category refers to fine postural action tremor that develops as a result of a
medication. Medications that have been reported to cause such an effect are
lithium, beta-adrenergic agonist med-ications, stimulants, dopaminergic medications,
anticonvulsant medications, antipsychotics, antidepressant medications and
methylxanthines (e.g., caffeine) (American Psychiatric Asso-ciation, 2000). The
psychotropic medication most typically as-sociated with such tremor is lithium,
and most of the available information on medication-induced tremor relates to
that caused by lithium.
muscle contractions are accompanied by tremor as a result of contractions of
muscle fiber recruitment. This tremor is typically low in amplitude and is referred
to as a physiological tremor. When these contractions are maintained, the
amplitude of the tremor increases and it becomes visible. This is referred to
as an enhanced physiological tremor. A number of medica-tions, including
lithium and bronchodilators, produce an en-hanced physiological tremor. The
pathophysiological mechanism of these tremors is not well understood but seems
to relate to adrenergic changes (probably mediated in the locus coeruleus) in
the mechanical properties of the skeletal muscle. The response of these tremors
to beta-adrenergic blocking agents and their ex-acerbation as a result of
beta-adrenergic agonists seem to lend support to the notion of adrenergic
Estimates of the frequency of lithium-induced tremor vary widely across the literature and range between 4 and 65%. Lifetime incidence of tremor is estimated to be 25 to 50% of patients start-ing lithium therapy. A number of possible risk factors have been proposed to predispose a person to development of a lithium-induced tremor. These include older age, greater serum lithium levels, concomitant use of antidepressant or antipsychotic medi-cation, greater caffeine intake, history of tremor, alcohol depend-ence and anxiety (American Psychiatric Association, 2000).
tremor may appear as soon as treatment is initi-ated. As the lithium level
increases, the tremor becomes more severe and coarse and may have associated
muscle twitching or fasciculations (American Psychiatric Association, 2000).
Com-plaints about the tremor are typically greatest at the beginning of
therapy. There is disagreement as to whether the tremor typically remains
stable or improves with time on lithium.
lithium-induced tremor is reasonably easy to diag-nose. It is a rhythmical
action tremor. It is most commonly seen in the hands or fingers but can
occasionally be seen in the head, mouth, or tongue (American Psychiatric
Association, 2000). The frequency of the tremor is typically 8 to 12 Hz and is
similar in appearance to an essential tremor. It may usually be seen by ask-ing
the patient to hold the affected body part in a stable position. The tremor is
made worse by anxiety, stress, fatigue, hypoglyc-emia, thyrotoxicosis,
pheochromocytoma, hypothermia, alcohol withdrawal, performance of voluntary
movements and concomi-tant administration of cyclic antidepressant medications.
difficult differential diagnosis involves distin-guishing a lithium-induced
tremor from a tremor that was pre-existing. To be classified as a
medication-induced tremor, it must have a temporal relationship to the
medication, it must relate to the serum level of the medication, and it must
not persist after the medication is discontinued. A similar postural tremor is
essential tremor, and differentiation between the two is nearly impossible
clinically without the medication history. Any of the factors listed that may
exacerbate a medication-induced tremor can also cause a similar tremor in the
absence of the medica-tion. Medication-induced tremor may resemble NIP. NIP,
how-ever, is generally worse at rest, is lower in frequency, and has other
associated features of parkinsonism (American Psychiatric Association, 2000).
literature suggests that there is some risk that tremor may be embarrassing for
certain patients and could impair activities that require delicate movements.
The actual percentage of patients who are bothered by their tremor is unknown.
There do not ap-pear to be any long-term sequelae as a result of having a
medica-tion-induced postural tremor. A sudden worsening of tremor may be
indicative of the beginning of lithium intoxication.
treatment options have been described for treatment of lithium-induced tremor.
Typically the tremor is benign, is not bothersome to the patient, and requires
no specific intervention. Some cases, however, require treatment because of the
patient’s concern about the side effect. Preliminary measures include pos-sibly
reducing the lithium dose (if clinically feasible), changing the lithium dose
to one-time evening administration, or chang-ing the lithium preparation.
Caffeine intake should be reduced or eliminated, and anxiety should be
pharmacologically or behav-iorally treated.
represent the best-studied method for gain-ing pharmacological control of the
tremor if the preliminary measures are ineffective. Arana and Rosenbaum (2000)
recom-mended starting propranolol on an as-needed basis. They sug-gested 10 to
20 mg a half-hour before the activity in which the tremor must not be present.
If a patient requires chronic relief from the tremor, propranolol should be
initiated at 10 to 20 mg b.i.d and increased until adequate dose for suppression
of the tremor is attained. Propranolol may decrease glomerular filtra-tion rate
and may result in a reduction in renal lithium clearance. This suggests that
patients who require long-term beta-blocker suppression for tremor need to have
lithium levels checked more regularly even when they are taking a stable dose
little information in the literature as to the pos-sible treatment of tremor
induced by medications other than lithium and further investigations are needed
to elucidate this syndrome.