Studies involving human subjects with chronic alcohol use have demonstrated reduced hippocampal volume (85–87), postmortem evidence of prior neuronal loss (88), and severely reduced hippocampal activity, including reductions in blood flow (89). Recently, one study comparing mild and heavy drinkers demonstrated no significant impairment of general cognition but an increased fMRI blood-oxygen-level-dependent (BOLD) response, an indicator of regional activity, in the hippocampus during correct responses to the visual encoding and memory task, implying a compensatory mechanism for cognitive function (90). However, tasks capable of identifying explicit hippocampal-sensitive cognitive impairments in adults, particularly those with substance dependency issues, are scarce beyond those investigating episodic memory. Episodic memory, or the function of remembering events in specific spatial and temporal context (in contrast to factual or semantic memory), is an important hippocampal function in humans (91, 92) and has been demonstrated to be significantly impaired in alcoholic patients (93–96). However, it should be noted that as described by Noel et al. (96), episodic memory is also sensitive to alcohol-induced damage to the PFC, so the findings of reduced episodic memory function cannot be explicitly attributed to impaired hippocampal function.
