This may not be surprising if the brain is viewed as having been constructed quintessentially for the processes of learning and remembering in order to enhance adaptation and survival efficacy. The diverse and spatially distributed neural systems subserving a great variety of learning and memory systems can give rise to equally numerous and diverse illnesses.

For example, attention deficit hyperactivity disorder (ADHD) has been conceptualized as a disturbance in emotional and reward-based learning, given the difficulty that children with ADHD have learning from prior mistakes, as well as their poor performance on delay aversion tasks, their preferences for smaller immediate rewards over larger delayed ones, and their more frequent risk-taking behaviors (Farmer and Peterson, 1995; Oosterlaan and Sergeant, 1998; Sonuga-Barke, Taylor, et al., 1992). Localized reductions in volumes of the amygdala have been reported in ADHD, primarily over the basolateral nuclear complex (Plessen et al., 2006). Structural disturbances in the basolateral complex may disrupt emotional learning and the affective drive to sustain attention to otherwise mundane sensory stimuli (Cardinal, Parkinson, et al., 2002; Holland and Gallagher, 1999). The basolateral complex is densely connected with the inferior prefrontal cortex (Baxter and Murray, 2002), another region in which reduced volumes have been reported in youth with ADHD (Sowell, Thompson, et al., 2003). Limbic-prefrontal circuits support the ability to tolerate delayed rewards and to suppress unwanted behaviors (Elliott, Dolan, and Frith, 2000), areas of difficulty that are defining hallmarks of ADHD (Barkley, Cook, et al., 2002; Rowland, Lesesne, and Abramowitz, 2002).

Disturbances in the extinction of conditioned fear responses have been postulated in the pathogenesis of a wide range of anxiety disorders. For example, fear is a normative response following exposure to trauma, and in most individuals it soon extinguishes completely. In a minority of individuals, however, fear will fail to extinguish, and they subsequently manifest symptoms of posttraumatic stress disorder (PTSD) (Yehuda, Flory, et al., 2006). Consequently, PTSD has been conceptualized as a disturbance of insufficient inhibitory control over conditioned fear responses (Liberzon and Sripada, 2008; Yehuda et al., 2006). Human imaging studies of PTSD patients have reported (1) exaggerated amygdala responses to a variety of emotional stimuli, presumably representing exaggerated fear responses; (2) deficient activation of frontal cortices, which is thought to mediate disordered fear extinction and impaired suppression of attention to trauma-related stimuli; and (3) reduced volumes and deficient activation of the hippocampus, which may mediate deficits in recognizing safe contexts (Bremner, Elzinga, et al., 2008; Rauch, Shin, and Phelps, 2006). Similar circuit-based disturbances have been postulated in other pediatric anxiety disorders, and they are thought to account for the minority of children whose anxiety disorders do not remit by adulthood (Pine, 2007). Preclinical and clinical studies have suggested that cognition-

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