Introduction

Bipolar disorder is a common psychiatric condition, affecting up to 3% of the world's population (Angst,1998; Narrow et al., 2002), and it is the sixth leading cause of disability worldwide (Murray and Lopez, 1996). Although bipolar disorder is defined by the occurrence of mania (type I disorder) or hypomania (type 2 disorder), in fact, the symptoms of bipolar disorder include affective instability, neurovegetative abnormalities, cognitive impairments, psychosis, and impulsivity. The likely neural basis of these symptoms, based on neuroimaging and other studies, has produced models of bipolar disorder that focus on dysfunction within so-called anterior limbic brain networks (Strakowski et al., 2004, 2005, 2007; Adler et al., 2006a; Brambilla et al., 2005). These networks consist of iterative prefrontal–striatal–pallidal–thalamic circuits that are modulated by amygdala and other limbic structures to direct social and emotional behaviors. An example of one such anterior limbic network model is provided in Figure 6.1 and is based on work that has been reviewed previously (Strakowski et al., 2005, 2007; Adler et al., 2006a). Indeed, recent advances in neuroimaging techniques, particularly those based on magnetic resonance imaging (MRI) and spectroscopy, have revolutionized the study of bipolar neurophysiology, leading to a proliferation of studies attempting to clarify the neural substrates of bipolar disorder.

One approach toward evaluating and extending functional neuroanatomic models of bipolar disorder is to use brain imaging to determine whether structural brain abnormalities within relevant networks can be identified.