Bipolar disorder (BD) affects about 1% of the population worldwide and is characterized by extreme variations in mood, motivation, and arousal (Belmaker, 2004). BD is distinguished from unipolar depression by the occurrence of manic or hypomanic symptoms during one or more episodes of the illness. Disturbances of gamma-amino butyric acid (GABA) (Benes and Berretta, 2001; Benes et al., 2000; Petty, 1995; Shiah et al., 1998), monoaminergic (Zubieta et al., 2000) and second messenger systems have been implicated in BD, but the underlying cellular mechanisms remain poorly understood (Belmaker, 2004). Neurobiological markers that are sensitive to the illness might provide a bridge between behavioral and neurobiological abnormalities (Lenox et al., 2002). Accumulating evidence suggests that disturbances in connectivity among brain regions may contribute to brain dysfunction in BD. Deep white matter (WM) hyperintensities are frequently observed in T2-weighted magnetic resonance imaging (MRI) (Kempton et al., 2008). Meta-analysis of whole-brain diffusion tensor imaging (DTI) studies demonstrated decreased fractional anisotropy (FA) affecting the right hemisphere WM near the parahippocampal gyrus and cingulate cortex (Vederine et al., 2011). Because signaling among brain regions is
