In the absence of preexisting neurodegenerative disorders, medication side effect is the predominant cause of dystonia. The prevalence of acute dystonia from antipsychotics is 10–30%. Ninety percent occur within 5 days of treatment [2]. Mild dystonia usually resolves without treatment. Anticholinergic agents are the mainstay of treatment for acute dystonia. Tardive dystonia is much rarer than acute dystonia. It has a worse prognosis, often persisting after stopping the offending agent. Tardive dystonia may also be seen as part of parkinsonism.

Akathisia is seen in up to 36% people on antipsychotics [2]. It is usually seen within 2 weeks of treatment and 90% occur within 10 weeks. It may be hard to differentiate from agitation secondary to psychotic symptoms, anxiety, substance withdrawal, restless leg syndrome, and acute delirium from metabolic abnormalities. Akathisia has features similar to restless legs syndrome but can usually be differentiated clinically. The latter presents mostly at night or during periods of inactivity; also, it mainly involves the legs and spares other parts of the body. Akathisia may also be seen as part of parkinsonism.

As with other EPS, higher potency typical antipsychotics are generally more likely than lower potency typical agents and atypical antipsychotics to cause akathisia. Among atypical antipsychotics, comparative incidence rates between agents vary across studies; risperidone and aripiprazole may have slightly higher rates [3].

Tardive dyskinesia (TD) refers to all syndromes that occur after prolonged exposure to treatment with dopamine -blocking agents. It includes tardive dystonia and akathisia but classic TD refers to the stereotypic movements of the face, limbs, and trunk. The majority of patients have oro-buccal-lingual dyskinesia that manifests as chewing, lip smacking, or tongue protruding movements. Symptoms are usually seen after 1–2 years of antipsychotic exposure though duration of exposure is variable. Most experts consider TD only after at least 3 months of antipsychotic exposure.

The incidence of TD varies across studies. The prevalence in patients on typical antipsychotics was 20% in a 1982 study [4]. As with other EPS, risk is highest with high-potency typical antipsychotics. But the risk with atypical agents appears to be higher than previously reported. A recent review reports annual rates as 5.5% for typical antipsychotics and 3.9% for atypical antipsychotics [5]. Risk is likely to be lower if lower potency typical antipsychotics or atypical antipsychotics are used. Among atypical agents, risperidone is the most likely and clozapine and quetiapine are least likely to cause TD [2].

Proposed risk factors for developing TD are older age, female gender, African-American race, history of other extrapyramidal symptoms, or other neurologic dysfunction. None have been consistently proven. Dose is not clearly correlated with TD prevalence though antipsychotic treatment with the lowest possible dose for a short duration is generally recommended. Though TD risk does increase with length of treatment, duration of antipsychotic exposure alone does not explain the differences in prevalence and severity of TD resulting from antipsychotic treatment across studies .

The course of TD is difficult to determine. TD can spontaneously resolve, especially in younger patients [6]. Stopping the medication resolves TD in some but not all patients. In the immediate period after stopping the antipsychotic, there may be a withdrawal dyskinesia and so patients have to be observed over a period of at least weeks to months to determine if TD has resolved.