We should evaluate all prescribed medications for their potential to induce catatonic symptoms and discontinued if possible. There is some ambiguity about the role of antipsychotics, but they generally encourage it to discontinue antipsychotic treatment in patients presenting with catatonia (46). In the presence of a catatonic state, both first and second-generation antipsychotics (SGA) may contribute to maintaining or worsening the catatonic state and increase the risk of developing NMS (51–54). During a prospective follow-up of 82 patients that had received antipsychotics at some point when catatonic, NMS developed in three cases (3.6%) (4), a substantially higher incidence than the estimated incidence of 0.07–1.8% in all antipsychotics-treated patients (55). The risk of worsening catatonia appears greater with neuroleptics and antipsychotics with higher D2-blockade and a higher potential of causing extrapyramidal side effects (56), but a worsening of catatonia and precipitation of NMS has also been reported in association with, e.g., olanzapine (57, 58).
Although it is generally accepted that neuroleptics are ineffective in catatonia (59), the role of the SGA in the treatment of catatonia is more ambiguous and based on cases mostly with schizophrenia (21). SGA has weak GABA-agonist activity and 5HT2-antagonism that could stimulate dopamine release in the prefrontal cortex and thus alleviate catatonic symptoms (11). Several authors have reported a beneficial effect of SGA, such as clozapine (60–63), olanzapine (64–66), risperidone (67–70), and quetiapine (71). In one randomized controlled trial, in 14 stuporous psychotic patients, risperidone (4–6 mg/day) was compared to ECT. ECT-treated patients showed significantly greater improvement than those receiving risperidone (72).
The use of antipsychotics in the presence of catatonia should be evaluated in any individual case. We support, however, the general notion to discontinue neuroleptics because of their inefficacy and their potential of aggravating the catatonic symptoms. Once treatment with benzodiazepines or ECT is started and catatonia improves, there may be a role for SGA to target residual psychotic symptoms such as delusions or hallucinations, especially in patients with schizophrenia (69), or as a prophylactic treatment in psychotic disorders and mood disorders. SGA with low D2 blockade (quetiapine, olanzapine) or with D2 partial agonism (aripiprazole) should be favored in these situations (54).
Patients presenting with both delirium and catatonia warrant special consideration (73, 74). Catatonia is a frequent feature of delirious mania, a severe syndrome characterized by the rapid onset of delirium, mania, and psychosis. Symptoms of catatonia and delirium overlap, complicating diagnosis. DSM states that catatonia should not be diagnosed if it occurs during a delirium. The issue is important because treatments for catatonia and delirium are different, albeit with overlap. While we typically treat delirium with (typical or atypical) antipsychotics, the emergence of catatonia may caution against the use of antipsychotics (75, 76). If we do not recognize catatonia in a delirious patient, the withdrawal or withholding of benzodiazepines sometimes thought to worsen delirium may induce catatonia or leave catatonia untreated. Further studies in delirious patients are needed to aid these treatment dilemmas (77).