Food addiction is characterized by poorly controlled intake of highly-palatable, calorically-dense, foods. While previous studies indicate that risk factors for food addiction are similar to substance use disorders (SUD), these studies have looked at food addiction and SUD in independent samples, limiting the ability to directly compare food addiction to SUD. The present study was conducted to assess rates of posttraumatic stress disorder (PTSD), depression, childhood and adult trauma exposure, as well as presence and severity of emotion dysregulation, in a sample of women (N = 229) who either meet criteria for no addiction, food addiction only or SUD only. The prevalence of food addiction was 18.3% and the prevalence of SUD was 30.6% in this sample. Women with food addiction and women with SUD endorsed more depression and PTSD symptoms when compared with individuals with no addiction. Individuals with food addiction and SUD had higher total emotion dysregulation scores, specifically with difficulties in goal directed behaviors, non-acceptance of emotional responses, impulse control, limited access to emotion regulation strategies, and lack of emotional clarity, when compared to individuals with no addiction (all p's < 0.05). There were no differences in PTSD and depression symptoms and emotion dysregulation scores between food addiction and SUD groups (all p > 0.05). However, women with SUD endorsed higher levels of total childhood (p < 0.01) and adulthood trauma (p < 0.01) as compared with women with no addiction or food addiction. These results suggest that women with food addiction and those with SUD share similar psychological characteristics and risk factors, with the exception of trauma histories. These findings have implications for the detection of risk for and treatment of these disorders.

Dissociative phenomena are frequently experienced by psychologically traumatized people. However, little is known about the cognitive profiles of highly dissociative traumatized individuals, and corresponding patterns of neural connectivity when attentional networks are engaged in the context of emotion. One hundred seventeen traumatized women completed the multiscale dissociation inventory (MDI) and neuropsychological testing; MDI scores were used to classify high- and low-dissociative participants. Forty-six participants also underwent fMRI during performance of an attentional control task that incorporates emotionally distracting images (Affective Number Stroop; ANS). Compared to low-dissociative participants, high-dissociative participants demonstrated better performance on an executive functioning task (F1,111 = 4.64, p = .03), worse performance on a task of visual memory (F1,111 = 9.52, p = .003), and similar performance on all other neuropsychological measures. In addition, dissociative symptoms were negatively correlated with functional connectivity between the amygdala and right anterior insula in response to trauma-related ANS trials. These findings indicate that highly dissociative traumatized people experience difficulties with attentional control in the context of emotionally evocative stimuli, but in a neutral context, their overall cognitive profiles are similar to low-dissociative people. Highly dissociative participants also demonstrated weaker connectivity between the amygdala and insula in response to trauma-relevant images. Evocative, trauma-relevant stimuli appear to disrupt neutral networks involved with attention to salient cues and interoception in highly dissociative traumatized individuals. (PsycINFO Database Record

Anhedonia emerges in some people after psychological trauma, reflected by a loss of interest, diminished affect, and detachment. Structural abnormalities in specific neural pathways at the time of trauma may influence the development of these posttraumatic anhedonia (PTA) symptoms. In this prospective study, we determined whether white matter connectivity at around one month post-trauma predicts PTA and other PTSD symptoms at six months post-trauma. Thirty men and women aged 19-62 were recruited from the emergency department of a Level I trauma center. Participants received diffusion tensor imaging at approximately one month post-trauma and clinical assessments at one and six months post-trauma. Probabilistic tractography was used to examine connectivity of select pathways. A replication sample (N = 57) in an independent, crosssectional dataset of traumatized women was similarly analyzed. Logistic regression results indicated that, after accounting for early PTSD symptoms (at one month) and other clinical risk factors, the integrity of the uncinate fasciculus (UF) uniquely predicted the presence of PTA at six months post-trauma (Beta = −225.6, p < .05). Together, these factors contributed to 76% of the variance in PTA. Integrity of the UF also predicted re-experiencing PTSD symptoms at six months post-trauma. These results were supported in our replication analyses. Our findings indicate that the integrity of the UF around 1 month post-trauma affects vulnerability for the development of anhedonic PTSD symptoms as well as re-experiencing symptoms. Connectivity of this amygdalaventromedial prefrontal pathway appears to be a salient predictor of anhedonia, above and beyond clinical risk factors.

Background: Attentional disruptions are common in PTSD, but findings across neuropsychological and neuroimaging studies have been variable. Few PTSD studies have investigated abnormalities in attention networks using a multi-modal imaging approach and attentional tasks that include emotionally-salient images. This study combined a behavioral task that included these images (emotional Stroop) with functional and structural neuroimaging (fMRI and diffusion tensor imaging; DTI) methods to comprehensively investigate attentional control abnormalities in a highly-traumatized civilian sample. Methods: 48 traumatized women with and without PTSD received clinical assessments, fMRI and DTI. During fMRI, the Affective Stroop (AS), an attentional control task that includes emotionally-salient distractor images (trauma-relevant, positive, neutral) and variable task demands, was administered. Results: In response to more difficult AS trials, participants with PTSD demonstrated lower activation in the dorsal and rostral anterior cingulate cortex and greater activation in the insula. This group also showed comparatively poorer performance on positive AS distractor trials, even after adjusting for trauma exposure. Performance on these trials inversely correlated with structural integrity of the cingulum bundle and uncinate fasciculus. Conclusions: Even after adjusting for trauma exposure, participants with PTSD showed worse performance on an attentional control task in the context of emotional stimuli. They also showed relatively lower cognitive control network activation and greater salience network activation. Fronto-parietal and fronto-limbic white matter connectivity corresponded with AS performance. Our findings indicate that attentional control impairments in PTSD are most evident in the context of emotional cues, and are related to decrements in function and structure of cognitive control and salience networks.

This study aims to determine whether sickle cell mice could recapitulate features of cognitive and neurobehavioral impairment observed in sickle cell patients and whether neuroinflammation could be a potential therapeutic target as in other non-sickle cell disease-related cognitive dysfunction. Cognitive (learning and memory) and behavioral (anxiety) deficits in 13- and later 6-month-old male Townes humanized sickle cell (SS) and matched control (AA) mice were evaluated using novel object recognition (NOR) and fear conditioning tests. Immunohistochemistry was performed to quantify peripheral immune cell (CD45+) and activated microglia (Iba1+) as markers of neuroinflammation in the dentate and peri-dentate gyrus areas. We evaluated cell fate by measuring 5'-bromodeoxyuridine and doublecortin fluorescence and phenotyped proliferating cells using either glial fibrillary acid protein (GFAP+), neuronal nuclei (NeuN+), CD45+, and Iba1+. In addition, Golgi-Cox staining was used to assess markers of neuroplasticity (dendritic spine density and morphology and density of dendrite arbors) on cortical and hippocampal pyramidal neurons. Compared to matched AA controls, 13-month-old SS mice showed significant evidence of cognitive and behavioral deficit on NOR and fear conditioning tests. Also, SS mice had significantly higher density of CD45+ and activated microglia cells (i.e. more evidence of neuroinflammation) in the dentate and peri-dentate gyrus area. Additionally, SS mice had significantly lower dendritic spine density, but a higher proportion of immature dendritic spines. Treatment of 13-month-old SS mice with minocycline resulted in improvement of cognitive and behavioral deficit compared to matched vehicle-treated SS mice. Also, treated SS mice had significantly fewer CD45+ and activated microglia cells (i.e. less evidence of neuroinflammation) in the dentate and peri-dentate gyrus, as well as a significant improvement in markers of neuroplasticity. Impact statement This study provides crucial information that could be helpful in the development of new or repurposing of existing therapies for the treatment of cognitive deficit in individuals with sickle cell disease (SCD). Its impact is in demonstrating for the first time that neuroinflammation and along with abnormal neuroplasticity are among the underlying mechanism of cognitive and behavioral deficits in SCD and that drugs such as minocycline which targets these pathophysiological mechanisms could be repurposed for the treatment of this life altering complication of SCD.