Neurophysiological biomarkers of response inhibition and the familial risk for borderline personality disorder

Abstract

Understanding of the biological factors that run in families affected with borderline personality disorder (BPD) is limited. The authors investigated the familial aggregation of neurophysiological biomarkers of response inhibition in the first-degree biological relatives of probands with BPD and associations with psychiatric diagnosis and impulsive traits. In the present study, psychiatric diagnoses and impulsive traits were measured in BPD probands (n = 86), psychiatrically affected and non-affected relatives (n = 60) and controls (n = 83). While undergoing neuroimaging using functional near-infrared spectroscopy, prefrontal cortex (PFC) activation was measured during a go/no-go response inhibition task and compared between probands, relatives and controls. Additionally, non-psychiatrically affected relatives and controls were contrasted to examine the potential impact of familial risk for BPD on response inhibition-related PFC activation in the absence of confounding psychiatric morbidity. Probands showed bilateral decreases in PFC activation during response inhibition compared to relatives and controls. Conversely, both affected and non-affected relatives displayed higher activation than controls and probands in left lateral/medial and right medial PFC, although non-affected relatives showed a lesser extent of activation than affected relatives. Probands and controls reporting greater impulsive traits displayed deactivation across the PFC during response inhibition, whereas relatives showed increased activation. In this first family study of neuroimaging biomarkers in BPD, we show that the familial risk for BPD is reflected in activation of the PFC during response inhibition, with lifetime psychiatric diagnosis and higher impulsive traits in relatives associated with larger increases in PFC activity. Higher PFC activity during response inhibition including among non-affected relatives could reflect a neurophysiological compensatory mechanism.