 8 times longer than the swing phase. The remaining 6 patients walked with an almost normal stride time and stance to swing ratio, but they were unable to voluntarily change the speed of the gait. Simultaneous E M G recordings showed that the normal phasic spindling related to the phase of gait was replaced in the hemiparetics by a low amplitude tonic activity, with occasional superimposed phasic spindles and loss of reciprocation between antagonists. Furthermore, clonic E M G bursts in triceps surae were present in a few patients. Spinal cord stimulation was followed by a decrease of the stride time and of the stance to swing ratio; a more phasic E M G activity with the appearance of the silent period and a better reciprocal relationship between antagonist muscles was
supraspinal pathway which was tested by tibial nerve stimulation. The leg muscle E M G responses induced by gait perturbations are suggested to be evoked by group II afferents and mediated by a spinal pathway. The CP evoked during gait most probably reflect the processing of these supraspinal motor centres for the coordination of widespread arm and trunk muscle activation, needed when body equilibrium becomes unstable.
P42.02 C O N T I N U O U S E X A M I N A T I O N O F T H E HEAD R I G H T I N G REACTION. M. Horie, T. Koike, H. Suzuki and A. Katada
P42.04 E L E C T R O M Y O G R A P H I C C O R R E L A T E S O F ACCURACY D U R I N G T H E P E R F O R M A N C E O F A BALLISTIC P R E C I S I O N GRIP SKILL.
(Saitama, Japan) J.M.M. Brown and R. Bronks
In order to investigate quantitatively the righting reaction of the head to tilting of the body in infants we used a special apparatus that was designed to give continuous angle changes of the tilting trunk axis and the displacement of the head position. The baby was seated on a stool of this device and supported by the examiner's hands so that both baby and stool were inclined manually. Surface E M G from neck muscles was also recorded. Four states of head righting were distinguishable; (1) welldeveloped head righting in which the head was maintained almost in the upright position, (2) with head raised more vertically than the tilting angle, but not enough to reach the vertical axis, (3) the head being lifted up at least along the trunk axis but unstably, and (4) the head being dropped down under gravity. A m o n g the subjects who showed weak or unclear reaction, however, instantaneous head lifting was observed temporarily through differentials of the head displacement, and the effort to lift the head was further confirmed from the neck muscular activity even in the fourth stage. The method was effective in the detailed examination of the suspected motor-retarded infant.
P42.03 A F F E R E N T C O N T R O L O F P O S T U R E AND GAIT.
(Brisbane, Australia) Changes in the electromyographic patterns of intrinsic and extrinsic hand muscles were evaluated during the performance of a ballistic isometric precision-grip skill. Ten subjects, aged 17 to 28 yrs, attempted to attain 50% of a predetermined criterion value over 100 trials. Feedback was provided by a visual percentage error display. Responses were placed in three groups; (1) accurate+ 5%, (2) overshoot 20% + , and (3) undershoot - 2 0 % or less. E M G potentials were obtained by 4 m m bipolar surface electrodes from 1st Dorsal lnterosseus (DI), Adductor Pollicius (AP), Abductor Pollicis (AbP), Long Flexors (LF) and Extensor Digitorum (ED) and amplified through Medelec AA6 amplifiers (band-pass 3.2Hz to 1.6kHz) and stored on a PDP 11/23 computer. During accurate trials, D1 and AP initiated the contraction and ceased activity after m a x i m u m force was reached (p < 0.05). However, in both over shoot and undershoot trials, their activity ceased at the same time as m a x i m u m force. ED ceased activity before DI and AP during accurate trials (p < 0.02) although this relationship was not evident in either overshoot or undershoot performance. The proportional contribution of the E M G of DI, AP and LF to the production of force did not change with accuracy, although there were some differences in the timing of muscle activity.
V. Dietz, W Berger and J Quintern
(Freiburg, W. Germany) The cerebral potentials (CP) evoked by electrical stimulation of the tibial nerve during stance and different phases of gait were compared with the CP and leg muscle E M G responses evoked by perturbation. During gait the CP evoked by an electrical stimulus appeared with a longer latency (first positive peak: mean 63 msec as against 43 msec) and a smaller amplitude compared to the stance condition. When the electrical stimulus was applied during stance under ischemia, the CP became similar to those evoked during gait. The CP evoked by perturbations were larger in amplitude but similar in latency and configuration. It is concluded that during gait the signals of group I afferents are blocked in their segmental as well as their
P42.05 T H E SCALING OF M U S C L E ACTIVATION AND M O V E M E N T A M P L I T U D E IN P A R K I N S O N ' S DISEASE. J.C. Rothwell, A. Berardelli, B.L. Day, J.P.R. Dick and C.D. Marsden
(London, U K ) Patients with Parkinson's disease cannot make arm movements as rapidly as normal subjects because the first burst of EMG activity in the agonist muscle is too small. The reason for the reduction in the agonist burst size is not clear. It could be due to saturation into the mechanism which produces the burst. To test this we asked patients with Parkinson's disease to perform movements of different amplitude, or against different loads,
$219 which are accomplinied in normal individuals by considerable changes in size of the agonist E M G burst. Wrist flexion movements of 150 or 600 were made with or without a large opposing load (2.2Nm). As in normal subjects, the size and duration of the agonist E M G burst increased with large or loaded movements, but always was smaller than normal. Thus the size of the agonist E M G burst was not saturated, at least for 150 unloaded movements. Nevertheless the movements still were slow. We suggest that the size of the agonist E M G burst in Parkinson's disease is scaled inappropriately to the size and load of the movements.
P42.06 V O L U N T A R Y M O T O R C O N T R O L IN PARKINSONISM.
S. Fujirnoto, N. Yanagisawa and R. Tanaka (Matsumoto, Japan) Quick-step mode tracking by pretibial muscles was studied in 17 Parkinsonism patients and 13 normal subjects to analyse rapid voluntary movement. Horizontal markers were presented on an oscilloscope, one with a 10mm width zone (T) as target and the other (F) as control cursor driven by a torque force obtained by isometric dorsiflexion around the ankle. T was moved quickly upwards from the centre. The subject was requested to move F into the range of T as quickly and accurately as possible. This task was performed in 4 torque conditions. In Parkinsonism, the torque obtained by maximal dorsiflection at the ankle decreased significantly in comparison with normal subjects (p < 0.01). Initial peak torque of ballistic catch-up movement (IPT) was smaller than in normal subjects; catch-up time (CT) from onset of movement until reaching the shifted target zone was prolonged significantly in Parkinsonism with weak contraction (p < 0.0l). As the required strength increased IPT was constant, but CT increased further in 11 cases with marked disabilities. In contrast, normal subjects accomplished each of the different required strengths in the same CT period: larger required strengths were made with larger IPTs. These disabilities in voluntary movement in Parkinsonism were clearly correlated with the grade of the clinical disabilities.
P42.07 CLINICAL, E L E C T R O P H Y S I O L O G I C A L A N D P H A R M A C O L O G I C A L I N V E S T I G A T I O N O F ASTERIXIS A N D NEGATIVE M Y O C L O N U S .
M. Osawa, I. Kobayashi and S. M a r u y a m a (London, U K and Tokyo, Japan) Asterixis is characterized by synchronous brief pauses in ongoing voluntary E M G activity. Apparently similar E M G pauses are called negative myoclonus when they are associated with a positive myoclonic jerk.
The purpose of this study is to compare negative myoclonus with asterixis occurring without any myoclonus clinically, electrophysiologically and pharmacologically. In 48 patients with asterixis startle reaction was not present, but disturbance of consciousness was seen: EEG background activity was slow or normal, somatosensory evoked potentials (SEPs) to median nerve stimulation were not enhanced, while C-responses were never induced at rest. Thyrotropin releasing hormone (TRH) suppressed asterixis, but clonazepam was not effective. Startle reaction was seen in one of the 8 patients with negative myoclonus: paroxysmal high voltage slow wave discharges with or without accompanying spikes a n d / o r photomyoclonic responses were recognized in the EEG of three patients: SEPs were enhanced in three patients, and in two patients C-responses were induced at rest. Clonazepam suppressed negative myoclonus, but T R H was not effective. Possible mechanisms of asterixis and negative myoclonus are discussed. It is speculated that the basic disturbance in asterixis is primary dysfacilitation probably in brain-stem reticular formation, while in negative myoclonus the basic disturbance is primary or secondary transient inhibition in excitatory cerebral cortex or disinhibited brain-stem reticular formation.
P42.08 E M G ANALYSIS O F GAIT IN H E M I P A R E T I C S A N D ITS I M P R O V E M E N T BY SPINAL C O R D S T I M U L A TION.
Beatrice Cioni, M. Meglio, R. Sgaramella and A. Zamponi (Rome, Italy) The gait patterns of 10 hemiparetic ambulatory patients have been studied and compared to those of 5 normal adults. Changes induced by spinal cord stimulation applied at cervical level through percutaneously inserted epidural electrodes were also analysed. E M G activity during standing and gait was recorded by surface electrodes placed over the bellies of quadriceps, adductors, hamstrings, tibialis anterior and triceps surae muscles on the hemiparetic side. A midfoot switch was employed to mark the phases of gait. 4 patients walked considerably slower than the controls and their stance phase was 5 to 8 times longer than the swing phase. The remaining 6 patients walked with an almost normal stride time and stance to swing ratio, but they were unable to voluntarily change the speed of the gait. Simultaneous E M G recordings showed that the normal phasic spindling related to the phase of gait was replaced in the hemiparetics by a low amplitude tonic activity, with occasional superimposed phasic spindles and loss of reciprocation between antagonists. Furthermore, clonic E M G bursts in triceps surae were present in a few patients. Spinal cord stimulation was followed by a decrease of the stride time and of the stance to swing ratio; a more phasic E M G activity with the appearance of the silent period and a better reciprocal relationship between antagonist muscles was