Original Publication Date: >2 November, 2015
Publication / Source: Future Neurology
Authors: Chin-Chuen Lin & Tiao-Lai Huang
The mechanisms of catatonia may involve the GABA system, dopamine system, glutamate/N-methyl-D-aspartate receptor system and brain-derived neurotrophic factor. In this article we will share our experiences in treating catatonia with benzodiazepines in Taiwan. We will look at catatonia and its association with anti-N-methyl-D-aspartate receptor encephalitis, and lastly, reports on predicting outcome of patients with catatonia will also be discussed.
Kahlbaum described catatonia in 1874 as a unique clinical phenomenon characterized by concurrent motor, emotional, vegetative and behavioral signs. Once free of catatonia, patients often report intense and uncontrollable anxieties. Over the past century, more than 40 motor signs of catatonia have been described, but the presence of two prominent features persisting for 24 h or longer is sufficient to identify the syndrome . Three forms of catatonia are generally described: retarded, excited and malignant. The retarded form presents with signs such as stupor, mutism and stereotyped movements, the excited form exhibits agitation and delirium, and the malignant form is marked by autonomic instability, which is often fatal . Even in the nonmalignant forms, catatonia requires immediate medical treatment due to possibility of severe complications. The etiologies of catatonia may be schizophrenia, mood disorders, general medical conditions, substance withdrawal, autism or idiopathic. Even street drugs such as ‘bath salts’ (i.e., cathiones) could cause catatonia . Catatonia was identified in 9.8 ± 1.4% (mean ± standard error of measurement) of adult admissions in 10 prospective studies from different sites around the world .