Onset Of Tremor Research Articles

Involvement of ionotropic glutamate receptors in the appearance of arecoline tremor in mice

Administration of the muscarinic cholinoreceptor agonist arecoline (6 mg/kg, s.c.) to mice induced long-lasting tremor. The ability of non-competitive antagonists of ionotropic glutamate receptors to suppress the onset of tremor was studied. These antagonists, i.e., adamantane and phenylcyclohexyl derivatives, selectively blocked NMDA-type receptor channels (monocations) or both NMDA-and AMPA-type channels (dications). Both types of blocker weakened arecoline tremor, though the dose-response relationships were different for mono-and dications. The effects of dications appeared only at low blocker doses (0.0001-0.01 micromol/kg) but gradually disappeared on dose elevation. These data lead to the conclusion that the mechanism of pathogenesis of arecoline tremor predominantly involves NMDA-type receptors. Moderate blockade of AMPA-type receptors could potentiate the preventive effect of mixed-action antagonists (anti-NMDA+anti-AMPA), though predominance of blocking action against AMPA-type receptors prevented this effect.

GRAVES DISEASE AND ISOLATED ORTHOSTATIC TREMOR

Orthostatic tremor (OT) is a rare neurologic condition characterized by a high-frequency tremor (13–18 Hz) predominantly involving the legs while standing, though tremor in the arms is also relatively common.1,2 Women are more frequently affected, and the age at onset can vary between 30 and 80 years.1-3 We describe a patient with Graves disease who presented with OT without other systemic manifestations. ### Case report. A 50-year-old woman with no significant medical history presented with a gradual onset of tremor in her right leg during standing, though no tremor was experienced on her left lower limb. The right leg tremor progressed in severity over a few months to an extent that she frequently experienced unsteadiness while standing. The tremor was completely relieved by sitting, walking, or leaning against the wall without bearing weight on her right lower limb. She did not notice tremors in her hands or other parts of her body. She did not have any other systemic symptoms such as loss of weight or appetite, intolerance of …

Loss of thalamic serotonin transporters in early drug-naïve Parkinson’s disease patients is associated with tremor: an [123I]β-CIT SPECT study

In vitro studies revealed serotonin transporter (5-HTT) decline in Parkinson’s disease (PD). Yet, few studies investigated thalamic 5-HTT in vivo and its effect on PD heterogeneity. We analyzed thalamic [123I]β-CIT binding (mainly reflecting 5-HTT binding) in 32 drug-naïve PD patients and 13 controls with SPECT. Twenty-six patients were examined twice (17 months apart). Based on UPDRS scores, we identified subgroups of patients with moderate/severe tremor (PDT) and without tremor (PDWT) at the time of clinical diagnosis. Additionally, depressive symptoms were evaluated using the Beck Depression Inventory (BDI) at baseline. Mean thalamic specific to non-specific [123I]β-CIT binding ratio was lower in patients when compared to controls, and further decreased during follow-up. At baseline, average thalamic ratio was significantly lower in the PDT than in the PDWT subgroup. No correlation was found between BDI scores and thalamic binding ratios. Our findings show decline of [123I]β-CIT binding to thalamic 5-HTT in PD and its possible contribution to tremor onset.

Hallucinations and tremors due to oral therapeutic doses of erythromycin and methylprednisolone

A 64-year-old electronic engineer, with a history of hypertension kept under control with irbesartan 300 mg/die and atenolol 100 mg/die, came to our observation 48 h after the onset of tremors and hallucinations. Six days before hospital admission the patient started amoxacillin-clavulanate 1 gr/tid for fever (37.5–38.5 C) and general discomfort, but this therapy was interrupted 3 days after for the onset of urticaria, and replaced with erythromycin (1 gr/bids) and methylprednisolone (16 mg/ bids), no antihistamines were used. Twenty-four hours after the beginning of this new therapy, the patient complained of visual and auditory hallucinations which he lived with particular anguish. Later, he also presented tremors that progressively compromised his common daily activities, i.e. eating, dressing, writing, walking and standing up. On admission, body temperature, heart rate and blood pressure were 36.7 C, 66/bpm rythmic and 105/70 mmHg, respectively. No signs of previous urticaria were present. Cardiovascular and respiratory examinations were normal. The liver was palpable at 2 cm below the right costal margin, without tenderness. There were neither clubbing nor superficial lymphadenopathies. Carotid pulses were symmetrically normal. The patient exhibited tremors of head and face, especially of mouth and tongue, and a postural tremor of upper and lower limbs, which increased during movement and altered stability during standing and walking. Alteration of balance and gait was due to the effect of tremor, not to cerebellar disorder or postural instability. Also writing was particularly difficult and uncertain (Fig. 1). Tremors were absent during sleep. The remaining neurological examination was normal, and in particular deep tendon reflexes, tactile, temperature and vibration sensation were normal. All laboratory exams (including thyroid and liver functions, and all electrolytes: sodium, potassium, chlorine, calcium, magnesium and phosphate) were normal. Blood, stool, and urine cultures were negative as well as an antibodies’ search for legionella, mycoplasma, chlamydia, toxoplasma and Epstein–Barr Virus. On the second day of hospitalization, an electroencephalogram showed a good organization of the activity, even if unstable due to drowsiness. Electrocardiogram, chest and cervical x-ray, abdominal ultrasound, echocolordoppler of carotid arteries and brain MRI scan were normal. In the hypothesis that the clinical situation could be due to the assumption of erythromycin and steroid therapy, we suspended these drugs immediately, and no other therapy was administrated. In the following days, the symptoms quickly improved with the disappearance of the hallucinations in about 48 h, and the progressive reduction of the tremors, with improvement in writing (Fig. 1), equilibrium M. Gallerani (&) B. Boari Division of Internal Medicine, Department of Medicine, St. Anna Hospital, Corso Giovecca, 203, 44100 Ferrara, Italy e-mail: m.gallerani@ospfe.it

Does Age of Onset in Essential Tremor Have a Bimodal Distribution? Data from a Tertiary Referral Setting and a Population-Based Study

Background/Aims: The distribution of age of onset of essential tremor (ET) is unclear, with discrepancies in the literature. Some data suggest a bimodal distribution and other data 1 late-life peak. We studied age of ET onset in 2 distinct settings: a population-based study and a tertiary referral center. Methods: Age of onset data were collected. Results: In the population, there was only a small peak at the age of ≤30 years (14.1% of cases) but a clear peak in later life (85.9% of cases). In the tertiary referral center, a bimodal distribution was apparent with 1 large peak (42.2% of cases) at the age of ≤40 years and the second large peak (57.8% of cases) in later life. Familial cases accounted for only 52.6% of young-onset cases from the population, yet 82.7% from the tertiary center. Discussion: In the population-based study, a peak in later life was clearly present but a young-onset peak was barely discernable, comprising few cases. By contrast, in a tertiary referral center, age of onset was clearly bimodal. While age of ET onset is often said to be bimodal, this may be due to the preferential referral to tertiary centers of patients with young-onset, familial ET.

123I]FP-CIT striatal binding in early Parkinson's disease patients with tremor vs. akinetic-rigid onset

We performed [123I]FP-CIT/SPECT in 20 drug-naive Parkinson's disease (PD) patients, 10 with unilateral akinesia/rigidity at onset (arPD) and 10 with additional tremor-at-rest (tPD), to evaluate whether resting tremor at onset is associated with differences in striatal dopamine transporter binding. Patients of the two cohorts were matched for age, disease duration (<3 years) and severity of non-tremor motor symptoms; 31 healthy participants served as controls. Mean striatal dopamine transporter binding reduction in PD patients vs. controls was 42% for arPD and 50% for tPD; mean ipsilateral striatum and caudate nucleus uptake values were lower by 12 and 24%, respectively, in tPD than arPD. We conclude that widespread degeneration of the nigrostriatal dopaminergic pathway might be necessary for the development of parkinsonian tremor-at-rest.

Pulmonary edema and respiratory failure associated with clenbuterol exposure

Background: Clenbuterol is a long-acting β 2-adrenergic agonist used outsidethe United States for treating pulmonary disorders and within the United States in veterinary medicine. Due to itspromotion of muscle growth and lipolysis ( β 3 effects), clenbuterol is illicitly exploited for livestock growth promotion and by bodybuilders. Recently, there have been reports of clenbuterol contamination of heroin and cocaine, resulting in prolonged tachycardia, hypokalemia, hypophosphatemia, and myocardial injury. We report a case of clenbuterol toxicity causing pulmonary edema and respiratory failure. Case report: The patient was a 33-year-old man who inhaled an unknown white powder and developed immediate onset of chest pain, palpitations, tremors, headache, nausea and vomiting. He presented to the emergency department, where the following initial vital signs were recorded: sinus tachycardia, 146 bpm; wide pulse pressure, 116/27 mm Hg; respiratory rate, 20/min; room air oxygen saturation, 99%. He was diaphoretic with a fine tremor and enlarged, reactive pupils. His electrocardiogram showed 1-millimeter ST depressions laterally. A working diagnosis of cocaine toxicity was made, and he was treated with 5 milligrams of intravenous lorazepam and 3 liters of normal saline without significant change in vital signs. Laboratory results were as follows: hypokalemia, 1.9 mmol/L; hypophosphatemia, 0.4 mg/dL; hyperglycemia, 230 mg/dL; lactate, 7.2 mmol/L; anion gap, 18. The patient was admitted to the intensive care unit, and treated with benzodiazepines and haloperidol for agitation, chest pain, and persistent tachycardia. Six hours after presentation, he desaturated to 64% on 100% oxygen. He was intubated for respiratory failure and CXR showed bilateral pulmonary edema. Ultrasound revealed bilateral oculated pleural effusions; creatinine kinase, 8880 U/L (normal rate, 25-185 U/L); creatinine kinase myocardial band, 57 ng/mL (normal rate, <5 ng/mL); troponin I, 1.18 ng/mL (normal rate, <0.4 ng/mL). He was extubated on hospital day 4 and discharged 9 days after initial presentation. His toxicology screen was negative for cocaine. His serum and urine analysis confirmed the presence of clenbuterol, at 6 and 874 ng/mL, respectively. Conclusion: Pulmonaryedema is a known complication of intravenous β 2-adrenergic agonists with a reported incidence of 5% in the obstetrics literature. The etiology is unknown but likely multifactorial, and can include cardiogenic mechanisms such as fluid overload and catecholamine-induced myocardial necrosis, and noncardiogenic mechanisms such as direct toxicity and increased pulmonary vessel permeability. This is the first documented case of pulmonary edema after inhalational β 2-adrenergic agonist exposure. Based on the recent epidemic of clenbuterol exposure, clinicians should be aware of the possibility of pulmonary edema and consequent respiratory failure.

Distinguishing psychogenic and essential tremor

In contrast to essential tremor (ET), psychogenic tremor (PT) is often manifested by shaking with variable amplitude and frequency, distractibility, suggestibility, and entrainment. The sensitivity and specificity of these findings in differentiating PT and ET have not been systematically examined. In order to determine clinical features that reliably distinguish PT from ET, we collected patient information regarding tremor onset, spontaneous remissions, family history, and employment history. A "blinded" rater evaluated video segments of subjects using a standardized protocol with special attention to distractibility, suggestibility, or entrainment. A total of 45 subjects with ET or PT were enrolled in this study: 33 met clinical criteria for ET with a mean age of 56.8+/-17.0 years and 12 met clinical criteria for PT with a mean age of 42.5+/-11.0 years. PT subjects were significantly more likely to relay a history of sudden onset (p=0.03), spontaneous remissions (p=0.03), and shorter duration of tremor (p=0.001). Family history of tremor was significantly more common in the ET group (p=0.001). A moderate-to-marked degree of distraction with alternate finger tapping (p=0.01) and mental concentration on serial 7 s (p=0.01) was more common in PT. Furthermore, suggestibility with a tuning fork (p=0.04) and exacerbation with hyperventilation (p=0.06) seemed predictive of PT. Entrainment was not different in the two groups. In conclusion, a history of tremor with sudden onset and spontaneous remissions along with distractibility and suggestibility on examination are good predictors of PT and help differentiate it from ET.

Risk of incident dementia in essential tremor: A population‐based study

Essential tremor (ET) is a late-life neurological disease. Mild cognitive deficits as well as an association with prevalent dementia have been reported in recent case-control studies. We determined whether ET was associated with an increased risk of incident dementia. In a population-based study of older people in central Spain (NEDICES), nondemented ET cases and controls were followed prospectively. Incident dementia at follow-up was diagnosed using DSM-IV criteria and the risk of incident dementia was estimated in ET cases versus controls using Cox proportional hazards models. 3,891 participants had a mean duration of follow-up of 3.2 years. Sixteen (7.8%) of 206 ET cases developed incident dementia versus 145 (3.9%) of 3,685 controls (unadjusted relative risk [RR]=2.08, 95% CI=1.24-3.50, P=0.006 and adjusted RR=1.66, 95% CI=0.99-2.80, P=0.054). In an adjusted model, ET cases with tremor onset after age 65 years were twice as likely to develop incident dementia than were controls (RR=1.98, 95% CI=1.14-3.45, P=0.01), whereas ET cases with tremor onset<age 65 years and controls were equally to develop incident dementia (RR=0.74, 95% CI=0.19-3.20, P=0.79). Although ET is often considered a benign condition, in this prospective, population-based study, elderly-onset ET was associated with an increased risk of incident dementia. The basis for this dementia, which is not known, requires additional study.

Neuropathological changes in essential tremor: 33 cases compared with 21 controls

Despite its being one of the most commonly observed neurological disorders, neuropathological studies of essential tremor (ET) are rare. There have been surprisingly few autopsy studies and even fewer case-control comparisons. The primary objective was to describe and quantify the pathological changes in 33 ET and 21 control brains. A secondary objective was to correlate clinical and pathological features. We examined autopsy tissue from the Essential Tremor Centralized Brain Repository. Eight (24.2%) of the 33 ET brains had Lewy bodies in the brainstem, mainly in the locus ceruleus. However, the majority of ET brains (25/33, 75.8%) had no Lewy bodies, but had pathological changes in the cerebellum. The mean number of Purkinje cells per 100x field was reduced in ET cases without Lewy bodies (6.6 +/- 2.4 versus 9.6 +/- 3.4, P < 0.01), and there were approximately 7x more Purkinje cell torpedoes per section (12.6 +/- 7.9 versus 1.7 +/- 1.4, P < 0.001) compared to controls. ET cases without Lewy bodies also had degeneration of the dentate nucleus (two cases). Other findings in ET cases were Purkinje cell heterotopias and dendrite swellings. Lewy body ET cases were older than ET cases without Lewy bodies. Several trends were observed in ET cases without Lewy bodies, including a younger age of onset of tremor and higher proportions with gait difficulty and family history of ET. The pathological changes of ET seem to be heterogeneous and degenerative. The majority have cerebellar changes without Lewy bodies; a smaller proportion has brainstem Lewy bodies. The clinical differences between cases with versus without Lewy bodies require additional study.

CGG repeat length correlates with age of onset of motor signs of the fragile X‐associated tremor/ataxia syndrome (FXTAS)

Fragile X-associated tremor/ataxia syndrome (FXTAS) is a late-onset neurological disorder among carriers of premutation CGG-repeat expansions within the FMR1 gene. Principal features of FXTAS include progressive action tremor and gait ataxia, with associated features of parkinsonism, peripheral neuropathy, dysautonomia, and cognitive decline. Although both clinical and neuropathologic features of FXTAS are known to be highly associated with CGG repeat length, the relationship between repeat length and age-of-onset is not known. To address this issue, the ages of onset of action tremor and gait ataxia were documented by history for 93 male carriers. For this cohort, the mean ages of onset were 62.6 +/- 8.1 years (range, 39-78 years) for tremor, and 63.6 +/- 7.3 years (range, 47-78 years) for ataxia; the mean CGG repeat number was 88.5 +/- 14 (range, 60-133). Analysis of the relationship between clinical onset and molecular measures revealed significant correlations between CGG repeat number and onset of both tremor (P = 0.001) and ataxia (P = 0.002), as well as overall onset (P < 0.0001). Our findings indicate that the CGG repeat number is a potential predictor of the age of onset of core motor features of FXTAS.

Neuroimaging Findings in a Case of Holmes Tremor

Holmes tremor, previously labeled “rubral tremor” or “midbrain tremor,” is a rare tremor of low frequency (mostly below 4.5 Hz) that appears at rest, becomes more severe on sustained posture, and increases with goal-directed movements. A variable delay is classically observed between lesion onset and occurrence of tremor (usually 4 weeks to 2 years). Impairment of the dopaminergic system is essential to the pathophysiology, the diagnosis, and the therapeutic approach of this tremor. We report the case of a 29-year-old patient with a typical posttraumatic Holmes tremor. I-123 FP CIT SPECT demonstrates complete unilateral dopaminergic denervation.

The effect of a high-fat meal on the pharmacodynamics of a model lipophilic compound that binds extensively to triglyceride-rich lipoproteins

A high-fat meal induces transient hyperlipidemia characterized by elevated triglyceride-rich lipoproteins (TRL) which are composed mainly of chylomicrons. The purpose of this work was to investigate the effect of this transient hyperlipidemia on the pharmacodynamics of lipophilic drugs, using DDT as a model compound since it binds extensively to TRL and has a distinct neurotoxic effect. The postprandial hyperlipidemia in rats was induced by oral administration of peanut oil and was monitored by measurement of plasma triglyceride levels. The control group received water instead of oil. The rats received a continuous intravenous infusion of DDT (10 mg/h) until onset of a predefined pharmacodynamic endpoint (facial muscle tremor). Plasma and brain samples were then obtained and assayed for DDT. Rats with postprandial hyperlipidemia required higher dose of DDT to induce onset of facial muscle tremor. At the pharmacodynamic endpoint, oil treated rats had significantly higher concentrations of DDT in plasma and in the chylomicron fraction, but DDT brain concentrations were the same in both groups. In conclusion, a high-fat meal induces postprandial hyperlipidemia that may significantly alter the pharmacological profile of lipophilic compounds that bind to TRL. This is due to alteration of the distribution characteristics of the lipophilic compound through its association with postprandial lipoproteins. However, this pharmacokinetic phenomenon did not affect the concentration–effect relationship at the site of action in the brain.

The Toxicity of Soman in the African Green Monkey (Chlorocebus aethiops)

ABSTRACTThis study determines soman toxicity in African green monkeys (Chlorocebus aethiops) and is the first step in exploring the suitability of this species as a model for nerve agent studies. Male African green monkeys were surgically implanted with telemetry devices to monitor electroencephalographic (EEG) and electrocardiographic (ECG) activity. Blood was taken at various times to measure whole blood acetylcholinesterase (AChE) activity and cardiac troponin I (cTnI). Blood AChE activity relative to baseline was 0.0% to 2.5% 6 h after soman exposure and recovered to 31.9% to 72.0% by 30 days after exposure. The 6 h postexposure cTnI levels varied from 0.64 to 6.55 ng/mL, suggesting cardiac damage. Soman was prepared in saline to a concentration of 100 μg/mL. Using an up-down design for small samples, subjects were exposed to 5.01, 6.31, or 7.94 μg/kg soman IM. The first subject was given 5.01 μg/kg soman IM and survived. Three subjects received 6.31 μg/kg soman IM and survived. Three subjects received 7.94 μg/kg soman IM and died within 25 min, 26 min, or 6 h. In all subjects, toxic signs of muscle fasciculation, tremors, chewing, and profuse salivation developed within 2 to 7 min. Tonic-clonic motor convulsions and EEG seizure began between 2 and 18 min after tremor onset. The 48 h IM LD50 of soman in saline in the African green monkey was calculated to be 7.15 μg/kg. The signs and speed of soman intoxication in African green monkeys were consistent with those described in rhesus, cynomolguscynomolgus, and baboons.

Interest in participating in clinical research: A study of essential tremor patients

Enrolling essential tremor (ET) patients in clinical research can be challenging. Investigators can maximize recruitment by targeting patient subgroups with greater interest in participation. Nothing has been published on factors that are associated with higher levels of interest in participation. The objective of this study was to identify factors associated with higher levels of interest in participating in clinical research on ET. A total of 149 ET patients were questioned about level of interest in participating in future research. Two questions were used, although one was of primary interest. Interest was rated from 0 to 10 (maximal). Data were collected on demographic factors, family history, and tremor-related disability. Tremor severity was assessed. The mean level of interest was 8.0 +/- 2.3. Level of interest was not related to age of tremor onset, tremor duration, tremor severity, extent of tremor-related disability, or use of tremor medication. Level of interest was related to family history of tremor (P < 0.05), concern that other family members might develop tremor (P < 0.05), >2 versus 0 live births in women (P < 0.05), the view that the tremor worsens with age (P < 0.05), and presence of head tremor (P = 0.05). A variety of factors were identified that were associated with greater interest in participating in clinical research. These observations should be assessed in additional patient samples. Investigators may use our observations to identify and target patients for clinical trials and other research.

Study of possible factors associated with age of onset in essential tremor

Factors associated with the age of onset of essential tremor (ET) have not been studied in detail. Identification of modifiable factors could lead to strategies to delay disease onset and identification of nonmodifiable factors would be useful while counseling at risk individuals. The objective of this study was to identify factors associated with age of onset of tremor in ET. One hundred ninety-five ET cases were enrolled in an environmental epidemiological study. Clinical questionnaires included questions on age of onset, demographics (age, sex, race, education), early-life exposures (birth order, childhood household size), exposures prior to tremor onset (head trauma, well water, rural living, estrogen replacement therapy), and family history. In unadjusted analyses, age of onset was associated with family history of tremor (40.9 +/- 22.0 years for cases with a family history of tremor vs. 57.3 +/- 18.4 years for cases without a history; P < 0.001), history of head trauma, younger current age, greater tremor severity, and white race. Ninety-one percent of cases with onset before age 20 years had a family history of tremor. Age ofonset was not associated with other variables of interest (e.g., sex, well water, rural living). In an adjusted linear regression model, age of tremor onset was strongly associated with family history of tremor (P < 0.001). The familial form of ET is characterized by an earlier age of onset than the sporadic form. This study did not detect any other exposures that modified the age of onset of ET. Follow-up studies are needed to examine additional factors of potential interest.

Side and type of motor symptom influence cognition in Parkinson's disease

It is well known that many patients with Parkinson's disease experience neuropsychological decline. However, the nature and extent of mental status change varies widely, with some patients showing mild or no cognitive impairments and others exhibiting frank dementia. Research has shown that several clinical disease parameters may differentially correlate with patterns of neuropsychological dysfunction. The present study examined side and type of motor symptom at disease onset and their relationship to cognition in idiopathic Parkinson's disease (PD). We identified 58 patients who initially presented with one of the following symptom profiles: right-side tremor onset (RSO-T; n = 15), right-side bradykinesia/rigidity onset (n = 12), left-side tremor onset (n = 19), and left-side bradykinesia/rigidity onset (n = 12). There were no differences between groups in disease duration, overall mental status, education, or depression severity. We administered a battery of neuropsychological measures to the four PD subgroups and a group of matched control subjects (n = 40). MANCOVAs controlling for age revealed patients with RSO-T performed significantly better than the other three PD subgroups across the entire neuropsychological battery. Further, the RSO-T subgroup performed comparably to controls. In contrast, the other three PD subgroups showed widespread cognitive deficits. These findings suggest an intricate relationship between motor symptom and side of disease onset and it is the combination of these factors that may influence the disease course and extent of cognitive deterioration. Furthermore, patients who develop tremor on the right side of their body represent a distinct subgroup of PD patients who exhibit relative sparing of cognitive function.

Sub-acute toxicity and biochemical effects of extracts of &lt;i&gt;Anaphe venata&lt;/i&gt; larvae in mice

Ataxia syndrome which is characterized by sudden onset of severe muscular tremor and gait ataxia has been shown to be associated with the consumption of the larvae of Anaphe venata in South Western part of Nigeria. In this report, the sub -acute toxicity and biochemical effects of polar and nonpolar extracts of Anaphe venata larvae were investigated in mice. The sub-acute toxicity study showed an increase in the behavioural components as tremor, jerking and stretching, after the administration of the extracts for 7 days, an indication of Ataxia syndrome. Also, no significant difference in these components occurred between polar and non-polar extracts, an indication of similarity in the chemical composition and level of toxicity. There was a corresponding increase in enzymatic activities coupled with increase in weight of essential organs investigated, but not significantly different from the controls. However, the involvement of receptors and neurotransmitters, in the action of the extracts to cause ataxia syndrome require further investigation. Keywords : anaphe venata, larvae, toxicity, free radicals, In vitro, Cissus quadrangularis , CCl 4 , antioxidant activity African Journal of Biomedical Research Vol. 8(2) 2005: 89-93

Essential tremor: predictors of disease progression in a clinical cohort

Objectives: To examine the utility of baseline factors to predict disease progression among a clinical cohort of patients diagnosed with essential tremor. Measures: Tremor Rating Scale (TRS). Methods: A clinical...

Essential tremor: predictors of disease progression in a clinical cohort

To examine the utility of baseline factors to predict disease progression among a clinical cohort of patients diagnosed with essential tremor. Tremor Rating Scale (TRS). A clinical series of 128 consecutive patients diagnosed with essential tremor was included for study. 45 (35%) patients had at least one follow-up exam (mean = 3.6 years). Baseline predictive factors examined included age, age at onset of symptoms, disease duration, sex, handedness, total tremor rating score, asymmetric tremor ratings, location of initial tremor onset, use of drugs for movement disorders, ETOH responsiveness of tremor, association of head or neck tremor, history of depression, familial history of essential tremor, Parkinson's disease, Alzheimer's disease and other movement disorders. On average, the TRS total score increased by <1 point per year before the first visit to the clinic and by about 2 points per year during the observed study period. The increase of 2 points per year during the observed study period represented an approximate 12% annual change from the mean TRS total score at the first clinic visit. Significant (p<0.05) predictive factors associated with increased tremor severity at the initial clinic visit included older age, longer disease duration, use of movement disorder drugs and the presence of voice tremor (r = 0.24, 0.27, 0.25, 0.19). The major factors associated with an increase in tremor severity from the initial clinic visit to the last follow up included asymmetrical tremor ratings, unilateral initial tremor onset and longer follow-up duration (r = 0.32, 0.31, 0.30). Multivariate regression analysis accounted for about 17-30% of the variance in tremor ratings (p<0.05). Essential tremor is a slow, progressive disease. The rate of disease progression and the factors associated with disease progression may vary throughout the disease course.