Invited ReviewEtiopathogenesis of Catatonia: Generalizations and Working HypothesesDhossche, Dirk M. MD, PhD*; Stoppelbein, Laura PhD*; Rout, Ujjwal K. PhD†Author Information From the Departments of *Psychiatry & Human Behavior and †Surgery, University of Mississippi Medical Center, Jackson, MS. Received for publication September 6, 2010; accepted September 8, 2010. Reprints: Dirk M. Dhossche, MD, PhD, Department of Psychiatry, University of Mississippi Medical Center, 2500 N State St, Jackson, MS 39216 (e-mail: firstname.lastname@example.org). There was no financial support received for this study. The authors have no proprietary or commercial interest to report. The Journal of ECT: December 2010 - Volume 26 - Issue 4 - p 253-258 doi: 10.1097/YCT.0b013e3181fbf96d Buy Metrics Abstract Catatonia has been rediscovered over the last 2 decades as a unique syndrome that consists of specific motor signs with a characteristic and uniform response to benzodiazepines and electroconvulsive therapy. Further inquiry into its developmental, environmental, psychological, and biological underpinnings is warranted. In this review, medical catatonia models of motor circuitry dysfunction, abnormal neurotransmitters, epilepsy, genetic risk factors, endocrine dysfunction, and immune abnormalities are discussed. Developmental, environmental, and psychological risk factors for catatonia are currently unknown. The following hypotheses need to be tested: neuroleptic malignant syndrome is a drug-induced form of malignant catatonia; Prader-Willi syndrome is a clinical GABAergic genetic-endocrine model of catatonia; Kleine-Levin syndrome represents a periodic form of adolescent catatonia; and anti-N-methyl-d-aspartate receptor encephalitis is an autoimmune type of catatonia. © 2010 Lippincott Williams & Wilkins, Inc.