According to Campanella and colleagues (2011), electrophysiological methods can guide the clinician to optimize the medication regimen tailored to a patient’s cognitive profile and adopt a kind of “personalized medicine” (Campanella et al. 2011). For example, alcoholic patients with attentional biases toward alcohol cues (indexed by increased P100 to probes replacing drug cues), but with intact inhibitory processes (indexed by normal No-Go P3 component), may hypothetically benefit more from acamprosate (which regulates the increased cerebral glutamate activity by restoring the balance between excitatory and inhibitory neurotransmission), by reducing the hyperexcitability that occurs during early abstinence. However, alcoholic patients with a reversed cognitive pattern (i.e., a deficient inhibitory mechanism with altered No-Go P3 but without any attentional biases toward alcohol cues indexed by normal P100) will likely improve with naltrexone (an opioid antagonist which blocks the release of alcohol-induced dopamine), which reduces or eliminates the positive reactions associated with the urge to drink and inhibits a dominant response (drinking) by reducing the reinforcing/reward effects of alcohol (Campanella et al. 2011). Although these hypothesized applications are intriguing, more studies are needed to
