The underlying etiology is not clear but many cases seem to be familial.^[23] It has been estimated that approximately one-half of the cases are due to a genetic mutation and the pattern of inheritance is most consistent with autosomal dominant transmission. No genes have been identified yet but genetic linkage has been established with several chromosomal regions.^[24][25] A number of environmental factors, including toxins, are also under active investigation and these may play a role in disease etiology.^[26] In terms of pathophysiology, clinical, physiological and imaging studies point to an involvement of the cerebellum and/or cerebellothalamocortical circuits.^[27] Recent postmortem studies have demonstrated the presence of degenerative changes, including Purkinje cell axonal swellings and Purkinje cell loss in the majority of cases and brainstem Lewy bodies in the remainder. These studies suggest that the disease is both heterogeneous and degenerative. In other words, ET might be a family of degenerative diseases rather than a single disease.^[28][29]

However, emerging research based on brain autopsies of 50 deceased ET patients (as of December 2009), showed clear degenerative and pathological abnormalities, including "messy" neurofilaments which can impede nerve impulses. Research by Dr. Elan Louis and colleagues revealed that 80% of autopsied brains also exhibited changes within the cerebellum particularly to neurons that produce GABA, a major inhibitory neurotransmitter. Further analysis showed elevated levels of two neurotoxins,lead and harmane, a heterocyclic amine. Heterocyclic amines (HCA) are chemicals found in some foods. Harmane has been detected in coffee and cigarettes (see:http://www.ncbi.nlm.nih.gov/pubmed/21776263), but is especially prevalent in meats that have been barbecued or exposed to high heat.^{[citation needed]}

Another research^[30] indicates there is a strong link between essential tremor in males and the amount of meat consumed, but the exact mechanism is yet unknown.

Changes in the cerebelleum could also be mediated by alcohol consumption. Purkinje cells are especially susceptible to ethanol excitotoxicity.^[31] The impairment could lead to the abnormal cerebellar circuitry seen in essential tremor and suggests that alcohol may also work as an exacerbating agent in the pathology of this disease.

Chronic ethanol consumption results in a loss of Purkinje cell synapses. However, these synapses are regained following a period of recovery that includes gradual weaning off of ethanol. Continued consumption of ethanol inhibits the recovery of synapses.^[32] This impairment of Purkinje synapses is a component of cerebellar degradation that could underlie essential tremor.^[31]

Chronic alcohol abuse has also been linked to other movement disorders such as myoclonus, ataxia, and dyskinesia.^[31]

Usually the diagnosis is established on clinical grounds. Tremors can start at any age, from birth through advanced ages (senile tremor).^[33][34] 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 patient's head to shake),tongue, and legs. A resting tremor of the hands is sometimes present.^[35][36] Tremor occurring in the legs might be diagnosable as Orthostatic Tremor.

ET does sometimes occur in combination with other neurological disorders such as dystonia, neuropathy, & dysautonomia.^[7] In addition, there may be a link between ET andParkinson's disease, with one study showing ET patients having an approximately 4 times greater likelihood of developing Parkinson's disease.^[37][38][39] Essential tremor also tends to co-occur with Orthostatic Tremor.

Treatment

There is no recognised cure for essential tremor. Many of the treatments available are to lower the severity of the condition. These may include:

Medication

This is where essential tremor & Parkinson's Disease probably differ the most.^[40][41] With Parkinson's Disease, treatment may include levodopa or dopamine agonists. Essential tremor may be treated with medications such as beta-blockers (propranolol and/or nadolol, for example), and/or antiepileptics, like primidone and/orgabapentin.^[42][43]

A trial of the benzodiazepine-anticonvulsant clonazepam (Klonopin, Rivotril) was found not to be an effective treatment;^[44] however, it is still recommended in some cases.^[45]

Topiramate has also been cited as a possible pharmaceutical treatment.^{[citation needed]}

Self-medication with small amounts of alcohol has been shown to give short term relief from tremor,^[46] although this form of self-medication is not recommended due to an increased risk of alcohol dependence or abuse.^[47] However, other alcohol groups such as 1-octanol are being researched to provide relief from essential tremor without providing the intoxication or toxicity that ethanol does.^[48]