An acute dystonic reaction (ADR; involuntary, intermittent, sustained muscle contractions) is an early-onset EPS and can occur after a single dose of an antipsychotic. Half of cases occur within 2 days of starting treatment and almost all within 1 week. While an ADR is much more likely with high-potency FGAs, this side effect can occur with all antipsychotics, including clozapine.

Patients complain about “cramping,” their “heads turning,” problems with their eyes “rolling back,” or a “thick” or protruding tongue. More dramatic manifestations, such as opisthotonus (body arching), torticollis, oculogyric crises (eyes rolling backward), or trismus (lockjaw), can occur. Patients can be distressed and overwhelmed with anxiety, but are not confused. Although distressing, dystonia is usually not dangerous except in cases of laryngeal-pharyngeal dystonia, which can result in respiratory compromise.

The clinical presentation of an ADR is usually acute and dramatic, and the diagnosis should not be difficult. Treatment with parenteral benztropine or diphenhydramine is highly effective.

ADR is preventable by giving prophylactic anticholinergics to high-risk patients. Do not forget to discharge patients who had an acute dystonic reaction in the emergency department (ED) with a brief course of an anticholinergic. If no further antipsychotic treatment is planned, 2 or 3 days of benztropine (Cogentin) 1 or 2 mg bid or diphenhydramine (Benadryl) 25 to 50 qid is sufficient. I have seen patients return to the ED the next day with another episode of ADR because they did not receive prophylaxis.

Akathisia literally means “unable to sit still.” It is an extremely unpleasant sense of inner restlessness with the desire to move about to relieve tension. As akathisia becomes more severe, you can observe the motor restlessness as patients may pace around, jiggle their feet, or be unable to sit and watch television for more than a few minutes at a time. It is one of the acute side effects, and I expect it to occur early in the course of treatment, sometimes after the first dose. Although FGAs, particularly high-potency antipsychotics like haloperidol or fluphenazine, can easily bring on akathisia, higher doses of second-generation antipsychotics can also cause it. The antipsychotics least likely to cause akathisia include quetiapine and clozapine.

The diagnosis of akathisia is usually straightforward. In the right clinical setting (i.e., after initiation of an antipsychotic), you should be alert for evidence of motor restlessness and always ask about an inner sense of restlessness. Some patients are objectively restless but deny the subjective component. In these circumstances I prefer to treat presumptively for akathisia. However, a diagnostic dilemma can occur when agitation in a very psychotic patient is either due to akathisia, requiring a reduction in antipsychotic treatment, or psychotic agitation, when increased treatment is needed.

Akathisia is not a side effect that patients should have to live with in the long run. If possible, lower the antipsychotic and hope the akathisia resolves. Otherwise, you might have to switch antipsychotics. Whatever you do, always treat akathisia symptomatically as well. Beta-blockers are considered the treatment of choice, and patients should be followed closely after initiation in case higher doses are required (start with propranolol 10 mg tid and titrate upward). Other effective medication classes include anticholinergics and benzodiazepines and, more recently, mirtazapine. In nonurgent cases I usually try to lower the antipsychotic dose while temporarily adding a benzodiazepine (e.g., clonazepam 1 mg bid).