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PubMed1997

Validity of long-term electromyography in the quantification of tremor.

We previously developed a method of tremor quantification using long-term electromyography registration of antagonistic forearm muscles that is reliable, sensitive, and specific for pathologic tremors. The present study demonstrates that tremor occurrence as measured by this method correlates well with clinical parameters of tremor in idiopathic Parkinson's disease (PD) and essential tremor (ET) (subscores of the Unified Parkinson's Disease Rating Scale for PD, tremor rating according to Bain et al. for ET). We conclude that the method is a valid and objective means of tremor quantification in PD and ET.

Activities of Daily Living↗
PubMed1998

Action tremor and weakness in Parkinson's disease: a study of the elbow extensors.

We have previously shown that action tremor persists during maximal wrist extension in patients with Parkinson's disease, and that this contributes to weakness at this joint by preventing the fully fused contraction of the forearm extensor muscles. Antiparkinsonian medication reduces the action tremor in torque and electromyographic (EMG) records, thereby improving strength at the wrist. In the present experiments, peak torque and action tremor were recorded during maximal extension of the elbow in nine patients with Parkinson's disease while they were on and off antiparkinsonian medication, and in eight age- and sex-matched healthy subjects. Peak torque and mean rectified EMG levels were reduced by 34% and 36%, respectively, during maximal elbow extension when patients off medication were compared to those in the treated state. Action tremor was visible in torque records and had a frequency of approximately 10 Hz both in parkinsonian patients and in normal controls. Activity of a similar frequency was often detected in EMG records, especially in patients off therapy. The absolute amplitude of action tremor in torque (A[torque]) and EMG (A[EMG]) records from the elbow was unaffected by therapy and was little different from that recorded in healthy controls. The relative action tremor in torque ([A(torque)/peak torque] x 100) and EMG ([A(EMG)/mean rectified EMG] x 100) was reduced by treatment, but this was the result of the increase in peak torque and mean rectified EMG. Thus, in contrast to the results at the wrist, antiparkinsonian medication has little effect on the 10-Hz action tremor at the elbow. Increased strength is produced by a different mechanism which allows recruitment of triceps motor units outside of this synchronizing influence.

Aged↗
PubMed1998

Pallidotomy for tremor.

We studied tremor-related activity in globus pallidus internus (GPi) neurons and the effects of pallidotomy on tremor in patients with Parkinson's disease. By using microelectrode recording, we identified GPi neurons with rhythmic firing at the frequency of contralateral tremor. There was a strong correlation between the tremor-related neuronal activity and limb tremor (r = 0.73). The majority of tremor-related neurons were located in the ventral one half of the caudal GPi, the area that is the target for pallidotomy. We found that pallidotomy produced striking improvements in off-period contralateral tremor. These effects were immediate and were maintained for > or = 2 years. This benefit is obtained despite the progressive nature of the illness and the often reduced dose of medications after surgery.

Globus Pallidus↗
PubMed1993

Orthostatic tremor: clinical and electrophysiologic characteristics.

Orthostatic tremor, sometimes known as "shaky legs syndrome," is a disorder of middle-aged or elderly people characterized by feelings of unsteadiness in the legs and a fear of falling when standing. Patients stand on a wide base but walk normally. These symptoms are due to high-frequency (13-18 Hz) burst firing in weight-bearing muscles. They are attenuated by walking and are abolished immediately by sitting. Some authors believe that the disorder is a variant of essential tremor. This study reports the clinical and electrophysiologic features of orthostatic tremor in 30 patients. The findings indicate that orthostatic tremor is distinct from essential tremor, both clinically and electrophysiologically. The major differences are the frequency of electromyographic burst firing, the invariable involvement of lower limb and paraspinal muscles, and the task-specific nature of the tremor in orthostatic tremor. The study shows that the diagnosis can be established rapidly with surface electromyographic recordings.

Acceleration↗
PubMed1994

Characteristics of tail-tremor induced by nicotine in rats.

To characterize the tail-tremor and locomotor hyperactivity induced by repeated nicotine administration, the effects of nicotinic, alpha-adrenergic and dopaminergic blockers were investigated in rats. Daily administration of nicotine (0.5 mg/kg, s.c.) induced tail-tremor from the 4th day, which became more marked in intensity by subsequent administration. Locomotor hyperactivity was also induced by nicotine, which was enhanced by daily administration. The tail-tremor and locomotor hyperactivity induced by repeated nicotine administration were inhibited by mecamylamine (0.1-1 mg/kg, i.p.) but not by hexamethonium (0.5 and 1 mg/kg, i.p.). Clonidine (0.02 and 0.04 mg/kg, i.p.) and prazosin (0.5 and 1 mg/kg, i.p.) reduced tail-tremor more markedly than hyperactivity. However, haloperidol (0.05-0.2 mg/kg, i.p.) and chlorpromazine (1-5 mg/kg, i.p.) reduced hyperactivity more markedly than tail-tremor. These results suggest that nicotine-induced tail-tremor and hyperactivity are due to an increased susceptibility of central nicotinic receptors of nicotine followed by catecholaminergic mechanisms, and that tail-tremor may be more associated with the noradrenergic system than the dopaminergic system.

Animals↗
PubMed1987

Comparative studies on the effects of beta-adrenergic blockers in essential tremor.

To establish the criteria for the selection of a beta-adrenergic blocking agent (beta-blockers) suitable for the long-term treatment of tremor, 20 patients with essential tremor were treated with five different types of beta-blockers. All beta-blockers were effective for essential tremor, but their efficacy differed. The weaker the intrinsic sympathomimetic activity (ISA) and the more marked the membrane stabilizing activity (MSA), the more marked was the anti-tremor effect. Propranolol, which showed the strongest anti-tremor effect, had no ISA, but its long-term administration induced symptoms of heart failure, such as pretibial oedema, in most cases. In most of these cases, when propranolol was replaced by indenolol, which showed a very slight ISA, the pretibial oedema subsided and well-controlled tremor was maintained over a long period. With regard to efficacy and usefulness, it was thought that the beta-blockers with a very slight ISA and a marked MSA, such as indenolol, was most suitable for the long-term treatment of essential tremor.

Adrenergic beta-Antagonists↗
PubMed1976

Modification of oxotremorine tremor and hypothermia by injections of drugs into the cerebral ventricles of the mouse.

1. The effect of various agents injected into the cerebral ventricles of the mouse, upon the tremor and hypothermia produced by oxotremorine (0.5 mg/kg i.p.) was studied. 2. Acetylcholine (0.1-10 mug) produced a dose-dependent potentiation of oxotremorine tremor in contrast to the multiphasic effect it had on the accompanying hypothermia. Both tremor and hypothermia were antagonised by very small doses (0.1-10 ng) of atropine. 3. Dopamine and apomorphine (0.1-10 mug) had no significant effect on oxotremorine tremor. A dose-dependent potentiation of hypothermia was, however, observed. 4. Noradrenaline (0.1-10 mug), phentolamine and propranolol (0.1-10 mug) produced no significant effect on tremor and inconsistent results were obtained on hypothermia. 5. Neither tremor nor hypothermia were affected by 5-hydroxytryptamine (1-20 mug). 6. Oxotremorine tremor appears to be due solely to the activation of cholinergic pathways, whereas the production of hypothermia is brought about via a system involving both cholinergic and dopaminergic components. 5-Hydroxytryptamine is not involved.

Acetylcholine↗
PubMed1993

GABA-gated chloride ion influx in brains of tremor rats.

We measured the GABA-gated chloride ion influx and GABA concentrations in the cerebral cortex and the hippocampus of young (5 weeks old) and older (15 weeks old) tremor rats. GABA-gated chloride ion influx in these tremor rats was significantly greater than in the controls of both the 5 week- and 15 week-old groups. GABA concentrations in the cerebral cortex and hippocampus of the tremor rats increased compared with controls of 5 weeks and decreased compared with controls of 15 weeks. These findings suggest that the GABAergic presynaptic neurons in the cortex and hippocampus of the tremor rat are disturbed with aging. This change may be related to the appearance of absence-like seizures in the rats. The increased GABA-gated chloride ion influx in tremor rats may be a compensatory mechanism against the genetically-determined seizure susceptibility of these rats. Furthermore, the increased GABA levels and GABA-gated chloride ion influx found in 5 week-old tremor rats may be related to the tremor movements.

Animals↗
PubMed2003

Kinaesthetic neurons in thalamus of humans with and without tremor.

Increased afferent input may alter receptive field sizes, properties and somatotopographic representation in the cortex. Changes in the motor thalamus may also occur as a result of altered afferent input. Such plasticity has been implicated in both sensory and movement disorders. Using tremor as a model of augmented afferent input to kinaesthetic/deep neurons representing the shaking limbs, we studied the representation and properties of these neurons in human thalamus in patients with resting tremor (RestTr) from Parkinson's disease, patients with action- or posture-induced tremor (ActionTr), and patients without tremor (NoTr). Data were collected during stereotactic thalamotomy or insertion of deep brain stimulators for relief of pain or movement disorder. Using microelectrode recording, 58 kinaesthetic neurons responding to wrist and/or elbow movement were studied by mapping the receptive field, carefully isolating each joint during testing. There were no significant differences in the proportions of single and multijoint responsive neurons in the different patient groups (RestTr, ActionTr and NoTr). The borders between tactile-cutaneous, deep-kinaesthetic and voluntary cell representations in the thalamus were mapped in 74 patients and compared between the different tremor groups. A significant difference in kinaesthetic representation was found: both the RestTr and ActionTr groups had a significantly greater kinaesthetic representation than the NoTr patients. There was an expansion of kinaesthetic representation in patients with chronic increased afferent drive from tremor, without alteration in RF size. No decrease in tactile representation was found, suggesting that the increase in kinaesthetic representation does not occur at the expense of tactile representation. These data suggest that plasticity can occur at the thalamic level in humans and may contribute to the pathogenesis of tremor.

Action Potentials↗
PubMed2003

Differential modulation of tremor and pulsatile control of human jaw and finger by experimental muscle pain.

Resting tremor is seen in both the limbs and in the trigeminal motor system. These rhythmical perturbations are the result of alternating activation of antagonistic muscles, and these increase in amplitude during slow, voluntary movements. In the present study, we examined the effect of experimental muscle pain on finger and jaw tremor. The tremor in the mandible and in the middle finger was measured on separate occasions, at rest and during two constant-velocity movements. Pain was then induced by the infusion of hypertonic saline into a jaw-closing muscle (masseter) or into a finger extensor muscle (extensor digitorum longus, EDL). During masseter pain, the power at the peak tremor frequency of the mandible decreased significantly both when the jaw was at rest and during voluntary jaw movements at two velocities. In contrast, pain in EDL resulted in a significant increase in the power of finger tremor only during the two speeds of voluntary movement. No change in the peak tremor frequency was seen in either the finger or the jaw during pain. The most likely explanation for these data is that muscle pain tonically modulates the amplitude of the outputs from the central "pulsatile control" generators that drive the alternating activation of antagonistic muscles which produce tremor at rest and during movements. This modulation is in the opposite direction for systems controlling jaw and hand, suggesting a specific interaction of the nociceptive afferents with separate central oscillators.

Adult↗
PubMed1998

Motor unit discharge and force tremor in skill- and strength-trained individuals.

We examined motor unit (MU) discharge properties (mean interspike interval, ISI, discharge variability, short-term synchronization, common drive) and force tremor in the first dorsal interosseous (FDI) muscle of five musicians (skill-trained), five weight-lifters (strength-trained) and six untrained subjects during low-force isometric abduction of the index finger. Mean MU ISI was slightly shorter in skill-trained subjects than in untrained subjects. Discharge variability of FDI MUs did not differ significantly between groups. The mean strength of MU synchronization (expressed as the frequency of extra synchronous discharges above chance) was different in skill-trained (0.22+/-0.02 s(-1), 162 MU pairs), untrained (0.32+/-0.02 s(-1), 199 MU pairs) and strength-trained subjects (0.44+/-0.03 s(-1), 183 MU pairs). FDI MU synchrony was weak and of equivalent strength in both hands of skill-trained subjects and the dominant (skilled) hand of untrained subjects. The stronger FDI MU synchrony in the non-dominant hand of untrained subjects was equivalent to that found in both hands of strength-trained subjects. The extent of common modulation of firing rates (common drive) was assessed for a subset of MU pairs and was weaker in skill-trained subjects (0.30+/-0.04, n=14) than untrained (0.43+/-0.3, n=14) and strength-trained (0.48+/-0.03, n=21) subjects. Force tremor was quantified for each hand in the same subjects during isometric index finger abduction at target forces of 0.5 N and 3.5 N. Tremor rms amplitude and peak power in the force frequency spectrum were significantly lower in skill-trained subjects than strength-trained subjects with the 3.5-N target force. The peak tremor frequency was similar in the three groups. The relatively more independent discharge of pairs of FDI MUs in skill-trained subjects was not responsible for the reduced tremor amplitudes in these subjects. Correlations between the overall extent of MU synchrony and common drive in FDI muscles and tremor measures obtained during the same experimental session were all non-significant. Differences in the central descending command signals are the most likely explanation for the more independent discharge of FDI MUs in skill-trained hands, while neural or peripheral muscular factors may be responsible for the weaker tremor.

Adolescent↗
PubMed1999

Dependence of peripheral tremor on mechanical perturbations: a modeling study.

The present study scrutinizes the popular view that tremors of central origin but not those of peripheral origin are largely resistant to mechanical perturbations. We explore the effects of perturbations in a well-established model of peripheral tremor and document that (a) tremor frequency can remain unchanged when spring or weight loads are added, (b) entrainment by external drives can be limited to drives of similar frequency, and (c) resetting of tremor phase by torque pulses can remain fractional. This resistance to mechanical perturbations arises in the model because peripheral neuromuscular dynamics act as a limit-cycle oscillator which, by its very nature, will absorb moderate changes to signals and parameters. We conclude from our study that resistance to mechanical perturbations is not an exclusive property of central tremors, but rather may also be found in peripheral tremors. Other criteria are therefore needed to distinguish between different origins of tremor.

Models, Biological↗
PubMed1999

Load dependence of simulated central tremor.

Previous studies have argued that tremors of central versus peripheral origin can be distinguished based on their load dependence: the frequency of peripheral tremor decreases when a weight is added to the tremulous limb, while the frequency of central tremors remains unchanged. The present study scrutinizes the latter statement. We simulated central tremor using a simple network of coupled neural oscillators, which receives proprioceptive feedback from the motor periphery. The network produced a self-sustained, stable oscillation. When the gain of proprioceptive feedback was high, oscillation frequency decreased in the presence of an inertial load. When the gain was low, the oscillation frequency was load independent. We conclude that load dependence is not an exclusive property of peripheral tremors but may be found in tremors of central origin as well. Therefore, the load test is not sufficient to reject a central tremor origin.

Central Nervous System↗
PubMed1984

Treatment of resting tremor by beta-adrenergic blockade.

The effect of nadolol, a peripherally acting beta-adrenergic blocker, on resting tremor was examined in eight patients with idiopathic Parkinson's disease. With the use of a double-blind, placebo-controlled study of crossover design, patients received 80 to 320 mg of nadolol for 6 weeks while continuing their previous treatment regimen. Accelerometer readings showed a progressive reduction in tremor amplitude, but no change in tremor frequency, with increasing nadolol dosage. Maximum benefit was achieved at 240 mg, when resting tremor improved 50% (p less than 0.01). Physician ratings confirmed these findings. The results suggest that response to beta-adrenergic blockade may not be limited to postural or intention tremor and that such agents may not reliably differentiate between the tremor of Parkinson's disease and essential tremor.

Adrenergic beta-Antagonists↗
PubMed1987

Stability of frequency during long-term recordings of hand tremor.

During recording of physiological postural hand tremor over a period of 60 min tremor peak frequency (PF) did not change in 14 normal subjects as long as the mechanical conditions were not changed. In contrast, tremor amplitude and synchronization of the corresponding EMG varied considerably. Any alteration in hand mechanics such as changing hand position or adding masses led to changes of PF according to the alteration in mechanical resonant properties. The results show that PF of physiological postural hand tremor is mainly determined by mechanical factors. There is no evidence for a systematic decrease of PF (Stiles et al. 1976) or for the emergence of a formerly described (Lippold 1981) 4-6 Hz tremor component with prolonged maintenance of posture. In the pathological tremor forms of Parkinson's disease or essential tremor PF also remained unchanged during prolonged maintenance of posture.

Adolescent↗
PubMed1989

24 hour continuous tremor quantification based on EMG recording.

A new method is described that allows continuous quantification of parkinsonian and essential tremor over a period of up to 24 h on the basis of surface EMG recording from antagonistic forearm muscles. Tremor extraction from EMG data and all other calculations are performed on a digital computer. The occurrence, intensity and frequency of tremor are calculated. The data evaluation is fully automatic, including quality control and elimination of artifacts. Since tremor changes considerably over a 24 h period, long-term quantification gives more reliable data to study diurnal variations and to control the effects of medical treatment on tremor. As an additional advantage tremor recording is not restricted to a laboratory environment. Tremor can be monitored under everyday conditions and in the presence of moderate voluntary EMG activity.

Electromyography↗
PubMed1975

Tremor production by intracaudate injections of morphine.

Pronounced resting tremor was produced in unanesthetized cats by injecting morphine (25-110 mug) into the caudate nucleus. The effects of morphine were antagonized by intracaudate (i.c.) injections of nalorphine (81-263 mug). Tremor activity was also inhibited by i.c. injections of dopamine (61-145 mug), Ca2+ (24-40 mug), scopolamine (88-121 mug) and hemicholinium-3 (HC-3; 73-129 mug) while serotonin (125 mug) was ineffective. Tremor inhibition by HC-3 was reversed by i.c. doses of acetylcholine (15-30 mug) which were subthreshold for tremor production in the absence of morphine. Morphine (55-110 mug) further increased the intensity of ongoing tremor activity induced by physostigmine (111 mug i.c.) I.c. injections of nalorphine antagonized the motor effects of morphine without affecting physostigmime tremor. Tremor production by morphine is attributed to a reduction in dopamine function which allows cholinergic activity in the caudate nucleus to predominate.

Acetylcholine↗
PubMed1984

Dependence of cerebellar tremor on proprioceptive but not visual feedback.

We studied the influence of proprioceptive and visual feedback on cerebellar tremor which occurred after arm perturbations and after voluntary elbow flexions. Cerebellar tremor was produced in monkeys by reversibly cooling through two probes implanted lateral and medial to the dentate nucleus. Cerebellar tremor was synchronized in different trials to torque pulse onset and to the end, but not the start, of voluntary movements. Addition of loads to the handle held by the monkey (increases in spring stiffness, viscosity, constant torque, and inertial load) changed the amplitude and frequency of tremor that follows arm perturbations or voluntary movements in the same way. In both situations EMG activity in each cycle of tremor followed stretch of its own muscle and attained a peak near peak velocity irrespective of the mechanical load. Removal of visual feedback did not alter the characteristics of the tremor or the associated EMG activity. We concluded that cerebellar intention tremor, which occurs when attempting to hold the arm in an intended position, is driven by stretch-evoked peripheral feedback and not by voluntary corrections based on vision.

Animals↗