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Essential Tremor

  • Author: Deborah A Burke, MD; Chief Editor: Selim R Benbadis, MD  more...
 
Updated: Jul 08, 2016
 

Practice Essentials

Essential tremor, the most common movement disorder, is a syndrome of unknown etiology characterized by a slowly progressive postural and/or kinetic tremor, usually affecting both upper extremities. Fundamental debate exists as to whether essential tremor is a neurodegenerative disease.

Signs and symptoms

In general, essential tremor is considered to be monosymptomatic (tremor only). Although some patients have abnormalities in gait and balance, most do not; therefore, carefully consider alternative diagnoses in the presence of gait abnormalities.

Patients with essential tremor may exhibit the following signs and symptoms:

  • Tremor begins in one upper extremity and then affects the other upper extremity; tremor rarely extends from an upper extremity to the ipsilateral lower extremity
  • Tremor may initially be intermittent, occurring during periods of emotional activation, and then becomes persistent over time
  • A mild degree of tremor asymmetry is not unusual
  • Tremor may also affect the head, voice, jaw, lips, and face
  • The tremor frequency is fixed at any point in time
  • The tremor amplitude is highly variable, worsened by emotion, hunger, fatigue, temperature extremes; the baseline amplitude gradually increases over several years; ethanol intake temporarily reduces tremor amplitude in about 50-70% of cases
  • Typically, there is a degree of voluntary control; tremor may be suppressed by performing skilled manual tasks
  • Tremor resolves when the body part relaxes as well as during sleep
  • Muscle tone and reflexes are normal; there is no bradykinesia or rigidity

See Clinical Presentation for more detail.

Diagnosis

Essential tremor is usually diagnosed based on family history and examination findings; thus, laboratory and imaging studies are usually not required. No biologic markers exist for essential tremor. Electromyography or accelerometry can be used to assess tremor frequency, rhythmicity, and amplitude but is not part of the routine evaluation.

Laboratory testing

If the patient’s family history and examination findings are not indicative of essential tremor, consider the following laboratory studies:

  • Standard electrolyte panel
  • Thyroid function tests
  • Blood urea nitrogen and creatinine levels
  • Liver function tests
  • Serum ceruloplasmin (for Wilson disease)

Imaging studies

Head computed tomography (CT) scanning and magnetic resonance imaging (MRI) findings are normal in essential tremor.

Perform MRI if the tremor has an acute onset or stepwise progression. MRI also helps to exclude structural and inflammatory lesions (including multiple sclerosis) and Wilson disease.

Single-photon emission CT (SPECT) scanning using 123I-ioflupain (DaTSCAN) may be used to support a diagnosis of parkinsonism, thereby reducing misdiagnosis of essential tremor as Parkinson disease.[1, 2, 3]

See Workup for more detail.

Management

Primidone and propranolol are the cornerstones of maintenance medical therapy for essential tremor. These medications provide good benefit, reducing tremor amplitude in approximately 50-70% of patients.[4, 5, 6]

Some patients require only intermittent tremor reduction (eg, to attend a meeting or engage in a social activity). For these patients, a cocktail or beer prior to the activity may be sufficient, or they may take propranolol (10-40 mg) approximately one half hour prior to the event.

Alcohol consumption is not an appropriate maintenance therapy for patients who seek tremor reduction throughout the day.[7]

Pharmacotherapy

The following medications are used in the management of essential tremor:

  • Nonselective beta-blockers (eg, propranolol hydrochloride)
  • Anticonvulsants (eg, primidone, topiramate)
  • Second-generation antipsychotics (eg, clozapine)
  • Antidepressants (eg, mirtazapine)

Surgery

Consider surgical intervention in patients with disabling, medically refractory upper extremity tremor. The procedures of choice are stereotactic thalamotomy and thalamic ventralis intermedius nucleus deep brain stimulation.

See Treatment and Medication for more detail.

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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. The etiology of essential tremor is not known, and fundamental debate exists as to whether essential tremor is a neurodegenerative disease. (See Etiology and Presentation.)

Inclusion and exclusion criteria

The Movement Disorders Society has proposed the following diagnostic criteria for classic essential tremor. Inclusion criteria are as follows (see Presentation and Workup):

  • Bilateral, largely symmetrical, postural (occurring with voluntary maintenance of a position against gravity) or kinetic (occurring during voluntary movement) 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

Association with other diseases

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. Moreover, 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. (See Etiology and Presentation.)[8]

Without biologic markers for these diseases, however, 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. (See Workup.)

An association between essential tremor and dystonia has also been suggested. Some patients with focal dystonia, such as torticollis, have mild, bilateral upper extremity postural tremors. Again, however, without biologic 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.

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Etiology

The etiology of essential tremor is not known. No pathologic 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 brainstem and involves the inferior olivary nucleus
  • The cerebellar-brainstem-thalamic-cortical circuits probably are involved
  • The pathophysiology of essential tremor is heterogeneous [9, 10]

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.[11] The most likely etiology appears to be alterations in metabolism rather than increased dietary intake.

In patients with essential tremor, [18 F]fluorodeoxyglucose positron emission tomography (18F-FDG-PET) scan studies identified increased glucose consumption in the medulla. In addition, [15 O]H2 O PET scan 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 pathologic abnormalities in the brainstem and cerebellum,[10] including Lewy bodies in the locus ceruleus, loss of Purkinje cells, and abnormalities of the dentate nucleus[12, 13] ; reduction in cerebellar cortical N-acetylaspartate/total creatine (NAA/tCR)[11] ; white matter changes on diffusion tensor imaging;[14] and clinical studies demonstrating an association with cognitive[15, 16] and gait changes.

Conflicting data argues against essential tremor being a neurodegenerative disease. This data includes improvement of gait abnormalities with ethanol administration,[17] lack of gray matter volume loss on voxel-based morphometry,[18] failure to confirm prominent presence of Lewy bodies in the locus ceruleus,[10] and other pathologic findings.[19]

Genetics

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.[20]

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 direct interviews of family members.

The following 3 susceptibility loci have been found:

  • 3q13 (EMT1) - Identified in 75 members of 16 Icelandic families; a Ser9Gly variant on the DRD3 gene has been associated with EMT1 [21]
  • 2p25-22 (EMT2) - Identified in 15 members of 4 generations of Americans; abnormalities found in 3 additional American families have been reported to map to this locus [22]
  • 6p23 - Identified in 2 families [23]

An association with a polymorphism in the HS1-BP3 gene has been reported, but this has not been confirmed.[20, 24]

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.

LINGO1 (leucine-rich repeat and Ig-containing domain 1) variant rs9652490 has been identified as a risk factor for familial essential tremor.[25, 26, 27]

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Epidemiology

Occurrence in the United States

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

International occurrence

Using a “door-to-door” method in Mersin Province, Turkey, 2253 individuals older than 40 years were examined by neurologists; 89 essential tremor cases were identified.[28]

Race-related demographics

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

Sex-related demographics

Essential tremor affects both sexes with equal frequency. However, head tremor may be more frequent in women, and postural hand tremor may be more severe in men. Childhood essential tremor may be more frequent in boys than in girls.[30]

Age-related demographics

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 center, with the population-based study revealing a significant peak only in older adults. This suggested that the bimodal peak may be attributable to preferential referral of young-onset essential tremor to tertiary centers.[31]

Essential tremor usually manifests by age 65 years and virtually always by age 70 years. Tremor amplitude slowly increases over time, but tremor frequency decreases with increasing age. An 8-12 Hz tremor is seen in young adults, and a 6-8 Hz tremor is seen in elderly individuals. Although essential tremor is progressive, no association has been found between age of onset and severity or disability.

Rare cases of essential tremor have been reported in newborns and infants. A strong correlation between age of onset before 20 years and family history of essential tremor was found in an environmental epidemiologic study of 195 essential tremor cases.[32]

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Prognosis

Mortality rates have been thought to be the same between patients with essential tremor and the general population. However, in a longitudinal, prospective study of patients aged 65 and older from 3 communities in central Spain, the risk of mortality in persons with essential tremor was found to be increased.[33] Further studies are needed to assess mortality rates in essential tremor.

Disability from essential tremor is common.[34] Of individuals with essential tremor, 85% report significant changes in their livelihood and socializing, and 15% report being seriously disabled by the condition.

Decreased quality of life results from loss of function and from 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.

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Contributor Information and Disclosures
Author

Deborah A Burke, MD Clinician, Sub-Investigator, Movement Disorder/Parkinson's Disease Center, University of South Florida College of Medicine; Investigator, Physician, Roskamp Institute Memory Clinic

Deborah A Burke, MD is a member of the following medical societies: American Academy of Neurology, International Parkinson and Movement Disorder Society

Disclosure: Nothing to disclose.

Coauthor(s)

Robert A Hauser, MD, MBA Professor of Neurology, Molecular Pharmacology and Physiology, Director, USF Parkinson's Disease and Movement Disorders Center, National Parkinson Foundation Center of Excellence, Byrd Institute, Clinical Chair, Signature Interdisciplinary Program in Neuroscience, University of South Florida College of Medicine

Robert A Hauser, MD, MBA is a member of the following medical societies: American Academy of Neurology, American Medical Association, American Society of Neuroimaging, International Parkinson and Movement Disorder Society

Disclosure: Received consulting fee from Cerecor for consulting; Received consulting fee from L&M Healthcare for consulting; Received consulting fee from Cleveland Clinic for consulting; Received consulting fee from Heptares for consulting; Received consulting fee from Gerrson Lehrman Group for consulting; Received consulting fee from Indus for consulting; Received consulting fee from University of Houston for consulting; Received consulting fee from AbbVie for consulting; Received consulting fee from Adama.

Theresa A McClain, RN, MSN, ARNP-BC Advanced Registered Nurse Practitioner and Investigator, Parkinson’s Disease and Movement Disorders Center, University of South Florida College of Medicine

Theresa A McClain, RN, MSN, ARNP-BC is a member of the following medical societies: Sigma Theta Tau International

Disclosure: Received consulting fee from Teva for consulting; Received consulting fee from Schering Plough for consulting; Received consulting fee from Biotie for consulting; Received consulting fee from Novartis for consulting.

Chief Editor

Selim R Benbadis, MD Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida College of Medicine

Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Medical Association, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Cyberonics; Eisai; Lundbeck; Sunovion; UCB; Upsher-Smith<br/>Serve(d) as a speaker or a member of a speakers bureau for: Cyberonics; Eisai; Glaxo Smith Kline; Lundbeck; Sunovion; UCB<br/>Received research grant from: Cyberonics; Lundbeck; Sepracor; Sunovion; UCB; Upsher-Smith.

Acknowledgements

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.

Daniel H Jacobs MD, FAAN, Associate Professor of Neurology, University of Florida College of Medicine; Director for Stroke Services, Orlando Regional Medical Center

Daniel H Jacobs 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

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

References
  1. Cuberas-Borrós G, Lorenzo-Bosquet C, Aguadé-Bruix S, et al. Quantitative evaluation of striatal I-123-FP-CIT uptake in essential tremor and parkinsonism. Clin Nucl Med. 2011 Nov. 36(11):991-6. [Medline].

  2. Antonini A, Berto P, Lopatriello S, Tamma F, Annemans L, Chambers M. Cost-effectiveness of 123I-FP-CIT SPECT in the differential diagnosis of essential tremor and Parkinson's disease in Italy. Mov Disord. 2008 Nov 15. 23(15):2202-9. [Medline].

  3. Tolosa E, Borght TV, Moreno E. Accuracy of DaTSCAN (123I-Ioflupane) SPECT in diagnosis of patients with clinically uncertain parkinsonism: 2-year follow-up of an open-label study. Mov Disord. 2007 Dec. 22(16):2346-51. [Medline].

  4. Koller WC, Vetere-Overfield B. Acute and chronic effects of propranolol and primidone in essential tremor. Neurology. 1989 Dec. 39(12):1587-8. [Medline].

  5. Winkler GF, Young RR. Efficacy of chronic propranolol therapy in action tremors of the familial, senile or essential varieties. N Engl J Med. 1974 May 2. 290(18):984-8. [Medline].

  6. Teräväinen H, Fogelholm R, Larsen A. Effect of propranolol on essential tremor. Neurology. 1976 Jan. 26(1):27-30. [Medline].

  7. Louis ED. Treatment of Essential Tremor: Are there Issues We are Overlooking?. Front Neurol. 2011. 2:91. [Medline]. [Full Text].

  8. Walter AR, Bower JH, Ahlskog JE et al. Increased risk of essential tremor in first-degree relative of patients with Parkinson’s disease. Mov Disord. Aug 15 2007. 22(11):

  9. Louis ED, Vonsattel JP. The emerging neuropathology of essential tremor. Mov Disord. 2008 Jan 30. 23(2):174-82. [Medline].

  10. Shill HA, Adler CH, Sabbagh MN, et al. Pathologic findings in prospectively ascertained essential tremor subjects. Neurology. 2008 Apr 15. 70(16 Pt 2):1452-5. [Medline].

  11. Louis ED, Zheng W, Mao X, Shungu DC. Blood harmane is correlated with cerebellar metabolism in essential tremor: a pilot study. Neurology. 2007 Aug 7. 69(6):515-20. [Medline].

  12. Louis ED, Honig LS, Vonsattel JP, Maraganore DM, Borden S, Moskowitz CB. Essential tremor associated with focal nonnigral Lewy bodies: a clinicopathologic study. Arch Neurol. 2005 Jun. 62(6):1004-7. [Medline].

  13. Louis ED, Vonsattel JP, Honig LS, Ross GW, Lyons KE, Pahwa R. Neuropathologic findings in essential tremor. Neurology. 2006 Jun 13. 66(11):1756-9. [Medline].

  14. Shin DH, Han BS, Kim HS, Lee PH. Diffusion tensor imaging in patients with essential tremor. AJNR Am J Neuroradiol. 2008 Jan. 29(1):151-3. [Medline].

  15. Bermejo-Pareja F, Louis ED, Benito-Leon J. Risk of incident dementia in essential tremor: a population-based study. Mov Disord. 2007 Aug 15. 22(11):1573-80. [Medline].

  16. Benito-Leon J, Louis ED, Bermejo-Pareja F. Elderly-onset essential tremor is associated with dementia. Neurology. 2006 May 23. 66(10):1500-5. [Medline].

  17. Klebe S, Stolze H, Grensing K, Volkmann J, Wenzelburger R, Deuschl G. Influence of alcohol on gait in patients with essential tremor. Neurology. 2005 Jul 12. 65(1):96-101. [Medline].

  18. Daniels C, Peller M, Wolff S, et al. Voxel-based morphometry shows no decreases in cerebellar gray matter volume in essential tremor. Neurology. 2006 Oct 24. 67(8):1452-6. [Medline].

  19. Ross GW, Dickson D, Cersosimo M. Pathological investigation of essential tremor. Neurology. Apr 2004. 62(7) S5:A537-A538.

  20. Ma S, Davis TL, Blair MA, et al. Familial essential tremor with apparent autosomal dominant inheritance: should we also consider other inheritance modes?. Mov Disord. 2006 Sep. 21(9):1368-74. [Medline].

  21. Deng H, Le W, Jankovic J. Genetics of essential tremor. Brain. 2007 Jun. 130:1456-64. [Medline].

  22. Higgins JJ, Pho LT, Nee LE. A gene (ETM) for essential tremor maps to chromosome 2p22-p25. Mov Disord. 1997 Nov. 12(6):859-64. [Medline].

  23. Shatunov A, Sambuughin N, Jankovic J, et al. Genomewide scans in North American families reveal genetic linkage of essential tremor to a region on chromosome 6p23. Brain. 2006 Sep. 129:2318-31. [Medline].

  24. Higgins JJ, Lombardi RQ, Pucilowska J, Jankovic J, Tan EK, Rooney JP. A variant in the HS1-BP3 gene is associated with familial essential tremor. Neurology. 2005 Feb 8. 64(3):417-21. [Medline].

  25. Thier S, Lorenz D, Nothnagel M, et al. LINGO1 polymorphisms are associated with essential tremor in Europeans. Mov Disord. 2010 Apr 30. 25(6):717-23. [Medline].

  26. Clark LN, Park N, Kisselev S, Rios E, Lee JH, Louis ED. Replication of the LINGO1 gene association with essential tremor in a North American population. Eur J Hum Genet. 2010 Jul. 18(7):838-43. [Medline]. [Full Text].

  27. Tan EK, Teo YY, Prakash KM, et al. LINGO1 variant increases risk of familial essential tremor. Neurology. 2009 Oct 6. 73(14):1161-2. [Medline]. [Full Text].

  28. Dogu O, Sevim S, Camdeviren H, et al. Prevalence of essential tremor: door-to-door neurologic exams in Mersin Province, Turkey. Neurology. 2003 Dec 23. 61(12):1804-6. [Medline].

  29. Louis ED, Barnes LF, Ford B, Pullman SL, Yu Q. Ethnic differences in essential tremor. Arch Neurol. 2000 May. 57(5):723-7. [Medline].

  30. Tan EK, Lum SY, Prakash KM. Clinical features of childhood onset essential tremor. Eur J Neurol. 2006 Dec. 13(12):1302-5. [Medline].

  31. Louis ED, Dogu O. Does age of onset in essential tremor have a bimodal distribution? Data from a tertiary referral setting and a population-based study. Neuroepidemiology. 2007. 29(3-4):208-12. [Medline].

  32. Louis ED, Ottman R. Study of possible factors associated with age of onset in essential tremor. Mov Disord. 2006 Nov. 21(11):1980-6. [Medline].

  33. Louis ED, Benito-Leon J, Ottman R, Bermejo-Pareja F. A population-based study of mortality in essential tremor. Neurology. 2007 Nov 20. 69(21):1982-9. [Medline].

  34. Rajput A, Robinson CA, Rajput AH. Essential tremor course and disability: A clinicopathologic study of 20 cases. Neurology. 2004 Mar 23. 62(6):932-6. [Medline].

  35. Thawani SP, Schupf N, Louis ED. Essential tremor is associated with dementia: prospective population-based study in New York. Neurology. 2009 Aug 25. 73(8):621-5. [Medline]. [Full Text].

  36. Chatterjee A, Jurewicz EC, Applegate LM, Louis ED. Personality in essential tremor: further evidence of non-motor manifestations of the disease. J Neurol Neurosurg Psychiatry. 2004 Jul. 75(7):958-61. [Medline].

  37. Miller KM, Okun MS, Fernandez HF, Jacobson CE 4th, Rodriguez RL, Bowers D. Depression symptoms in movement disorders: comparing Parkinson's disease, dystonia, and essential tremor. Mov Disord. 2007 Apr 15. 22(5):666-72. [Medline].

  38. Benito-Leon J, Louis ED, Bermejo-Pareja F. Reported hearing impairment in essential tremor: a population-based case-control study. Neuroepidemiology. 2007. 29(3-4):213-7. [Medline].

  39. Ondo W, Jankovic J, Schwartz K, Almaguer M, Simpson RK. Unilateral thalamic deep brain stimulation for refractory essential tremor and Parkinson's disease tremor. Neurology. 1998 Oct. 51(4):1063-9. [Medline].

  40. Stolze H, Petersen G, Raethjen J, Wenzelburger R, Deuschl G. The gait disorder of advanced essential tremor. Brain. 2001 Nov. 124:2278-86. [Medline].

  41. Deeb J. Gannon K. Shah M, et al. Comparison of datscan imaging and smell testing in essential tremor and Parkinson disease. Jr Neurol, Neurosurg. & Psych. Sept 2007. 78(9):1018-1019.

  42. Findley LJ, Shah M. Muhammed N, et al. Olfactory tests distinguish essential from parkinsonian tremor. Evidence of enhanced detection and age resistance in familial essential tremor. J Neurol Neurosurg Psych. Jan 2006. 77(1):140.

  43. Doep F. Plotkin M, Siegel L. Brain parenchyma sonography and 123I-FP-CIT SPECT in Parkinson’s disease and essential tremor. Mov. Disord. Dec 7 1007. 23(3):(405-410).

  44. Stockner H, Sojer M, K KS, et al. Midbrain sonography in patients with essential tremor. Mov Disord. 2007 Feb 15. 22(3):414-7. [Medline].

  45. Luo WF, Zhang YC, Sheng YJ, Fang JC, Liu CF. Transcranial sonography on Parkinson's disease and essential tremor in a Chinese population. Neurol Sci. 2011 Dec 11. [Medline].

  46. Kim JS, Oh YS, Kim YI, Koo JS, Yang DW, Lee KS. Transcranial sonography (TCS) in Parkinson's disease (PD) and essential tremor (ET) in relation with putative premotor symptoms of PD. Arch Gerontol Geriatr. 2012 Jan 23. [Medline].

  47. Fytagoridis A, Sandvik U, Aström M, Bergenheim T, Blomstedt P. Long term follow-up of deep brain stimulation of the caudal zona incerta for essential tremor. J Neurol Neurosurg Psychiatry. 2011 Dec 28. [Medline].

  48. Benabid AL, Pollak P, Gao D, et al. Chronic electrical stimulation of the ventralis intermedius nucleus of the thalamus as a treatment of movement disorders. J Neurosurg. 1996 Feb. 84(2):203-14. [Medline].

  49. [Guideline] Zesiewicz TA, Elble RJ, Louis ED, et al. Evidence-based guideline update: treatment of essential tremor: report of the Quality Standards subcommittee of the American Academy of Neurology. Neurology. 2011 Nov 8. 77(19):1752-5. [Medline]. [Full Text].

  50. O'Brien MD, Upton AR, Toseland PA. Benign familial tremor treated with primidone. Br Med J (Clin Res Ed). 1981 Jan 17. 282(6259):178-80. [Medline]. [Full Text].

  51. Elias WJ, Huss D, Voss T, Loomba J, Khaled M, Zadicario E, et al. A pilot study of focused ultrasound thalamotomy for essential tremor. N Engl J Med. 2013 Aug 15. 369(7):640-8. [Medline].

  52. Goldman MS, Ahlskog JE, Kelly PJ. The symptomatic and functional outcome of stereotactic thalamotomy for medically intractable essential tremor. J Neurosurg. 1992 Jun. 76(6):924-8. [Medline].

  53. Kondziolka D, Ong JG, Lee JY, Moore RY, Flickinger JC, Lunsford LD. Gamma Knife thalamotomy for essential tremor. J Neurosurg. 2008 Jan. 108(1):111-7. [Medline].

  54. Pahwa R, Lyons KL, Wilkinson SB, et al. Bilateral thalamic stimulation for the treatment of essential tremor. Neurology. 1999 Oct 22. 53(7):1447-50. [Medline].

  55. Schuurman PR, Bosch DA, Bossuyt PM, et al. A comparison of continuous thalamic stimulation and thalamotomy for suppression of severe tremor. N Engl J Med. 2000 Feb 17. 342(7):461-8. [Medline].

  56. Taha JM, Janszen MA, Favre J. Thalamic deep brain stimulation for the treatment of head, voice, and bilateral limb tremor. J Neurosurg. 1999 Jul. 91(1):68-72. [Medline].

  57. Tasker RR. Deep brain stimulation is preferable to thalamotomy for tremor suppression. Surg Neurol. 1998 Feb. 49(2):145-53; discussion 153-4. [Medline].

  58. Jeffrey, S. FDA Okays Brio Neurostimulation System for PD, ET. Medscape Medical News. Available at http://www.medscape.com/viewarticle/846456. June 12, 2015; Accessed: June 17, 2015.

 
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