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S-7-4 Sensorimotor integration and movement disorder: the role of neurophysiological techniques
Symposium 8. Control of muscle tone and its disorders but durations of E M G activities were prolonged in the patients because of co-contractions of the antagonists. The task-specific CNV amplitude loss reflects a failure of neural activities preparing for a phasic neck movement, resulting in co-contraction of the agonists and the antagonist. Dystonia is associated with defective retrieval or retaining of specific motor programs or subroutines in response to sensory stimuli, and therefore is a valuable tool for investigating normal mechanisms for controlling automatic mot,;r tasks.
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Saccadic eye movements in basal ganglia disorders
Masaya Segawa. Segawa Neurological Clinic for Children, Tokyo Saccadic eye movements (SEMs) are mediated by the direct and the indirect striatal projections, and arc controlled by the nigrostriatal dopamine neurons. Evaluation of two kinds of SEMs, visually guided saccade (VS) and memory guided saccade (MS, in various types of basal ganglia disorders and in normal subjects of various ages revealed to show abnormalities, particular for each type and their age dependent modulation. Hereditary progressive dystonia with marked diurnal fluctuation (HPD) - - 7 cases, Dopa-responsive dystonia (DRD) other than HPD - - 2 cases, dystonic type juvenile parkinsonism (dJP) - 2 cases, Parkinson's disease (PD) - - 4 cases, chronic motor tics (CMT) including Tourette syndrome - - 57 cases and symptomatic torsion dystonia (STD) - - 6 cases were subjected to this study. Ninety-five normal subjects (aged 5-68 years) were examined as controls. Eye movements were estimated with target positions at 5, 10, 20 and 30 degrees. In the MS task the subjects were required to make saccade promptly (within 600 ms) to the remembered location where a target cue was previously flashed. Normal children below the age of 15 years often failed to make a MS and tended to break the fixation immediately in response to the anticipated cue (saccade to cue, CS). At these ages, MS, if present, tended to be hypometric. Similar characteristics were observed in subjects above age 60 years. No apparent age related variation was observed in VS. Patients with various basal ganglia disorders showed abnormalities in MS rather than in VS. These abnormalities were mostly marked in STD. In HPD, VS was also affected and abnormalities in MS were alleviated with age. D R D showed similar tendencies while JP and PD showed abnormalities predominantly in MS. In CMT, the increase in frequency of CS was prominent. These results suggest that evaluation of SEMs is uselul for detecting the pathophysiology of basal ganglia disorders and the neural mechanisms for MS, with its age variation might have important roles for higher order functions of the basal ganglia.
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Sensorimotor integration and movement disorder: the role of neurophysiological techniques
P.M. Rossini. Ospidale Fatebenefratelli, lsola Tiberina, Roma, Italy and L R. C. C.S. "Santa Lucia ", Roma Neurophysiological protocols combining SEPs and muscular reflexes in healthy humans during different motor performances and in patients with movement disorders have helped to clarify some neural mechanisms underlying movement and sensorimotor integration processes. Contra- and ipsilateral pre- and post-rolandic median nerve SEPs recorded during full relaxation ( = "baseline" condition) were compared to SEPs during a) a self-improvised sequence of
S15
finger movements ( = "internal" condition); b) finger movements according to a sequence of numbers ( = "external"); c) mental ideation without any motor execution ( = "imagined") and d) passive displacement of fingers. The parietal P14-N20 and N33-P45 were not significantly affected in any conditions; P25-N33 was significantly reduced (i.e., gating) in a), b), c) and d); the N20-P25 was reduced in a) and d). N30 and P40 were significantly decremented (20-75%) in a) and b), mainly in the c~,ntralateral electrodes. Gating of frontal and parietal waves was combined with enhanced late muscular responses during active contraction. Decreased frontal SEPs have been described in Parkinsonian (PD) subjects during "relaxation" and, together with parietal SEPs alterations, also in choreic patients; an opposite behaviour was reported in dystonia, Moreover, Apomorphine induced a transient increase of P22-N30 amplitude both in PD and, to a lower extent, in patients with parkinsonism, while parietal SEPs were little affected. Patients with enhanced late muscular responses also exhibited lower than normal frontal N30. Altogether, this findings confirm that the cortico-subcortical loop (M1-SMA-Basal ganglia-Thalamus-Sl) can be explored via neurophysiological techniques and strongly suggest that this circuitry is playing a pivotal role in programming and execution of movements.
S-8. CONTROL OF MUSCLE TONE AND ITS DISORDERS
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Clinical aspects of the pathophysiology of muscle tone
Robert R. Young. Department of Neurology, University of
California, Irvine Muscle tone is defined as tension in a muscle that is not being voluntarily contracted. Tone is evaluated by manipulating joints to stretch several muscles at one time. Weak thixotropic tone is present in all normal relaxed muscles (i.e., muscles without EMG). Stronger rigor-like tone also occurs without EMG. Fibrous contracture must be differentiated from involuntary muscle contraction, the latter being the basis for true increased tone. Although it is usually hard to appreciate, less tone than normal is found with cerebellar deficits and severe denervation. Spasticity is defined as a velocity sensitive increase in tone and rigidity is considered to be length sensitive. Both are thought to be mediated by increases in tonic stretch reflexes. Spastic patients usually have mixtures of velocity and length sensitive increases in tone. There is no evidence to support the hypothesis that increased spindle Ia input is responsible for the increased stretch reflexes. However, increased nociceptive (and? proprioceptive) input does increase tone. Segmental spinal mechanisms which underlie all these increases intone malfunction because of rostral lesions or disorders. Normal humans are able to inhibit their tonic stretch reflexes when told to "relax". Failure of this ability occurs with diffuse cerebral dysfunction and results in gegenhalten. Failure also occurs with Parkinson's disease, spasticity and so on. Relaxation appears to be an active p h e n o m e n o n - - n o t just the absence of voluntary, postural or reflex activation of motor neurons. W h e n mechanisms underlying this active form of relaxation are elucidated, increases in muscle tone will be understood. Meanwhile important discoveries are being made concerning the function and dysfunction of segmental spinal circuits.
~-]
Saccadic eye movements in basal ganglia disorders
Masaya Segawa. Segawa Neurological Clinic for Children, Tokyo Saccadic eye movements (SEMs) are mediated by the direct and the indirect striatal projections, and arc controlled by the nigrostriatal dopamine neurons. Evaluation of two kinds of SEMs, visually guided saccade (VS) and memory guided saccade (MS, in various types of basal ganglia disorders and in normal subjects of various ages revealed to show abnormalities, particular for each type and their age dependent modulation. Hereditary progressive dystonia with marked diurnal fluctuation (HPD) - - 7 cases, Dopa-responsive dystonia (DRD) other than HPD - - 2 cases, dystonic type juvenile parkinsonism (dJP) - 2 cases, Parkinson's disease (PD) - - 4 cases, chronic motor tics (CMT) including Tourette syndrome - - 57 cases and symptomatic torsion dystonia (STD) - - 6 cases were subjected to this study. Ninety-five normal subjects (aged 5-68 years) were examined as controls. Eye movements were estimated with target positions at 5, 10, 20 and 30 degrees. In the MS task the subjects were required to make saccade promptly (within 600 ms) to the remembered location where a target cue was previously flashed. Normal children below the age of 15 years often failed to make a MS and tended to break the fixation immediately in response to the anticipated cue (saccade to cue, CS). At these ages, MS, if present, tended to be hypometric. Similar characteristics were observed in subjects above age 60 years. No apparent age related variation was observed in VS. Patients with various basal ganglia disorders showed abnormalities in MS rather than in VS. These abnormalities were mostly marked in STD. In HPD, VS was also affected and abnormalities in MS were alleviated with age. D R D showed similar tendencies while JP and PD showed abnormalities predominantly in MS. In CMT, the increase in frequency of CS was prominent. These results suggest that evaluation of SEMs is uselul for detecting the pathophysiology of basal ganglia disorders and the neural mechanisms for MS, with its age variation might have important roles for higher order functions of the basal ganglia.
[•
Sensorimotor integration and movement disorder: the role of neurophysiological techniques
P.M. Rossini. Ospidale Fatebenefratelli, lsola Tiberina, Roma, Italy and L R. C. C.S. "Santa Lucia ", Roma Neurophysiological protocols combining SEPs and muscular reflexes in healthy humans during different motor performances and in patients with movement disorders have helped to clarify some neural mechanisms underlying movement and sensorimotor integration processes. Contra- and ipsilateral pre- and post-rolandic median nerve SEPs recorded during full relaxation ( = "baseline" condition) were compared to SEPs during a) a self-improvised sequence of
S15
finger movements ( = "internal" condition); b) finger movements according to a sequence of numbers ( = "external"); c) mental ideation without any motor execution ( = "imagined") and d) passive displacement of fingers. The parietal P14-N20 and N33-P45 were not significantly affected in any conditions; P25-N33 was significantly reduced (i.e., gating) in a), b), c) and d); the N20-P25 was reduced in a) and d). N30 and P40 were significantly decremented (20-75%) in a) and b), mainly in the c~,ntralateral electrodes. Gating of frontal and parietal waves was combined with enhanced late muscular responses during active contraction. Decreased frontal SEPs have been described in Parkinsonian (PD) subjects during "relaxation" and, together with parietal SEPs alterations, also in choreic patients; an opposite behaviour was reported in dystonia, Moreover, Apomorphine induced a transient increase of P22-N30 amplitude both in PD and, to a lower extent, in patients with parkinsonism, while parietal SEPs were little affected. Patients with enhanced late muscular responses also exhibited lower than normal frontal N30. Altogether, this findings confirm that the cortico-subcortical loop (M1-SMA-Basal ganglia-Thalamus-Sl) can be explored via neurophysiological techniques and strongly suggest that this circuitry is playing a pivotal role in programming and execution of movements.
S-8. CONTROL OF MUSCLE TONE AND ITS DISORDERS
~-~
Clinical aspects of the pathophysiology of muscle tone
Robert R. Young. Department of Neurology, University of
California, Irvine Muscle tone is defined as tension in a muscle that is not being voluntarily contracted. Tone is evaluated by manipulating joints to stretch several muscles at one time. Weak thixotropic tone is present in all normal relaxed muscles (i.e., muscles without EMG). Stronger rigor-like tone also occurs without EMG. Fibrous contracture must be differentiated from involuntary muscle contraction, the latter being the basis for true increased tone. Although it is usually hard to appreciate, less tone than normal is found with cerebellar deficits and severe denervation. Spasticity is defined as a velocity sensitive increase in tone and rigidity is considered to be length sensitive. Both are thought to be mediated by increases in tonic stretch reflexes. Spastic patients usually have mixtures of velocity and length sensitive increases in tone. There is no evidence to support the hypothesis that increased spindle Ia input is responsible for the increased stretch reflexes. However, increased nociceptive (and? proprioceptive) input does increase tone. Segmental spinal mechanisms which underlie all these increases intone malfunction because of rostral lesions or disorders. Normal humans are able to inhibit their tonic stretch reflexes when told to "relax". Failure of this ability occurs with diffuse cerebral dysfunction and results in gegenhalten. Failure also occurs with Parkinson's disease, spasticity and so on. Relaxation appears to be an active p h e n o m e n o n - - n o t just the absence of voluntary, postural or reflex activation of motor neurons. W h e n mechanisms underlying this active form of relaxation are elucidated, increases in muscle tone will be understood. Meanwhile important discoveries are being made concerning the function and dysfunction of segmental spinal circuits.