Binge eating disorder (BED) is the most prevalent of all eating disorders and is characterized by recurrent episodes of eating a large amount of food in the absence of control. There have been various kinds of research of BED, but the phenomenon remains poorly understood. This thesis reviews the results of research on BED to provide a synthetic view of the current general understanding on BED, as well as the neural correlates of the disorder and treatments. Research has so far identified several risk factors that may underlie the onset and maintenance of the disorder, such as emotion regulation deficits and body shape and weight concerns. However, neuroscientific research suggests that BED may characterize as an impulsive/compulsive disorder, with altered reward sensitivity and increased attentional biases towards food cues, as well as cognitive dysfunctions due to alterations in prefrontal, insular, and orbitofrontal cortices and the striatum. The same alterations as in addictive disorders. Genetic and animal studies have found changes in dopaminergic and opioidergic systems, which may contribute to the severities of the disorder. Research investigating neuroimaging and neuromodulation approaches as neural treatment, suggests that these are innovative tools that may modulate food-related reward processes and thereby suppress the binges. In order to predict treatment outcomes of BED, future studies need to further examine emotion regulation and the genetics of BED, the altered neurocircuitry of the disorder, as well as the role of neurotransmission networks relatedness to binge eating behavior.

Compulsive eating behavior is a transdiagnostic construct that shares many behavioral, neurobiological, and theoretical features with compulsive drug use. The focus of this dissertation is to progress a framework for compulsive eating behavior, including identification of risk factors for its development and examination of functional neuroadaptations to brain reward systems in an animal model of compulsive eating. We first investigated impulsivity (impulsive choice and impulsive action) as a potential vulnerability factor for the development of binge and compulsive eating behavior. Impulsivity has been implicated in drug addiction as well as eating disorders and obesity, but its exact role in the conferment of risk for compulsive eating is unknown. To achieve this, we measured impulsive choice (i.e. delay discounting) and impulsive action (i.e. motor impulsivity) and subsequent binge-like eating. We observed no effects of impulsive choice behavior on binge-like eating of palatable food; however, impulsive action predicted higher binge-like eating, higher motivation for palatable food, and increased compulsive-eating behavior. Therefore, impulsive action, but not impulsive choice, predicted the development of binge- and compulsive-like eating behaviors. The second aim of this dissertation was to investigate functional neuroadaptations to brain reward pathways in rats with a history of palatable diet alternation, a model of compulsive eating. Overeating of palatable food, similar to exposure to drugs of abuse, is hypothesized to cause reward deficits via downregulation of mesolimbic dopamine systems. To investigate this, we measured sensitivity to d-Amphetamine using behavioral and neurochemical methods. To identify potential neuroadaptations to the dopamine and dopamine transporter (DAT) systems, we assessed baseline NAc-shell dopamine and DAT function in vivo. In rats with a history of palatable diet alternation, we observed deficits in the stimulating, reward-enhancing, and rewarding effects of d-Amphetamine, and impaired d-Amphetamine-induced dopamine efflux in the NAc-shell. Furthermore, dopamine and dopamine transporter systems were downregulated evidenced by decreased extracellular NAc-shell dopamine at baseline and decreased DAT function. These results contribute to an overall framework for compulsive eating behavior where initial impulsivity predisposes compulsive eating and compulsive eating results in the emergence of reward deficits. / 2021-06-14T00:00:00Z

Temporal discounting can be used to evaluate impulsivity in various populations. One assessment measure that can be used is a monetary choice questionnaire in which individuals are provided with an option to select a specified amount of money now, or a different amount following a temporal delay. This study examines the convergent validity of a long monetary choice questionnaire consisting of 189 questions and a brief monetary choice questionnaire consisting of 7 questions, in which participants can select all of the amounts they would prefer to acquire. The results of this study suggested that there is convergent validity between the two surveys through the use of Pearson’s correlation (r=.648, p< .001) and a paired samples t- test that demonstrated that the difference between the AUC scores was not significant (p=.287). Keywords: discounting, convergent validity, impulsivity, self- control, temporal discounting

Highly organised and differentiated neural circuits form and unite to link the cortex with the basal ganglia and thalamus to mediate movement, cognition and behaviour. Previous assertions that the basal ganglia primarily acted to filter cortical information to facilitate motor outputs only have since given way to an understanding of the basal ganglia as a relay and gating structure with functionally and structurally segregated inputs, functions and outputs. Thus, cortical – basal ganglia circuits can be segregated into three broadly separable functional domains mediating motor (primary and supplementary motor cortex (SMA) and putamen), cognitive (dorsolateral prefrontal cortex (dlPFC) and caudate), and limbic (ventromedial prefrontal cortex and ventral striatum (VS)) processes. In addition, cognitive and behavioural programs that pass through the cortical – basal ganglia circuitry can be subject to filtering by the subthalamic nucleus (STN), which receives direct projections from the cortex. This work first demonstrated the functional organisation of segregated intrinsic cortical – basal ganglia circuits in humans, alongside a detailed map of functional subzones within STN, a small and technically inaccessible midbrain structure. The behavioural relevance of the defined cortical – basal ganglia circuits was investigated by examining the cognitive constructs of impulsivity and compulsivity. Waiting impulsivity, a tendency towards rapid premature responses that has been associated with compulsive drug use, was associated with connectivity between limbic regions including subgenual anterior cingulate cortex, VS and STN. However, motor impulsivity, in the form of stopping ability, was associated with motoric regions including pre-SMA and STN. Compulsivity was captured as deficits in: reversal learning, implicating lateral orbitofrontal cortex; attentional shifting, implicating dlPFC; and habit learning, implicating SMA. Neural circuit changes were also examined in individuals with alcohol dependence and binge drinkers. Waiting impulsivity was elevated in both groups and the functional connectivity, microstructural integrity and anatomical connectivity of the neural circuit underlying waiting impulsivity were associated with problematic drinking behaviours in both groups. Together, this work establishes that discrete functional subzones of small subcortical regions can be differentiated in humans and that their behavioural correlates can be similarly mapped. The definition of intrinsic network architecture underlying a particular behaviour and the demonstration its disturbance in psychiatric groups will crucially inform the development of future diagnostic and therapeutic models.

Impulsivity, venturesomeness, and pride variables were examined as potential moderators of the associations between childhood trauma and physical aggression, alcohol use and physical aggression, and drug use and physical aggression. Participants (n = 457) were college students recruited from a university in the Southeast. It was hypothesized that childhood trauma, alcohol use, and drug use would be associated with increased scores of physical aggression. In addition, it was hypothesized that impulsivity, venturesomeness, authentic pride, and hubristic pride would moderate these relationships. Linear, multivariate hierarchical regression analyses were used to examine these variables as potential moderators. Hypotheses concerning hubristic pride as a moderator of the relationship between alcohol use and physical aggression as well as the relationship between drug use and physical aggression were supported. In addition, the hypothesis concerning authentic pride as a moderator of the relationship between alcohol use and physical aggression was supported albeit in the opposite direction than predicted. Hypotheses concerning the moderating roles of impulsivity and venturesomeness were not supported. Findings support the idea that the deleterious psychological effects of substance use can be compounded by personality factors such as authentic and hubristic pride. The discussion encompasses why interventions should target attributions and cognitions and why simply encouraging someone to have a more “healthy pride” is likely to be ineffective at reducing physical aggression in the context of drug use and alcohol use.

Licensed drivers arrested for driving under the influence (DUI) of alcohol have increased rates of vehicle crashes, moving violations, traffic tickets, and contribute to an estimated 120 million occurrences of impaired driving per year (Evans, 2004; Jewett et al., 2015). Survey research on DUI offenders indicates traits of impulsivity (e.g., sensation seeking). Together, these pieces of evidence suggest that DUI offenders display patterns of impulsive action and risk-taking while driving. However, to-date DUI offenders are rarely studied in a laboratory setting, and not much is known about how they respond to a dose of alcohol. The present study examined the degree to which DUI offenders display an increased sensitivity to the acute impairing effects of alcohol on mechanisms of behavioral impulsivity, skill and risk-based driving simulations, and subjective evaluations of driving fitness and perceived intoxication following alcohol consumption. A sample of 20 DUI offenders were compared to a demographically-matched sample of 20 control drivers. All participants attended two dose sessions in which they received either a 0.65 g/kg dose of alcohol or a placebo dose, counterbalanced, on separate days. Results indicated that alcohol affected all of the behavioral outcome measures. More specifically, alcohol increased impulsive choice responses and decreased response inhibition on the behavioral impulsivity tasks. Alcohol also increased risky driving behaviors and decreased driving-related skills. Furthermore, alcohol generally decreased participants’ self-reported willingness and ability to drive a motor vehicle, and increased levels of intoxication and BAC estimations relative to placebo. With regard to group differences, DUI offenders showed an increased sensitivity to the disrupting effects of alcohol on impulsive choices, such that DUI offenders showed a significantly greater preference for impulsive choices under alcohol relative to placebo than controls. Taken together, these findings provide some of the first pieces of evidence that compared to controls, DUI offenders display an increased tendency for impulsive decisions under alcohol, which likely contributes to risky decisions to drive after drinking, despite clear evidence for their behavioral impairment. These findings could have important implications for understanding the mechanisms underlying maladaptive behaviors in this high-risk population, and sheds light on possible targets for intervention to reduce DUI recidivism.

tDCS brain stimulation does not always work in the intended direction. It has been found to sometimes worsen behavior rather than improve it. A preliminary study shows that people high on sensation-seeking and lack of premeditation were prone to reverse effects of tDCS on performance on a Stop Signal Task. Both of these constructs are related to dopamine levels. Study 2 seeks to intentionally cause a reverse effect of tDCS by increasing participants’ dopamine levels via caffeine. There was not a significant interaction between tDCS and caffeine on errors on the Stop Signal Task in this study. However, other factors interacted with tDCS and caffeine including lack of premeditation. This two study package suggests the effects of tDCS are variable across individuals, with personality and neurochemistry both affecting behavioral outcomes of tDCS.

Complex cognitive functions require interactions within and between different brain regions by direct anatomical connections or synchronous activation. As such, damage to any region involved in a cognitive process has the potential to affect its function. Impulsivity is a multifaceted construct that, when dysfunctional, contributes to many psychiatric conditions. The striatum has been implicated as an integral part of the neural circuitry of impulsivity. The current work aims to contribute to the understanding of neural dysfunction underlying disorders of impulsivity by examining how striatal damage affects impulsive behavior. It also aims to improve our understanding of whether neural processes involved in impulsivity are also involved in maintaining awareness of one's thoughts and actions. No studies have systematically examined the extent to which damage to the striatum correlates with both changes in impulsive behavior and changes in self-awareness of impulsive personality. In the first experiment, I examined the effects of focal unilateral striatal damage on self-awareness of impulsivity and other personality traits. I predicted that participants with striatal damage (SD) would have less self-awareness of changes in impulsivity and other personality traits after brain damage, as compared to brain damage comparisons (BDC), due to indirect disruption of neural networks responsible for self-referential processing. I tested this prediction using self and collateral versions of the Barratt Impulsiveness scale (BIS) and the Iowa Scales of Personality Change. In partial support of my hypothesis, there were mean differences in self- and collateral-reported impulsivity on the BIS, with self ratings higher than collateral ratings in the SD group. There were no significant differences in the correlations between self- and collateral-reports for current impulsivity, change in impulsivity, or change in other personality traits. In the second experiment, I examined the effects of focal unilateral striatal damage on laboratory measures of impulsivity. I predicted that participants with striatal damage would exhibit lower levels impulsivity than brain damaged comparisons due to structural loss of regions involved in reward/motivation and motor activity. I tested this using impulsive action tasks (Go/NoGo and Stop Signal Tasks) and impulsive choice tasks (Delay and Probability Discounting). In contrast to my hypothesis, SD participants did not exhibit less impulsive action or impulsive choice than BDC participants. In the third experiment, I examined the effects of focal unilateral striatal damage on the integrity of frontostriatal resting state functional connectivity. I predicted that participants with striatal damage would exhibit alterations in functional connectivity between the remaining regions of the frontostriatal network. I tested this by comparing the strength of functional connectivity of the caudate head and ventromedial prefrontal cortex. While my hypothesis was not directly supported, the data showed interesting trends that warrant further exploration. These included stronger caudate-vmPFC resting state functional connectivity on the lesion side, and weaker functional connectivity on the non-lesioned side in striatal participants compared to brain damaged comparisons. Together, these experiments suggest that although unilateral striatal damage does not appear to affect subjective reports or laboratory measures of impulsivity, it may affect the underlying neural networks utilized by the striatum, as evidenced by changes in frontostriatal resting state functional connectivity. This work extends our understanding of the neurobiology of impulsive behavior and self-awareness, at systems level, and may help pave the way for treatments of those with brain injury, such as traumatic brain injury and stroke patients, or psychiatric disorders involving impulsivity.

This study compared the impact of instructional and improvisational music therapy approaches on the level of motor impulsivity displayed by adolescent boys who have Attention Deficit Hyperactivity Disorder (ADHD). Measures included numbers of errors made on a Synchronised Tapping Task (STT); and Conners' Rating Scales (Conners, 1997). Participants (n=13), aged 11 - 16 years, were enrolled in a special residential school. A combination of a multiple contrasting treatment and an experimental control group design was used. Students were randomised to three groups; control (Group A) and two treatment groups. Students in Group B received eight sessions of improvisational music therapy followed by eight sessions of instructional music therapy, while the order was reversed for Group C.There was no statistical difference between the impacts of the contrasting music therapy approaches on the level of motor impulsivity displayed by the students as measured by the STT and the Restless-Impulsive and Hyperactive-Impulsive Conners' subscales. However all students significantly improved on the STT across each phase of treatment and improvement was slightly greater during the instructional treatment periods for both groups. During these same periods teachers reported a small decrease in restless and impulsive behaviours. The results therefore cautiously imply that the instructional approach might contribute to a reduction in motor impulsivity in the classroom.Significant improvement on STT without the corresponding improvement in motor impulsivity suggested that increased accuracy on the STT might be attributable to progress in other developmental domains. Teacher report of significant improvement for treatment groups on the DSM-IV Total Subscale adds weight to this suggestion, and implies that combined music therapy approaches might have contributed to a reduction in DSM-IV symptomology in the classroom.Rickson's (2001) tentative suggestion that creative music-making might over-arouse students with ADHD was not confirmed. Students did make more errors when tested on the STT a second time on the same day but this was regardless of whether they had been involved in instructional, improvisational or no music therapy programme. It is possible that students who have ADHD are easily aroused by the general school milieu and classroom or music room interactions with peers.

Numerous cognitive, personality and situational factors have been found to be related to aggression. Understanding how these factors interrelate is essential to predicting violence and critical to the assessment and treatment of offenders with violent histories. Previous research has suggested a potential role for social problem solving as a mediator between impulsivity and aggression (McMurran et al., 2002). Additionally, it is well established that aggression is more likely to occur in the context of alcohol use (Collins, 1993; Reiss & Roth, 1993; Lipsey, Wilson, Cohen & Derzon 1997). Based on existing literature, a model of aggression was developed involving impulsivity, social problem solving and alcohol dependency. Utilizing path analysis with multiple regression, a mediational model of aggression was assessed on a sample of 179 provincially incarcerated offenders, 87% of whom were Aboriginal and 45% of whom had a previous conviction of domestic abuse. The data suggest that social problem solving, alcohol dependency and impulsivity are all important in understanding and predicting aggression. Social problem solving does not appear to act as a mediator in the relationship between impulsivity and aggression, although preliminary results suggest that impulsivity, may serve the function in this relationship and in the manifestation of aggression. The implications of these findings for our understanding about human factors contributing to aggression and for further advancement of treatment programs are provided.