Understanding the pathophysiology of postpartum psychosis: Challenges and new approaches

Abstract

Postpartum psychosis is a severe psychiatric condition which affects 1-2 of every 1000 mothers shortly after childbirth. Whilst there is convincing evidence that the condition is precipitated by a complex combination of biological and environmental factors, as yet the pathophysiological mechanisms remain extremely poorly defined. Here, I critically review approaches that have been, or are being, employed to identify and characterise such mechanisms; I also review a recent animal model approach, and describe a novel biological risk model that it suggests. Clarification of biological risk mechanisms underlying disorder risk should permit the identification of relevant predictive biomarkers which will ensure that “at risk” subjects receive prompt clinical intervention if required.

Keywords: CCN3; Immune system; Steroid sulfatase; Nephroblastoma-overexpressed; Mouse; Animal model; Risk factor

Core tip: Postpartum psychosis is a severe psychiatric condition affecting a small proportion of women shortly after childbirth. The pathophysiological mechanisms underlying risk for the condition are extremely poorly-defined, but may include perturbed immune function, altered tryptophan metabolism and serotonergic dysfunction. Here, I critically review evidence underlying these assumptions, and discuss a novel model for postpartum psychosis risk, involving maternal deficiency for the enzyme steroid sulfatase, and overexpression of the CCN gene family, based upon emerging data from a recently-developed mouse animal model. Identifying and characterising predictive biomarkers for postpartum psychosis risk will help to ensure prompt clinical intervention if required.