eMedicine Specialties > Neurology > Movement and Neurodegenerative Diseases

Essential Tremor

Author: Deborah A Burke, MD, Consulting Staff, Sub-investigator, Clinician, Movement Disorder/Parkinson's Disease Center, University of South Florida; Investigator, Physician, Roskamp Institute Memory Clinic
Coauthor(s): Robert A Hauser, MD, MBA, Professor of Neurology, Molecular Pharmacology and Physiology, Director, Parkinson's Disease and Movement Disorders Center, University of South Florida; Clinical Chair, Signature Interdisciplinary Program in Neuroscience; Theresa McClain, MSN, ARNP, Parkinson's Disease and Movement Disorders Center, University of South Florida
Contributor Information and Disclosures

Updated: Mar 31, 2009

Introduction

Background

Essential tremor is the most common movement disorder. It is a syndrome characterized by a slowly progressive postural and/or kinetic tremor, usually affecting both upper extremities.

Pathophysiology

The pathophysiology of essential tremor is not known. No pathological findings are known to be consistently associated with essential tremor. However, the following has been hypothesized:

  • Essential tremor is the result of an abnormally functioning central oscillator, which is located in the Guillain Mollaret triangle near the brain stem and involves the inferior olivary nucleus.
  • The cerebellar-brainstem-thalamic-cortical circuits probably are involved.
  • The pathophysiology of essential tremor is heterogeneous.1,2

Harmane, a heterocyclic amine (HCA), is a potent tremor-producing neurotoxin. It is often found in the human diet. Blood concentrations have been found to be elevated in patients with essential tremor as compared with controls.3 The most likely etiology appears to be alterations in metabolism rather than increased dietary intake.

In patients with essential tremor, [18 F]fluorodeoxyglucose PET studies identified increased glucose consumption in the medulla. [15 O]H2 O PET studies demonstrated an increase in medullary regional cerebral blood flow in subjects with essential tremor, only after the administration of ethanol, and bilateral overactivity of cerebellar circuitry.

Fundamental debate exists as to whether essential tremor is a neurodegenerative disease. Data suggesting that it is neurodegenerative includes postmortem findings of pathological abnormalities in the brainstem and cerebellum2 , including Lewy bodies in the locus ceruleus, loss of Purkinje cells, and abnormalities of the dentate nucleus4,5 ; reduction in cerebellar cortical NAA/tCR3 ; white matter changes on diffusion tensor imaging6 ; and clinical studies demonstrating an association with cognitive7,8 and gait changes. Conflicting data argues against essential tremor being a neurodegenerative disease. This data includes improvement of gait abnormalities with ethanol administration9 , lack of grey matter volume loss on voxel-based morphometry10 , failure to confirm prominent presence of Lewy bodies in the locus ceruleus2 , and other pathological findings11 .

Frequency

United States

Assessments of prevalence and incidence vary widely depending on ascertainment methodology and diagnostic criteria. The prevalence of essential tremor is estimated at 0.3-5.6% of the general population. A 45-year study of essential tremor in Rochester, Minnesota, reported an age- and sex-adjusted prevalence of 305.6 per 100,000 and an annual incidence of 23.7 per 100,000. An estimated 0.5-11.1% of affected individuals seek medical attention.

International

Using a “door-to-door” method in Mersin Province, Turkey, 2253 individuals older than age 40 years were examined by neurologists; 89 essential tremor cases were identified.12

Mortality/Morbidity

Mortality rates have been thought to be the same between patients with essential tremor and the general population. However, in a recent, longitudinal prospective study of patients age 65 and older from 3 communities in central Spain, the risk of mortality was found to be increased.13  Further studies are needed to assess mortality rates in essential tremor.

Disability from essential tremor is common.

  • Of individuals with essential tremor, 85% report significant changes in their livelihood and socializing and15% report being seriously disabled by essential tremor.
  • Decreased quality of life results from both loss of function and embarrassment. In a study of hereditary essential tremor, 60% of affected individuals did not seek employment; 25% changed jobs or took early retirement; 65% did not dine out; 30% did not attend parties, shop alone, partake of a favorite hobby or sport, or use public transportation; and 20% stopped driving.

Race

Race has not been extensively studied in essential tremor. One evaluation of a multiethnic group (White, African American, and Hispanic) found differences in presence or absence of head tremor and variable tremor score among the subgroups. White subjects had a tremor score that was 5.3 points lower than nonwhites. Head tremors were present in 25% of Whites, 29% of Hispanics, and absent in African Americans.14

Sex

Essential tremor affects both sexes with equal frequency.

  • Head tremor may be more frequent in women.
  • Postural hand tremor may be more severe in men.
  • Childhood essential tremor may be more frequent in boys than in girls.15

Age

The prevalence of essential tremor increases with age.

  • Data has suggested bimodal peaks in age of onset—one in late adolescence to early adulthood and a second in older adulthood. The mean age at presentation is 35-45 years. One comparison of a population-based cohort with patients at a tertiary care center found a significant bimodal presentation only at the latter, suggesting preferential referral of young-onset essential tremor to tertiary centers.16
  • Essential tremor usually manifests by age 65 years and virtually always by 70 years. Tremor amplitude slowly increases over time. Tremor frequency decreases with increasing age. An 8- to 12-Hz tremor is seen in young adults and a 6- to 8-Hz tremor is seen in elderly individuals.
  • Rare cases of essential tremor have been reported in newborns and infants. Although essential tremor is progressive, no association has been found between age of onset and severity or disability
  • A strong correlation between age of onset before 20 years and family history of essential tremor was found in a environmental epidemiological study of 195 essential tremor cases.17

Clinical

History

  • Tremor usually begins in one upper extremity and soon affects the other. essential tremor rarely extends from the upper extremity to the ipsilateral leg.
  • A mild degree of asymmetry is not unusual.
  • In about 30% of cases, tremor involves the cranial musculature; the head is involved most frequently, followed by voice, jaw, and face.
  • Tremor may be intermittent initially, emerging only during periods of emotional activation. Over time the tremor becomes persistent.
  • At any point of time the frequency of tremor is relatively fixed, but amplitude is highly variable depending on the state of emotional activation. Tremor amplitude is worsened by emotion, hunger, fatigue, and temperature extremes. The baseline tremor amplitude slowly increases over several years.
  • A degree of voluntary control is typical, and the tremor may be suppressed by skilled manual tasks.
  • The tremor resolves during sleep.
  • Ethanol intake temporarily reduces tremor amplitude in an estimated 50-70% of cases.
  • A family history of essential tremor is noted in 50-60% of cases.
  • Visible tremor is generally pathologic, but distinguishing between essential tremor and enhanced physiologic tremor can be difficult. Causes of enhanced physiologic tremor, including medications, stimulants such as caffeine, hyperthyroidism, fever, and anxiety, should be excluded.

Physical

essential tremor generally is considered to be monosymptomatic (tremor only), although some patients have abnormalities in gait and balance. If patients have such abnormalities, the diagnosis should be carefully considered because most patients with essential tremor do not have gait abnormalities.

The tremor is characteristically postural (occurring with voluntary maintenance of a position against gravity) and kinetic (occurring during voluntary movement). It usually resolves when the body part relaxes.

  • Both upper extremities are typically affected.
  • Mild asymmetry is not uncommon.
  • Tremor also may affect the head, voice, and lips.
  • Tone and reflexes are normal.
  • Parkinsonian features such as bradykinesia and rigidity are absent.
There are data calling into question the tenet that essential tremor is truly monosymptomatic. Findings associated with essential tremor include changes in cognition (see above), personality,18 mood,19 hearing,20,21 and motor symptoms associated with cerebellar outflow.22

Causes

Essential tremor probably represents a syndrome and multiple etiologies will likely be identified. Most or all of these causes are probably genetic.

  • Essential tremor is familial in at least 50-70% of cases. Transmission is autosomal dominant, with incomplete penetrance. Some cases are sporadic with unknown etiology. Twin studies suggest that genetic and environmental factors contribute to the pathogenesis. Non-Mendelian transmission in kindreds with an apparent autosomal dominant inheritance of essential tremor was demonstrated in one study.23
    • Variations in methodology (ie, assessment procedures and diagnostic criteria) account for the wide variation in findings; reported studies have found that 17% to almost 100% of cases are familial.
    • One study demonstrated that the frequency of having an affected relative increased from 67.7% to 96% after repeated and varied questioning followed by directly interviewing family members.
  • Three susceptibility loci have been found.
    • A locus at 3q13 (EMT1) was identified in 75 members of 16 Icelandic families. A Ser9Gly variant on the DRD3 gene has been associated with EMT1.24
    • Another locus, 2p25-22 (EMT2), was identified in 15 members of 4 generations of Americans. Abnormalities found in 3 additional American families have been reported to map to this locus.
    • A locus on 6p23 was identified in 2 families.25
    • An association with a polymorphism in the HS1-BP3 gene has been reported but this has not been confirmed.26,23
    • In one family with levodopa-responsive, autosomal dominant, Lewy body parkinsonism, a chromosome arm 4p haplotype that segregates with the disease was identified. This haplotype also occurred in individuals in the family who did not have parkinsonism but rather a postural tremor consistent with essential tremor. This suggests that in some cases postural tremor can be an alternative phenotype of the same mutation.
  • Associations between essential tremor and Parkinson disease  and essential tremor and dystonia have been suggested.
    • Essential tremor has been hypothesized to be a risk factor for the development of Parkinson disease. Some patients with Parkinson disease report a long-standing history of bilateral upper extremity postural tremor. Without biological markers for these diseases, determining whether long-standing postural tremor is part of a Parkinson disease syndrome or reflects the presence of both essential tremor and Parkinson disease is not possible.
    • Some patients with focal dystonia, such as torticollis, have mild bilateral upper extremity postural tremors. Without biological markers for these diseases, determining whether postural tremor is part of a focal dystonia syndrome or reflects the presence of both dystonia and essential tremor is not possible.
    • In a large cohort study by the Mayo Clinic, the risk of essential tremor was significantly increased in relatives of patients with Parkinson disease with younger onset and in relatives of patients with tremor-predominant Parkinson disease.27
  • The Movement Disorders Society has proposed the following diagnostic criteria for classic essential tremor:
    • Inclusion criteria are as follows:
      • Bilateral, largely symmetric postural or kinetic tremor involving hands and forearms that is visible and persistent
      • Possible additional or isolated tremor in head but absence of abnormal posturing
    • Exclusion criteria are as follows:
      • Other abnormal neurologic signs, especially dystonia
      • The presence of known causes of enhanced physiologic tremor, including current or recent exposure to drugs that are known to cause tremor or a drug-withdrawal state
      • Historic or clinical evidence of psychogenic tremor
      • Convincing evidence of sudden onset or evidence of stepwise deterioration
      • Primary orthostatic tremor
      • Isolated voice tremor
      • Isolated position- or task-specific tremors, including occupational tremors and primary writing tremor
      • Isolated tongue or chin tremor
      • Isolated leg tremor

More on Essential Tremor

Overview: Essential Tremor
Differential Diagnoses & Workup: Essential Tremor
Treatment & Medication: Essential Tremor
Follow-up: Essential Tremor
References
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  86. Zirh A, Reich SG, Dougherty PM, Lenz FA. Stereotactic thalamotomy in the treatment of essential tremor of the upper extremity: reassessment including a blinded measure of outcome. J Neurol Neurosurg Psychiatry. Jun 1999;66(6):772-5. [Medline].

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Further Reading

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Keywords

essential tremor, essential tremor treatment, movement disorder, benign essential tremor, familial tremor, senile tremor

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Contributor Information and Disclosures

Author

Deborah A Burke, MD, Consulting Staff, Sub-investigator, Clinician, Movement Disorder/Parkinson's Disease Center, University of South Florida; Investigator, Physician, Roskamp Institute Memory Clinic
Deborah A Burke, MD is a member of the following medical societies: American Academy of Neurology and Movement Disorders Society
Disclosure: Nothing to disclose.

Coauthor(s)

Robert A Hauser, MD, MBA, Professor of Neurology, Molecular Pharmacology and Physiology, Director, Parkinson's Disease and Movement Disorders Center, University of South Florida; Clinical Chair, Signature Interdisciplinary Program in Neuroscience
Robert A Hauser, MD, MBA is a member of the following medical societies: American Academy of Neurology, American Medical Association, American Society of Neuroimaging, and Movement Disorders Society
Disclosure: Allergan Sales, LLC Honoraria Speaking and teaching; Bayer Shering Pharma AG Honoraria Consulting; Boehringer Ingelheim France Honoraria Consulting; Centapharm Honoraria Speaking and teaching; Genzyme Corporation Honoraria Consulting; GlaxoSmithKline Honoraria Consulting; IMPAX Laboratories, Inc.  Consulting; Kyowa Pharmaceuticals, Inc. Honoraria Consulting; Novartis Pharmaceuticals Corp. Honoraria Consulting; Prestwick Pharmaceuticals, Inc. Honoraria Consulting

Theresa McClain, MSN, ARNP, Parkinson's Disease and Movement Disorders Center, University of South Florida
Theresa McClain, MSN, ARNP is a member of the following medical societies: Sigma Theta Tau International
Disclosure: Teva Consulting fee Consulting; GSK Consulting fee Consulting; Valeant Pharm Consulting fee Consulting

Medical Editor

Daniel H Jacobs, MD, Associate Professor of Neurology, University of Central Florida College of Medicine
Daniel H Jacobs, MD is a member of the following medical societies: American Academy of Neurology, American Society of Neurorehabilitation, and Society for Neuroscience
Disclosure: Teva Pharmaceutical Grant/research funds Consulting; Biogen Idex Grant/research funds Independent contractor; Serono EMD Royalty Speaking and teaching; Pfizer Royalty Speaking and teaching; Berlex Royalty Speaking and teaching

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Nestor Galvez-Jimenez, MD, MSc, MHA, Chairman, Department of Neurology, Program Director, Movement Disorders, Department of Neurology, Division of Medicine, Cleveland Clinic Florida
Nestor Galvez-Jimenez, MD, MSc, MHA is a member of the following medical societies: American Academy of Neurology, American College of Physicians, and Movement Disorders Society
Disclosure: Nothing to disclose.

CME Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association
Disclosure: Nothing to disclose.

Chief Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association
Disclosure: Nothing to disclose.

 
 
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