Unipolar depression is an episodic disorder characterized by decreased hedonic and motivational responsiveness to events previously associated with positive outcomes (Akiskal and McKinney, 1973
; Depue and Iacono, 1989
). These symptoms implicate dysfunction of incentive motivation and positive affectivity (Watson et al.
) that involve alterations in cognition and neurophysiology via multiple brain pathways and circuits (Davidson et al.
; Mayberg, 2003
Although there is broad evidence that depression is associated with disruption of appetitive/approach motivation (Dickson and MacLeod, 2004
; McFarland et al.
), most studies of motivational deficits in depression have focused on temperament-based mechanisms for approach and avoidance (Fowles, 1988
; Gray, 1994
). However, recent studies also suggest that dysfunction of self-regulation
, defined as the psychological and neurophysiological processes that underlie personal goal pursuit (Carver, 2004
), constitutes both a risk factor for and a consequence of depression (Kasch et al.
). The present study tested the hypothesis that depression would be associated with dysfunction in neural mechanisms underlying the representation and processing of two important classes of personal goals.
Regulatory focus theory (RFT) identifies two distinct classes of goals representing desired end-states toward which people self-regulate (Higgins, 1997
). The two types of goals are associated with different cognitive, motivational and strategic inclinations. Promotion
goals involve accomplishment, advancement or aspiration—that is, ‘making good things happen’. Prevention
goals involve security, safety or responsibility—that is, ‘keeping bad things from happening’. Pursuit of promotion and prevention goals involves strategic
rather than spatiotemporal approach and avoidance respectively and can be activated intentionally as well as automatically (e.g. when a stimulus ‘primes’ a goal representation). RFT predicts that perceived progress toward a promotion goal is associated with feelings of happiness while perceived failure is associated with sadness and dejection; in contrast, perceived progress toward a prevention goal leads to quiescence while perceived failure leads to agitation and anxiety (Higgins et al.
). Chronic perceived failure to attain promotion goals is associated with depressive symptoms, whereas failure to attain prevention goals is associated with symptoms of anxiety (Strauman, 1992
). The psychological mechanisms that underlie pursuit of promotion and prevention goals emerge during development primarily as a function of socialization (Manian et al.
) and can be distinguished reliably from the temperament-based mechanisms described in biobehavioral theories of approach and avoidance (Strauman and Wilson, in press).
Although there is considerable evidence from behavioral studies supporting the predictions of RFT regarding promotion and prevention goal pursuit, data regarding the neural correlates of promotion/prevention goal activation are just beginning to appear. Using EEG, Amodio and colleagues (2004
) found that chronic promotion focus was associated with greater left frontal activity while chronic prevention focus was associated with greater right frontal activity. Using functional magnetic resonance imaging (fMRI), Cunningham et al.
) found that individual differences in promotion/prevention focus were associated with patterns of neural activation in response to a valence judgment task. In a recent study, we used fMRI to identify brain regions activated during incidental priming of promotion and prevention goals (Eddington et al.
). Based on evidence of cortical asymmetry associated with individual differences in regulatory focus (Amodio et al.
), we predicted that promotion and prevention goal priming would be associated with activation in the left and right orbitofrontal cortices (OFC), respectively. Promotion goal priming discriminantly activated a region of left OFC (BA 11), and variability in activation of this region following promotion goal priming was correlated with individual differences in the strength of participants’ self-reported orientation to promotion goals.
To our knowledge, the Eddington et al.
study was the first to use fMRI to link idiographically assessed personal goal representation and priming with changes in cerebral blood flow in the OFC—a region implicated in decision making, in performance monitoring and in representing the hedonic value of primary as well as abstract (secondary) reinforcers (Kringelbach, 2005
). Furthermore, the left OFC activation following promotion goal priming was detected while participants were performing a task unrelated to personal goal pursuit, supporting the postulate of RFT that promotion and prevention goals, as highly accessible knowledge structures, can be activated implicitly. Other investigators have found evidence linking OFC with goal-pursuit-related cognitive and motivational processes such as integrating information regarding the current state of the organism with previously acquired social knowledge in order to guide behavioral choices and strategies (Furuyashiki and Gallagher, 2007
; Petrides, 2007
). Thus, the OFC may be an important component of a neural system that instantiates personal goal representations and, via interactions with other brain regions, determines incentive values and guides hierarchically organized goal-directed behaviors (Holland and Gallagher, 2004
If promotion goal priming is associated with left OFC activation, and individuals experiencing chronic failure to attain promotion goals are vulnerable to depressive symptoms, then depression might be characterized by a dysfunction in left OFC activation following promotion goal priming. Such a deficit would be consistent with behavioral findings linking chronic perceived failure in promotion goal pursuit with vulnerability to depression (Strauman, 2002
), as well as with the observation that compared with nondepressed controls, depressed individuals manifest decreased left OFC activation in response to affectively salient visual stimuli (Tremblay et al.
). In addition, recent clinical data indicated that a self-regulation-based treatment was differentially efficacious for patients diagnosed with primary major depressive disorder or dysthymic disorder characterized by chronically poor promotion goal pursuit (Strauman et al.
In the current study, we hypothesized that incidental priming of promotion goals during a social judgment task would reliably induce left OFC activation among individuals with no history of depression (replicating the findings of Eddington et al.
), but that depressed patients would show an attenuated left OFC response to promotion goal priming. We also hypothesized, consistent with previous studies showing frontal asymmetry related to negative/positive affectivity (Allen and Kline, 2004
; Davidson, 2004
) and with recent perspectives on depressive/anxious comorbidity (Strauman, 2002
; Watson, 2005
), that priming prevention goals would lead to increased activation in the right PFC in depressed patients, reflecting compensatory hypersensitivity to prevention goals due to hypoactivation of promotion goals (Strauman, 2002
). Finally, we predicted that despite these differences in response to personal goal priming, the two participant groups would show similar patterns of cortical activation in response to the judgment task itself.