Resting frontal electroencephalographic (EEG) asymmetry has been hypothesized as a marker of risk for major depressive disorder (MDD) but the extant literature is based predominately on female samples. Resting frontal asymmetry was assessed on 4 occasions within a two-week period in 306 individuals age 18-34 (31% male) with (n = 143) and without (n = 163) DSM-IV defined lifetime MDD. Lifetime MDD was linked to relatively less left frontal activity for both sexes using a current source density (CSD) reference, findings that were not accounted for solely by current MDD status or current depression severity, suggesting that CSD-referenced EEG asymmetry is a possible endophenotype for depression. In contrast, results for average and linked mastoid references were less consistent, but demonstrated a link between less left frontal activity and current depression severity in women.

Frontal electroencephalographic (EEG) alpha asymmetry is widely researched in studies of emotion, motivation, and psychopathology, yet it is a metric that has been quantified and analyzed using diverse procedures, and diversity in procedures muddles cross-study interpretation. The aim of this article is to provide an updated tutorial for EEG alpha asymmetry recording, processing, analysis, and interpretation, with an eye towards improving consistency of results across studies. First, a brief background in alpha asymmetry findings is provided. Then, some guidelines for recording, processing, and analyzing alpha asymmetry are presented with an emphasis on the creation of asymmetry scores, referencing choices, and artifact removal. Processing steps are explained in detail, and references to MATLAB-based toolboxes that are helpful for creating and investigating alpha asymmetry are noted. Then, conceptual challenges and interpretative issues are reviewed, including a discussion of alpha asymmetry as a mediator/moderator of emotion and psychopathology. Finally, the effects of two automated component-based artifact correction algorithms-MARA and ADJUST-on frontal alpha asymmetry are evaluated.

The role of interoception and its neural basis with relevance to drug addiction is reviewed. Interoception consists of the receiving, processing, and integrating body-relevant signals with external stimuli to affect ongoing motivated behavior. The insular cortex is the central nervous system hub to process and integrate these signals. Interoception is an important component of several addiction relevant constructs including arousal, attention, stress, reward, and conditioning. Imaging studies with drug-addicted individuals show that the insular cortex is hypo-active during cognitive control processes but hyperactive during cue reactivity and drug-specific, reward-related processes. It is proposed that interoception contributes to drug addiction by incorporating an “embodied” experience of drug uses together with the individual’s predicted versus actual internal state to modulate approach or avoidance behavior, i.e. whether to take or not to take drugs. This opens the possibility of two types of interventions. First, one may be able to modulate the embodied experience by enhancing insula reactivity where necessary, e.g. when engaging in drug seeking behavior, or attenuating insula when exposed to drug-relevant cues. Second, one may be able to reduce the urge to act by increasing the frontal control network, i.e. inhibiting the urge to use by employing cognitive training.