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PubMed1995

A positron emission tomography study of cerebral activation associated with essential and writing tremor.

OBJECTIVE: To compare the abnormal patterns of cerebral activation associated with essential and writing tremors. DESIGN: Positron emission tomography using oxygen 15-labeled water was utilized to determine regional cerebral blood flow. Positron emission tomography images that were taken of the brain in individual patients were coregistered with magnetic resonance images of the same brain to ascertain accurate localization of cerebral activation in single patients. Patients with essential tremor underwent scanning at rest, during involuntary postural tremor, and during passive wrist oscillation. Normal control subjects underwent scanning at rest and during voluntary and passive wrist oscillation. Patients with writing tremor underwent scanning while they were holding a pen to paper with consequent involuntary tremor and again while they were holding a pen in the same supinated arm without tremor. SETTING: Research hospital. PATIENTS OR OTHER PARTICIPANTS: Seven patients with essential tremor, six patients with writing tremor, and six matched control subjects. INTERVENTIONS: None. MAIN OUTCOME MEASURES: Regional cerebral blood flow. RESULTS: Essential tremor was associated with abnormal bilateral cerebellar, red nuclear, and thalamic activation. Writing tremor was also associated with abnormal bilateral cerebellar activation. Voluntary wrist oscillation in control subjects caused only ipsilateral cerebellar activation. These findings were evident in single patients, when positron emission tomography images were coregistered with magnetic resonance images and on group analysis of the pooled positron emission tomography data after transformation into stereotaxic space. CONCLUSION: These results indicate that both essential and writing tremors are associated with abnormal bilateral overactivity of cerebellar connections.

Adult↗
PubMed1993

A positron emission tomography study of essential tremor: evidence for overactivity of cerebellar connections.

The origin of essential tremor is unknown. Animal models have suggested that the inferior olivary nucleus may act as a tremor generator. We used positron emission tomography to study changes in regional cerebral blood flow associated with involuntary postural tremor and passive wrist oscillation in patients with essential tremor. Activation due to voluntary wrist oscillation and arm extension without tremor was studied in normal control subjects. The essential tremor group had bilaterally increased cerebellar blood flow at rest (without tremor) compared with the control group. Involuntary postural tremor was associated with further bilateral cerebellar activation, and also contralateral striatal, thalamic, and sensorimotor cortex activation. Voluntary wrist oscillation, maintained arm extension without tremor, and passive wrist oscillation were all associated with significant ipsilateral rather than bilateral cerebellar activation. We conclude that essential tremor is associated with increased bilateral cerebellar activity both at rest and during tremor.

Adult↗
PubMed2002

Pathophysiology of nonparkinsonian tremors.

Patients with nonparkinsonian tremors are the second largest group treated with functional neurosurgery. We summarize the present pathophysiological knowledge of these conditions. Essential tremor (ET) may be due to oscillations within the olivocerebellar circuit. There is experimental evidence from animal models for such a mechanism, and clinical data indicate an abnormal function of the cerebellum in ET. Cerebellar tremor may be closely related to the tremor seen in advanced ET. The malfunction of the cerebellum causes a pathological feed-forward control. Additionally an oscillator within the cerebellum or its input/output pathways may cause cerebellar tremor. Almost nothing is known about the pathophysiology of dystonic tremor. Holmes tremor is based on a nigral and a cerebellar malfunction and presents clinically as the combination of tremor in Parkinson's disease and cerebellar tremor. Neuropathic tremor can be extremely disabling and is thought to be due to an abnormal interaction of the disturbances within the periphery and abnormal cerebellar feedback. Unlike the case of Parkinson's disease, functional neurosurgery of nonparkinsonian tremors is not yet based on a solid pathophysiological background.

Brain↗
PubMed2006

Online movement control in multiple sclerosis patients with tremor: effects of tendon vibration.

Patients with intention tremor due to multiple sclerosis (MS) exhibit an increased reliance on visual feedback in the sensorimotor control of slow goal-directed movements. In the present study, the use of proprioceptive information was investigated in MS patients with intention tremor compared to MS patients without tremor and healthy controls. Tendon vibration was applied to the wrist extensor muscles during a memory-guided slow wrist step-tracking task to investigate the use of muscle spindle afferent information in online movement control. A significant reduction of movement amplitude was induced by tendon vibration in all three groups, but the effect was found to be smaller in MS patients with tremor (28%) than in subjects without tremor (50%). Vibration also induced an increase of overall tremor amplitude in the MS tremor group; however, its effect on movement amplitude was not directly related to (changes in) tremor severity. The results suggest that the decreased online use of proprioceptive information in MS patients with tremor reflects an adaptation over time to cope with a tremor-related noisy background. Abnormalities in proprioceptive processing may explain why MS patients with tremor show an increased reliance on visual feedback for online motor control.

Adult↗
PubMed1992

Noise-induced psychogenic tremor associated with post-traumatic stress disorder.

Tremors in post-traumatic stress disorders have not been previously well characterized. A 67-year-old man has a 46-year history of a noise-induced exaggerated startle reflex followed by a large amplitude rest, postural and kinetic tremor that may persist for up to 3 days. This tremor is superimposed on a continuous mild organic postural/kinetic tremor whose electrophysiological characteristics are different from those of the overlying tremor. We attribute the exaggerated startle reflex and the noise-induced tremor to Post-Traumatic Stress Disorder (PTSD) and postulate a psychogenic origin for the noise-induced tremor. The patient also believes the noise-induced tremor to be psychologically based and to be produced by the fear and anxiety he experiences when he hears loud, unexpected noises. The sudden onset of the noise-induced tremor, its intermittent character, its temporary disappearance on distraction despite the patient's inability to suppress it, inconsistencies in handwriting and figure drawing, and the fact that the noise-induced tremor is stimulus specific and persists long after the offending stimulus (noise) is no longer present all suggest a tremor of psychogenic origin.

Accidents↗
PubMed1998

Diagnostic and pathophysiological aspects of psychogenic tremors.

Psychogenic tremor has become a rare movement disorder. Twenty-five patients from our movement disorder unit presented either with obviously nonorganic body shaking during stance or with extremity tremors. A sudden onset and a variable but rarely remitting course of the condition was common. The "coactivation sign of psychogenic tremor" and absent finger tremor were the most consistent criteria to separate them from organic tremors. Quantitative analysis of tremor shows decreasing amplitudes in most organic tremors when the extremity is loaded with additional weights. In contrast, we found an increase of tremor amplitude for most of the cases with psychogenic tremor. This might be caused by increased coactivation to maintain the oscillation. These clinical and electrophysiological features suggest a clonus mechanism induced by coactivation as the pathophysiological basis of psychogenic extremity tremor. Psychiatric evaluation did not show overt signs of hysteria for the majority of the patients. However, we found depression and functional somatic or psychosomatic conditions to be frequent among the patients. A reduced ability to cope with stressful situations may play a significant role. The clinical course of the condition is usually far from benign. We conclude that psychogenic tremor can be positively diagnosed by means of neurologic signs in the majority of patients and is not only a diagnosis of exclusion. The poor outcome makes early and serious neuropsychiatric attempts at therapy necessary.

Adaptation, Psychological↗
PubMed1998

Pathology of symptomatic tremors.

Symptomatic tremors are labeled in the literature under different names including rubral tremor, midbrain tremor, thalamic tremor, myorhythmia, Holmes' tremor, cerebellar tremor, and goal-directed tremor. The most common tremor is a delayed-onset postural and action tremor with a low frequency of 3 Hz and a proximal distribution. Resting irregular tremor is sometimes present. Mild cerebellar dysmetria is often detected. The lesions are mainly located in the thalamus, the brain stem, and the cerebellum, with secondary interruption and degeneration of various pathways and olivary hypertrophy. The more consistent lesions are found in the cerebello-thalamo-cortical and dentato-rubro-olivary pathways. The role of superimposed dysfunction of the nigrostriatal system may account for the rest component. The role of the basal ganglia in the emergence and control of tremor is poorly understood.

Cerebellum↗
PubMed1984

Mandibular postural tremor during relaxation and during volitional innervation of the jaw muscles.

Jaw tremor was recorded as the changes in the vertical distance between mandible and maxilla. Two states of motor performance of the jaw muscles were chosen: relaxed and actively positioning of the mandible close to toothcontact, referred to as respectively rest- and activity tremor. Rest tremor contained a strong ballistocardiac component (bc power = 50%) and was of small amplitude (9.4 micron rms). Activity tremor revealed increased amplitudes (19.2 micron rms) with a predominant neuromuscular component (nm power = 75%). Bc tremor patterns differed significantly from nm tremor patterns. A negative linear relationship, which apparently was similar for rest and for activity tremor (P greater than 0.10), existed between the estimated bc contribution and tremor amplitude. As tremor amplitude increased neuromuscular activity appeared increasingly time locked to bc activity, which should be attributed to synchronization of spindle activity, either through the stretch reflex or through vascular pulsation. The average bc contribution to tremor amplitude remained of almost constant magnitude (7.0 micron rms), with no differences between rest and activity for the group as a whole. During resting conditions, complete relaxation of the jaw muscles was not attained by the majority of the subjects. The latter revealed a heart rate arrhythmia that was strongly correlated with motor (nm) activity (P less than 0.001). During activity conditions no such correlation was present. The present results demonstrate that for the understanding and the interpretation of the underlying mechanisms of jaw tremor genesis, both the recording technique, i.e., differential jaw displacements, and the signal analysis procedure, i.e., autocorrelograms and power spectra over extended record length, were of crucial importance.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Assessing the impact of essential tremor on upper limb function.

We compared the impact of essential tremor on the performance of three manual tasks: drawing spirals, holding a cup full of water and a joystick-controlled tracking test. Tremor amplitude and frequency were measured by accelerometry during the tracking test, when holding the cup and whilst a standard posture was maintained. The inter-relationships between tremor amplitude, frequency and task impairment were then examined. The results showed that the amplitude and frequency of essential tremor (measured from the principal spectral peak) changed with different activities, with the mildest postural tremors changing most in frequency (by up to 4-5 Hz). The amplitude of tremor decreased in almost every case during the tasks, relative to posture, and this decrement was greatest for the most severe tremors. We also demonstrate that for practical purposes, such as routine clinical situations and therapeutic trails, the effect of essential tremor upon upper limb function can be usefully assessed by two simple complementary techniques: rating spirals and measuring the volume of water split from a cup. The impairments in carrying out these tasks and the tracking test were highly correlated with one another and also with the amplitude and frequency of postural tremor. The concept of tremor "suppressability" is introduced: the relative percentage decrease in the amplitude of a particular tremor during the performance of a specific task compared to that recorded whilst holding a standard posture.

Acceleration↗
PubMed1997

Role of central nicotinic and beta-adrenergic receptors in the onset and further development of tail-tremor induced by repeated nicotine administration to rats.

The effects of nicotinic and beta-adrenergic receptor antagonists on tail-tremor induced by repeated nicotine administration were investigated in rats. The daily administration of nicotine (0.5 mg/kg/day, s.c.) for 8 days resulted in an augmentation of tail-tremor. However, repeated administration of dimethyl phenyl piperazinium iodide (1 mg/kg/day, s.c.) for 8 days did not cause tail-tremor. Mecamylamine (0.5 mg/kg, i.p), administered before the nicotine injection on each day, abolished the tail-tremor. After discontinuation of the mecamylamine treatment, nicotine injections caused tail-tremor augmentation. Propranolol (20 mg/kg, i.p.), administered before the nicotine on each day, suppressed the appearance of tail-tremor. After the discontinuation of propranolol treatment, the degree of tail-tremor induced by a single injection of nicotine on day 9 was much greater in the propranolol-treated group than in the saline-treated control group. Neither carteolol (20 mg/kg, i.p.) nor metoprolol (20 mg/kg, i.p.) treatment showed such effects. Intraspinal injection of 6-hydroxydopamine markedly enhanced the tail-tremor induced on the first day of nicotine injection. This effect became more intense on subsequent administration of nicotine. The enhanced tail-tremor following 6-hydroxydopamine treatment was abolished by mecamylamine (0.5 and 1 mg/kg, i.p.), and was suppressed by propranolol (5-20 mg/kg, s.c.) in a dose-dependent manner. These results suggest that central nicotinic receptors are essential for the onset and for the further development of tail-tremor induced by the repeated administration of nicotine, and that beta 2-adrenoceptors are associated with the tremor mechanism. Moreover, spinal noradrenergic mechanisms may be involved in the manifestation of this phenomenon.

Adrenergic Agents↗
PubMed2002

The origins of physiological tremor as deduced from immersions of the finger in various liquids.

To investigate the influence of gravity on physiological tremor during a holding stretch of the finger, tremor during immersion of the finger in liquids was measured. Liquids with various densities and various coefficients of viscosity were used. Tremor was detected using an acceleration sensor, and power spectrum analysis was performed on the acceleration signal of the tremor. The total power of the tremor spectrum decreased with an increase of the density and an increase of the coefficient of viscosity, the high frequency domain of the tremor spectrum showing a larger decrease than the low frequency domain. Linear regression analysis showed that the viscosity of the liquid had a larger effect on tremor than the buoyancy due to the liquid. A model was proposed for tremor during immersion of the finger in liquid. The effect of the buoyancy and the viscosity on tremor was examined using the proposed model. The origin of two frequency bands in the tremor spectrum was verified by both the immersion experiment and the proposed model. The stretch-reflex system via the spinal cord produced a high frequency band around 25 Hz, while the supraspinal system caused a low frequency band around 10 Hz. The neuromuscular function of the human body was evaluated using the amplitude and the frequency of tremor.

Acceleration↗
PubMed1995

The role of brain acetylcholine in phenol-induced tremor in mice.

The relation between phenol-induced tremor and brain acetylcholine levels, and the effects of cholinergic drugs on the tremor were investigated, using male ddY mice weighing 28-35 g. The magnitude of phenol-induced tremor was graded on a 4-point scale: 0, normal; 1, slight; 2, moderate; 3, severe, and acetylcholine levels were measured by high-performance liquid chromatography with electrochemical detection. The magnitude of tremor and the decrease in acetylcholine levels in the striatum and cerebral cortex induced by s.c. injection of phenol (50, 100, 200 mg/kg) were dose-dependent, and both showed parallel time courses. Intracerebroventricular (i.c.v.) injection of phenol (100 micrograms/mouse) caused a decrease in acetylcholine levels in the striatum but did not induce tremor. Intraperitoneal injection of pentobarbital (10 mg/kg), which inhibits the release of acetylcholine, weakened both the magnitude of the tremor and the decrease in acetylcholine levels induced by phenol (200 mg/kg), whereas i.c.v. injection of pentobarbital (120 micrograms/mouse) attenuated the decrease in acetylcholine levels induced by phenol, but did not affect the magnitude of the tremor. Intraperitoneal (20 mg/kg) or i.c.v. (60 micrograms/mouse) injection of mecamylamine further strengthened the tremor. Intraperitoneal (0.3 mg/kg) injection of physostigmine strengthened the tremor, while i.c.v. injection (1 microgram/mouse) caused a reduction in its magnitude. These results suggest that the tremor is caused directly by the phenol-induced increase in acetylcholine release in the peripheral nervous system (motor nerve endings), that the decrease in brain acetylcholine levels may be due to phenol-induced increases in acetylcholine release within the central nervous system, and that the resultant reduction in brain acetylcholine levels indirectly suppresses the tremor.

Acetylcholine↗
PubMed1984

Quantitative analysis of drug-induced tremor in mice.

A method of analyzing tremor in mice was developed using a power spectral analysis of the random current induced by the movement of a magnet attached to a mouse, on a wire coil. The power spectral density function defined the frequency composition of the tremor, and the mean square value of the data in any frequency range of concern was determined. It was possible to determine qualitative differences in the tremor caused by various tremorgenic agents, and to differentiate the drug-induced tremor from spontaneous motor activity. The power spectral densities of the tremorine- and oxotremorine-induced tremors were tentatively expressed as the sum of 3 main components (Cauchy distribution) with different peak frequencies, consisting of the spontaneous motor activity component and two tremor components. On the other hand, the power spectral densities of the harmaline-induced tremor were expressed as the sum of two components with two peak frequencies, and the plots of the power spectral densities versus frequency, consisting of the spontaneous motor activity component and a tremor component. The frequency of the peak spectral density was almost independent of the dose of tremorgenic agents, but changed slightly with the lapse of time after their injection. The severity of the tremor was determined quantitatively in terms of the sum of the mean square value. The sum of the mean square value for a period of 45 min after the injection of tremorine, changed in a dose-dependent manner. The severity of the tremor was different for each of the mouse strains. The method studied in the present paper is expected to be utilized for the quantitative examination of the fine motor movement of the experimental animal, particularly, for the screening test of new anti-tremor drugs.

Alkaloids↗
PubMed2001

[Postural tremor: clinical and neurophysiological study in a consecutive series of 300 patients].

BACKGROUND: There are few studies analysing the clinical and neurophysiological characteristics of postural tremor in Spain. PATIENTS AND METHOD: We studied prospectively 300 consecutive patients referred to a Movement Disorders Section because of postural tremor of the upper limbs. Syndromic diagnosis of postural tremor was made according to clinical criteria with the aid of neurophysiological criteria (accelerometric and EMG data). In patients diagnosed with essential tremor (ET), diagnostic sensitivity studies, correlation studies of clinical and neurophysiological data and multivariate analysis were performed. RESULTS: Most frequent syndromic diagnoses were ET (77%), parkinsonian postural tremor (10%) and exaggerated physiological tremor (6%). Fifty percent of ET patients reported having affected relatives, and 7% reported that their tremor improved with alcohol. Mostly specific variables for the diagnosis of ET were: affected relatives (77%), cephalic tremor (80%), alcohol improvement (100%), and synchronous EMG pattern (79%). The presence of affected relatives and a synchronous EMG pattern were significant predictive variables on a multivariate analysis. We found a significant correlation between age at time of consulting and frequency (rs = 0.561; p < 0.0005) and amplitude (rs = 0.470; p < 0.0005) of tremor. CONCLUSIONS: In the present study, ET was the most common cause of reference for postural tremor. Selective clinical data and neurophysiological evaluation are useful for the diagnosis of postural tremor.

Aged↗
PubMed2001

Regularity of force tremor in Parkinson's disease.

OBJECTIVES: The study examines the time-dependent structure of force tremor to investigate two hypotheses: (1), the regularity of tremor can help in discriminating normal aging from that of Parkinson's disease (PD); and (2), there is increased tremor regularity with increases in the severity of PD. METHODS: Eight young (21-29 years), eight elderly (68-80 years), and eight PD (68-80 years) subjects produced constant grip force at 5, 25 and 50% of their maximal voluntary contraction by squeezing two load cells with their index finger and thumb under a vision and no vision condition. Spectral analysis and approximate entropy (ApEn) were used, respectively, to analyze the frequency and time-dependent structure of tremor. RESULTS: The analyses showed that there were no differences in the amplitude and modal frequency of force tremor between groups. The ApEn was significantly lower in the PD group compared with the controls. For the PD group, the linear relations between the total scores taken from the Unified Parkinson's Disease Rating Scale-motor section and the dependent variables were r(2)=0.71 (P<0.01) for ApEn, r(2)=0.20 (P>0.05) for the modal frequency, and r(2)=0.23 (P>0.05) for the standard deviation. Surrogate analyses revealed that the time-dependent structure of tremor provided additional information beyond that of amplitude and modal frequency analyses. CONCLUSIONS: These findings indicate that tremor analyses should not be limited to just the frequency and amplitude of the oscillation, and that the time-dependent structure of tremor is useful in differentiating tremor in healthy people from those with PD. The hypothesis that more regular tremor in PD is due to a loss of multiple neuronal oscillators contributing to the tremor output is discussed.

Adult↗
PubMed2001

Clinical and electromyographic examinations of patients with tremor after chronic occupational lead exposure.

Tremor is considered to be a clinical sign of patients with chronic lead exposure. However, the type of tremor and its pathophysiological mechanisms are controversial. The aim of this study was to examine the clinical and electromyographic characteristics of tremor in patients with chronic lead exposure. Twenty-three men, 27-49 years old, participated in the study. The tremor activity was detected using surface electrodes from a pair of antagonistic hand muscles. Serum lead concentrations were measured on the day of examination. Our results revealed 12 Hz postural and kinetic tremor, with characteristics of enhanced physiological tremor. Different pathophysiological mechanisms might be responsible for the enhanced physiological tremor of patients with chronic lead exposure. In conclusion, the tremor of patients with chronic lead exposure is an enhanced physiological one. It is probable that this tremor could be influenced by beta-blockers, known to influence the enhanced physiological tremor in anxiety. This will be of benefit for patients disturbed by persistent tremor.

Adult↗
PubMedDate not supplied

Ambulatory objective assessment of tremor in Parkinson's disease.

Continuous ambulatory multichannel accelerometry (CAMCA) has recently been validated for the assessment of hypo-and bradykinesia and body position in patients with Parkinson's disease (PD). This study aims to validate CAMCA for the assessment of resting tremor in patients with PD. First, in seven patients with PD with varying degrees of tremor severity, a tremor detection algorithm was developed. Second, 59 patients with PD and 43 age-matched controls were assessed with CAMCA during 24 hours. Duration and intensity of resting tremor, and measures reflecting hypo-and bradykinesia and body position were calculated for the diurnal period. In part 1 of the study, the tremor detection algorithm had a high sensitivity (0.82) and specificity (0.93). Ambulatory monitoring revealed that categories with higher clinical tremor severity had increased objective values for duration and intensity of tremor. Duration and intensity of tremor were correlated with the clinical score for resting tremor (Spearman's rank correlation: 0.66-0.77). Measures for hypo-and bradykinesia differed between patients and controls, but not between groups of patients defined by tremor severity. This study has validated continuous ambulatory multichannel accelerometry for the assessment of tremor in PD, while simultaneously measuring hypo-and bradykinesia and body position.

Aged↗
PubMed2001

Changes in quantitatively assessed tremor during treatment of major depression with lithium augmented by paroxetine or amitriptyline.

Tremor is a relatively frequent side effect of lithium and of antidepressants with serotonergic properties. It can be expected that combinations of lithium (which is itself serotonergic) with such antidepressants will enhance not only efficacy, but also the incidence of side effects, including tremor. To quantitatively monitor the effect of antidepressant augmentation of ongoing lithium therapy on tremor, lithium-maintained patients with a breakthrough episode of major depression were randomly assigned under double-blind conditions to receive paroxetine 20 mg/day (N = 14) or amitriptyline 75 mg/day (N = 17). The initial dosages could be increased after 2 weeks to 40 mg/day and 150 mg/day, respectively, and the patients were treated for 6 weeks. Tremor activity was assessed weekly, quantitatively by accelerometry and qualitatively with the Dosage Record and Treatment Emergent Symptom Scale. Statistical analysis detected no significant difference between the treatment groups with respect to changes in mean tremor activity relative to baseline. However, analysis of the pooled data showed that tremor increased significantly during the course of combined lithium and antidepressant therapy, with the greatest increments occurring independent of dosage approximately 3 weeks after initiation of combination treatment. Although the mean tremor activity subsided toward the end of treatment, tremor activity on the whole was still significantly greater after 6 weeks of combined lithium and antidepressant treatment than at the start of combination therapy. Increased tremor was not associated with decreased medication compliance, and no patient discontinued treatment because of increased tremor. Tremor frequency was not affected by the study treatments.

Adult↗