A special type of postural action tremor, closely related to the enhanced physiologic tremor, occurs as the most prominent feature of the early stages of withdrawal from alcohol or other sedative (benzodiazepines, barbiturates) following a sustained period of use. LeFebvre-D’Amour and colleagues have described two tremors of slightly different frequency, one of which is indistinguishable from essential tremor. Either of these may occur as the individual emerges from a relatively short period of intoxication (“morning shakes”). A number of alcoholics, on recovery from the withdrawal state, exhibit a persistent tremor of essential (familial) type, described below. The mechanisms involved in alcohol withdrawal symptoms are discussed in the chapter on Disorders of the Nervous System Caused by Alcohol, Drugs, Toxins, and Chemical Agents.
Action tremors are seen in a number of other clinical settings. A large number of drugs can cause tremor either as direct or an idiosyncratic effect. At times it is difficult to determine if the drug is simply exaggerating a preexisting tremor, but most often the tremor is only evident with the drug and ceases when the drug is withdrawn. The main examples are antiepileptic medications, particularly valproate; bronchodilators and adrenergic drugs such as aminophylline, cocaine, thyroxine; gastrointestinal drugs such as metoclopramide and cimetidine; psychiatric drugs, mainly lithium but also amitriptyline, the selective serotonin reuptake inhibitors and haloperidol; and immunosuppressants such as tamoxifen, tacrolimus, cyclosporine, and interferon-alpha. A more complete discussion of drug-induced tremors can be found in the review by Morgan and Sethi. A coarse action tremor, sometimes combined with myoclonus, accompanies various types of meningoencephalitis (e.g., in the past it was quite common with syphilitic general paresis) and certain intoxications (methyl bromide and bismuth).
This, the commonest type of tremor, is of lower frequency (4 to 8 Hz) than physiologic tremor and is unassociated with other neurologic changes; thus it is called “essential.” It is usually at the lower end of this frequency range and of variable amplitude. Aside from its rate, the identifying feature is its appearance or enhancement with attempts to maintain a static limb posture or to produce a smooth trajectory of movement. Like many other tremors, essential tremor is worsened by emotion, exercise, and fatigue. One infrequent type of essential tremor is faster and of the same frequency (6 to 8 Hz) as enhanced physiologic tremor. Essential tremor may increase in severity to a point where the patient’s handwriting becomes illegible and he cannot bring a spoon or glass to his lips without spilling its contents. Eventually, all tasks that require manual dexterity become difficult or impossible. The pathophysiology of this tremor and its treatment are discussed further on.
Typical essential tremor occurs in several members of a family, for which reason it has been called familial or hereditary essential tremor. Inheritance is in an autosomal dominant pattern with high penetrance. The idiopathic and familial types cannot be distinguished on the basis of their physiologic and pharmacologic properties and probably should not be considered as separate entities. This condition had been referred to as “benign essential tremor,” but this is hardly so in many patients in whom it worsens with age and interferes with normal activities.