Catatonia is a severe but treatable neuropsychiatric syndrome known since the middle of the nineteenth century. It has been considered for a long time as a subtype of schizophrenia, even though this association occurs only in 10% of cases. In contrast, it is frequently observed in bipolar patients. First-line treatment consists of benzodiazepines, while in case of resistance electroconvulsive therapy (ECT) and clozapine have shown positive results. In addition, recent studies reported the efficacy of some atypical antipsychotics. The present case shows the clinical response to augmentative asenapine in a catatonic manic patient with a partial response to clozapine. 1. Introduction The term Catatonia, coined in 1874 by Karl Kahlbaum, is a severe psychomotor syndrome characterized by the presence for more than 24 hours of at least two among a list of symptoms including stupor/immobility, rigidity, excessive motor activity (purposeless), staring, posturing, and autonomic alterations. Even though catatonia has been considered for a long time a subtype of schizophrenia, this syndrome frequently occurs over other conditions including mood disorders [1, 2]. According to international guidelines, high dosages of benzodiazepines are the first-line treatment for catatonia; Electroconvulsive Therapy (ECT) is to be taken into consideration when patients do not respond to benzodiazepines or rapid resolution is necessary [3]. In recent studies, some atypical antipsychotics such as risperidone and olanzapine have been successfully used, while clozapine should be reserved to resistant cases [4, 5]. In this paper we report the case of a bipolar catatonic patient who showed response to augmentative asenapine after partial response to clozapine. 2. Case Presentation R. was a 46-year-old man, with a 24-year history of bipolar disorder and manic psychotic episodes requiring hospitalization. The first catatonic episode occurred in 2001 and responded to high dosages of clozapine (600？mg/day) after 6 weeks of hospitalization. During the following ten years, the patient maintained an adequate level of functioning, attending most of daily activities despite of his limited social relationships. Given that the subjective well-being had been continuing for many years, the patient decided to stop assuming clozapine in May 2012. As a consequence, a recurrence of the previous symptoms occurred, reaching its peak in September 2012, when he was admitted to our inpatients service. At the admission, R. showed euphoric mood, purposeless excessive motor activation, stereotyped movements,
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