Catatonia as a Syndrome Characterized by GABAergic Interneuronal Dysfunction Mediated by NMDA Receptors

Abstract

Efforts to elucidate the pathophysiology of catatonia have hitherto been unsuccessful largely due to its variegated clinical presentation and seemingly disparate treatment modalities. Catatonia manifests with marked behavioral and cognitive changes, often producing a significant decrease in speech and motor output. Generally, catatonia can be treated with GABA-agonists with impressive symptomatic relief. ECT is also used as a second-line therapeutic intervention if GABA-agonists fail to produce significant symptomatic relief. However, there is uncertainty regarding additional treatment if the aforementioned therapeutic interventions fail to provide symptomatic relief. In the present paper, suggest utilizing pharmacotherapy that modulates NMDAR activity on the basis that catatonia can be fundamentally a syndrome characterized by excessive glutamatergic stimulation of NDMAR on cortical GABAergic interneurons leading to a dysregulation of horizontal and vertical processing.