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Proposed mechanisms for cerebellar coordination, stabilization and monitoring of movements and posture.

In this paper cerebellar mechanisms have been proposed for the coordination of all movements, for the learning effect of training on movements, for the effect of mental set on posture and voluntary movements, for the detection of velocity and acceleration, and for the stabilization of movements and posture. Coordination of agonist, antagonist, fixation and synergistic muscles during a movement could occur via a cerebellar matrix which connects agonist efferent feedback from the Motor Cortex to the appropriate antagonist motor cortical neurons. Improved efficiency through repetition (learning) occurs through suggested changes at the molecular and synaptic levels. The Inferior O-live-Climbing Fibre System is seen as a dynamic oscillator; indicating when a movement begins, its velocity and acceleration, and its stability. According to this view, the cerebellum stabilizes movements, and adds the effect of mental set on posture and voluntary movements, by inducing changes in the gain of stretch reflexes. Inhibitory interneurons add versatility to movements, while excitatory collaterals from cerebellar afferents directly to cerebellar deep nuclei improve sensitivity of the system. These mechanisms work for all movements whether active, passive, or reflexive.

Action Potentials↗

Methods of time and frequency domain examination of physiological tremor in the human jaw.

This paper discusses, using the human jaw as a model, some of the commonly used techniques for examining physiological tremor. The EMG component driving mandibular physiological tremor approximately 7Hz can be revealed in the time domain manifestation of EMG by demodulation. The co-occurrence of approximately 7Hz physiological tremor (PT) in force and EMG can also be seen in the frequency domain representations of these signals and coherence analysis provides a method by which the degree of co-occurrence can be statistically investigated. Additionally, estimation of time lags between the signals by phase and cumulant density analysis provides evidence of the direction of dependence. Data presented herein using these techniques illustrates that for the human jaw, PT arises from a rhythmic component of EMG. This component is frequency and amplitude invariant across a range of bite forces indicating that it is not due to interaction between the stretch reflex and the mechanical resonance of the system.

Biomechanical Phenomena↗

Control of single-joint movements with a reversal.

We studied the kinematic and electromyographic (EMG) patterns during single-joint elbow flexion movements with a reversal and tested two hypotheses. First, that the amplitude of the second phase of the movement (M(2)) will be controlled by two different means, a drop in the second flexor burst for a small M(2) and an increase in the integral of the extensor burst for larger M(2). Second, based on the muscle stretch-shortening cycle (SSC), that movements reversing without a delay will show a larger extensor burst, as compared to movements that reverse after a delay. Changes in EMG patterns with M(2) amplitude supported the first hypothesis and could be interpreted within the framework of the equilibrium-point hypothesis. The observations also corroborate a hypothesis that discrete movements represent outcomes of an oscillatory control process stopped at a particular phase. In Experiment-2, even the shortest delay at the target led to a significantly larger extensor burst. However, there were no differences in the peak velocity of M2 with and without the delay. These observations do not support a major role of stretch reflexes in the SSC effects during such movements. However, they are compatible with the idea of peripheral factors, such as peripheral muscle and tendon elasticity, playing a major potentiating role in the SSC.

Adaptation, Physiological↗

Plasticity from muscle to brain.

Recognition that the entire central nervous system (CNS) is highly plastic, and that it changes continually throughout life, is a relatively new development. Until very recently, neuroscience has been dominated by the belief that the nervous system is hardwired and changes at only a few selected sites and by only a few mechanisms. Thus, it is particularly remarkable that Sir John Eccles, almost from the start of his long career nearly 80 years ago, focused repeatedly and productively on plasticity of many different kinds and in many different locations. He began with muscles, exploring their developmental plasticity and the functional effects of the level of motor unit activity and of cross-reinnervation. He moved into the spinal cord to study the effects of axotomy on motoneuron properties and the immediate and persistent functional effects of repetitive afferent stimulation. In work that combined these two areas, Eccles explored the influences of motoneurons and their muscle fibers on one another. He studied extensively simple spinal reflexes, especially stretch reflexes, exploring plasticity in these reflex pathways during development and in response to experimental manipulations of activity and innervation. In subsequent decades, Eccles focused on plasticity at central synapses in hippocampus, cerebellum, and neocortex. His endeavors extended from the plasticity associated with CNS lesions to the mechanisms responsible for the most complex and as yet mysterious products of neuronal plasticity, the substrates underlying learning and memory. At multiple levels, Eccles' work anticipated and helped shape present-day hypotheses and experiments. He provided novel observations that introduced new problems, and he produced insights that continue to be the foundation of ongoing basic and clinical research. This article reviews Eccles' experimental and theoretical contributions and their relationships to current endeavors and concepts. It emphasizes aspects of his contributions that are less well known at present and yet are directly relevant to contemporary issues.

Animals↗

Experimental benznidazole encephalopathy: I. Clinical-neurological alterations.

Benznidazole (N-benzyl-2-nitro-1-imidazoleacetamide) is an antiprotozoan agent of the nitroimidazole group used extensively in South America to treat Chagas' disease. In humans, its most important side effect is peripheral polyneuropathy, the frequency of which is dose related. To evaluate this effect, we administered benznidazole to adult, male, mongrel dogs at doses ranging from 5 to 40 mg/kg/day (0.5 to 4 times the dose used to treat chagasic patients). Subsequent neurological examination revealed apathy, ataxia, spastic tetraplegia with hyperreflexia of stretching reflexes, balance disorders and asymmetrical gait. These alterations appeared earlier and were more intense at the higher doses. Drug withdrawal also left dose- and time-dependent sequelae like ataxia, hypertonia, hyperreflexia and alterations of balance. No peripheral neuropathy was detected. The present findings suggest that a careful reevaluation of the side effects of benznidazole in humans is necessary.

Animals↗

Effects of limb loading on the lower-limb electromyographic activity during orthotic locomotion in a paraplegic patient.

The relationship between limb loading and lower-leg electromyographic (EMG) activity was examined during orthotic locomotion in a complete paraplegic patient. The level of limb loading was modified by a hanging system. Surface EMG in the lower-leg extensor and flexor muscles was unilaterally recorded together with the load signal on the ipsilateral sole. The motion of the knee and the ankle joints was minimized, which means that the change in length of the examined muscles was minimum. The muscles were activated synchronously with the locomotor movement and the magnitude of the extensor activity was changed relative to the peak load on the sole. It is conceivable that the spinal cord interpreted the load information and modified the EMG output in the anti-gravity muscles even in the absence of stretch reflexes.

Adult↗

Orthodontic forces exerted by activators with varying construction bite heights.

The present study was conducted to investigate the nature of forces induced with activators by measuring strains, electromyogram (EMG) and electroencephalogram (EEG) during a 2-hour sleep period. Fifteen adolescent patients with Class II and Class III malocclusions, (30 subjects) were used. Four types of activators were made for each patient with construction bites taken at incisal edge clearances of 2, 4, 6, and 8 mm vertically. The magnitude of forces generated by passive tension of soft tissues increased significantly (p < 0.01) from approximately 80 to 160 gf in the Class II group and from approximately 130 to 200 gf in the Class III group with varying construction bite heights from 2 to 8 mm. Higher construction bites also significantly changed (p < 0.01) the direction of forces by passive tension from vertical to posterior and from vertical to anterior in relation to the reference plane in the Class II and Class III groups, respectively. Duration of forces generated by passive tension was most significantly longer than that of active contraction of the jaw closing muscles, irrespective of the construction bite heights. It is concluded that passive tension, derived from viscoelasticity of soft tissues, plays a more important role in inducing changes that phasic stretch reflex during jaw orthopedic therapy with activators.

Activator Appliances↗

Inhibition of masseteric electromyographic activity during oral respiration.

Although the effects of oral respiration on the growth and development of craniofacial structure have been studied previously, little is known about how altered respiration affects the activity of the jaw-closing muscles. Obstruction of the nasal airway in the cat significantly inhibited the masseteric stretch reflex and discharges of masseteric motor units but did not affect the electromyographic activity of the diaphragm. This inhibition was greater during inspiration than during expiration. In addition, the amplitude of the masseteric monosynaptic reflex elicited by electrical stimulation of the mesencephalic trigeminal nucleus showed no significant change in association with the altered respiratory mode. These findings suggest that masseteric electromyographic activity is inhibited during oral respiration and that the gamma-system is involved in this inhibition.

Action Potentials↗

Treatment of spasticity with tizanidine in multiple sclerosis.

Spasticity is a frequent and often disabling symptom in MS patients. Current drugs used as antispastic agents include Dantrolene Sodium, Baclofen and Diazepam. Tizanidine (5-chloro-4-(2imidazolin-2 yl amino)-2,1,3-benzothialdiazole) is a new antispasticity agent that has purported central action. A double blind placebo controlled trial was performed to study the efficacy of this drug in MS patients. Sixty-six patients entered an eight week therapeutic trial and fifty-nine completed the trial. Patients were assessed at 0, 2, 3 and 8 weeks of therapy for clinical effects. Electrophysiologic tests were performed at 0 and 8 weeks. A statistically significant benefit was noted in spastic muscle groups in the legs with concomitant significant reduction in hyperactive stretch reflexes and ankle clonus. Side effects most frequently cited included dry mouth and drowsiness. Two patients developed elevated liver function test that decreased with cessation of therapy. Other clinical details, side effects and electrophysiologic data will be presented. Tizanidine appears to reduce clinical spasticity and hyperreflexia in MS patients although no change in functional status was detected. Tizanidine may well serve as an alternate antispastic agent, alone or in combination with other agents.

Adolescent↗

Locomotor pattern in paraplegic patients: training effects and recovery of spinal cord function.

Recent studies have shown that a locomotor pattern can be induced and utilized by paraplegic patients under conditions of body unloading using a moving treadmill. The present study investigated the behaviour of the locomotor pattern and also the relationship of its development to the spontaneous recovery of spinal cord function assessed by clinical and electrophysiological (tibial nerve somatosensory evoked potentials and motor evoked potentials) examinations. The earliest time that spinal locomotor activity could be induced was when signs of spinal shock had disappeared. This activity was distinct from spinal stretch reflex activity. In complete paraplegic patients the locomotor pattern improved spontaneously without training. This was coincident with both an increase of gastrocnemius electromyographic activity during the stance phase of gait and a decrease of body unloading. These effects reached a plateau after about 5 weeks. In complete and incomplete paraplegic patients a near linear increase of gastrocnemius electromyographic activity occurred during the stance phase of a step cycle with daily locomotor training over the whole training period of 12 weeks. This was also coincident with a significant decrease of body unloading. In contrast to this, neither clinical nor electrophysiological examination scores improved after the onset of training in both patient groups. Only in incomplete paraplegic patients was there recovery, albeit statistically insignificant, of spinal cord function according to the sensory and motor scores obtained in the neurological examination during the time period before onset of training. An improvement of locomotor function by training was also seen in patients with paraplegia due to a cauda lesion. Such training effects on muscles and tendons could be separated from those on the spinal locomotor centres. The findings of this study may be relevant for the future clinical treatment of paraplegic patients.

Adolescent↗

Effect of cold air therapy in relieving spasticity: applied to spinalized rabbits.

STUDY DESIGN: Before-After trial measured prior to cold air therapy, immediately following, after 30 and 60 min. OBJECTIVE: To determine the effect of cold air therapy in relieving spasticity, the optimal intramuscular temperature, and the duration of spasticity relief attained by cold air therapy. SETTING: Clinical research laboratory, Seoul, Korea. SUBJECT: Forty-six spastic paraplegic rabbits with spinal cord injury. METHODS: Spastic paraplegia was induced by transection of spinal cord in 46 rabbits. Cold air was applied to triceps surae muscles for 30 min at three different intramuscular temperatures (25, 30 and 32.5 degrees C). Clinical parameters of spasticity (muscle tone, Babinski's sign, muscle stretch reflex and ankle clonus) and electrophysiologic parameters (F/M ratio and H/M ratio) were measured immediately following, after 30 and 60 min. RESULTS: In the 32.5 degrees C group, relief in spasticity lasted less than 30 min. In the 30 and 25 degrees C groups, the decrease in spasticity lasted for at least 30 min clinically. The spasticity relief was observed only immediately following treatment when measured electrophysiologically. However, six out of 16 cases (37.5%) in the 25 degrees C group showed complete motor conduction block. CONCLUSION: To relieve spasticity with cold air therapy, the intramuscular temperature should be maintained at 30 degrees C. The duration of spasticity relief lasted from between 30-60 min after cold air therapy. We certify that all applicable institutional and governmental regulations concerning the ethical use of animals were followed during the course of this research.

Animals↗

The importance of posture on the isokinetic assessment of spasticity.

OBJECTIVE: To measure spasticity of the knee flexors and extensor muscles in two different hip positions. SETTING: Swiss Paraplegic Center Nottwil, Switzerland. METHODS: Twenty spinal cord injured (SCI) patients with complete lesions were tested with a torque-velocity dynamometer in the following positions: (1) supine with a hip angle of 0 degrees; (2) sitting with a hip angle of 90 degrees. The excursion of the knee was measured for both positions using a goniometer. Two flexion/extension movements of the knee were performed at a speed of 10 degrees per sec. A further four flexion/extension movements over the same trajectory were made at a speed of 120 degrees per sec. Eccentric peak torques were measured continuously during movement of both legs for both speeds. RESULTS: At a speed of 120 degrees per second, there was a significant difference in stretch reflex of the hamstrings and quadriceps femoris muscles for the two positions (Wilcoxon's paired t-test, P<0.05). Excitability was higher for the quadriceps femoris muscles in supine than in sitting position. For the hamstrings, the effect was reversed. Significant differences between sitting and supine position were not found for the speed of 10 degrees per sec. Test-retest reliability was high for the movements of 120 degrees per sec but low for 10 degrees per sec. CONCLUSIONS: Our findings indicate that for a reliable and comparable measurement of spasticity, an exact description of test position and procedure is essential.

Adult↗

Correlation of polyelectromyographic patterns and clinical upper motor neuron syndrome in hemiplegic stroke patients.

OBJECTIVE: To investigate the correlation between movement patterns, measured by polyelectromyography (PEMG), and clinical upper motor neuron (UMN) syndrome in stroke patients. DESIGN: PEMG patterns, recorded from pairs of flexor-extensor muscles during voluntary maneuvers, and motor outcomes were assessed approximately 1 month after stroke (early stage). Motor outcomes were reassessed 6 months later (late stage). PARTICIPANTS: Thirty-nine hemiplegic stroke patients and 18 healthy control subjects. MAIN OUTCOME MEASURES: Passive stretch reflexes (PSRs), Brunnstrom's stages, and walking ability. RESULTS: Six PEMG patterns, varying from complete reciprocal to complete synchrony, were identified. Higher PEMG pattern scores were associated with better Brunnstrom's stages (r > .80), walking ability (r > .39), and some PSRs (r < -.37). PEMG patterns could separate patterns 1 and 2 from patterns 3 and 4 for patients with early Brunnstrom's stages 1 and 2. Patterns 1 and 2 (reduced agonist electromyographic activities) indicated weakness and resulted in the worst motor outcomes. Patterns 3 and 4 (cocontraction and coactivation) indicated spasticity and associated synergistic movements. Patients with patterns of 5 and 6 (reciprocal electromyographic activities) had more selective motor control. CONCLUSIONS: PEMG patterns correlate with clinical UMN syndromes and may allow treatment strategy planning on the basis of underlying motor control, as well as the prediction of final motor outcomes soon after stroke, even in patients who cannot move their legs initially.

Aged↗

Postural control in elderly subjects.

The postural stability of 23 subjects aged 85 years or over was studied with a force platform. The sensory function of the lower limbs was disturbed with small vibrators placed on both calf muscles and/or by placing the subjects on a platform covered with foam plastic. When compared with a group (n = 100) of 50-60-year-old subjects, the elderly subjects had significantly higher sway velocities even during nonperturbed conditions. The perturbation of muscle spindles with vibration and/or pressoreceptor function with foam plastic did not increase the postural instability of the elderly subjects. Visual deprivation had a significant effect on postural stability, and the visual influx contributed about 50% of the postural stability. Postural control is reduced as a result of loss of sensory cues of pressoreceptors and also deterioration in function of stretch reflexes initiated from muscle spindles. The very elderly seem to rely on visual control of posture; this is slow, which can be one reason for susceptibility to falls.

Age Factors↗

The effect of posterior column lesions on servo responses from the human long thumb flexor.

Lesions of the posterior column pathways, in which muscle spindle afferents run towards the brain, are associated with loss of servo responses in the long flexor of the thumb, in the absence of motor weakness and with tendon jerks preserved. This evidence is consistent with the hypothesis that the long-latency stretch reflex (on which servo responses are based) uses a supraspinal, possibly a transcortical, reflex arc.

Adult↗

Different types of disturbed motor control in gait of hemiparetic patients.

The pattern of muscle activation in walking was studied in a group of 26 hemiparetic patients. Electromyograms were taken with surface electrodes from 6 muscle groups of the paretic leg and analysed after rectification and time averaging. The sagittal rotations in hip, knee and ankle joint were determined with intermittent light photography. The muscle activation pattern of each patient was compared to that in healthy subjects as well as to the movements performed by the patient and to the normal movement pattern. The normal patterns of movement and muscle activation were assessed from compiled data from 10 healthy female volunteers and average values of angular displacements and amplitude of intergrated EMG were determined at each 5 per cent of the gait cycle. Change of muscle length was determined with a length recording transducer. Gait capacity varied highly in the group of patients studied and the movement pattern also varied markedly. Three types of abnormal muscle activation pattern were disclosed in the patients. In 9 patients, the calf muscles were prematurely activated in the stance phase, probably due to enhanced stretch reflexes (Type I). In another 9 patients, EMG activity was abolished or extremely low in 2 or more of the muscles examined (Type II). In 4 patients, there was a pathological coactivation of several or all of the muscles during part of the gait-cycle, thus disrupting the normal sequential shift of activity in antagonistic muscles (Type III). In the remaining 4 patients, the muscle activation pattern was more complex and no common pattern was discerned.

Adult↗

The coexistence of bradykinesia and chorea in Huntington's disease and its implications for theories of basal ganglia control of movement.

Investigation of motor function in a group of 17 patients with Huntington's disease reveals that, in addition to the chorea that many patients exhibit, defects in voluntary motor performance also are evident. Fast simple wrist flexion movements to 15 degrees or 60 degrees were slower, and individual movements showed greater variability than seen in normal subjects. This bradykinesia was most pronounced in those patients who were akinetic and rigid, but also was seen in those with chorea alone; bradykinesia was independent of the drug treatment that the patients were receiving (and was therefore not due to drug-induced parkinsonism). The electromyographic activity of the agonist muscles during such simple but slow movement differed from that seen in Parkinson's disease. The performance of complex movements revealed further deficits. Some patients were unable to combine two movements in a simultaneous or sequential movement task of squeezing the hand and flexing the elbow. Those who could perform these complex movements exhibited slowing of the velocity of the movement and prolongation of the interval between movements. These abnormalities were present in patients with chorea who were not taking neuroleptic drugs. It is argued that they represent an abnormality of motor programming of complex movements, over and above the defect in executing simple movements. The long latency stretch reflexes in wrist flexor muscles and flexor pollicis longus were reduced or absent, but this did not correlate with changes in motor performance, or with the reduced size of the early components of cortical sensory evoked potentials. Bradykinesia is thus shown to be an integral component of the motor disorder of Huntington's disease, in addition to the chorea. The coexistence of bradykinesia and chorea in this illness is compatible with current theories of the role of the basal ganglia in the control of movement.

Adult↗

Relationship between electromyographic activity and clinically assessed rigidity studied at the wrist joint in Parkinson's disease.

The electromyographic (EMG) patterns recorded from wrist muscles during manually applied, repetitive flexion and extension movements of the wrist joint, used for simultaneous clinical assessment of rigidity, were studied in patients with Parkinson's disease and healthy subjects. Recordings were made whilst patients/subjects attempted voluntarily to relax the muscle of the arm whose wrist joint was manipulated. Individual patients were investigated before and at varying times after their routine daily medication as their clinical rigidity underwent associated modulations. It was often possible to induce additional alterations in clinical rigidity by instructing patients to perform an activation or Jendrassik-like manoeuvre (clenching the contralateral fist). In rigid patients, the approximately sinusoidal wrist displacements (60 deg, 1-1.5 Hz) typically elicited pronounced, cyclic modulations of EMG activities in wrist flexors and extensors; increases in EMG activity were phase-locked to the respective periods of muscle stretch. Stretch-related EMG activity reduced or disappeared as rigidity was abolished by drug therapy. The EMG patterns of patients showing cogwheel rigidity featured discrete, phasic bursts superimposed upon more generalized stretch-related increases in activity. In healthy subjects, showing no clinical rigidity, the pronounced cyclic modulations of EMG activity characteristic of rigid patients were absent during similar manually applied wrist displacements. Quantitative EMG measurements for individual patients, made 'on' and 'off' medication and as their rigidity fluctuated, indicated that mild (grade 1) and moderate (grade 2) rigidity was consistently associated with increased stretch-related activity compared with non-rigid conditions. Pair-wise statistical analysis indicated such increases in EMG to be significant. Similarly, the ratios of EMG activities in the stretched versus released muscles were significantly greater for grades 1 and 2 rigidity than in the absence of rigidity. Overall, the present findings support the view that enhancement of stretch reflex activity has a major role in the genesis of parkinsonian rigidity.

Aged↗