- Email: [email protected]
6.3 Effects of Trauma Exposure on Fear Inhibition Circuitry in the Developing Brain
SYMPOSIA 6.1 — 6.4
6.1 AUTOBIOGRAPHICAL MEMORY AND LATENT VULNERABILITY TO PSYCHIATRIC DISORDER FOLLOWING CHILDHOOD MALTREATMENT Eamon McCrory, PhD, PsyD, University College London, e. [email protected] Objectives: Altered autobiographical memory (ABM) functioning has been implicated in the pathogenesis of depression and PTSD and may represent one mechanism by which childhood maltreatment elevates psychiatric risk. The aim of the current study was to investigate the impact of childhood maltreatment on ABM functioning. Methods: ABM functioning was investigated in 67 children: 34 with maltreatment experiences documented by social services (MT group); and 33 nonmaltreated comparison children matched on age, gender, handedness, pubertal status, IQ, and socioeconomic status. All participants performed a standard Autobiographical Memory Task (AMT) to assess over-general memory outside the scanner. Participants also recalled specific ABMs in response to emotionally valenced cue words during fMRI. Results: Maltreated children showed greater recall of over-general memories on the AMT, even in the absence of overt psychopathology, relative to nonmaltreated peers [t(55) ¼ 2.46, P ¼ 0.02]. The MT group also showed reduced hippocampal and increased middle temporal and parahippocampal activation during positive ABM recall compared with peers. During negative ABM recall, they exhibited increased amygdala activation and greater amygdala connectivity with brain regions critical for processing salience. Conclusions: Childhood maltreatment is associated with altered ABM functioning, specifically reduced activation in areas encoding specification for positive memories, and greater activation of the salience network for negative memories. This pattern may confer latent vulnerability to future depression and PTSD.
CAN, IMAGS, PSP http://dx.doi.org/10.1016/j.jaac.2017.07.606
6.2 HARSH PHYSICAL PUNISHMENT AND AGGRESSION: NEUROBIOLOGICAL MEDIATORS AND INFLUENCES OF OTHER FORMS OF ENVIRONMENTAL RISK W. Dustin Albert, PhD, Bryn Mawr College, walbert@ brynmawr.edu Objectives: Consistent links exist between harsh physical punishment during childhood and risk for later aggressive and violent behavior in adolescence. Recent work has focused on how changes in brain regions such as the amygdala may mediate the linkage between harsh physical punishment and later aggression and violence. Past research has found that forms of early life stress, such as child maltreatment, are related to higher amygdala activity to facial displays of threat, but few links have been reported between amygdala activity and problem behavior in these sample groups. Methods: We tested links between childhood exposure to harsh physical punishment, amygdala activity, and aggressive behavior in adolescence, using data from a longitudinal study of individuals followed from middle childhood (n ¼ 73; 43 males; mean age at scan ¼ 15.4 years). Unique to the work, we sought to examine harsh physical punishment, as well as other sociodemographic and parenting risk factors. To evaluate amygdala activity, we used a well-validated, face-matching neuroimaging task with facial displays of threat. Results: In line with past reports, exposure to harsh physical punishment during childhood was related to heightened right amygdala reactivity in adolescence (b ¼ 0.34, P ¼ 0.018). Interestingly, amygdala reactivity (left and right) was not related to other risk factors, including household income, parental rejection, and parental hostility (all P > 0.27). Next, higher amygdala reactivity was related to greater aggressive behavior, as assessed by higher delinquency, higher aggression, and lower prosocial behavior (b ¼ 0.34, P < 0.005). Finally, using statistical mediation, amygdala reactivity partially explained the connection between early harsh physical punishment and aggressive and violent behavior in adolescence (z ¼ 2.06, P ¼ 0.04).
JOURNAL OF THE AMERICAN ACADEMY OF CHILD & ADOLESCENT P SYCHIATRY VOLUME 56 NUMBER 10S OCTOBER 2017
Conclusions: These results provide increased understanding of the deleterious effects of harsh physical punishment. We replicated past reports showing heightened amygdala activity in relation to harsh physical punishment. We also note how variations in amygdala activity were not associated with other sociodemographic and parenting risk factors. These findings provide important directions for future investigations aimed at understanding how various forms of stress and environmental experiences can become embedded in our neurobiology.
AGG, CAN, IMAGS Supported by NIDA Grants R01DA033369, R01DA031579, P30DA023026, and P30DA027827 and Eunice Kennedy Shriver National Institute of Child Health and Human Development Grant T32HD0737625 http://dx.doi.org/10.1016/j.jaac.2017.07.607
6.3 EFFECTS OF TRAUMA EXPOSURE ON FEAR INHIBITION CIRCUITRY IN THE DEVELOPING BRAIN Tanja Jovanovic, PhD, Emory University, [email protected] Objectives: Impaired inhibition is increasingly considered a biomarker of PTSD, and prior research has demonstrated a possible shared neural circuitry for fear and response inhibition in traumatized adults. Childhood trauma has been associated with impaired inhibition; however, most neuroimaging studies have been retrospective. The current study investigated the effects of violence exposure on brain activation during an emotional response inhibition task in children and whether altered brain response was associated with impaired fear inhibition. Methods: Children (N ¼ 40) were recruited from an ongoing study in an African American, highly traumatized, inner-city population. Participant measures included the following: trauma interviews using the Violence Exposure ScaleRevised (VEX-R); PTSD symptom assessment using the University of California, Los Angeles (UCLA) PTSD Reaction Index (PTSD-RI); an emotional Go/NoGo fMRI task; and a fear-potentiated startle task. The amygdala, ventromedial prefrontal cortex (vmPFC), and hippocampus were used as regions of interest for our analyses. Fear-potentiated startle was measured using electromyography recordings of the eyeblink muscle during a differential fear conditioning task. Results: The average VEX-R total score was 9.89, and the average PTSD-RI score was 16.71, with none of the children meeting the criteria for PTSD based on a UCLA cutoff score of 38. Positive associations were found between violence exposure and activation in amygdala (r ¼ 0.47, P < 0.02), vmPFC (r ¼ 0.41, P < 0.05), and hippocampus (r ¼ 0.50, P ¼ 0.01) during response inhibition (NoGo > Go), as well as between violence exposure and amygdala (r ¼ 0.46, P < 0.02) and hippocampus (r ¼ 0.45, P < 0.02) activation during emotional response inhibition (NoGo Fear > Go Neutral). vmPFC activation during emotional response inhibition was negatively correlated with fearpotentiated startle to a conditioned safety cue (r ¼ 0.51, P < 0.05). Conclusions: The association of decreased vmPFC activation with increased fear-potentiated startle to safety presents a possible shared neural circuitry for response and fear inhibition in children. Increased amygdala, vmPFC, and hippocampal activation, with violence exposure in this high-trauma, low-symptom population, may represent adaptive responses at this stage of development, although longitudinal research is required to determine their future effects.
AGG, COG, IMAGS Supported by NIMH Grant R01MH100122 and a NARSAD Independent Investigator Grant http://dx.doi.org/10.1016/j.jaac.2017.07.608
6.4 EPIGENETIC ABNORMALITIES ASSOCIATED WITH ALTERED EMOTION PROCESSING CIRCUITRY IN PEDIATRIC POSTTRAUMATIC STRESS DISORDER Ryan Herringa, MD, PhD, University of Wisconsin School of Medicine and Public Health, [email protected] Objectives: Epigenetic changes represent candidate mechanisms contributing to PTSD in youth. Studies of adult PTSD suggest differential DNA
www.jaacap.org
S309
6.1 AUTOBIOGRAPHICAL MEMORY AND LATENT VULNERABILITY TO PSYCHIATRIC DISORDER FOLLOWING CHILDHOOD MALTREATMENT Eamon McCrory, PhD, PsyD, University College London, e. [email protected] Objectives: Altered autobiographical memory (ABM) functioning has been implicated in the pathogenesis of depression and PTSD and may represent one mechanism by which childhood maltreatment elevates psychiatric risk. The aim of the current study was to investigate the impact of childhood maltreatment on ABM functioning. Methods: ABM functioning was investigated in 67 children: 34 with maltreatment experiences documented by social services (MT group); and 33 nonmaltreated comparison children matched on age, gender, handedness, pubertal status, IQ, and socioeconomic status. All participants performed a standard Autobiographical Memory Task (AMT) to assess over-general memory outside the scanner. Participants also recalled specific ABMs in response to emotionally valenced cue words during fMRI. Results: Maltreated children showed greater recall of over-general memories on the AMT, even in the absence of overt psychopathology, relative to nonmaltreated peers [t(55) ¼ 2.46, P ¼ 0.02]. The MT group also showed reduced hippocampal and increased middle temporal and parahippocampal activation during positive ABM recall compared with peers. During negative ABM recall, they exhibited increased amygdala activation and greater amygdala connectivity with brain regions critical for processing salience. Conclusions: Childhood maltreatment is associated with altered ABM functioning, specifically reduced activation in areas encoding specification for positive memories, and greater activation of the salience network for negative memories. This pattern may confer latent vulnerability to future depression and PTSD.
CAN, IMAGS, PSP http://dx.doi.org/10.1016/j.jaac.2017.07.606
6.2 HARSH PHYSICAL PUNISHMENT AND AGGRESSION: NEUROBIOLOGICAL MEDIATORS AND INFLUENCES OF OTHER FORMS OF ENVIRONMENTAL RISK W. Dustin Albert, PhD, Bryn Mawr College, walbert@ brynmawr.edu Objectives: Consistent links exist between harsh physical punishment during childhood and risk for later aggressive and violent behavior in adolescence. Recent work has focused on how changes in brain regions such as the amygdala may mediate the linkage between harsh physical punishment and later aggression and violence. Past research has found that forms of early life stress, such as child maltreatment, are related to higher amygdala activity to facial displays of threat, but few links have been reported between amygdala activity and problem behavior in these sample groups. Methods: We tested links between childhood exposure to harsh physical punishment, amygdala activity, and aggressive behavior in adolescence, using data from a longitudinal study of individuals followed from middle childhood (n ¼ 73; 43 males; mean age at scan ¼ 15.4 years). Unique to the work, we sought to examine harsh physical punishment, as well as other sociodemographic and parenting risk factors. To evaluate amygdala activity, we used a well-validated, face-matching neuroimaging task with facial displays of threat. Results: In line with past reports, exposure to harsh physical punishment during childhood was related to heightened right amygdala reactivity in adolescence (b ¼ 0.34, P ¼ 0.018). Interestingly, amygdala reactivity (left and right) was not related to other risk factors, including household income, parental rejection, and parental hostility (all P > 0.27). Next, higher amygdala reactivity was related to greater aggressive behavior, as assessed by higher delinquency, higher aggression, and lower prosocial behavior (b ¼ 0.34, P < 0.005). Finally, using statistical mediation, amygdala reactivity partially explained the connection between early harsh physical punishment and aggressive and violent behavior in adolescence (z ¼ 2.06, P ¼ 0.04).
JOURNAL OF THE AMERICAN ACADEMY OF CHILD & ADOLESCENT P SYCHIATRY VOLUME 56 NUMBER 10S OCTOBER 2017
Conclusions: These results provide increased understanding of the deleterious effects of harsh physical punishment. We replicated past reports showing heightened amygdala activity in relation to harsh physical punishment. We also note how variations in amygdala activity were not associated with other sociodemographic and parenting risk factors. These findings provide important directions for future investigations aimed at understanding how various forms of stress and environmental experiences can become embedded in our neurobiology.
AGG, CAN, IMAGS Supported by NIDA Grants R01DA033369, R01DA031579, P30DA023026, and P30DA027827 and Eunice Kennedy Shriver National Institute of Child Health and Human Development Grant T32HD0737625 http://dx.doi.org/10.1016/j.jaac.2017.07.607
6.3 EFFECTS OF TRAUMA EXPOSURE ON FEAR INHIBITION CIRCUITRY IN THE DEVELOPING BRAIN Tanja Jovanovic, PhD, Emory University, [email protected] Objectives: Impaired inhibition is increasingly considered a biomarker of PTSD, and prior research has demonstrated a possible shared neural circuitry for fear and response inhibition in traumatized adults. Childhood trauma has been associated with impaired inhibition; however, most neuroimaging studies have been retrospective. The current study investigated the effects of violence exposure on brain activation during an emotional response inhibition task in children and whether altered brain response was associated with impaired fear inhibition. Methods: Children (N ¼ 40) were recruited from an ongoing study in an African American, highly traumatized, inner-city population. Participant measures included the following: trauma interviews using the Violence Exposure ScaleRevised (VEX-R); PTSD symptom assessment using the University of California, Los Angeles (UCLA) PTSD Reaction Index (PTSD-RI); an emotional Go/NoGo fMRI task; and a fear-potentiated startle task. The amygdala, ventromedial prefrontal cortex (vmPFC), and hippocampus were used as regions of interest for our analyses. Fear-potentiated startle was measured using electromyography recordings of the eyeblink muscle during a differential fear conditioning task. Results: The average VEX-R total score was 9.89, and the average PTSD-RI score was 16.71, with none of the children meeting the criteria for PTSD based on a UCLA cutoff score of 38. Positive associations were found between violence exposure and activation in amygdala (r ¼ 0.47, P < 0.02), vmPFC (r ¼ 0.41, P < 0.05), and hippocampus (r ¼ 0.50, P ¼ 0.01) during response inhibition (NoGo > Go), as well as between violence exposure and amygdala (r ¼ 0.46, P < 0.02) and hippocampus (r ¼ 0.45, P < 0.02) activation during emotional response inhibition (NoGo Fear > Go Neutral). vmPFC activation during emotional response inhibition was negatively correlated with fearpotentiated startle to a conditioned safety cue (r ¼ 0.51, P < 0.05). Conclusions: The association of decreased vmPFC activation with increased fear-potentiated startle to safety presents a possible shared neural circuitry for response and fear inhibition in children. Increased amygdala, vmPFC, and hippocampal activation, with violence exposure in this high-trauma, low-symptom population, may represent adaptive responses at this stage of development, although longitudinal research is required to determine their future effects.
AGG, COG, IMAGS Supported by NIMH Grant R01MH100122 and a NARSAD Independent Investigator Grant http://dx.doi.org/10.1016/j.jaac.2017.07.608
6.4 EPIGENETIC ABNORMALITIES ASSOCIATED WITH ALTERED EMOTION PROCESSING CIRCUITRY IN PEDIATRIC POSTTRAUMATIC STRESS DISORDER Ryan Herringa, MD, PhD, University of Wisconsin School of Medicine and Public Health, [email protected] Objectives: Epigenetic changes represent candidate mechanisms contributing to PTSD in youth. Studies of adult PTSD suggest differential DNA
www.jaacap.org
S309