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Researchers proposed a hypothesis linking dysfunctions in the striatum and the dorsal diencephalic connection system (DDCS) to classic tardive dyskinesia (TD).
The following is a summary of “Putative role of immune reactions in the mechanism of tardive dyskinesia,” published in the November 2023 issue of Psychiatry by Loonen et al.
Extrapyramidal disorders (EPDs) encompass conditions like Parkinson’s disease and Huntington’s disease, as well as a range of extrapyramidal side effects (EPS) of antipsychotics, including tardive dyskinesia (TD).
Researchers conducted a retrospective analysis to summarize the current understanding of the association between cytokine levels and TD.
They discovered data through systematic searches on Pubmed and Embase. The constraints of these studies posed a significant hurdle to interpretation. Following the delineation of pertinent factors of the neuroinflammatory reactions and the neuroanatomical backgrounds of EPS, they introduced a new hypothesis for the origin of TD, emphasizing dysfunctions in the striosomal section of the striatum and the dorsal diencephalic connection system (DDCS).
The results showed a postulated increase in oxidative stress, partly immunologically induced, and a dopamine-dependent immune response in classic TD, primarily proceeding via the DDCS, activated from evolutionarily older parts of the forebrain. The choroid plexus of the third ventricle’s proximity to the habenula may contribute to neuroinflammatory responses.
Investigators concluded that while direct evidence for the role of inflammation in TD remains elusive, existing findings warrant further investigation of this potential link.
Source: sciencedirect.com/science/article/pii/S2666354623001011
