Catatonia is currently viewed as a unique syndrome that consists of specific motor signs responding to benzodiazepines and electroconvulsive therapy (ECT). Advances in catatonia may provide a new window into the mechanism of ECT. Findings on catatonia are updated and related to the mechanism of ECT.
Selective literature review.
There are several putative models and mechanisms of catatonia concerning motor circuitry dysfunction, abnormal neurotransmitters, epilepsy, genetic risk factors, and endocrine and immune dysfunction. Fear and vagal nerve models are presented casting catatonia in an evolutionary-based autonomic neural substrate of social behaviors, engagement, and disengagement according to perceived level of danger. Benzodiazepines and ECT are thought to have autonomic and vagal effects.
Advances in catatonia provide a new window into the mechanism of ECT. Fear and vagal nerve models call for further anatomical, functional, and clinical studies on the vagal nerve and for further studies on the use of anticholinergic medications in catatonia, on vagal function in catatonia, and on the effects of benzodiazepines, ECT, and induced seizures on cholinergic and vagal function.
From the Department of Psychiatry, University of Mississippi Medical Center, Jackson, MS.
Received for publication January 3, 2014; accepted March 17, 2014.
Reprints: Dirk M. Dhossche, MD, PhD, Department of Psychiatry, University of Mississippi Medical Center, 2500 North State St, Jackson, MS 39216 (e-mail: firstname.lastname@example.org).
This work received no funding.
The author has no conflict of interest or financial disclosures to report.