Catatonia and the immune system: a review

Area of Science:

• Neuroscience
• Immunology
• Psychiatry

Background:

• Catatonia is a psychomotor disorder characterized by stupor, posturing, and echophenomena.
• Immune dysregulation is increasingly implicated in the pathophysiology of catatonia.
• The neurovegetative features of catatonia, such as mutism and psychomotor retardation, may involve innate immune system activation.

Purpose of the Study:

• To examine the evidence linking immune dysregulation to catatonia.
• To explore the role of innate and autoimmune processes in catatonic symptoms.
• To investigate the association between N-methyl-D-aspartate receptor (NMDAR) encephalitis and catatonia.

Main Methods:

• Review of existing literature on immune system activation in catatonia.
• Analysis of evidence for acute-phase reactant involvement.
• Examination of infectious and autoimmune causes of catatonia, with a focus on NMDAR encephalitis.

Main Results:

• Evidence for acute-phase immune activation in catatonia is sparse and conflicting, with its relation to immobility unclear.
• Infections, particularly central nervous system infections, are associated with catatonia.
• N-methyl-D-aspartate receptor (NMDAR) encephalitis is the most common cause of autoimmune catatonia, presenting the full spectrum of symptoms.

Conclusions:

• Autoimmunity, specifically NMDAR encephalitis, is a significant cause of catatonia.
• Autoimmune catatonia may result from specific antibody actions rather than systemic inflammation.
• The link with NMDAR encephalitis supports a hypothesis of glutamatergic hypofunction in catatonia.