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Neuroleptic-induced catatonia (NIC), manifested in an extrapyramidal-catatonic syndrome, has been sporadically reported in the literature. Confusion surrounds its relationship to neuroleptic malignant syndrome (NMS) and extrapyramidal reactions to neuroleptics. This study examined (a) its clinical presentation and response to benzodiazepines, (b) the hypothesis that NIC and NMS are on the same spectrum with a continuum of symptom progression, and (c) its possible relationship to extrapyramidal reactions. Of 127 episodes of acute catatonia prospectively identified, 18 were diagnosed with NIC. All catatonia episodes received benzodiazepines. The NIC episodes were analyzed noting their clinical presentations, laboratory findings, and responses to treatments. Their responses to benzodiazepines were compared, with retrospective rating on a 7-point scale, to that for catatonia episodes associated with mania and schizophrenia. The progression of symptoms in each NIC episode was reviewed. The NIC episodes presented predominantly in the stuporous form associated with parkinsonism. Delirium, autonomic abnormality, and elevated serum creatine phosphokinase were all common. Neuroleptic malignant syndrome was diagnosed in 3 episodes (17%). The 3 catatonia groups did not differ significantly in their benzodiazepines responses: 78% (14/18) of NIC, 75% (12/16) of manic catatonia, and 67% (34/51) of schizophrenic catatonia episodes showed full responses. A spectrum of presentation across episodes was noted with simple NIC without delirium, autonomic disturbances, or fever at one end and NMS or malignant NIC at the other end. Symptoms in individual episodes showed a similar continuum progression. No extrapyramidal reactions immediately preceded the NIC episodes. Findings of this study support the hypothesis that NIC and NMS are disorders on the same spectrum and reveal no indication that extrapyramidal reactions progress to NIC.

Neuroleptic malignant syndrome (NMS) is usually a self-limited disorder, with most cases resolving within 2 weeks after antipsychotic drug discontinuation. However, the course of NMS may not always be short-lived. In this report, the authors describe five patients who developed a residual catatonic state that persisted after acute hyperthermic symptoms of NMS had subsided and compare them with 27 similar cases in the literature. Two of our patients recovered gradually with supportive treatment. Three patients were treated with electroconvulsive therapy (ECT). Of these, two showed a positive response, although one died later of intercurrent pneumonia. A third patient did not respond to ECT, but recovered gradually thereafter. Although dopamine agonists or benzodiazepines have been advocated for the treatment of residual symptoms in previous case reports, ECT was the treatment most often associated with a rapid response and no mortality, even in patients refractory to pharmacotherapy. In conclusion, catatonic and parkinsonian symptoms of NMS may persist as a residual state lasting for weeks to months after more fulminant acute symptoms abate. These residual symptoms may be more likely to develop in patients with pre-existing structural brain disorders. Although patients may improve gradually with supportive care or pharmacotherapy, ECT can often be highly effective in treating the residual catatonic state that follows NMS.

The use of benzodiazepine medication is associated with a variety of acute and well-recognized withdrawal syndromes including anxiety, agitation, insomnia, and confusion. Catatonia has not previously been described. We report five patients who became catatonic after withdrawal of benzodiazepines. All five were older individuals (53-88 years) who had acutely become immobile, mute, and rigid with refusal or inability to eat or drink. Each of the five showed pronounced and rapid improvement after administration of low-dose lorazepam, which has previously been reported to be effective in the treatment of catatonia. Careful review of the records showed that each of the patients had been taking benzodiazepine medication for anywhere from 6 months to 15 years and that it had been rapidly tapered or abruptly discontinued 2 to 7 days before the onset of catatonia. These cases illustrate that severe and potentially life-threatening catatonia can develop in the wake of benzodiazepine withdrawal. Older individuals may be particularly vulnerable to this side effect.

The authors describe a patient with major affective disorder, unipolar depressed type, recurrent, psychosis who went into a catatonic stupor state while being treated with maprotiline hydrochloride and thiothixene. The article also deals with findings on electroencephalogram, response to treatment, a review of other similar case reports, and the clinical significance and relevance based upon which other clinicians can take some precautionary measures while prescribing this newer antidepressant, especially in combination with a neuroleptic.

Presented here are four cases of catatonic reactions which were felt to be neuroleptic induced. Intravenous lorazepam was rapidly effective in reversing the catatonia and attendant symptoms. Lorazepam's previous uses and pharmacological profile are discussed. Reviewed briefly are catatonia and its neuroleptic-induced forms. Possible mechanisms responsible for the therapeutic effect of intravenous lorazepam in these cases are then examined.