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PubMed1997

Neurophysiological investigations in patients with head tremor.

We studied 30 patients whose primary complaint was head tremor in an attempt to characterize neurophysiological aspects of their abnormal movement. Based on family medical history and physical examination, 23 patients had definite or probable essential tremor (essential head tremor, EHT). The remaining seven had mild dystonic signs accompanying their head tremor (head tremor plus dystonic signs, HT + DS). We recorded head movement and the electromyographic (EMG) activity of the sternomastoid and splenius capitis muscles, determined the spontaneous blinking rate, and measured the excitability recovery curve of the blink reflex and of the masseteric inhibitory reflex. All patients had tremor bursts at a frequency ranging between 3 and 9 Hz in at least one of the muscles examined. The predominant pattern seen when patients were sitting relaxed and facing forward was that of synchronized EMG bursts in both splenius capitis muscles. Maintenance of extreme head postures demonstrated two types of additional abnormalities: type 1 (enhancement of tremor), which was observed in 11 patients (47.8%) with EHT and in two (28.5%) with HT + DS; and type 2 (activation of neck muscles not required for maintenance of the posture), which was observed in two patients (8.7%) with EHT and in five (71.5%) with HT + DS (chi 2 = 26.4; p < 0.001). Mean blinking rate per minute was 24.9 +/- 14.6 in patients with EHT and 42.3 +/- 10.5 in patients with HT + DS (paired t test, p = 0.001). The blink reflex and masseteric inhibitory reflex excitability recovery curves showed an abnormal interneuronal excitability enhancement in seven (30.4%) of the 23 patients with EHT and in two (28.5%) of the seven with HT + DS (chi 2 = 3.1; p > 0.05). Abnormal patterns of EMG activity of the neck muscles correlated well with the presence of mild dystonic signs. However, the analysis of brainstem interneuronal excitability did not enable recognition of those patients with head tremor who could potentially develop cervical dystonia. The enhancement of brainstem interneuronal excitability found in approximately 30% of patients with head tremor could be related to plastic changes triggered by increased activity of the cranial muscles.

Adult↗
PubMed1997

Tremor in Latin texts of Dutch physicians: 16th-18th centuries.

In his monograph An essay on the shaking palsy (1817), James Parkinson mentioned tremor and propulsion to be the most important signs of the disease that he was describing. In this article, we study aspects of the history of one of the signs that he mentioned, that is, tremor, and see how the meaning of this term evolved since its description by Galen, particularly in the period from the 16th to the 18th centuries. We'll pay attention to the development of a distinction made between action tremor and rest tremor. Work by the following authors is covered: Pratensis and Forestus (16th century); Tulp, Van Beverwijck, an Sylvius (17th century); and Boerhaave and Van Swieten (18th century). Not all authors made the distinction, originally noticed by Galen, between action tremor and rest tremor. Parkinson tremor probably was observed but was classified among the tremors of the elderly. The meaning of palpitation changed through the ages and finally was applied only to pathologic heart and artery pulsations. Sylvius and Van Swieten were the only authors in this study who clearly distinguished between action and rest tremor. They are discussed in Parkinson's monograph.

Geriatrics↗
PubMed1997

Cerebellar axial postural tremor.

Three cases are presented with a predominantly axial postural tremor, without visible palatal tremor. Tremor varied in frequency between 3 and 10 Hz, often jumping from one frequency to another in this band. All three patients had evidence of cerebellar pathology. Cases 1 and 2 developed tremor in the setting of a late-onset cerebellar degeneration and after excision of a right cerebellar haemangioblastoma, respectively. Etiology was unclear in Case 3. Nevertheless, this patient had a cerebellar dysarthria. The tremor was similar to that sometimes seen in conjunction with palatal tremor, and EMG studies in Case 3 demonstrated a subclinical modulation of palatal muscle activity simultaneous with the truncal tremor. It is suggested that an axial postural tremor may be due to pathology of the cerebellum and its outflow pathways, despite the absence of clinically apparent palatal tremor.

Adult↗
PubMed1998

Orthostatic tremor: an electrophysiological analysis.

Orthostatic tremor (OT) is a clinically defined syndrome of leg tremor while standing. Controversy surrounds whether OT is a distinct syndrome or is an essential tremor (ET) variant. We report two patients with OT. Electrophysiological testing included polymyography, accelerometry, nerve conduction, and evoked potential studies. The effects of various maneuvers and body positions on the tremor were assessed. The findings included rapid (15-17 Hz) lower-extremity tremor burst frequency evoked by standing but not by walking or swaying; rapid upper-extremity burst pattern synchronous with lower-extremity bursts; and failure of electrical stimulation or mental concentration to "reset" the tremor. Additionally, there was the novel finding of accelerometric recordings in the legs revealing the same rapid frequency (16-17 Hz) as the electromyographic tremor bursts. Some prior reports have suggested that OT is related to ET by emphasizing a considerable disparity and variability between the accelerometric tremor frequency and the electromyographic burst frequency. In our patients, however, the rapid (15-17 Hz) accelerometer-recorded tremor synchronous with the electromyographic bursts, and also the clinical improvement with clonazepam but not beta blockers or mysoline, and the lack of a family history of ET provide support that OT is distinct from ET.

Aged↗
PubMed1993

Tremor in healthy volunteers after bambuterol and terbutaline CR-tablets.

Bambuterol tablets, 10 and 20 mg, and terbutaline CR-tablets, 5 and 7.5 mg, have been compared for their capacity to produce subjectively determined tremor in a randomised, double-blind, cross-over study in 40 healthy volunteers. The duration of each treatment was one week, with an intervening washout period of at least 2 weeks. On the second and the last treatment days in each period, tremor was subjectively assessed on six occasions. In addition, an overall assessment of night and day tremor was made each morning and evening. Analyses were made for the second and last treatment days and during the treatment week. Paired comparisons for tremor during daytime showed a significant difference between the treatments, with the exception of bambuterol 20 mg and terbutaline 5 mg. Bambuterol 10 mg caused less tremor and terbutaline 7.5 mg caused more tremor than the other treatments. At the end of the week, the differences were smaller and were only significant when comparing bambuterol 10 mg with the 20 mg dose and with high dose terbutaline. Terbutaline 7.5 mg caused more tremor at night than the other treatments. The tremor experienced was generally mild, and after bambuterol 10 mg it was almost negligible (mean 0.13 after the first dose). Two subjects recorded a score of 3 after terbutaline 7.5 mg. The results indicate that, in doses equipotent with regard to bronchodilation, tremor is less pronounced after bambuterol as compared to controlled release tablets of terbutaline.

Administration, Oral↗
PubMed1983

Physiological evidence for central modulation of voice tremor.

The present report presents an attempt to define the physiological parameter used to describe "voice tremor" in psychological stress evaluating machines, and to find its sources. This parameter was found to be a low frequency (5-20 Hz) random process which frequency modulates the vocal cord waveform and (independently) affects the frequency range of the third speech formant. The frequency variations in unstressed speakers were found to be the result of forced muscular undulations driven by central nervous signals and not of a passive resonant phenomenon. In this paper various physiological and clinical experiments which lead to the above conclusions are discussed. a) It is shown that induced muscular activity in the vocal tract and vocal cord regions can generate tremor in the voice. b) It is shown that relaxed subjects exhibit significant tremor correlation between spontaneously generated speech and EMG, with the EMG leading the speech tremor. c) Tremor in the electrical activity recorded from muscles overlapping vocal tract area was correlated with third formant demodulated signal and vocal cord demodulated pitch tremor was correlated with first formant demodulated tremor. d) Enhanced tremor was found in Parkinson patients and diminished tremor in patients with some traumatic brain injuries.

Electromyography↗
PubMed1983

Drugs for Parkinson's disease reduce tremor induced by physostigmine.

The effects of anticholinergic and dopaminergic drugs used for Parkinson's disease were studied on the tremor induced by physostigmine (0.3-3.0 mg/kg) in rats. For the measurement of tremor a new electronic device was employed. Atropine (0.3-1.2 mg/kg) and biperiden (0.01-1.0 mg/kg) reduced the physostigmine-induced tremor in a dose-related manner and could abolish it. Biperiden was less potent than atropine. Methylatropine in a dose of 1.2 mg/kg slightly inhibited the tremor. Amantadine (0.3-3.0 mg/kg) reduced the tremor but only to a certain degree. Bromocriptine (0.1-10.0 mg/kg) reduced it in a manner that was not dose-related. Pimozide potentiated the tremor in the dose of 0.2 mg/kg but not in larger doses. At the onset of the tremor, a small decrease in rectal temperature occurred. The hypothermia lasted significantly longer than the tremor. Neither the anticholinergic nor the dopaminergic anti-Parkinson drugs altered the hypothermic effect of physostigmine. The results show that those anti-Parkinson drugs, which act by increasing the dopaminergic activity can counteract the tremor induced by physostigmine. However, these drugs are clearly less active than th anticholinergic anti-Parkinson drugs.

Amantadine↗
PubMed1983

Spectral analysis of tremorine and cold tremor electromyograms in animal species of different size.

In 14 mice (36.2 +/- 5.4 g), 17 rats (425 +/- 46.4 g), and 11 rabbits (3,200 +/- 340 g) a comparative electromyographic analysis of tremorine tremor and cold tremor was performed in gastrocnemius and tibialis anterior muscles using spectral analysis. The mean frequency of cold tremor decreased with increasing body weight (mice: 40.2 +/- 4.5 Hz; rats: 31.3 +/- 4.9 Hz; rabbits: 16.4 +/- 3.2 Hz). With tremorine tremor no such allometric correlation was found for tremor frequency and body weight (mice: 17.7 +/- 3.6 Hz; rats: 19.6 +/- 5.1 Hz; rabbits: 15.9 +/- 2.1 Hz). Cross spectral analysis revealed that during cold tremor the flexor muscle (tibialis anterior) and the extensor muscle (gastrocnemius) of rabbits are activated alternately. The mean phase shift between the activation of flexor and extensor muscle was -155.5 degrees. Stronger activation was observed in the flexor muscle. Tremorine tremor was characterized by synchronous activation of flexor and extensor muscles with a mean phase angle of 3.0 degrees and a predominance of the extensor muscle. The results suggest that the nervous mechanisms for the generation of tremorine tremor and cold tremor are different.

Animals↗
PubMed1991

Semidominant expression of absence-like seizure in tremor rats.

Tremor rats (tremor homozygous rats) exhibit spontaneous absence-like seizure, which is characterized by a sudden immobility with staring and the appearance of 5- to 7-Hz spike and wave complexes in cortical and hippocampal electroencephalogram (EEG). In this study, we examined the development of the seizure and the mode of inheritance. All tremor homozygous and heterozygous rats exhibited the seizure by 14 and 26 weeks of age, respectively. The frequency and total duration in tremor heterozygous rats were significantly lower in comparison with those in tremor homozygous rats. None of the seven tremor wild-type homozygous rats exhibited the seizure. In an EEG study of backcross progeny of (BN/fMaiKyo x tremor heterozygous rats)F1 (tm/+) x tremor heterozygous rats at 5 months of age, the ratio of rats with and without the seizure was 23:7 (chi 2 = 0.09 for 3:1 ratio). These results suggest that the absence-like seizure is semidominantly expressed, in contrast to other recessive mutant traits in tremor rats.

Animals↗
PubMed2000

Essential tremor: an overdiagnosed condition?

The diagnosis of essential tremor (ET) and its differentiation from other types of tremor is often difficult. In 1994 Bain et al. defined a classical phenotype by studying 20 patients with pure essential tremor and similarly affected family members in at least three generations. We assessed how many of the patients diagnosed by different neurologists at our institution as having ET conformed to this defined phenotype. We randomly selected 50 patients who were diagnosed with ET by any neurologist at the National Hospital for Neurology and Neurosurgery since the publication of the Bain et al. report, and determined the number of patients who had clinical features compatible with the phenotype that it had defined. Only 25 (50%) of these patients had ET so defined. Ten patients clearly had alternative diagnoses: four had clear additional dystonia, two neuropathic tremor, two had unilateral leg tremor, one drug-induced tremor, and one sudden onset after head trauma. The remaining 15 patients also had atypical features including myoclonus (one), onset in a body part other than the arms (six), sudden onset (two), rest tremor (seven), onset after the age of 65 years (four), a family member with an isolated head tremor (one), or reduced armswing (two). The diagnosis of ET is overused even among experienced neurologists, and other types of tremor should be considered in atypical patients before making this diagnosis.

Adolescent↗
PubMed1987

Reflex origin of parkinsonian tremor.

The 8-Hz wrist tremor seen in normal subjects results from an oscillation in the spinal stretch reflex arc but the resting 4-Hz tremor of Parkinson's disease is believed to result from synchronization of motor unit activity by periodic descending inputs driven by an oscillator which resides within the brain. Accelerometer and smoothed EMG (0.8 to 16.0-Hz pass) recordings of resting tremor were taken from the upper limbs of 10 volunteers with Parkinson's disease for several different limb positions and while the limb was fixed to prevent tremor movements. The smoothed EMG and accelerometer records produced a complex periodic waveform with prominent 4- and 8-Hz components. Spectral analysis of both records produced large peaks at those frequencies which were harmonically related. The appearance of the regular tremor waveform in accelerometer and smoothed EMG records was greatly altered by changes in limb posture in all patients. Fixing of the shoulder and elbow joints only, also altered the smoothed EMG waveform and reduced the tremor amplitude. Fixing of the entire limb removed all signs of synchronization of motor unit activity in raw and smoothed EMG records. Similarly, the prominent 4- and 8-Hz peaks, found in the smoothed EMG power spectra from trembling muscles, were eliminated if the limb was effectively prevented from trembling. These experiments showed that the synchronization of motor unit activity at Parkinson's tremor frequency is wholly dependent on the oscillation in limb position and thus proprioceptive reflex activity. It is suggested that the known properties of the 4-Hz resting tremor of Parkinson's disease can be attributed to a flip-flop oscillation involving the mutually inhibitory connections between the spinal stretch reflexes of antagonist muscles. The supraspinal contribution to the tremor may thus be confined to an "aperiodic" descending facilitation of spinal reflex pathways.

Arm↗
PubMed1993

Effects of beta-adrenergic blockers on drug-induced tremors.

We studied the effect of various kinds of beta-adrenergic blockers on oxotremorine-, harmaline- and thyrotropin-releasing hormone (TRH)-induced tremors in mice. To investigate what property of beta-blockers plays the main role in suppressing tremor, we employed five beta-blockers (propranolol, atenolol, butoxamine, pindolol, and arotinolol). All drugs suppressed oxotremorine-induced tremors but none reduced harmaline-induced tremors. Even though TRH-induced tremors were decreased significantly only by propranolol and high doses of arotinolol, all drugs had a tendency to reduce the tremor. We concluded that neuropharmacological mechanisms underlying to harmaline-induced tremors were different from those of TRH- and oxotremorine-induced tremors and that features of beta-blockers (beta 1- or beta 2-selectivity, intrinsic sympathomimetic activity, and membrane stabilizing activity) did not primarily contribute to the suppression of tremors.

Adrenergic beta-Antagonists↗
PubMed2006

Digitised spirography as an evaluation tool for intention tremor in multiple sclerosis.

This study investigated validity and reliability of digitised circle and square spiral drawing for quantifying intention tremor severity and related disability in patients with multiple sclerosis (MS). The tremor amplitude was measured as the standard deviation of the drawing velocity of the arm in the radial and tangential direction for circle spiral drawing, and in the horizontal and vertical direction for square spiral drawing. Results were compared with those of MS patients without tremor and healthy controls, and correlated with clinical assessments of tremor severity and arm functionality including Fahn's tremor rating scale, Test d'Evaluation des Membres supérieurs des Personnes Agées (TEMPA) and the nine-hole-peg test to examine validity. Comparison of patient's performance between four repeated trials examined short-term test-retest reliability. All digitised spirography variables discriminated between the MS-tremor and both MS-no-tremor and healthy control groups. Validity was also shown by high spearman correlation coefficients between spirography variables and clinical ratings. Tremor appeared to be most profound in the radial and vertical direction during circle and square spiral drawing, respectively. The consistency and high correlations between four repeated executions indicated short-term test-retest reliability. We conclude that the digitised spirography provide a useful instrumentation for quantifying MS intention tremor.

Adult↗
PubMedDate not supplied

The direction of oscillation in spiral drawings can be used to differentiate distal and proximal arm tremor.

The assessment of the extent of involvement of the distal and proximal joints in a complex arm tremor is important clinically, as tremor generated around the distal and proximal arm joints can be differentially alleviated by surgical intervention to the thalamic and subthalamic targets, respectively. We observed that the tremor present in spiral drawings shows a diagonal directional preference. We hypothesized that the directional preference of tremor within spiral drawings could be related to the involvement of different arm joints. In this study, we tested this hypothesis by: (1) studying simulated tremulous drawings performed by healthy subjects with the joints selectively restrained; (2) recording surface EMGs from the forearm extensor and deltoid muscles during drawing; and (3) mathematical modelling the kinematics of the arm in 2D drawings. Our data showed that a "main diagonal" axis of orientation of the tremor along the orientation of the forearm indicates a predominantly proximal tremor driven by the shoulder, and a "cross diagonal" axis of orientation of tremor (i.e. perpendicular to the forearm) indicates that the tremor is predominantly distal and driven by the elbow or wrist. We conclude that the spiral drawing task can be used as an objective and quantitative method for differentiating the involvement of the proximal and distal arm joints in complex arm tremors.

Activity Cycles↗
PubMed1997

Anti-tremor activity of talipexole produced by selective dopamine D2 receptor stimulation in cynomolgus monkeys with unilateral lesions in the ventromedial tegmentum.

The anti-tremor activity of talipexole (6-allyl-2-amino-5,6,7,8-tetrahydro-4H-thiazolo[4,5-d]azepine dihydrochloride, B-HT 920 CL2, Domin), a non-ergot dopamine D2 receptor agonist which possesses alpha 2-adrenoceptor agonistic and 5-HT3 receptor antagonistic properties, was examined in monkeys with a unilateral lesion in the ventromedial tegmentum. Talipexole dose dependently suppressed the tremor and had ED50 values of 34 micrograms/kg s.c. and 84 micrograms/kg p.o. The anti-tremor effect of talipexole occurred at much lower doses than that of an ergot dopamine receptor agonist, bromocriptine (2-bromo-alpha-ergocryptine mesilate, ED50; 2.5 mg/kg s.c.), and talipexole acted synergistically in combination with L-DOPA (3,4-dihydroxyphenylalanine). In ventromedial tegmentum-lesioned monkeys, anti-tremor doses of talipexole did not cause emetic behavior, but had sedative effects. Conversely, monkeys given bromocriptine exhibited oral movement, salivation and vomiting when anti-tremor effects were observed, but not marked sedative behavior at any of the doses investigated. During repeated administration of talipexole (a daily dose of 50 micrograms/kg s.c. for 21 days), the extent and duration of the anti-tremor effect did not change, but those of the sedative effect decreased gradually. The anti-tremor effect of talipexole was significantly suppressed by sulpiride, but not by SCH 23390 (7-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-1H-3-benzazepine-7-ol) or yohimbine, while the sedative effect was inhibited by sulpiride and yohimbine. The main metabolites of talipexole had no anti-tremor or sedative effects. These results indicate that talipexole exerts its anti-tremor activity via selective dopamine D2 receptor stimulation.

Administration, Oral↗
PubMed2000

Acute hypoxia activates human 8-12 Hz physiological tremor.

Hypoxia causes arousal. Therefore, we hypothesized that hypoxia activates the human somatomotor system and should augment tremor. We determined the effects of hypoxia, PET(O2) = 45+/-2.2 mm Hg, hypocapnia, and the hypocapnic-hypoxic interaction on finger tremor during elastic loading. A total of 12 healthy male volunteers were studied during five conditions: eupnea, hypocapnic hypoxia, eucapnic hypoxia, hypocapnic normoxia, and eucapnic normoxia. Acceleration power spectra were computed to quantify 8-12 Hz tremor. Hypoxia significantly augmented 8-12 Hz physiological tremor (P=0.002). Furthermore, six subjects (50%) exhibited significantly more tremor during hypocapnic hypoxia (hH) than during eucapnic hypoxia (eH). We conclude that acute hypoxia augments 8-12 Hz physiological tremor, and hypocapnia further augments this tremor in some subjects. As such, hypoxic tremor is activated physiological tremor, and entrainment of spinal alpha-motoneuron activity may be the final common pathway.

Acute Disease↗
PubMed2000

Effects of serotoninergic drugs on tremor induced by physostigmine in rats.

We investigated the effects of various serotoninergic drugs and serotonin (5-HT) depletion on physostigmine-induced visible tremor in rats. Physostigmine (0.25-1.5 mg/kg) caused dose-dependent tremor, initiated at 3-5 min (latency decreases as dose increases) and lasted for 30-35 min. Serotonin agonists, 8-hydroxy-2-(di-n-propylamino) tetralin (2.5 mg/kg) and buspirone (5 mg/kg) augmented the tremor response caused by physostigmine. The 5-HT(1)/5-HT(2) receptor antagonist, metergoline (1 mg/kg), and 5-HT(2) blocker, cyproheptadine (10 mg/kg) significantly decreased the duration (40%) as well as intensity (45-50%) of physostigmine-tremor. The 5-HT(2a)/5-HT(2c) antagonist ritanserin (5 mg/kg) significantly reduced the duration (60%) without affecting the intensity of the tremor. In 5-HT depleted rats (p-chlorophenylalanine; 300 mg/kg, for 3 days), physostigmine failed to produce tremor. Interestingly, in these animals, administration of a non-specific 5-HT agonist, 5-methoxy-N,N-dimethyl tryptamine, caused high intensity tremor. These results suggest that presence of 5-HT at the pre-synaptic terminals is needed for the tremor response by physostigmine and the response is greatly mediated via post-synaptic 5-HT receptors. The overall data indicated a direct involvement of central 5-HT system in the cholinergic tremor induced by physostigmine.

Animals↗
PubMed2003

Effects of topiramate in patients with cerebellar tremor.

PURPOSE: To evaluate the safety and potential beneficial effect of topiramate (TPM) as monotherapy or adjunctive therapy to carbamazepine (CBZ) in patients with cerebellar tremor. METHODS: Nine patients with cerebellar tremor participated a 4-week, open-label, prospective-controlled trial. TPM was given as monotherapy (n=7 cases), or in combination with CBZ (n=2 cases), at dosages ranging from 25 mg twice daily to 100 mg twice daily. The severity of tremor was assessed clinically on a 0-4 scale, by tremograms, by the Patients Global Impressions Scale, and by a "free writing" task at baseline and after 4 weeks. RESULTS: TPM was discontinued in four patients due to adverse effects (sedation=2; cognitive impairment=2; increased aggressiveness=2; asthenia=1). During TPM, all patients improved. The mean tremor amplitude, compared with the baseline period, was reduced from 20% to 75%. After TPM, mean clinical scores of postural tremor and kinetic tremor decreased from 2.1+/-0.8 to 0.9+/-0.9 and from 2.1+/-1 to 1.4+/-1 (P<.05), respectively. All patients with head tremor improved. Writing, eating, and drawing were improved with TPM. Four patients chose to keep taking the drug. CONCLUSIONS: Our study indicates that TPM may be useful for the management of cerebellar tremors. A prospective placebo-controlled trial of TPM in this kind of tremor is warranted. TPM dosages should be titrated slowly to avoid the potential side effects of the drug. The range and the frequency of adverse events might limit the clinical usefulness of TPM.

Adult↗