Despite an extensive body of research examining brain-behavior relationships underlying Antisocial Personality Disorder (APD), the findings have neither been consistent in terms of the strengths of these relationships nor the underlying mechanisms or processes being studied. This is because APD is comprised of a heterogeneous constellation of symptoms, and includes dimensions of implicit personality characteristics (lacking empathy and egocentricity) and explicit behaviors (impulsivity and poor behavioral control), which in turn are driven by cognitive (poor executive functioning and inhibition) and affective (lack of emotion) deficits. Dinn and Harris (2000) suggest that different manifestations of APD are best explained by deficits in different parts of an interactive network, as opposed to localized areas in the frontal lobe or amygdala. This paper argues that two theories in particular are useful for understanding this neuropathophysiology, and how dysfunction in different areas of the brain accounts for various manifestations of APD: 1) Damasio's (1996) Somatic Marker Hypothesis, and 2) Baron-Cohen's (1998) Social Cognition Model.