Impulsivity and neural correlates of response inhibition in bipolar disorder and their unaffected relatives: A MEG study

Abstract

BackgroundResponse inhibition is a core cognitive impairment in bipolar disorder (BD), leading to increased impulsivity in BD. However, the relationship between the neural mechanisms underlying impaired response inhibition and impulsivity in BD is not yet clear. Individuals who are genetically predisposed to BD give a way of identifying potential endophenotypes. MethodsA total of 97 participants, including 39 patients with BD, 22 unaffected relatives (UR) of patients with BD, and 36 healthy controls performed a Go/No-Go task during magnetoencephalography. We carried out time-frequency and connectivity analysis on MEG data. ResultsDecreased beta power, prolonged latency and increased peak frequency in rIFG, decreased beta power in pre-SMA and reduced rIFG-to-pre-SMA connectivity were found in BD relative to healthy controls. In the UR group, we found a decrease in the beta power of pre-SMA and prolonged latency of rIFG. Furthermore, increased motor impulsiveness in BD was related to abnormal alterations in beta oscillatory activity of rIFG and functional connectivity between rIFG and pre-SMA. ConclusionsHypoactivity activity in rIFG and impaired dominant role of rIFG in the prefrontal control network may underlie the neuropathology of response inhibition dysfunction, resulting increased motor impulsivity in BD. Our findings point to measuring rIFG dysfunction as a potential means of identifying individuals at genetic high risk for transition to BD disease expression.