Delirium in hospitalized and intensive care unit patients is an emerging condition due to its rapid-onset requiring fast action to mitigate a worse clinical outcome. Although several causes and conditions are known, the association between delirium and neural autoantibodies has often been neglected in cohort studies and reviews as causing delirium. The aim of our review is to delineate the occurrence and type of neural autoantibodies and to depict other biological markers of autoimmunity in relationship to delirium.
For this narrative review Pubmed research was done to select articles about delirium and neural autoantibodies.
We can report on several cell-surface autoantibodies such as anti-α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors, anti-contactin associated protein 2, anti-Leucin rich glioma inactivated protein 1, anti-dipeptidyl-peptidase-like 6 protein, anti-glycine receptor and anti-myelin autoantibodies, as well as intracellular autoantibodies such as anti-glutamic acid decarboxylase 65 (GAD65), anti-CV2 and anti-Hu associated with delirium in patients. Our case reports and case series screening revealed that 20 of 63 patients with delirium presented neural autoantibodies, thus revealing a 32% frequency of autoantibody-associated delirium in delirium patients. Our main finding is that delirium’s hyperactive form is associated with neural autoantibodies. Diagnosing delirium differentially is difficult, as in patients with delirium and GAD65 autoantibodies, as it must be distinguished from other psychopathological excitation states such as mania. We also describe autoimmune delirium’s potential pathophysiologic pathways.
The existence of neural autoantibodies in delirious patients is scientifically and clinically highly relevant in its diagnosis, therapy, and pathogenesis. More large-scale studies should be conducted to evaluate their significance and prevalence in delirium.

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