[Pharmacological treatment of acute catatonia]

Catatonia is a neuropsychiatric syndrome of psychomotor dysregulation that can be present in a broad spectrum of clinical situations. Advances made over the last decades have progressively contributed to its clinical differentiation and its conceptual delimitation. Both Benzodiazepines (BZD) and Electroconvulsive therapy (ECT) have been consolidated as first-line therapy. In this regard, a BZD response rate ranging from 70 to 90 per cent has been reported in different case series. Furthermore, NMDA receptor antagonists represent an emerging strategy in the therapeutic approach to the disorder. Most of the evidence that supports the aforementioned treatment recommendations arises from descriptive observational studies. Traditionally, catatonia pathophysiological research focused on the study of subcortical brain structures. Currently there exists compelling evidence that supports a cortical origin of the syndrome, emphasizing the role of the prefrontal cortex. Neuropsychiatric catatonia models that integrate clinical, pathophysiological, and neurobiological findings have been postulated. The aim of the present review is to summarize up-to-date available evidence associated with the pharmacotherapeutic approach to acute catatonia as well as the neurochemical basis of its effectiveness. Likewise, general measures intended to prevent morbimortality are subject to discussion herein.