Immune Dysfunction and Catatonia

Catatonia is a neuropsychiatric disorder affecting movement, speech and complex behaviour. There is no unified theory of the pathophysiology of catatonia and concepts mostly rely on the effects of GABA-ergic and glutamatergic therapies. Several movement disorders have an established autoimmune aetiology, or at least an inflammatory component to pathophysiology, these include: stiff person syndrome and Sydenham’s chorea. Numerous suspected infective organisms have been associated in the literature with the development of catatonia, most of which are organisms known to affect the central nervous system. In addition, a wide range of inflammatory disorders have been associated with catatonia, though the vast majority of reported cases are accounted for by NMDA receptor encephalitis. A number of cases have also been reported in association with systemic lupus erythematosus. Raised creatine kinase and reduced serum iron have been reported in several studies of catatonia, but there is little evidence for raised peripheral inflammatory markers. We conclude that catatonia may not have a unifying pathophysiology, but it does appear that there is a subgroup of patients where autoimmunity plays a role, potentially through actions on glutamatergic pathways. Future studies must compare inflammatory and neuroimmunological markers amongst large cohorts of individuals with and without catatonia.