Childhood Adversity Is Associated with Left Basal Ganglia Dysfunction During Reward Anticipation in Adulthood

Functional MRI studies show differences in centrally-driven reward processing that could mediate ELA-related risk of psychopathologies and substance use-related illnesses.

“Functional MRI studies show differences in centrally-driven reward processing that could mediate ELA-related risk of psychopathologies and substance use-related illnesses [40, 41].”

Similar findings have been observed in prospective cohorts following childhood adversity, suggestive of a possible causal relationship between childhood adversity and alterations of the dopamine system.

“and similar findings have been observed in prospective cohorts following childhood adversity (Dillon et al., 2009) suggestive of a possible causal relationship between childhood adversity and alterations of the dopamine system.”

People with a history of early-life maltreatment show dampened behavioral reward responsiveness and reduced activation in striatal structures.

“Dillon et al., (2009) found that participants with a history of early-life maltreatment displayed dampened behavioral responsiveness to reward and reduced activation in striatal structures.”

Previous reports suggest decreased striatal activity during reward anticipation in adults and adolescents with a history of childhood adversity.

“Our finding of reduced activation in the ventral striatum is largely consistent with previous reports, suggesting decreased striatal activity during reward anticipation in adults and adolescents with a history of childhood adversity.36–39”

A previous fMRI study showed significantly decreased left basal ganglia activity during reward anticipation, which was associated with anhedonia symptoms in adulthood.

“Similarly, a previous fMRI study assessing the effects of early-life maltreatment on reward-related learning37 showed significantly decreased left basal ganglia activity during reward anticipation, which was associated with anhedonia symptoms in adulthood.”

Four monetary incentive delay studies reported lower basal ganglia activity during reward anticipation in people exposed to institutionalization or early adversity before adolescence.

“Using the monetary incentive delay task, four studies demonstrated decreased activity in regions of basal ganglia during the anticipation phase, suggesting reduced approach motivation in individuals who were exposed to institutionalization or early life adversity prior to adolescence (Boecker et al., 2014; Boecker-Schlier et al., 2016; Dillon et al., 2009; Mehta et al., 2010).”

Two studies reported longer reaction times on the monetary incentive delay task in people with prior ELS, while children with reactive attachment disorder had shorter reaction times on a gambling task; other studies either did not assess behavior or found no differences.

“Dillon et al. (2009) and Boeker et al. (2014) found increased reaction times in individuals with prior ELS in the monetary incentive delay task, while decreased reaction times were noted in children with reactive attachment disorder in a gambling task (Takiguchi et al., 2015), although the remainder of studies either did not measure behavior (Casement et al., 2015, 2014; Goff et al., 2013; Hanson”

Many human studies link lower basal ganglia activation during reward anticipation or receipt to depressive symptoms, and this activation often mediates the ELS-depression relationship.

“in many of the human studies reviewed, decreased activation in regions of the basal ganglia to the anticipation or receipt of reward was not only associated with depressive symptoms (Dillon et al., 2009; Goff et al., 2013), but often found to mediate the relationship between ELS and depression (Corral-Frías et al., 2015; Hanson et al., 2015).”

fMRI studies have linked ELA to blunted subjective responses to reward-predicting cues and to altered connectivity in the extended reward network, leading to increased vulnerability to FA and obesity later in life.

“Functional magnetic resonance imaging (fMRI) studies have linked ELA to blunted subjective responses to reward-predicting cues [29], and to altered connectivity in the extended reward network, leading to increased vulnerability to FA and obesity later in life [30].”

Functional magnetic resonance imaging studies have linked early life adversity to blunted subjective responses to reward-predicting cues and dysfunction in the left basal ganglia regions implicated in reward-related learning and motivation.

“Functional magnetic resonance imaging (fMRI) studies have linked ELA to blunted subjective responses to reward-predicting cues and dysfunction in the left basal ganglia regions implicated in reward-related learning and motivation [121].”

This case illustrates the link between ELA and FA which is likely mediated by biological mechanisms including altered DA signaling.

“This case illustrates the link between ELA and FA which is likely mediated by biological mechanisms including altered DA signaling [121,122,192,193,194].”

ELA leads to weaker reward responsivity, and deprivation may increase substance use to overcome this blunted reward response.

“Behavioral and neurobiological studies indicate that ELA leads to blunted reward responsivity (i.e. lower neural response to reward in reward-processing brain regions such as the ventral striatum (VS)), an effect that persists across the lifespan.67–70”