Essential tremor (ET), also called benign tremor, familial tremor, and idiopathic tremor, is a medical condition characterized by involuntary rhythmic contractions and relaxations (oscillations or twitching movements) of certain muscle groups in one or more body parts of unknown cause. It is typically symmetrical, and affects the arms, hands, or fingers; but sometimes involves the head, vocal cords, or other body parts. Essential tremor is either an action (intention) tremor—it intensifies when one tries to use the affected muscles during voluntary movements such as eating and writing—or it is a postural tremor, which occurs when holding arms outstretched and against gravity. This means that it is distinct from a resting tremor, such as that caused by Parkinson's disease, which is not correlated with movement. Unlike Parkinson's disease, essential tremor may worsen with action.

Essential tremor is a progressive neurological disorder, and the most common movement disorder. Though not life-threatening, it can certainly be debilitating. Its onset is usually between 40 and 50 years of age, but it can occur at any age. The cause is poorly understood. Diagnosis is made by observing the typical pattern of the tremor coupled with the exclusion of known causes of such a tremor. There is currently no medical test available to identify an essential tremor.

While essential tremor is distinct from Parkinson's disease, which causes a resting tremor, essential tremor is nevertheless sometimes misdiagnosed as Parkinson's disease.

In mild cases, ET can manifest as the inability to stop the tongue or hands from shaking, the ability to sing only in vibrato, and difficulty doing small, precise tasks such as threading a needle. Even simple tasks such as cutting in a straight line or using a ruler can range from difficult to impossible, depending on the severity of the condition. In disabling cases, ET can interfere with a person's activities of daily living, including feeding, dressing, and taking care of personal hygiene. Essential tremor generally presents as a rhythmic tremor (4–12 Hz) that occurs only when the affected muscle is exerting effort. Any sort of physical or mental stress tends to make the tremor worse.

The tremor may also occur in the head (neck), jaw, and voice, as well as other body regions, with the general pattern being that the tremor begins in the arms and then spreads to these other regions in some people. Women are more likely to develop the head tremor than are men, and it is also found to be more severe in women than men. In people with essential tremor (ET), the head tremor can be either vertical ("yes-yes") or horizontal ("no-no") and is typically accompanied by tremors in the hands or voice. Other types of tremor may also occur, including postural tremor of the outstretched arms, intention tremor of the arms, and rest tremor in the arms. In one study, men had more severe postural hand tremor when compared to women. Abnormal tandem gait was more commonly observed in older ET people and those with more than 5 years of disease duration.

ET-related tremors do not occur during sleep, but people with ET sometimes complain of an especially coarse tremor upon awakening that becomes noticeably less coarse within the first few minutes of wakefulness. Tremor and disease activity can intensify in response to fatigue, strong emotions, low blood sugar, extreme cold and heat, caffeine, lithium salts, some antidepressants, stress, and other factors.

Parkinson's disease and parkinsonism can also occur simultaneously with ET. A non-motor feature such as hearing impairment has been shown to have higher prevalence in those with ET compared with those that are healthy or with Parkinson's. Cochlear pathologies which affect the inner ear are proposed as the potential cause, but there is still insufficient information regarding retrocochlear pathologies (affects central or neural nerve) and central auditory processing.

Walking difficulties in essential tremor are common. About half of patients have associated dystonia, including cervical dystonia, writer's cramp, spasmodic dysphonia, and cranial dystonia, and 20% of the patients had associated parkinsonism. Olfactory dysfunction (loss of sense of smell) is common in Parkinson's disease, and has also been reported to occur in patients with essential tremor. A number of patients with essential tremor also exhibit many of the same neuropsychiatric disturbances seen in idiopathic Parkinson's disease. The similarity in characteristics between parkinsonism and essential tremor can make it difficult to distinguish between the two at times. as well as dementia, although the link between these conditions, if any, is still not understood. Familial cases of ET tend to present at younger ages, whereas older ages of onset are linked to faster progression of the disease.

Essential tremor has two tremor components, central and peripheral. These two tremor components were identified by measuring the tremor of ET patients once with no weights on their hands and then with 1-pound weights on their hands. The addition of the weights resulted in a tremor spectrum with two peaks, one that maintained the same frequency (the central tremor) and one that decreased in frequency (the peripheral tremor). Only with the addition of the weights was the peripheral tremor distinguishable from the central tremor.

The frequency of essential tremor is 4 to 12 Hz, depending on which body segment is affected. Previously, it was 4 to 11 Hz according to the American Family Physician on Classification of Tremors and Treatment Update. Proximal segments are affected at lower frequencies, and distal segments are affected at higher frequencies.

Cause

Essential tremor was once thought to be a single disease state, however, research shows that there are multiple factors that are associated with causing essential tremor. This leads to the consideration that essential tremor is more akin to a family of diseases, due to the presence of both genetic (familial) and sporadic essential tremors. Currently, there are multiple main hypotheses behind essential tremor, being the degeneration of the cerebellum, inheriting the tremor, ingestion of toxins, or the presence of Lewy Bodies in the brainstem. However, post mortem studies showed that only a small number of patients had Lewy Bodies, and was more common for patients not to exhibit them.

<big>Cerebellar</big>

It is unknown how the degeneration of the cerebellum leads to essential tremor, however, it is hypothesized that it may be due to the loss of Purkinje cells, as they release gamma-aminobutyric acid (GABA), which is an inhibitory neurotransmitter meant to control the firing of neurons in the cerebellum. In certain essential tremor clinical studies which augment the GABA pathway, only some participants exhibited a reduction of tremor. Some patients have responded to alcohol, claiming alcohol has reduced the tremor, however the reduction is only short term. About half of the cases are due to a genetic mutation and the pattern of inheritance is most consistent with autosomal dominant transmission, meaning patients with essential tremor have around a 50% chance to pass it on to their children. There are multiple gene mutations and presentations on various chromosomes that lead to essential tremor. These include genes present on chromosomes 1–3, 6, 11, and 16. Each presentation or mutation of different genes were associated with families from different regions. For example, presentation of a gene associated with essential tremor on chromosome 6 has been noted in North American families, while a Canadian family was noted with mutations in the fused in sarcoma/translated in liposarcoma (FUS/TLS) gene. and GABA receptors in the cerebellum of people with essential tremor. HAPT1 mutations have also been linked to ET, as well as to Parkinson's disease, multiple system atrophy, and progressive supranuclear palsy.

Poisons and toxins

Some environmental poisons, including toxins, are also under active investigation, as they may play a role in the disease's cause. Exposure to heavy metals, specifically lead, has been associated with causation of ET. Lead is a heavy metal that can cross the central nervous system's (CNS) main line of defense, the blood–brain barrier, even increasing its permeability, allowing other harmful substances to access the CNS. This allows lead access to the CNS, permitting it to disturb processes that utilize calcium, including synaptic activity, and causes intracellular disruption, both of which may lead to irreversible damage to the CNS. This would include cerebellar damage which could cause ET. There are other poisons that work in a similar manner to lead such as other heavy metals like mercury and aluminum, as well as toxic chemicals like certain pesticides and alcohol. In particular, excessive alcohol consumption can worsen essential tremor due to damage to the cerebellum.

Pathophysiology

Essential tremor is one of the most prevalent and poorly-understood neurological disorders. Clinical, physiological and imaging studies point to involvement of the cerebellum and/or cerebellothalamocortical circuits. However, recent studies, especially those examining brain tissue, propose a new hypothesis that ET may be a neurodegenerative disease focused in the cerebellum, differing from the old theory. Impairment of Purkinje synapses is a component of cerebellar degradation that could underlie essential tremor. ET cases that progress to Parkinson's disease are less likely to have had cerebellar problems. Recent neuroimaging studies have suggested that the efficiency of the overall brain functional network in ET is disrupted.

In 2012, the National Toxicology Program concluded that sufficient evidence exists of an association between blood lead exposure at levels >10 μg/dl and essential tremor in adults, and limited evidence at blood lead levels >5 μg/dl.

Diagnosis

Usually, the diagnosis is established on clinical grounds. Although ET was long considered a single-symptom illness, recent studies have shown that some patients also experience other additional motor symptoms and non-motor features. According to recent medical literature, besides isolated essential tremor, there are two additional classifications: 'ET plus' and 'ET-PD.' 'ET plus' is diagnosed when patients show cognitive impairments or other motor symptoms like ataxia, dystonia, or resting tremor. 'ET-PD' is used for those who meet the criteria for both ET and Parkinson's disease. The clinical features of tremor in a patient include medical history (such as age of onset, family history, progression over time, and exposure to drugs or toxins), tremor characteristics (like which parts of the body are affected, when the tremor occurs, and its frequency), and any associated signs (such as signs of systemic illness, neurological signs, and soft signs). For some types of tremors, additional tests like recording tremor frequency, imaging for lesions, receptor imaging, and biomarkers in blood or tissue may help identify the cause. Tremors can start at any age, from birth through advanced ages (senile tremor). Any voluntary muscle in the body may be affected, although the tremor is most commonly seen in the hands and arms and slightly less commonly in the neck (causing the person's head to shake), tongue, and legs. A resting tremor of the hands is sometimes present. Tremor occurring in the legs might be diagnosable as orthostatic tremor. Tremors in the lower limbs are quite rare in ET and are more likely to indicate Parkinson's disease.

ET occurs within multiple neurological disorders besides Parkinson's disease. This includes migraine disorders, where co-occurrences between ET and migraines have been examined. People with mild tremors that do not interfere with daily activities and psychological well-being do not require pharmacological treatments. People with persistent tremors which impact daily functions and social interactions should be treated with the appropriate pharmacological therapies. In addition, getting adequate sleep and utilizing relaxation techniques can also help improve and reduce tremor symptoms in individuals who reported an increase in tremors following physical activities. different non-pharmacological therapeutic techniques are available that can support patients with the management of tremors including occupational therapy, speech therapy, and psychotherapy. Since GABA can decrease neural activity, it is believed that alcohol can increase the activity of GABA which then can reduce involuntary muscle movements or tremors. However, the duration of action of alcohol on ET is around 3–4 hours, alcohol also had been associated with the rebound of tremor, not to mention the risk of development of long-term alcohol consumption and abuse.

!Drugs

!Mechanism of action

!Efficacy

!Side-effects

|-

! colspan="4" |First-line therapies

FDA-approved or supported by double-blinded, placebo-controlled studies (class I evidence)

|-

|propranolol (60-800 mg/d)

| rowspan="2" |non-selective β-adrenergic receptor antagonist (probable mechanism: antagonism at peripheral β<sub>2</sub> receptors)

|50-70% (>50% response)

|frequent (>60%): hypotension, bradycardia, fatigue, dizziness, exertional dyspnea

|-

|propranolol long-acting (80-320 mg/d)

|30-38%

|skin eruption, transient dizziness

|-

|primidone (up to 750 mg/d)

|antiepileptic barbituric acid-derivative (probable mechanism: interaction with voltage-gated sodium channels or opening and potentiating GABA receptors)

|50-70% (30-50% response)

|sedation, fatigue, drowsiness, dizziness, ataxia, confusion, gastrointestinal upset, loss of coordination, anorexia

|-

! colspan="4" |Second-line therapies

Supported by double-blinded, placebo-controlled trials (class II evidence or lower)

|-

|topiramate (up to 400 mg/d)

|voltage-gated sodium channel and high voltage-activated calcium channels (antitremor mechanism unknown)

|20-37% (30-40% response)

|paresthesias, trouble concentrating, gastrointestinal upset, somnolence, fatigue, confusion (discontinuation rate: 30%)

|-

|gabapentin (1.2-1.8 g/d), pregabalin

|α<sub>2</sub>δ subunit voltage-gated calcium N-type channel blockers (antitremor mechanism unknown)

|30-40% (30-50% response)

|sleepiness, dizziness, ataxia, nausea, weight gain, psychiatric disturbances (including suicidal ideation)

|-

|alprazolam (0.125-3 mg/d), clonazepam (0.5-6 mg/d)

|benzodiazepines

|30-50% (>50% response)

|sedation, cognitive impairment, tolerance, dependency and abuse, withdrawal effects (discontinuation rate: 50%)

|-

|atenolol (50-15 mg/d)

| rowspan="2" |competitive β1-adrenergic antagonist

|37%

| rowspan="2" |similar to propranolol

|-

|metoprolol

|single dose efficacy equal to propranolol (no effect after chronic use)

|-

|nadolol (120-240 mg/d), sotalol (75-200 mg/d), indenolol, artinolol, timolol

|non-selective β-adrenergic receptor antagonists

|effective only in patients responsive to propranolol

|similar to propranolol with additional reduction of alertness

|-

|theophylline

Nicardipine single-dose reduces tremor, but does not work long-term

|somnolence, headache, dizziness, mood disturbances (including suicidal thoughts), coordination difficulties

|-

|zonisamide

|complex mechanism

|tremor amplitude reduction, mixed evidence for reduction of total score in Fahn-Tolosa-Marin Tremor Rating Scale

|multiple side effects common in patients taking zonisamide (see: article about zonisamide)

|-

|isoniazid (up to 1.2 g/d)

|}

Beta-adrenergic Blockers

thumb|Chemical structure of Propranolol, one of the most effective medication for treating ET

When symptoms are sufficiently troublesome to warrant treatment, the first choice medication is propranolol, a non-selective beta-blocker, which has been shown effective in reducing tremor by 70% in 50% of patients in clinical studies. Based on the guidelines from the American Academy of Neurology and the Italian Movement Disorders Association, propranolol is most effective in limb tremors, also there is little to no effect on head tremors. The recommended doses of propranolol range from 60 to 360&nbsp;mg daily, and it is based on the patient's specific factors. In patients that have contraindicated comorbidities to propranolol, other beta-blockers such as Atenolol, pindolol, Sotalol, and nadolol have shown some potential efficacy, but they are not very well studied and have limited evidence in their efficacy on the treatment of ET. a 2017 review of zonisamide found insufficient information to assess efficacy and safety, and a 2016 review of pregabalin determined the effects to be uncertain due to the low quality of evidence.

Botulinum Toxin (BoNT)

Botulinum toxin is a neurotoxin produced by a gram-positive, rod-shaped bacteria called Clostridium botulinum. BoNT works by inhibiting acetylcholine release at the presynaptic terminal by inactivating the SNARE proteins (SNAP-25), which interfere with muscle contraction. BoNT type A injections have shown benefits in several clinical trials for the treatments of limb, voice, and head. However, the associated side effects included muscle weakness, stiffness reported within studies of limb tremors, and neck muscle pain, weakness, and dysphagia in clinical trials of head tremors.

Additional procedures

Ultrasound

thumb|Frontal MRI four days after MRgFUS (MRI-guided high-intensity focused ultrasound): Left ventral intermediate nucleus (Vim) thalamotomy. 79-year-old man with essential tremor.

Additionally, MRI-guided high-intensity focused ultrasound is a nonsurgical treatment option for people with essential tremor who are medication refractory. MRI-guided high-intensity focused ultrasound does not achieve healing, but can improve the quality of life by reducing the tremor manifestation. While its long-term effects are not yet established, the improvement in tremor score from baseline was durable at 1 year and 2 years following the treatment. To date, reported adverse events and side effects have been mild to moderate. Possible adverse events include gait difficulties, balance disturbances, paresthesias, headache, skin burns with ulcerations, skin retraction, scars, and blood clots. This procedure is contraindicated in pregnant women, persons who have non-MRI compatible implanted metallic devices, allergy to MR contrast agents, cerebrovascular disease, abnormal bleeding, hemorrhage and/or blood clotting disorders, advanced kidney disease or on dialysis, heart conditions, severe hypertension, and ethanol or substance abuse, among others. At one year following the surgical intervention with DBS, patients showed 66% improvement and 48% improvement at 10 years. This stimulation has been explored using different stimulation intensities, either above the motoneuron activation threshold (thus directly activating the muscles in peripheral limbs), or below the motoneuron activation threshold but above the sensory afferent neuron threshold. While electrical stimulation above the activation motoneuron threshold can reduce tremor by up to 73%, it causes muscle fatigue and discomfort. Stimulating below the motoneuron activation threshold on the other hand requires precise timing to counteract the descending pathological neuronal signals driving ET in the peripheral limbs. Thus, while this treatment option shows promise it still requires rigorous investigation.

Prognosis

Although essential tremor is often mild, people with severe tremor have difficulty performing many of their routine activities of daily living. ET is generally progressive in most cases (sometimes rapidly, sometimes very slowly), and can be disabling in severe cases.

Epidemiology

Essential tremor (ET) is a common neurological disorder, affecting up to 5% of the global population, with approximately 24.91 million people affected worldwide in 2020. The prevalence of ET increases significantly with age, particularly in individuals aged 60 and above. ET is more common in males than females across all age groups. While the likelihood of developing ET increases with age, it can also occur in younger individuals, especially if there is a family history of the disorder. Although not all studies show this trend; the majority of studies (70%) indicate that there are no sex differences in prevalence.

Society and culture

Actress Katharine Hepburn (1907–2003) had an essential tremor, possibly inherited from her grandfather, that caused her head—and sometimes her hands—to shake. The tremor was noticeable by the time of her performance in the 1979 film The Corn Is Green, when critics mentioned the "palsy that kept her head trembling". Hepburn's tremor worsened in her later life.

Director-writer-producer-comedian Adam McKay was diagnosed with essential tremor.

Downton Abbey creator Julian Fellowes has the condition, as does Jim Carter the show's character Charlie Carson.

In 2022, Matthew Caws of Nada Surf and his son made a PSA called "Living with a Mild Essential Tremor".

Research

Harmaline is a widely used model of essential tremor (ET) in rodents. Harmaline is thought to act primarily on neurons in the inferior olive. Olivocerebellar neurons exhibit rhythmic excitatory action when harmaline is applied locally. Higher levels of the neurotoxin are associated with greater severity of the tremors. Harmane is particularly abundant in meats, and certain cooking practices (e.g., long cooking times) increase its concentration, but at least one study has shown that harmane blood concentrations do not go up after meat consumption in ET patients with already elevated harmane levels, whereas the control group's harmane levels increase accordingly, suggesting that another factor, such as a metabolic defect, may be responsible for the higher harmane levels in ET patients.

Caprylic acid is being researched as a possible treatment for essential tremor. It has currently been approved by the FDA and designated as GRAS, and is used as a food additive and has been studied as part of a ketogenic diet for treatment of epilepsy in children. Research on caprylic acid as a possible treatment for ET began because researchers recognized that ethanol was effective in reducing tremor, and because of this, they looked into longer-chain alcohols reducing tremor. They discovered that 1-octanol reduced tremor and did not have the negative side effects of ethanol. Pharmacokinetic research on 1-octanol lead to the discovery that 1-octanol metabolized into caprylic acid in the body and that caprylic acid actually was the tremor-reducing agent. Many studies of the effects of caprylic acid on essential tremor have been done, including a dose-escalation study on ET patients and a study testing the effects of caprylic acid on central and peripheral tremor. In February 2026, Praxis Precision Medicines submitted a New Drug Application (NDA) to the FDA. The FDA accepted the application for review in April 2026 and set a target action date of January 2027. Detailed Phase 3 results were subsequently presented at the April 2026 American Academy of Neurology (AAN) Annual Meeting, demonstrating that the drug significantly improved patients' activities of daily living compared to placebo.

A major factor attributed to the clinical success of the ulixacaltamide Phase 3 program was a paradigm shift in efficacy assessment methodology. Historically, essential tremor drug trials relied heavily on clinic-based performance snapshots, most notably the evaluation of Archimedes spiral drawings. However, recent methodological critiques presented at the 2026 AAN Annual Meeting highlighted that relying on brief, 90-second clinical tasks creates a "sampling theorem" problem.