Drug-induced Movement Disorders

Treatment

Prevention and Recognition
As iatrogenic conditions, DIMD are typically treated by discontinuation or reduction of the offending drug, if possible. However, when the use of antipsychotic agents results in a DIMD, a dilemma arises in which the patient's need for treatment of the essential psychiatric condition must be weighed against a requisite level of tolerable dyskinetic movements. No pharmacologic treatment has been proven to be universally or even typically effective in this situation. Therefore, the treatment of a DIMD in this setting, as in all others, is instead aimed at preventing, recognizing, and managing the movements.

Discontinuing or reducing the level of the causative agent may lead to a reduction in the movements; however, this may occur at the expense of exacerbating the psychiatric illness. An apparently contradictory practice holds that DRBD may be used to treat OBLD caused by antipsychotic drugs, an effect that actually occurs through suppression and not treatment of the movements; however, this method typically leads to a rebound phenomenon and exacerbation of the movements. When the use of a typical antipsychotic medication leads to TD, switching to an atypical antipsychotic medication, particularly clozapine, may prove to be the most efficacious strategy. Studies have shown that the resolution of the symptoms of tardive disorders vary from 33% for OBLD, to 12% and 8% for tardive dystonia and akathisia, respectively.

The Use of Medications in the Treatment of DIMD
Amine-depleting agents such as reserpine (Serpalan®, Serpasil®) and tetrabenazine (Nitoman®) block the reuptake of dopamine, norepinephrine, and serotonin, thereby depleting central availability of these neurotransmitters. They are most effective in treating tardive dystonia (~60% to 90%), tardive akathisia (~75%), and tardive dyskinesia (~50% to 90%) of patients whose symptoms are not resolved through the discontinuation of the causative agent.1 Few studies have been undertaken to evaluate the effectiveness of these drugs in the treatment of tardive DIMD, although they are in widespread use in clinical practice. Tetrabenazine, a monoamine-depleting drug acting as an inhibitor of vesicular monoamine transporter (VMAT₂), is not currently available in the United States.15-17 Amine-depleting agents seem to be most effective when not used concomitantly with neuroleptic therapy but, instead, when they are used after the neuroleptic drug is withdrawn. Significant side effects limit the use of these drugs.

When treatment with amine-depleting drugs is not indicated, e.g., symptoms are mild or the patient has depression or another contraindication to the use of amine-depleting drugs, other medications may be effective but have not been well studied or have not been proven unequivocally in studies to provide benefit.18 These medications include anticholinergic agents,19 dopamine agonists,20 GABAergic agents,21 beta-adrenergic receptor blocking agents, branched chain amino acids,11,12 essential fatty acids,22 and vitamins B623 and E.24 In addition, chemodenervation with botulinum toxin injection therapy may be used to treat drug-induced focal dystonia.25