“…Conversely, a subgroup of patients to whom alcohol acts as negative reinforcer, potentially because of elevations of brain glutamate levels should respond best to a compound known for its antiglutamatergic action (e.g., acamprosate). Moreover, earlier publications reported drug mechanisms and "putative subgroup dysfunction" [1], such as the role of alcohol-cue-induced brain activation in the ventral striatum as a predictor of naltrexone response [4], as well as the acoustic startle response to distinguish between naltrexone and acamprosate responders [5].…”