Akathisia: a comprehensive review and treatment summary

Akathisia can be a quite common and very troubling side effect of psychotropic treatment. Clinicians have become steadily more aware of this disorder, owing to original descriptions of restless movement disorder dating back to the first half of this century. Delineation of acute akathisia from other movement disorders, such as tardive dyskinesia, is crucial for providing patients with the best interventions. The pathophysiology of akathisia is not completely understood, but likely arises from complex interactions in subcortical and possibly spinal dopamine/norepinephrine systems. There are now valid and reliable methods to assess akathisia using standardized scales; doing so helps track the progress of treatment interventions. The secondary complications of akathisia are numerous. The most notable ones are non-compliance and assaultive or suicidal ideation or behavior. Iron status may play a pivotal role in the pathophysiology and development of acute akathisia due to the possible interaction of iron with the D2 receptor, but practical clinical significance of this is not yet clear. Causative agents of akathisia include all currently available neuroleptics, various other psychoactive medications, and occasional other non-psychotropics. Treatment first should include stopping the offending agent (if possible), lowering the dose, or changing to a lower potency neuroleptic. If these are not feasible, then there are a host of medications which are variably effective. The most common are beta-blockers, anticholinergics, clonidine, or benzodiazepines. Less commonly prescribed agents such as opiates, amantadine, buspirone, piracetam, amitriptyline, and dopamine depleters can be tried in more treatment-refractory patients. An overall treatment algorithm incorporating knowledge to date is presented at the end of this review.