Esensial Tremor

7/31/2019 Esensial Tremor

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Background

Essential tremor is the most common movement disorder. It is a syndrome characterized by aslowly 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 aposition 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 posturingExclusion criteria are as follows:

Other abnormal neurologic signs, especiallydystonia 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 upperextremity 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.)[1]

Without biologic markers for these diseases, however, determining whether long-standingpostural 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.
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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 essentialtremor is not possible.

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 islocated in the Guillain Mollaret triangle near the brainstem and involves the inferiorolivary nucleus

The cerebellar-brainstem-thalamic-cortical circuits probably are involved The pathophysiology of essential tremor is heterogeneous[2, 3]

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 essentialtremor as compared with controls.

[4]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 overactivityof 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 abnormalitiesin the brainstem and cerebellum,

[3]including Lewy bodies in the locus ceruleus, loss of Purkinje

cells, and abnormalities of the dentate nucleus[5, 6]

; reduction in cerebellar cortical N-acetylaspartate/total creatine (NAA/tCR)[4] ; white matter changes on diffusion tensor imaging;[7]

and clinical studies demonstrating an association with cognitive[8, 9] and gait changes.

Conflicting data argues against essential tremor being a neurodegenerative disease. This data

includes improvement of gait abnormalities with ethanol administration,[10]

lack of gray matter

volume loss on voxel-based morphometry,[11]

failure to confirm prominent presence of Lewy

bodies in the locus ceruleus,[3]

and other pathologic findings.[12]

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


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transmission in kindreds with an apparent autosomal dominant inheritance of essential tremor

was demonstrated in one study.[13]

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 onthe DRD3 gene has been associated with EMT1

[14]

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 6p23 - Identified in 2 families[15]

An association with a polymorphism in the HS1-BP3 gene has been reported, but this has notbeen confirmed.[13, 16]

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 bean alternative phenotype of the same mutation.

Epidemiology

Occurrence in the United States

Assessments of the prevalence and incidence of essential tremor vary widely depending onascertainment 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 yearswere examined by neurologists; 89 essential tremor cases were identified.

[17]

Race-related demographics


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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 tremorand 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.[18]

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.[19]

Age-related demographics

The prevalence of essential tremor increases with age. Data has suggested bimodal peaks in age

of onsetone 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 ata 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 bimodalpeak may be attributable to preferential referral of young-onset essential tremor to tertiary

centers.[20]

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.[21]

Prognosis

Mortality rates have been thought to be the same between patients with essential tremor and thegeneral 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.[22]

Further studies are needed to assess mortality rates in essential tremor.

Disability from essential tremor is common.[23]

Of individuals with essential tremor, 85% report

significant changes in their livelihood and socializing, and 15% report being seriously disabledby the condition.

Decreased quality of life results from loss of function and from embarrassment. In a study ofhereditary essential tremor, 60% of affected individuals did not seek employment; 25% changed


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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.

History

The following characteristics can be noted in patients with essential tremor:

A family history of essential tremor is noted in 50-60% of cases 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 emotionalactivation

Over time the tremor becomes persistent At any point in time, the frequency of the tremor is relatively fixed The amplitude of the tremor is highly variable, depending on the state of emotional

activation; tremor amplitude is worsened by emotion, hunger, fatigue, and temperatureextremes

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

Visible tremor is generally pathologic, but distinguishing between essential tremor and enhanced

physiologic tremor can be difficult. Causes of enhanced physiologic tremor, includingmedications, stimulants such as caffeine,hyperthyroidism, fever, and anxiety, should be

excluded.

Like a previous population-based study from Spain, a community-based cohort study from New

York by Thawani et al found an association between essential tremor and dementia. In cross-

sectional analyses, dementia was present in 31 of 124 subjects with essential tremor versus 198of 2,161 controls (25% vs 9.2%). In prospective analyses, dementia developed in 17 of 93

subjects with essential tremor versus 171 of 1,963 controls (18.3% vs 8.7%).[24]

Physical Examination

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 gaitabnormalities.
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The tremor is characteristically postural (occurring with voluntary maintenance of a position

against gravity) and kinetic (occurring during voluntary movement). It usually resolves when thebody part relaxes. Other characteristics of essential tremor include the following:

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, personality,[25] mood,[26]

hearing,[27, 28]

and motor symptoms associated with cerebellar outflow.[29]

Conditions to consider in the differential diagnosis of essential tremor include the following:

Cerebellar tremor

Dystonia and dystonic tremors Enhanced physiologic tremor Isolated chin tremor Isolated voice tremor Movement disorders Orthostatic tremor Palatal tremor Rubral tremor Writer's tremor and other task-specific tremors Psychogenic tremor

Drug-induced tremors can result from the following:

Antidepressants, especially tricyclics Beta agonists Depakote Dopamine Lithium Metoclopramide Neuroleptics Theophylline Thyroid hormones Withdrawal of drugs

Metabolism-related tremors can result from the following disorders:

B-12 deficiency Hyperthyroidism Hyperparathyroidism


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Hypocalcemia Hyponatremia Kidney disease Liver disease

Toxin-related tremors can result from the following :

Alcohol Arsenic Caffeine Dichlorodiphenyltrichloroethane (DDT) Lead Nicotine Toluene Withdrawal of alcohol, cocaine

Differential Diagnoses

Multiple System Atrophy Neurologic Effects of Caffeine Neurological Manifestations of Thyroid Disease Parkinson Disease Parkinson-Plus Syndromes Torticollis Wilson Disease

Imaging StudiesFindings on computed tomography (CT) scanning and magnetic resonance imaging (MRI) of the

head are normal in essential tremor. MRI helps to exclude structural and inflammatory lesions

(including multiple sclerosis) and Wilson disease. MRI should be performed if the tremor hasacute onset or stepwise progression.

Midbrain ultrasonography has been suggested as a tool to differentiate essential tremor fromParkinson disease as a result of a study finding that high substantia nigra hyperechogenicity has a

high positive predictive value for Parkinson disease. However, another study found a significant

increase in substantia nigra hyperechogenicity in patients with essential tremor compared with

controls.

[32, 33, 34]

Approach Considerations

No biologic markers exist for essential tremor. If the family history and examination findings are

indicative of essential tremor, no laboratory or imaging studies are required. However, if the

family history and examination findings are not indicative of essential tremor, laboratory and

imaging studies should be considered.[30, 31]
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Laboratory investigations include the following:

Standard electrolyte panel Thyroid function tests Blood urea nitrogen (BUN)

Creatinine Liver function tests Serum ceruloplasmin (for Wilson disease)

Procedures

Electromyography or accelerometry can be used to assess tremor frequency, rhythmicity, and

amplitude but is not part of the routine evaluation.

Approach Considerations

Primidone and propranolol are the cornerstones of maintenance medical therapy for essentialtremor. These medications provide good benefit, reducing tremor amplitude in approximately50-75% of patients.

Some patients require only intermittent tremor reduction, such as when attending a meeting orengaging in a social activity. For these patients, a cocktail or beer prior to the activity may be

sufficient. An alternative is 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.

Surgery

For patients with disabling, medically refractory upper extremity tremor, surgery is considered.

Stereotactic thalamotomy and thalamic ventralis intermedius nucleus deep brain stimulation are

the procedures of choice. Both procedures offer high rates of tremor reduction in thecontralateral arm. Information suggests that they are also useful in reducing head and voice

tremor.[35]

Bilateral thalamotomy is associated with a relatively high risk of dysarthria, occurring in as

many as 29% of patients, and a risk of cerebral hemorrhage. The potential advantage of thalamic

stimulation is that it is adjustable. If the stimulation causes an adverse effect, the rate of

stimulation can be modified or discontinued.

In 1996, Benabid et al initially proposed that thalamic stimulation might be a useful procedure onthe opposite side in patients who have already had a unilateral thalamotomy, in an effort to avoid

the potentially serious complications of bilateral thalamotomy.[36] Thalamic stimulation now is

considered the procedure of choice.

Practical Management of Pharmacologic Therapy


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For patients who require daily maintenance treatment for essential tremor, a decision is made

whether to start with primidone or propranolol. Usually, propranolol is started first in youngerpatients and primidone is started first in older individuals. Generally, propranolol carries more

risk of serious adverse effects in older patients than in younger ones. Additionally, younger

patients, particularly those who are in school or working, find the sedating and cognitive side

effects of primidone more troublesome than older patients do.

If the patient has a relative contraindication to propranolol, such as pulmonary disease or heartblock, starting with primidone is preferable.

The chosen medication, primidone or propranolol, is introduced at a low dose and increasedslowly until sufficient benefit is achieved or the usual maximum dosage is reached. If no benefit

is derived, the patient is completely weaned off the drug before the alternative medication is

started. If a partial benefit from the first drug occurs, the second medication is added and slowly

increased until sufficient benefit is achieved or the usual maximum dosage is reached. If noadditional benefit occurs, the patient is weaned off the second medication.

If sufficient benefit is not achieved with primidone or propranolol, other medications are

considered based on the severity of the residual tremor. A beta1-receptor antagonist can be tried

if necessary; in general, however, beta1-receptor antagonists are more effective than placebo but

are not as effective as beta2-receptor antagonists. (Metoprolol, a relatively selective beta1-receptor antagonist, may be useful in patients with asthma or other pulmonary conditions.)

If the tremor is mild and more of a nuisance than it is disabling, a benzodiazepine (usuallyclonazepam) is considered. For patients with head tremor, cervical injections of botulinum toxin

may be given.

Propranolol

Winkler first noted remarkable tremor reduction in a patient treated with propranolol forparoxysmal atrial tachycardia.

In a double-blind, crossover study, propranolol at doses from 60-240 mg/day reduced tremor in75% of patients with essential tremor. In a dose-response study, 240-320 mg/day was found to be

the optimal dose range, with no additional benefits above 320 mg/day.

Average tremor reduction is 50-75%, but while some patients experience marked tremor

reduction, others derive no benefit from the drug. The mechanism of action probably is related to

peripheral beta2-receptor antagonism.

Once an effective maintenance dose of propranolol is achieved, switching to the long-acting

preparation is considered. The long-acting formulation of propranolol has an efficacy similar tothat of the standard formulation and may allow the patient to take fewer daily doses. An

alternative is to use the long-acting formulation from the beginning, but this requires multiple

prescriptions and is more cumbersome.


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Primidone

O'Brien et al initially observed that primidone, when administered to a patient with epilepsy andessential tremor, reduced tremor. In a placebo-controlled study, primidone significantly reduced

tremor in otherwise untreated patients and patients treated with propranolol. Doses greater than

250 mg/day did not provide additional benefit.[37]

Primidones mechanism of action is unknown. Active metabolites are phenylethylmalonamide(PEMA) and phenobarbital. PEMA has no effect on tremor, and phenobarbital has only modest

effect on tremor. Tremor reduction is not correlated with serum levels of primidone or

phenobarbital.

Adverse effects, if any, usually occur early in the course of treatment, possibly with the first

dose. Acute adverse effects are minimized by starting at a very low dose and then slowly

increasing the dose. However, some patients are unable to tolerate primidone even at very lowdoses.

Topiramate

Topiramate is an anticonvulsant medication that enhances gamma-aminobutyric acid (GABA)

activity, carbonic anhydrase inhibition, antagonism of alpha-amino-3-hydroxy-5-

methylisoxazole-4 propionic acid/kainite receptors, and blockage of voltage-dependent calciumand sodium channels.

Multiple studies indicate that tremor is reduced by an average of approximately 20% in

comparison with placebo. However, clinical trials indicate a fairly substantial dropout rate of

40% because of adverse effects such as cognitive difficulty and somnolence.

Alcohol

The mechanism of tremor reduction by alcohol is unknown. In a double-blind study, the 6-carbon alcohol methylpentynol did not have any effect on tremor. This suggests that the alcohol

group of ethanol is not the element that provides antitremor activity and that the antitremor effect

of ethanol is not due to sedation.

Restricted intra-arterial ethanol administration does not reduce tremor in the perfused limb. This

suggests that ethanols effect is mediated centrally.

Additional Medications

Many other medications have been reported to be of benefit in the treatment of essential tremor.Most of the evidence, however, has come from case reports and small, open-label studies.

Clozapine


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In a randomized, double-blind, crossover study, tremor was reduced significantly by clozapine in

13 of 15 patients with drug-resistant essential tremor. The investigators compared a single 12.5mg dose of clozapine with placebo.

A significant reduction of tremor was reported with long-term (open-label) clozapine therapy

(39.9 mg/day). No tolerance was observed over 15 months.

Mirtazapine

In a small, open-label case series, mirtazapine was reported to reduce tremor in patients with

essential tremor and Parkinson disease.

Gabapentin

A double-blind, crossover trial comparing gabapentin (400 mg tid) with propranolol (40 mg tid)found that both drugs demonstrated significant and comparable reductions in tremor compared

with baseline. However, a double-blind, placebo-controlled, crossover study identified nodifference between gabapentin and placebo.

Benzodiazepines

Benzodiazepines, particularly clonazepam and alprazolam, are used commonly in the treatment

of essential tremor, but their effectiveness is limited. They probably work to reduce the anxiety

that can amplify tremor amplitude.

Botulinum toxin

Botulinum toxin has been evaluated for the treatment of essential tremor. Its use in the treatmentof tremor of the upper extremities is limited because it commonly causes weakness. It is moreuseful in the treatment of head tremor because it often provides benefit without unwanted,

troublesome weakness.

Thalamotomy

A retrospective study by Jankovic et al evaluated 60 patients who underwent thalamotomy formedically intractable tremor and found that, of those patients with essential tremor, most showed

improvement in tremor and in function. In the study, 42 patients had Parkinson disease, 6 had

essential tremor, 6 had cerebellar tremor, and 6 had posttraumatic tremor. Patients were observedfor a mean period of 53.4 months and for as long as 13 years.

Cessation or moderate to marked improvement in contralateral tremor with improvement infunction occurred in 86% of patients with Parkinson disease, 83% of patients with essential

tremor, 67% of patients with cerebellar tremor, and 50% of patients with posttraumatic tremor.

Fourteen of the 60 patients had a total of 18 persistent complications, including weakness in 9


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patients, dysarthria in 6, contralateral ataxia in 1, blepharospasm in 1, and pulmonary embolus

resulting in death in 1.

In a study by Goldman et al of thalamotomy in 8 patients with moderate to severe essential

tremor, the condition in all of the patients was reduced to a mild tremor or disappeared

completely. Mild persistent dysarthria was seen in 2, and a "mild verbal cognitive defect" wasseen in 1.

Stereotactic thalamotomy is less expensive than deep brain stimulation, no hardware remains,

and it has been demonstrated to provide long-term efficacy. Potential adverse effects include

intracerebral hemorrhage, motor weakness, dystonia, speech disturbance, and memory loss.

Thalamic Deep Brain Stimulation

In a multicenter study, measures of function improved significantly in patients with essentialtremor, following the administration of high-frequency, unilateral thalamic stimulation. In the

study, the results of such stimulation were assessed in 29 patients with essential tremor and 24individuals with Parkinson disease. A blinded evaluation at 3 months with patients randomizedto stimulation on or stimulation off demonstrated a significant reduction in essential tremor and

Parkinson disease contralateral tremor with stimulation on. However, stimulation was commonly

associated with transient paresthesias. Other adverse events were mild and well tolerated.

In a study of 14 patients with essential tremor, Ondo et al reported an average 83% reduction in

contralateral arm tremor following unilateral thalamic deep brain stimulation.[28]

Pahwa et al reported good results with bilateral thalamic deep brain stimulation in 9 patients with

essential tremor. Patients experienced 68% improvement in hand tremor following the first

surgery and 75% improvement in the opposite hand following the second surgery. Complicationswere noted in 5 patients and included asymptomatic intracranial hematoma (1 patient),

postoperative seizures (1 patient), hematoma over the implanted pulse generator (1 patient), leadrepositioning (1 patient), and implantable pulse generator (IPG) malfunction (1 patient). Adverse

effects related to stimulation were mild and resolved with the adjustment of stimulation

parameters.

Thalamotomy Versus Deep Brain Stimulation

In a retrospective comparison study of deep brain stimulation and thalamotomy in essential

tremor and Parkinson disease, Tasker demonstrated complete contralateral tremor abolition in42% of patients treated with either procedure, near abolition in 69% of the thalamotomy group

and 79% of the deep brain stimulation group, and recurrence in 15% of the deep brain

stimulation group and 5% of the thalamotomy group. None of the deep brain stimulationimplants and 15% of the thalamotomies had to be repeated.

In the study, adverse effects, including ataxia, dysarthria, and gait disturbance, were more

common with thalamotomy (42%) than with deep brain stimulation (26%); adverse effects were


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persistent in 31% of people undergoing thalamotomy; and those occurring after deep brain

stimulation were almost always controlled by adjusting stimulation parameters. Paresthesiaswere persistent in 19% of patients undergoing thalamotomy and were avoidable in deep brain

stimulation by stimulation modification.

Taha et al evaluated thalamic deep brain stimulation contralateral to thalamotomy in 23 patients(6 with Parkinson disease, 15 with essential tremor, and 2 with multiple sclerosis); of 20 patients

with bilateral limb tremor, 85% improved to having no tremor or only stress-induced tremor.

In a prospective study, Schuurman et al concluded that, although thalamotomy and thalamic

stimulation are equally effective for tremor suppression, stimulation results in greater functionalimprovement and has fewer adverse effects. In the study, the investigators compared thalamic

stimulation and thalamotomy in a prospective, randomized study of 68 patients with Parkinson

disease, essential tremor, or multiple sclerosis.

The investigators found that functional status improved more in the thalamic stimulation group.

Tremor was suppressed completely or almost completely in 30 of 33 patients who underwentthalamic stimulation, compared with 27 of 34 patients in the thalamotomy group. One patient in

the stimulation group died perioperatively after an intracerebral hemorrhage.

In a long-term study of a series of patients who underwent thalamic stimulation, the rates of

stimulator reoperations, explants, and device failures were relatively high, suggesting that long-term evaluations may be necessary to assess definitively the relative benefits and complications

of these procedures.

Another study found gamma knife thalamotomy to be safe and effective in patients who were not

eligible for open surgical techniques and had medically refractory tremor.

The main advantage of thalamic deep brain stimulation is that it is adjustable; adverse effectsfrom stimulation can be controlled by reducing stimulation. Disadvantages of deep brain

stimulation include expense, the use of a foreign body implant, the need to optimize parameters,

and hardware maintenance, including battery replacement after several years.[35]

Follow-Up

Essential tremor is slowly progressive; therefore, medication doses may need to be adjusted overtime. Additionally, loss of medication benefit and long-term adverse effects are not uncommon.

Adverse effects, including depression and male impotence, should be monitored in patients on

propranolol.

Ongoing attention to activities of daily living, as well as to social and psychological adaptation,

is warranted. The frequency of follow-up must be individualized.

Essential tremor is often familial; follow-up with family members may be appropriate. Concerns

about disability arising in family members may need to be addressed.

Esensial Tremor

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