In addition, emerging concepts in neuroimaging studies have suggested that pathophysiology of AUD involves the interaction of motivational, affective, and cognitive processes and multiple brain regions, rather than impairment in solely the cognitive process (5, 10). This is further supported by the clinical manifestation of AUD that includes a variety of symptoms such as disrupted reward anticipation, negative emotionality, dysfunctional cue reactivity, impulsivity, and compulsivity in addition to impaired executive function (5). Thus, there is a significant need for clinical and research work to comprehensively identify the alteration in neural networks relevant to motivational, affective, and cognitive processes to understand the neurophysiological mechanisms underlying the multiple symptoms of AUD.
