Catatonia is a clinical syndrome characterized by a range of psychomotor abnormalities. It was first described in 1875 by Kahlbaum (1) who reported 25 patients with a “brain disease” characterized by four of the following signs: long periods of immobility, mutism alternating with verbigeration, staring, withdrawal and refusal to eat or drink, negativism, posturing and grimacing, echolalia, echopraxia, stereotypy, and waxy flexibility (seeTable 1). Kahlbaum observed that these otherwise immobile patients could become very agitated or excited and were often found to have extremes of mood disturbance in the form of “melancholy” or “mania.” This phenomenon of marked, polar alterations in the predominant psychomotor state eventually led to division of the syndrome into retarded and excited types (2). The excited form has been much more difficult to characterize and distinguish from mania (3). In rare instances, patients with severe motor excitement develop fever, autonomic disturbances, stupor, and rhabdomyolysis and may succumb to cardiovascular collapse. This clinical state has been referred to as lethal or malignant catatonia (4,5) and the clinical and laboratory similarities to neuroleptic malignant syndrome (NMS) has generated considerable interest and discussion (6,7).