Event Related Potential Abnormalities in Major Depression Disorder Paper

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Event-related potential (ERP) abnormalities in major depression disorder (MDD): From cognition to motivation

In a typical P300 task, participants listen to frequent standard sounds, and must count or respond to relatively infrequent target sounds; the P300 is evident 300 to 500 ms following infrequent target stimuli as an increased positive potential at parietal sites. Bruder and colleagues report a mean effect size (i.e., Cohen’s d) of .85 across many studies documenting a reduced P300 in MDD and link this abnormality to cognitive deficits in depression: the increased P300 to targets has been postulated to reflect cognitive processes that include memory and related constructs such as context updating [4].

An increased P300 has also been observed following the presentation of emotional compared to neutral stimuli [5]-[7]. When participants view both pleasant and unpleasant compared to neutral stimuli, the ERP is also characterized by a sustained positivity at midline parietal sites that has been referred to as the late positive potential [LPP; 8]. We have argued that the P300 and LPP both reflect attentional engagement with salient environmental stimuli – and that salience can be determined by either task relevance (e.g., in an oddball task) or stimulus content (Proudfit, Jackson, Ferri, & Weinberg, in press). We focus on the LPP in this paper; our view is that the reduced LPP in MDD may reflect deficits in attentional engagement with salient environmental stimuli, and might best be understood in terms of emotional and motivational abnormalities.

Very early studies using emotional words reported that individuals with MDD had a reduced LPP to both pleasant and unpleasant emotional words—but the LPP did not differ in response to neutral words [9]. Using pictures of dermatological disease, Kayser and colleagues [10] found that patients with MDD were characterized by a reduced LPP to unpleasant pictures.

These early studies are supported by a growing body of literature indicating that both clinical diagnoses of depression and depressive symptoms are associated with reduced LPPs to positive and negative emotional stimuli in children and adults. For example, in a passive viewing paradigm, adults with MDD exhibited reduced LPPs to angry and fearful faces compared to healthy controls [11]. Relatedly, in clinical samples, depression predicted blunted LPPs to both unpleasant and pleasant emotional scenes (A MacNamara et al., in preparation; A Weinberg et al., in preparation). The effects of depression on the LPP appear to be most apparent for participants with an early onset depression (i.e., before age 18) or suicidality (A Weinberg et al., in preparation). Little work has evaluated the LPP and depression across development; however, there is evidence of similar patterns in youth, with greater depressive symptoms associated with a reduced LPP to threatening faces in children and adolescents (A Kujawa et al., under review).

Lastly, reduced LPPs to positive and negative emotional faces and scenes have been observed among never-depressed offspring of parents with histories of depression, even in children as young as six years old [14; Nelson B et al., under review], suggesting that the LPP may be a vulnerability marker for depression. That is, reduced emotional reactivity is evident before the onset of depression in at-risk youth, and the LPP could be useful for identifying children most in need of prevention and early intervention.

Reward dysfunction in anhedonia

A defining feature of MDD is anhedonia, defined as markedly diminished interest or pleasure in normally enjoyable activities. In recent years, there has been growing interest in translating findings from basic neuroscience to characterize anhedonia in terms of dysfunction in reward-related brain circuitry, and in anhedonia as a potential endophenotype for MDD [15]. ERP research in this area has focused primarily on the electrocortical differentiation at frontocentral electrode sites that occurs approximately 300 ms following feedback indicating monetary reward versus loss. After losses, the ERP is characterized by an N2-like negative deflection previously referred to as the feedback negativity, or FN; following reward, a relative positivity (the Reward Positivity or RewP) is observed [16]. The RewP amplitude captures sensitivity to reward outcomes, and is correlated with indicators across other units of analysis, including self-reported reward sensitivity and reward learning behavior [17]. Source localization and combined ERP/fMRI indicate that RewP amplitude reflects—either directly or indirectly—activation of the basal ganglia by reward delivery [18-21].

Recent studies consistently demonstrate that RewP amplitude is a neurophysiological indicator of diminished reward sensitivity in MDD. In non-clinical samples, RewP amplitude is blunted among individuals with depressive symptomatology [22], an effect which is driven specifically by reduced neural activity to monetary gains [23]. In clinical samples, RewP amplitude is blunted in patients with an MDD diagnosis compared to never-depressed controls [24,25]. These studies are consistent with fMRI findings of reduced activity in reward circuitry, including the dorsal/ventral striatum and orbitofrontal cortex [15]. Moreover, RewP amplitude is also associated with variability in reward functioning within MDD samples: In one study of patients with MDD, reduced RewP amplitude was associated with severity of self-reported anhedonia, even after adjusting for illness severity [24]. In a separate clinical study, the effect of MDD diagnosis on RewP amplitude was found to be driven by a subgroup of patients who reported impaired mood reactivity to positive life events, a core feature of melancholic MDD—but not the full, DSM-defined melancholic subtype [25]. These data suggest that reduced RewP amplitude may be a biomarker for an anhedonic/melancholic phenotype, accounting for heterogeneity within MDD populations that is not captured by the current diagnostic system.

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