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PubMed1981

Harmaline-induced tremor. II. Unit activity correlation in the interposito-rubral and oculomotor systems of cat.

Units were recorded extracellularly in the cat brainstem under the effect of tremogenic doses of harmaline. They were localized post mortem and the units discharging at the harmaline tremor frequency were mapped. Harmaline-sensitive neurons were found in the bulbo-pontine reticular formation, in particular, in the lateral reticular nucleus and the nucleus reticularis tegmenti pontis. The nucleus interpositus as well as the red nucleus also displayed numerous units discharging at the tremor frequency, indicating that the cerebello-interposito-rubro-spinal system controlling the flexor muscles participate in harmaline tremor. Participation of the oculomotor system in the harmaline-induced tremor was tested at the level of the vestibular neurons relaying the vestibulo-ocular reflex, the motoneurons, the eye muscles and the eye movements. No rhythmic discharge at the tremor frequency nor eye movements could be detected, indicating that harmalie tremor does not affect the oculomotor system.

Alkaloids↗

PubMed1988

Twenty-four-hour tremor recordings in the evaluation of the treatment of Parkinson's disease.

A new method of prolonged recording of EMG provides a good estimate of spontaneous and induced diurnal variations in resting tremor in Parkinson's disease. It provides a record and a measure of the effects of treatment. Tremor intensity shows considerable variations even over short periods of time. Therefore short-term measurements of tremor are unhelpful. Long-term recordings agree better with the patient's assessment than with the clinical rating score. Repeated recordings over a similar 10-h period on 3 consecutive days in one patients showed fairly constant measures of occurrence and intensity of tremor. In contrast to accelerometer measurements of tremor, artefacts caused by movements and general activity of the patient do not materially interfere with tremor evaluation using surface EMG.

Adult↗

PubMed1993

Myo-electric signals from two extrinsic hand muscles and force tremor during isometric handgrip.

The objective of the present study was to investigate the myo-electric signs of muscle fatigue and the isometric force tremor of two extrinsic hand muscles, extensor digitorum communis and flexor digitorum superficialis, during isometric power grip. In addition, the synergy between flexor and extensor muscles and hand differences in a right-handed population have been studied. During isometric hand-dynamometry the myo-electric signal was recorded using surface electrodes and isometric force tremor was recorded using a special load cell. Eight subjects participated in this study and contractions were performed at 20%, 40%, 60% and 80% of maximal voluntary contraction (MVC) with left and right hands. The decrease of mean power frequency (MPF) with duration of contraction was greater in the left extensor as compared to the ipsilateral flexor muscle. No differences in the decrease in MPF with the duration of the contraction were found between the right extensor and flexor muscles. Isometric force tremor root mean square did not change during contractions at a given contraction level. Isometric tremor amplitude increased from 20% to 60% MVC and decreased at higher contraction levels. Tremor amplitude was higher in the left hand at all contraction levels but 60% MVC. These data would suggest differences in fatiguability and muscle fibre composition between the dominant and nondominant hand, which may be due to preferred use. The significance of force tremor for the evaluation of recruitment order and muscle fatigue is discussed.

Adult↗

PubMed1985

DDT-induced tremor in rats: effects of pharmacological agents.

Rats given a tremorigenic dose of DDT (75 mg/kg, PO) were treated with pharmacological agents either 30 min prior to DDT or 1-2 h prior to testing at the time of peak effect (12 h postdosing). The administration of mephenesin (a centrally acting muscle relaxant) or Dilantin (an anticonvulsant) prior to DDT significantly attenuated tremor. Pretreatment with pizotifen (a serotonergic receptor antagonist) had no significant effect on tremor. Administration of the same agents 1-2 h prior to measurement had minimal effects. Trihexyphenidyl (a muscarinic cholinergic receptor antagonist) exacerbated the tremor produced by DDT. These data suggest that cholinergic neurotransmitter systems may be involved in DDT-induced tremor. That DDT-induced tremor was significantly attenuated by mephenesin and Dilantin is in accord with the conclusion that DDT-induced tremor is a manifestation of repetitive discharge due to interference with ionic conductance.

Analysis of Variance↗

PubMed1985

Serotonergic potentiation of muscarinic agonist evoked tremor and salivation in rat and mouse.

The dose-effect of oxotremorine upon the onset, duration and magnitude of tremor and salivation was studied in both mice and rats. The threshold doses of oxotremorine (SC) for eliciting tremor were above 50 micrograms/kg in mice and above 150 micrograms/kg in rats and the threshold doses for eliciting salivation were above 75 micrograms/kg in mice and above 200 micrograms/kg in rats. Alaproclate, a nontricyclic 5-HT uptake inhibitor, when injected 30 min prior to the administration of the cholinergic agonist, produced a dose-dependent enhancement of tremor and salivation in both rats and mice. Alaproclate itself did not produce these effects in the absence of a muscarinic cholinergic stimulant such as oxotremorine, arecoline or the acetylcholine esterase inhibitor physostigmine. Both salivation and tremor could be fully blocked by atropine at any dose of the cholinergic stimulant and of alaproclate used. The potentiating effects of alaproclate on salivation and tremor could also be blocked by two serotonin receptor antagonists, metitepine and danitracen, but not by metergoline or cinanserin. Other compounds which inhibit the uptake of 5-HT such as fluoxetine, citalopram, norzimeldine, zimeldine and the non-tricyclic antidepressant, iprindol, did not enhance the cholinergic agonist induced tremor or salivation under the same conditions as did alaproclate. It is suggested that alaproclate exerts the potentiating effect at a hitherto undefined serotonergic receptor site.

Alanine↗

PubMed1989

The effectiveness of different isomers of octanol as blockers of harmaline-induced tremor.

Intracellular recording in the guinea-pig brainstem slice has demonstrated that high molecular weight alcohols block the low threshold calcium channel (LTCC) in the inferior olive (IO). These alcohols thus provide a tool for understanding the function of the pacemaking cellular networks of the olivo-cerebellar system, since the LTCC has been implicated in the oscillatory behavior of these neurons. Aspects of normal and pathological tremor are also believed to be mediated by these circuits, and thus development of effective ways of blocking the LTCC in vivo may eventually lead to novel treatments for essential tremor. The present experiments evaluated the effectiveness of the isomers of octanol in decreasing harmaline-induced tremor in vivo in the rat. Harmaline was used in this study because its tremorgenic action is mediated at the level of IO; octanol was found to be a potent antagonist of harmaline-induced tremor. Significant differences between the isomers further suggested conformational differences. This, taken in conjunction with the lack of effect of octanol in both IO lesioned rats and oxotremorine-induced tremor, implied that the action of the alcohol may be mediated at a specific binding site. These findings thus support the conclusions that the antagonism of harmaline-induced tremor by octanol occurs in the IO, and, in view of the previously reported in vitro data, that octanol may be an effective blocker of the LTCC in vivo.

Alkaloids↗

PubMed2003

The detection of tremor during slow alternating movements performed by patients with early Parkinson's disease.

The present study demonstrates that tremor can be detected during slow alternating movements (SAM) performed by patients with early Parkinson's disease (PD) and that its relative amplitude is strongly correlated with patients' rest and postural hand tremor amplitudes (Rho=0.80 and 0.61, respectively, P<0.05). However, the tremor detected during SAM did not influence the accuracy of patients because of its relatively low amplitude. These results imply that the presence of tremor during movement is not restricted to advanced PD, but can also be detected in patients with early PD having relatively low amplitude tremor. Evidence that the tremor detected at rest, during posture and during voluntary movement share similar or overlapping neural substrates is also presented.

Age of Onset↗

PubMed2000

Evidence that ventrolateral thalamotomy may eliminate the supraspinal component of both pathological and physiological tremors.

Ventrolateral (VL) thalamotomy produced a marked reduction of oscillations related to the supraspinal components of Parkinson's disease tremor (4-7 Hz) and physiological tremor (8-12 Hz). Finger tremor was examined in nine patients undergoing unilateral VL thalamotomy and in nine age-matched controls. In comparison to the preoperative state, the relative percentage of power within the 7.6-12.5 Hz band did not increase after the surgical procedure. Furthermore, the amount of absolute power within the 7.6-12.5 Hz band was much lower for post-surgical patients in comparison to matched controls when periods of tremor having equal amplitudes were compared. These results suggest that VL thalamotomy interrupts a common circuit involved in the supraspinal component of both physiological and pathological tremors. We provide evidence that the thalamus may be involved in circuits generating physiological tremor in humans.

Adult↗

PubMed2000

Significance of peripheral afferent input to the alpha-motoneurone pool for enhancement of tremor during an isometric fatiguing contraction.

The objective of this study was to investigate the contribution of peripheral afferent input to the enhancement of isometric tremor during a sustained submaximal isometric contraction. It was hypothesised that during muscle fatigue, when excitatory drive is high, peripheral afferent input may augment oscillations in the stretch reflex arc and result in bursting motor-unit activity and increased tremor. Nine healthy subjects maintained isometric plantar flexions at 30% of their maximum voluntary contraction until the limit of endurance, under three test conditions. Two paradigms were used to reduce afferent input to the triceps surae alpha-motoneurone pool: (1) continued vibration of the Achilles tendon, and (2) ischaemic partial block of the tibial nerve. These were compared to a control experiment, in which there was no intervention. By recording H-reflexes from the gastrocnemius and soleus muscles, it was possible to assess the effectiveness of reducing the afferent input. When H-reflex suppression had stabilised, the fatiguing contraction was commenced and tremor was computed from the continuously recorded torque signal. Superimposed maximum twitches were elicited as indirect measures of excitatory drive. The increase in tremor root mean square throughout the fatiguing contraction was significantly less for both the vibration and ischaemic conditions. Furthermore, tremor mean power frequency decreased significantly with endurance time in the control experiment, while no significant change was seen in the other two experimental conditions. It is concluded that the enhancement of isometric tremor seen during a fatiguing submaximal isometric contraction is facilitated by peripheral afferent input to the alpha-motoneurone pool.

Adult↗

PubMed2001

Physiological tremor of the upper limb segments.

The acceleration signal produced by physiological tremor from four different upper limb segments (the finger, hand, forearm and upper limb) was measured by an acceleration sensor during holding posture and was analyzed by power spectrum analysis. Two prominent peaks appeared in the power spectrum, suggesting that the tremor in the four different limb segments was composed of two frequency components. The frequency of one peak at 8-12 Hz did not change between the different limb segments, while the frequency of the other peak decreased with the increase in the mass of the limb segment. A model with two reflex pathways was developed for the tremor in the four limb segments. The model includes two reflex pathways, a spinal pathway and a supraspinal pathway. The theoretical values of the frequency and the amplitude of the tremor predicted by the model were in good agreement with the experimental results. Analysis of the model revealed that one of the two frequency components of the tremor was of spinal origin and was dependent upon the mass of the limb segment, and the second was of supraspinal origin, corresponding to the frequency at 8-12 Hz. In the normal subject, it is possible that the tremor could be used to evaluate the change in neuromuscular function produced by prolonged work involving just part of a limb segments (e.g., typing). It may also be used to evaluate the neuromuscular function of patients suffering from neurological diseases such as muscular dystrophy and Parkinson's disease.

Adult↗

PubMed2002

Pathological tremors as diffusional processes.

Two types of pathological tremors, essential and Parkinsonian, are studied using dynamical systems theory. It is shown that pathological tremors can be characterized as diffusional processes. The time-scale range for the diffusional scaling law to be valid starts from about one to several tens of the mean oscillation period. This time-scale range contrasts sharply with the predictable time scale for deterministic chaos, which is usually only a small fraction of the mean oscillation period. The diffusions in pathological tremors are usually anomalous. A number of quantities are designed to characterize the diffusions in the tremor. Their relevance to potential clinical applications is discussed. It is argued that in order to discriminate between Parkinsonian and essential tremors, quantities not of purely dynamical origin may be more useful, since purely dynamical quantities emphasize more the dynamical similarities between the two types of tremors.

Essential Tremor↗

PubMed1988

Comparison of cerebellar intention tremor under isotonic and isometric conditions.

The characteristics of cerebellar intention tremor were investigated by comparing the properties of tremor following movements about the elbow with that following isometric contractions of biceps and triceps brachii. Cerebellar dysfunction was produced by local, reversible cooling of the dentate and interposed nuclei in three Cebus monkeys. Cerebellar nuclear cooling disrupted isometric contractions to the aimed target and produced oscillations in torque. Whereas the cerebellar tremor that followed movements was regular and had a frequency of 3-5 Hz, the oscillations in the isometric task were irregular and were often of a lower frequency. In addition, cycles of tremor following movements were in phase from trial to trial, while the oscillations that occurred following isometric contractions did not show this phase-relationship. It is concluded that a cerebellar tremor can occur in an isometric situation but that movement about a joint is required for development of a rhythmic 3-5-Hz cerebellar intention tremor.

Animals↗

PubMed1975

The importance of extrapyramidal function for the induction and antagonism of harmine tremor.

The brain lesion technique was used to investigate the role of the paleostriatum and the nigro-neostriatum in harmine-induced tremor and in its antagonism by dopaminergic agonists, apomorphine, 1-dopa, piribedil, d- and l-amphetamine. Bilateral lesions of the caudate--putamen or substantia nigra failed to modify the intensity of tremor or its antagonism by dopaminergic agonists. Bilateral lesions of the globus pallidus markedly reduced the intensity of tremor and the results indicated that such lesions were also able to reduce the effectiveness of dopaminergic agonists as tremor antagonists. The data suggest that the integrity of the paleostriatum is more important than that of the neostriatum for the mediation of harmine tremor and its antagonism by dopaminergic agonists. The results are discussed in relation to the proposed clinical relationship between paleostriatal dopamine dysfunction and tremor mechanisms.

Alkaloids↗

PubMed1976

Charcot-Marie-Tooth disease associated with "essential tremor": Report of 7 cases and a review of the literature.

A study of 7 cases of Charcot-Marie-Tooth disease associated with a dyskinesia resembling benign essential tremor is presented. In 4 patients, the family history strongly suggested an autosomal mode of transmission, 2 cases were sporadic without an established genetic pattern and 1 was probably recessive. The distal parts of the upper and lower limbs showed imparied muscle strength with slight or no atrophy in 4 patients and conspicuous weakness and wasting in another 2. One patient was a chairbound. Although essential tremor and the tremor seen in these patients are clinically (phenotypically) similar it seems possible that they result from two different genotypes. Further, it seems that cases with Charcot-Marie-Tooth disease and "essential tremor" are not the result of the association of two separate dominant characteristics which are generally inherited as mendelian dominant traits. In spite of the diversity of the clinical manifestations of the peripheral neuropathy, the semiologically different types of essential tremor and the electrophysiological data, it is concluded that patients who develop a peripheral neuropathy on a familial basis and who exhibit clinical features of similar character, suffer from a common type of pathological disorder. Stress is laid upon the fact that Friedreich's ataxia and Charcot-Marie-Tooth disease share many clinical features. It is suggested that when Friedreich's ataxia and Charcot-Marie-Tooth disease seem to be present in the same individual and/or alternate in different members of the same family, the process is likely to be one of Charcot-Marie-Tooth disease. The value of the type of inheritance, natural history, clinical examination and electrophysiological data in differentiating Charcot-Marie-Tooth disease (with or without essential tremor) from other degenerative disorders is analyzed.

Adolescent↗

PubMed1995

Altered brain contents of neuropeptides in spontaneously epileptic rats (SER) and tremor rats with absence seizures.

Immunoreactive- (IR-) somatostatin (SRIF), neuropeptide Y (NPY) and corticotropin-releasing factor (CRF) contents were investigated in the brain of tremor rats with absence-like seizure and spontaneously epileptic rats (SER), which is a genetically defined double-mutant (zi/zi, tm/tm) obtained by mating zitter homozygote (zi/zi) with tremor heterozygote (tm/+) and shows both absence-like seizure and tonic convulsions. Increased levels of IR-NPY and IR-CRF were observed in several regions including the amygdala and hippocampus in homozygous SER compared to heterozygous SER (zi/zi, tm/+ or +/+). Homozygous tremor rats (tm/tm) showed lower levels of IR-NPY and IR-CRF contents mainly in the hippocampus and mesolimbic system (entorhinal and pyriform cortex and nucleus accumbens) than heterozygous tremor rats. IR-SRIF contents of homozygous SER were higher in frontal cortex than heterozygous SER and in amygdala than homozygous tremor rats. No change of IR-SRIF between groups was noted in the hippocampus among brain structures underlying epileptogenicity. The results suggest that the change of neuropeptide levels, most conspicuous in NPY among three peptides tested, may be involved in the phenotypical manifestation of seizures in SER and tremor rats, and that the development of tonic convulsion and absence seizures may be differently associated with the change of brain neuropeptide levels.

Animals↗

PubMed1991

Structure-activity studies of neurotensin on muscular rigidity and tremors induced by 6-hydroxydopamine lesions in the posterolateral hypothalamus of the rat.

It has previously been reported that intracerebroventricular administration of neurotensin (30 micrograms) reduced muscular rigidity and tremors, induced by a neurochemical lesion with 6-hydroxydopamine in the posterolateral hypothalamus of rats. In the present study, the effects of two fragments (NT1-10 and NT8-13) and two analogues ([D-Tyr11]-NT and [Ala11]-NT) of neurotensin on the grasping time (index of muscle rigidity) and tremors in 6-hydroxydopamine-lesioned rats are reported. Intracerebroventricular administration with 120 micrograms of NT1-10 and [Ala11]-NT had no effect on the muscle rigidity and tremors induced by the neurochemical lesion. The administration of NT8-13 60 micrograms) significantly attenuated both behavioural responses. The analogue [D-Tyr11]-NT produced a much greater attenuation of the muscle rigidity and tremors. The dose of 1.8 micrograms of [D-Tyr11]-NT significantly reduced the grasping time, while the number of tremors was attenuated with the threshold dose of 0.9 micrograms. Together, these results suggest that the effects of neurotensin on muscle rigidity and tremors, induced by pretreatment with 6-hydroxydopamine injected into the posterolateral hypothalamus, were not caused by non-specific effects but largely depended on the carboxy terminal of the peptide. The tyrosine residue in position 11 of the molecule plays a critical role in the action of neurotensin, as shown with the high potency and duration of action of the analogue [D-Tyr11]-NT. As previously suggested, the greater effect with [D-Tyr11]-NT may be due to greater resistance of the analogue to enzymatic degradation because of the incorporation of the D-Tyr amino acid, in position 11 of neurotensin.

Animals↗

PubMed1989

Nicotine-induced tail-tremor and drug effects.

Tail-tremor induced by repeated and daily administration (0.5 mg/kg SC x 6 times/day) of nicotine as well as effects of various drugs on this response were investigated in Wistar strain male rats. Daily administration of nicotine in doses of 0.5 mg/kg SC caused tail-tremors to appear beginning on the 3rd day. Tail-tremor induced by the first injection of each day gradually increased with the daily injections, however, the heightened effect of this first injection at the beginning of each day decreased during the day upon repeated administration of 6 times/day at 2-hr intervals. Basically, tail-tremor appeared about 5 min after SC administration of nicotine and reached a peak approximately 7-9 min after injection, declining to zero afterwards. Different drugs showed various effects on this response. While mecamylamine (0.5 and 1.0 mg/kg IP) abolished nicotine-induced tail-tremor, arecoline (0.5 and 1.0 mg/kg IP), atropine (2.5 and 5.0 mg/kg IP), scopolamine (1.0 and 2.0 mg/kg IP) and hexamethonium (0.5 and 1.0 mg/kg IP) showed no such effects. Furthermore, physostigmine (0.1 mg/kg IP) actually potentiated this action. These results suggest that tail-tremor induced by nicotine may be mediated through central nicotine receptor system.

Animals↗

PubMed1994

Modification of 2,2',2''-tripyridine-induced tremor in mice by serotonergic agonists and antagonists and benzodiazepines.

The administration of 2,2',2''-tripyridine produced generalized tremor, myoclonus, and hindlimb abduction, similar to the "5-hydroxytryptamine (5-HT) syndrome," in mice. Pretreatment with mianserin, cyproheptadine, methysergide, or metergoline ameliorated, whereas 5-hydroxytryptophan (5-HTP), 5-methoxy-N,N-dimethyltryptamine (5-MeODMT), or 8-hydroxy-2-[di-n-propylamino]tetraline hydrobromide (8-OH-DPAT) augmented the 2,2',2''-tripyridine-induced tremor. Furthermore, diazepam and flunitrazepam exhibited a dose-dependent protection against 2,2',2''-tripyridine-induced tremor in mice, but pentobarbital only had a slightly protective effect. The inhibitory effects of diazepam and flunitrazepam on the 2,2',2''-tripyridine-induced tremor were potentiated in mice pretreated with p-chlorophenylalanine (PCPA). These observations suggest a serotonin-mediated action of 2,2',2''-tripyridine in its tremor action and that the benzodiazepine agonist attenuation of the 2,2',2''-tripyridine-induced tremor is probably mediated through the GABAergic inhibition of serotonergic neurons.

Animals↗