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The brain appears to process food differently in people with eating disorders. Most consistently, these studies have identified altered responses to food images in the ventral striatum for both AN and BN. Similarly, people with BN have shown heightened activation in response to food images in reward regions 54 as well as reduced activation in response to the taste of food in the insula and medial frontal gyrus.

First, they engaged a conditioning procedure to train subjects to expect a specific association a particular visual stimuli cued either administration of sucrose or artificial saliva , but on some trials the association was altered to create an unexpected event no sucrose given for the sucrose stimulus or sucrose given for a saliva stimulus.

They found that the BN subjects showed less activation in the insula, the ventral putamen, the amygdala and the lateral orbitofrontal cortex, when that association was disrupted. This supports the idea that actual reward may be less important than the expectation or idea of a reward in BN. Additionally, the responsivity of reward regions for people with BN appears to depend more strongly on emotional state with more ventral striatum responses when anticipating a positive food reward than observed in HC.

They found differences in the orbitofrontal cortex in BED, and differences in the anterior cingulate and insula in BN in response to food images.

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Weygandt et al 59 then examined this dataset using machine-learning techniques to diagnostically differentiate the groups. These differences related to food responses in the amygdala, the ventral striatum, and the anterior cingulate in both eating disorder groups, suggesting that eating disorder patients show greater engagement of cognitive control regions in response to food than healthy people.

Understanding whether differences in reward are solely related to eating and food or extend into the neural responses to other stimuli may help determine if biological differences related to experiencing reward may underlie or contribute to development or maintenance of disordered eating behaviors. To assess this, several studies have probed the neural responses to monetary rewards in subjects with eating disorders Table 1. In AN, many of these comparisons focus on women in weight recovery from AN recAN and to mitigate the effects associated with acute starvation.

First, Wagner et al 60 found that recAN women did not show different neural responses in the ventral striatum for positive and negative feedback, unlike healthy women. Using the same paradigm, recBN women also failed to differentiate positive and negative feedback in both the ventral striatum and the dorsal caudate. Balodis et al 63 examined ventrostriatal activations in BED, HC of normal weight, and HC that were overweight using a monetary incentive task. There, overweight HC differed from both other two groups, with elevated ventrostriatal activity when anticipating a reward.

Most recently, the neural responses to monetary reward were examined in hungry and satiated individuals in recovery from AN and compared to those in healthy women. Structural studies have also identified differences in the size of brain regions in the reward pathway in eating disorders. Similarly, Mettler et al 66 reported reduced fractional anisotropy in the corona radiata in BN, suggesting differences in the connectivity of regions related to taste and reward. Frank et al 67 identified alterations in brain structure in both AN and BN, with increased gray matter GM in medial orbitofrontal cortex and insula and reduced dorsal striatal volumes.

Importantly, dorsal striatum volumes were also positively related to sensitivity to reward in both illnesses, with greater volume of the dorsal striatum corresponding to greater sensitivity to reward. Finally, Titova et al 68 recently completed a meta-analysis combining nine separate studies of brain volumes in AN, identifying specific deficits in GM in the hypothalamus, caudate, and right lentiform nucleus.

Brooks et al 69 connected the size of the dorsolateral prefrontal cortex with dietary restraint, a finding that suggests top-down cortical feedback may serve to suppress subcortical regions related to experiencing primary rewards. In total, all of these studies suggest that reward responses may be less salient in patients with eating disorders.

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Problems in decision-making can amplify the symptoms of mental disease, particularly issues with high temporal discounting for rewards, 70 a common problem in addictive disorders 71 and borderline personality disorder. One important characteristic of the reward system is a close sensitivity of the timing of reward relative to decisions and choices. Many of these clusters overlapped with areas previously identified using the reward meta-analysis: the left caudate vox , the right caudate vox , two clusters in the medial prefrontal cortex 63 and 85 vox , the right inferior frontal gyrus and insula 81 vox , and the left inferior frontal gyrus and insula 54 vox.

Only one new region was engaged: the dorsal anterior cingulate vox. In sum, activations of subcortical reward regions are closely related to decisions and decision-making, with the addition of a portion of frontal cortex. Eating disorders are characterized by recurrent problems in decision-making, leading to poor behavioral choices about consuming food, both eating too little or too much, as well as overexercising and engaging in purging behaviors. The Iowa Gambling Test asks participants to select cards with different values of money on them. The objective is to choose cards with larger long-term monetary gain, and those who do are deemed to have better decision-making skills.

Several researchers have examined decision-making using behavioral measures from this task in eating disorder patients.

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Cavedini et al 75 reported that patients with AN have poor performance compared to HC but that there was no relationship between the severity of illness and the degree of poor performance. Thus, poor decision-making may be a state-based phenomenon. Only a few neuroimaging studies have directly accessed decision-making in eating disorders Table 2. Decker et al 80 examined decision-making in AN with fMRI at two time points, at treatment initiation and after weight-recovery, using a delayed-discounting task.

Participants provided their preference about receiving some money now or a different amount of money at a future time point, allowing an individual discounting rate for each participant to be obtained, while examining neural activity during their decisions. Their data suggest that while underweight, patients with AN prefer future rewards to current rewards compared to healthy women, although the opposite phenomena occurred in the Iowa Gambling Task.

These data suggest that starvation impacts not only subcortical reward regions but also higher cortical regions engaged to evaluate decisions. Making decisions involves collecting and synthesizing information prior to acting on it. As such, impulsivity is a specific personality trait that sabotages decisions and frequently appears altered in psychopathology, particularly in addictions.

That study found increased frontal and anterior cingulate activations in the binge—purge group, which was interpreted as inefficient processing. Impulsivity may be related to altered engagement of frontal regions as well as the bingeing and purging behaviors in EDs. They found that the AN group had increased prefrontal cortex responses to the active people, suggesting alterations in frontostriatal circuits for stimuli related to the illness. There is considerably less overlap in the social map than the reward and decision maps showed, with social studies activating many more cortical clusters.

The only overlapping regions were areas in the medial prefrontal cortex 2, vox and bilateral clusters in the inferior frontal gyri and insula R, vox; L, vox. These regions have frequently shown alterations in both BN and AN. Of note, these social regions include both regions engaged in reward processing the ventral striatum, orbitofrontal cortex and regions activated during decision-making dorsolateral prefrontal cortex, inferior frontal gyri, and dorsal anterior cingulate.

Activations of many regions included in this social network can be altered based on sociocultural factors. Izuma and Adolphs 97 showed that exposure to the preferences of peers and an anti-peer group sex offenders about T-shirts over the course of short, single scanner session, not only altered brain activity in the dmPFC that day, but that these changes in the dmPFC persisted for 4 months.

Eating disorder ED behaviors have been related to the adoption of Western values and the exposure to Western media, supporting an idea that brain differences related to social factors might be present in this illness. Anne Becker 98 studied Fijian girls mean age 17 in and The first wave was surveyed in when Western television had been accessible on the island for less than a month.

The wave had been exposed to television for 3 years and had radically different attitudes regarding body image and eating. Several imaging studies have examined neural responses to social stimuli in EDs Table 3. During imaging tasks probing general social behaviors, subjects with AN and BN have shown reduced modulation of the inferior frontal gyri, the medial temporal gyrus, the temporoparietal junctions, and the medial prefrontal cortex.

Cowdrey et al presented emotional faces to 16 weight-recovered AN subjects and 16 HC and found no neural differences. In contrast, using a similar task but with 31 underweight AN subjects and 31 HC, Fonville et al found elevated responses in the fusiform gyrus in the AN subjects while viewing neutral, happy, and very happy expressions relative to healthy women.

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Ashworth et al found reduced neural responses in the precuneus for angry and disgusting expression in subjects with BN compared to healthy women, as well as reduced amygdala activation to angry expressions. In concert, these data suggest that the patients currently meeting criteria for eating disorders are more likely to show altered neural responses to basic social and emotional stimuli than patients recovered from an eating disorder.


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Considering social and body image descriptive adjectives related to oneself or others are a social cognitive task that can engage neural regions related to self-knowledge, typically the midline cortical structures. Miyake et al found that AN subjects showed elevated frontal activations for negative social adjectives relative to the HC subjects. Further, the amount of alexithymia in the AN group correlated with the activation of both the anterior and posterior cingulate cortex, suggesting that emotional processing of negative stimuli in these self-referential neural regions may be specifically impaired in AN.

Suda et al also observed reduced activation in the medial prefrontal cortex and right fusiform gyrus in an AN group, in response to viewing individuals engaging in body checking, an ED behavior. All of these studies suggest that self-knowledge may be specifically altered in EDs, consistent with the recently proposed idea that our self may be largely defined by what is rewarding to us. We examined the neural differences in adults with AN and BN using a pair of self-appraisal tasks. A recent meta-analysis has identified activations of the precuneus as primarily related to other processing.

Interestingly, Cabanis et al recently examined positive and negative social attributions in healthy people and identified the posterior precuneus as a region specifically associated with positive self-attributions. In concert, these data suggest that there may be significant differences in neural function of the precuneus in relation to both self and other processing in patients with eating disorders.

Eating disorders are complex psychiatric illnesses that include alterations in the neural systems related to reward, decision-making, and social processing.

The Neurobiology of Drug Addiction Part 1

At this point, we cannot determine if the neural differences identified in eating disorders cause or are caused by the eating disorder. This does not lessen the importance of understanding the effects of these differences in the patients. First, providers must continually reiterate the expected neurobiological changes in brain function that relate to impaired nutrition: fatigue, concentration, mood swings, insomnia, impulsivity, anhedonia and learning impairments are the expected sequelae of starvation.

Ideally, research will be conducted examining the impact of treatments on neural function of these pathways and regions, to help identify the changes leading to recovery. One major translational result emerging across these studies is that people with eating disorders show less of a connection between their physiological need for food and their reward pathway responses to food than healthy people. Eating disorders appear to disrupt both hunger and hedonic responses to food. This suggests that treatments that do not require patients to identify appropriate amounts of food based on internal cueing are more likely to be more effective, as the internal cueing related to hunger and satiety is disrupted.

This is consistent with most inpatient and partial hospital programs for AN and BN in which a dietician generally creates a meal plan for the patients as well as outpatient family therapy in which the authority to select appropriate foods and their amounts is given to the parents or caregivers.

Another important translational consideration are the findings that neural responses to food stimuli depend on the emotional state of eating disorder patients. This clinical study supports the importance of mood symptoms as a possible mediator of eating disorder behaviors, just as observed in neuroimaging activations described in Bohon and Stice. Nook and Zaki asked college students to rate how much they liked a variety of both healthy and hedonic foods.

They then repeated the task without the immediate peer feedback. This study demonstrates that peer values related to food preference can significantly and immediately alter both subcortical NA and cortical vmPFC activations. We would like to consider this study in the context of the development and treatment of eating disorders. In concert with the proliferation of eating disorder support, social media, and eating disorder promotion groups on the internet, people with eating disorders seek out information related to the valuation of both hedonic and healthy foods.

As a caution, these data also suggest that exposure to eating disorder beliefs about food from peers eg, all fats are unhealthy might intensify some symptoms of this disease. The studies of reward Table 1 also suggest that the subcortical levels of reward responses may be less salient in response to the direct food stimuli in patients who have had eating disorders.