Explain the physiology of emotional response in terms of the structures and The limbic system is the area of the brain most heavily implicated in emotion and . The limbic system is comprised of brain structures that are involved in our structures are involved in many of our emotions and motivations. Learn about how neuropsychologists and neuroscientists are advancing our knowledge of the brain and the regions where motivation originates.
It is likely that at least some of the observed motivation-related dysfunction associated with anxiety and depression is related to the EF deficits that also characterize these disorders. Adaptive motivational processing relies on intact EF, such that goals can be selected based on their predicted value, behaviors can be initiated to achieve these goals, and goal-directed action can be maintained across time, particularly in the face of distraction Spielberg et al.
Many of the abnormal approach- and avoidance-related behaviors associated with anxiety and depression are likely due at least in part to dysfunction in specific EFs. For example, depressed individuals have difficulty sustaining reward responsiveness over time Heller et al. Heller and colleagues found that problems in reward responsiveness were linked to dysfunction in frontal and subcortical areas, which interact to implement goal-directed behavior.
Just as EFs appear to influence motivational processes, there is also evidence that motivation affects these cognitive processes in anxiety and depression. In healthy individuals, altering motivational processing via monetary incentives has been associated with enhancements of various EFs, including cognitive control, attention, set-shifting, and working memory Pochon et al.
In contrast, depressed adults and adolescents failed to adaptively adjust their performance during EF tasks in order to optimize their chances of winning money in rewarding and punishing contexts Henriques and Davidson, ; Jazbec et al. Similarly, high trait-anxious individuals did not improve their performance during a demanding EF task when monetary incentives were offered, while low trait-anxious individuals demonstrated the expected enhanced performance in the reward condition Eysenck, In a sample of anxious adolescents, incentive-related modulation of performance on a cognitive control task was significantly weaker than in healthy adolescents Hardin et al.
Motivation and the Brain
The failure of motivational manipulations to appropriately modulate EFs in individuals with anxiety and depression is likely related to the observed dysfunction in brain networks associated with incentive processing and task-relevant cognitive processing. As reviewed above, anxiety and depression are associated with dysfunction in areas involved in processing both positive, rewarding stimuli and negative, punishing stimuli e.
Furthermore, it is likely that networks involved in implementing motivation-related processes and EFs fail to interact appropriately in order to integrate various functions and successfully execute goal-driven behavior. Relationships among EF, emotion, and motivation Evidence reviewed above establishes many interactions among cognition, emotion, and motivation and clearly indicates that these interactions contribute to psychopathology.
Although it is generally assumed that deficits in cognition and EF are caused by emotional and motivational disturbances, it has also been postulated that deficits in specific EFs e. For example, a bias to attend to negative information in anxious and depressed individuals may be driven in part by difficulties inhibiting distracting information or shifting attention to relevant aspects of a task. EFs may affect motivational processes, such that they alter ability to evaluate potentially pleasurable stimuli or activities or implement approach-related behaviors.
EF deficits make it difficult to select goals based on their anticipated benefits and to implement strategies aimed at achieving these goals, particularly when distractions are present in the environment Banich, Some support for EF deficits contributing to emotion-related symptoms of psychopathology has been provided by recent research. Bredemeier and Berenbaum in press found that, when controlling for initial levels of worry, reduced working memory capacity predicted worry levels several weeks later.
Similarly, research in our laboratory found that self-reported working memory difficulties predicted increases in symptoms of depression several months later, above and beyond the effects of initial depression Letkiewicz et al. Alexopoulos and colleagues found evidence that scores on measures of initiation and perseveration predicted early relapse, recurrence of depression, and the course of depressive symptoms post-remission.
Interestingly, a treatment study of the response of depressed individuals to the antidepressant fluoxetine found that nonresponders performed significantly worse on pre-treatment measures of EF Wisconsin Card Sorting Task, Stroop task; Dunkin et al. Determining which deficits come first, or understanding the causal and temporal mechanisms of the relationship between difficulties in EF and psychopathology, will depend in part on the availability of longitudinal data.
Regardless of the nature of causality among these psychological and biological processes Miller,the relationships among EFs, emotion, and motivation in anxiety and depression are likely related to dysfunction in brain networks that are involved in integrating aspects of these processes, particularly DLPFC and ACC Gray et al.
Further, research in our laboratory showed that DLPFC regions associated with approach and avoidance motivation demonstrated increased connectivity with OFC, ACC, amygdala, and basal ganglia during an EF task involving goal maintenance in the face of distraction Spielberg et al. ACC also seems a likely candidate for integrating aspects of emotion, motivation, and EF, evidenced by its connectivity to both the amygdala and nucleus accumbens, as well as OFC and ventral striatum Pessoa,key areas involved in emotion and motivation.
Hence, subregions of ACC are involved in assessing events for their emotional and motivational relevance, error and conflict monitoring, and predicting value of potential rewards and punishments Rushworth et al. Other research explicitly examining functional connectivity between regions also suggests that anxiety and depression are associated with dysfunctional communication between regions. For example, individuals with MDD exhibited decreased connectivity in a fronto-parietal network relative to healthy controls during a working memory task Vasic et al.
Individuals with social phobia displayed less functional connectivity between the amygdala, medial OFC, and PCC than healthy individuals during rest Hahn et al. Thus, it is likely that the dysfunction observed in individuals with anxiety and depression is related to problematic communication between regions, rather than just altered activity in isolated regions.
Intervention and neuroplasticity Numerous interventions, both psychological and biological, have been developed to target disruptions in cognition, emotion, and motivation interactions associated with anxiety and depression.
In addition, a growing body of research has aimed to elucidate the mechanisms of neuroplasticity by characterizing the experience-dependent functional and structural changes in the brain associated with these interventions.
As reviewed above, anxiety and depression are associated with impaired executive control, dysfunctional relationships among cognitive, emotional, and motivational processes, and abnormal activity in brain regions that are part of networks implementing these processes. Importantly, they appear to normalize function and structure in the brain regions and networks that exhibit dysfunction prior to treatment in individuals who respond to treatment. Although a large body of literature demonstrates improvements in psychological symptoms associated with various types of interventions, it should be noted that not everyone responds to one or more of these treatments.
Less than half of individuals with depression who receive either psychotherapy or pharmacotherapy are able to attain full remission Casacalenda et al.
Further, many individuals who respond initially to treatment ultimately relapse, regardless of the type of treatment received. However, there is evidence that psychotherapy leads to lower relapse rates than does pharmacotherapy Gould et al. There continues to be great room for improvement in treatments in order to increase recovery rates and prevent relapse. If we can better understand the psychological and neural mechanisms through which treatment is effective for responders, this knowledge can be used to improve treatments, as well as match specific treatments to those who are likely to benefit from it.
Cognitive behavioral therapy CBT is one of the most effective psychological treatments for anxiety and depression and addresses emotion-cognition and motivation-cognition interactions that are altered in these disorders.
The cognitive component of CBT and CT emphasizes changing problematic patterns of thinking and maladaptive beliefs, which leads to improvements in emotional and motivational function and enhances approach behavior. The behavioral component of CBT and a related therapeutic approach, Behavioral Activation BAtarget problematic behavioral patterns e. In addition to increasing more adaptive, approach-related behaviors, these behavioral strategies lead to alterations in cognition and emotion.
Some studies have found that CBT and CT for depression are associated with decreased amygdala activation and increased prefrontal activation during tasks that recruit various cognitive, emotional, and motivational processes relative to pre-treatment activation see DeRubeis et al. Others have found that prefrontal activation decreased during a resting-state condition e.
It has been suggested that maintaining lower frontal resting-state activity is adaptive in that it allows for more flexible activity during EF task conditions, with the amount of activity depending on the context and task demands DeRubeis et al.
Similar to CBT studies of depression, studies of successful CBT for anxiety disorders highlight the neuroplasticity of several brain regions that play key roles in cognition, emotion, and motivation.
For example, individuals diagnosed with posttraumatic stress disorder PTSD were given treatment involving imaginal exposure to feared situations and cognitive restructuring, two key components of CBT for PTSD that target avoidance behaviors and distortions in thought patterns Felmingham et al. Researchers found that treatment was associated with PTSD-symptom improvement, as well as increased rACC activation and decreased amygdala activation when viewing fearful versus neural faces.
Thus, treatment normalized dysfunctional pre-treatment activity in regions involved in emotional experience and regulation. Treatment for obsessive-compulsive disorder OCD that focused on changing maladaptive behavior patterns was associated with decreased caudate activity during rest Schwartz et al.
Individuals with spider phobia exhibited decreased symptoms post-CBT along with significant reductions of pre-treatment hyperactivity in insula and ACC Straube et al. Clark and Beck reviewed studies of CBT for anxiety disorders and reported that treatment leads to increased activity in ventral and dorsal ACC, mPFC, and VLPFC, regions that exhibit pre-treatment hypoactivity relative to controls, as well as decreased activity in amygdala, hippocampus, and anterior and medial temporal cortex, which show pre-treatment hyperactivity.
Thus, CBT alters activity in regions involved in diverse cognitive, emotional, and motivational processes, including more bottom-up, stimulus-driven processing and top-down processing Clark and Beck, Successful antidepressant treatment has been associated with decreased activation in regions involved in threat and punishment-related responses such as the amygdala, subgenual cingulate, and striatum in response to affective stimuli Mayberg et al. Prior to treatment, these regions appeared to be hyperactive relative to healthy individuals.
In addition, antidepressant treatment has been shown to increase activation in several cognitive control regions that are typically hypoactive in depressed individuals, including prefrontal cortex and rACC Mayberg et al. It has been proposed that antidepressant medication does not target prefrontal activity directly; rather, it targets amygdala activity, which in turn prompts prefrontal disinhibition DeRubeis et al.
Further, antidepressant medication appears to enhance functional connectivity among brain regions in depressed individuals Anand et al. Antidepressant medication has been used to treat anxiety as well. Studies examining its effects on neural activity in individuals with anxiety disorders have found that it also appears to normalize activity in regions and networks that were dysfunctional prior to treatment in medication responders.
For example, obsessive-compulsive disorder OCD has been associated with hyperactivity in frontal-subcortical circuits relative to healthy individuals, and antidepressant treatment has been shown to decrease activity in OFC and caudate nucleus Saxena et al.
In addition, antidepressant treatment has been associated with decreased activity in medial temporal cortex in individuals with PTSD Seedat et al. Further, after antidepressant treatment, individuals with social phobia displayed attenuated activity in amygdala, hippocampus, and parahippocampal cortex during a public speaking task Furmark et al.
These functional changes associated with successful medication and psychotherapy treatment are supported by structural changes. Antidepressants appear to reverse various structural abnormalities observed in depression and anxiety. For example, there is evidence that chronic antidepressant treatment enhances neurogenesis, prevents neuronal atrophy, and promotes neuronal sprouting and dendritic branching Vaidya and Duman, ; Pittenger and Duman, It also stimulates new synapse formation, strengthens synaptic connectivity, and alters neurotrophic signaling cascades Manji et al.
These cellular and molecular changes are associated with more macro-level changes, including increased regional brain volume e. There is little direct evidence of cellular and regional changes associated with psychotherapy specifically; however, such changes have been observed after various learning-related experiences similar to those involved in psychotherapy Kolb and Whishaw, ; Liggan and Kay,and the neuroplastic effects of structured behavioral interventions more generally are well established e.
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Studies examining the neurobiological effects of pharmacological versus psychological treatments have been inconsistent, with some reporting similar results e. Seminowicz and colleagues asserted that different types of treatment e.
Regardless, psychotherapy and antidepressant medication appear to have at least some similar effects, though they likely have distinct mechanisms of change e. This hypothesis is consistent with anecdotal reports that medication can be helpful in diminishing the intensity of emotional and motivational symptoms in a way that allows more intentional cognitive strategies to be deployed effectively. This may explain why the combination of antidepressants and CBT is more effective than either alone in difficult-to-treat cases of depression Keller et al.
To our knowledge, no research has examined the neural changes associated with combined medication and psychotherapy treatment. Future research in this area will be useful to determine if pharmacotherapy and psychotherapy have additive or interactive effects on brain activation.
The studies reviewed above are limited in that they reflect neural changes in individuals who responded to treatment and showed at least some symptom improvement. Although uncommon, a few studies have examined neural patterns in treatment nonresponders. For example, Mayberg and colleagues found that, relative to responders, nonresponders showed an inverse activation pattern in some areas e. In addition, an exciting line of research has begun to examine how findings from studies of neural mechanisms involved in psychological and pharmacological interventions can be used to inform treatment selection for individuals, given that not everyone responds.
Numerous studies have found that pre-treatment activity in rACC and subgenual portions of ACC sgACC is consistently predictive of who will respond to treatment for a review, see Mayberg, For example, Siegle and colleagues scanned depressed individuals prior to 16 sessions of CBT while they performed an emotional information processing task. They found that low pre-treatment sgACC and high amygdala activation in response to negative words were associated with increased response to CBT.
The results regarding sgACC were replicated in two separate samples Siegle et al. Such evidence of pretreatment psychophysiological reactivity predicting psychotherapy response adds to a long tradition of such literature e.
Similar to CBT, several antidepressant studies have found that greater pre-treatment activity in rACC consistently predicted better response to antidepressant treatment in individuals with anxiety and depressive disorders Mayberg et al. Activity in other regions, including OFC and amygdala, has also been found to predict greater improvement with treatment Saxena et al. In addition, patterns of connectivity between regions in a network shown to be dysfunctional in depression e.
Although much work remains to be done before routinely applying such findings to clinical practice, matching individuals with treatments likely to be effective based on pretreatment psychophysiological and neuroantatomical characterization is a promising method that can be used in the future to enhance response rates.
Cognitive bias modification Another line of research has explored improving response rates with strategies other than treatment-matching. Some researchers have argued that using methods that more directly target cognitive processes, specifically the biases observed in anxiety and depression, will improve current treatment approaches.
Thus far, evidence suggests that decreasing cognitive biases leads to enhanced emotional function for review, see Koster et al. This literature developed in part to test the theory that cognitive biases play a role in the etiology of anxiety and depressive disorders and are an important target for therapeutic intervention.
Numerous studies have now provided support that cognitive biases 1 play a causal role in psychopathology, 2 can be modified, and 3 lead to improvements in clinical symptoms and emotional reactivity to stress when these biases are reduced or alleviated. In fact, cognitive bias modification CBM has received so much recent attention that a special section in Journal of Abnormal Psychology VolumeNumber 1 was devoted to it, numerous reviews have already been published e.
This literature encompasses a variety of experimental procedures, typically computerized, that are used to systematically alter cognitive processing styles. Given the prolific research focusing on the role of attentional bias in anxiety, it is not surprising that there is also a large CBM literature investigating the alteration of this bias for review, see Bar-Haim, For example, individuals with GAD exhibited reduced anxiety symptoms after undergoing a training procedure involving a probe task that induced a bias to orient attention away from threatening information toward neutral words Amir et al.
These results provide support for the assertion that an attentional bias to negative information plays a causal role in the development of GAD symptoms.
Similarly, individuals who suffered from recurrent depression exhibited significant reductions in depression, anxiety, automatic negative thoughts, and rumination after undergoing attention training involving monitoring external auditory stimuli under conditions of selective attention, attention switching, and divided attention Papageorgiou and Wells, Primary reinforcers motivate behavior without any learning while secondary reinforcers only motivate after learning — or conditioning - takes place.
They trained rats to press a lever to obtain food pellets, for example. This is called instrumental learning. From these animal experiments, neuroscientists have extrapolated primary and secondary reinforcers of human behaviors. Humans learn cues that lead to positive and negative outcomes, becoming motivated by actions and behaviors that produce positive results. Individuals also quickly learn what elicits negative outcomes, and try to decrease or avoid behaviors leading to adverse results.
However, research studies using humans have remained obscure mainly as a result of ethical consequences. For example, keeping food from humans, or punishing them with options such as electric shock to teach them to avoid certain behaviors are not viable options. The social context also plays a part in human learning. For instance, in some experimental situations, humans will make choices to avoid looking stupid.
However, neuropsychologists now use effective tools to measure human motivation. The Iowa Gambling Task is one such example, now the most widely used tool for understanding how humans use rewards and punishments to alter behavior. Test participants select cards from the decks, which, unknown to them, are marked accordingly: Researchers tell participants that each time they select a card that they will win game money, but occasionally selecting a card will cause them to lose some money.
The high-risk decks offer the highest money rewards but also the greatest penalties. The object is to earn as much money as possible, and participants quickly learn that by selecting from the high-risk decks they earn large amounts of money, but can lose the largest amounts as well. Over the course of the game, participants will earn the most and have the lowest amount of penalties by selecting from the low-risk decks.
Normal participants selecting cards from each deck learn after about 40 or 50 selections which decks have the steadiest income with the least penalties. However, these results are still being debated in the scientific community, with many still not convinced in a direct causal link between OFC dysfunction and consequence planning.The Psychology of Motivation and Emotion
A number of neuropsychological researchers use the Iowa Gambling Task in combination with functional magnetic resonance imaging, or fMRI, to observe the brain regions as they complete the Iowa Gambling Task using different research paradigms. For instance, some observe only normal volunteers while others observe those with psychiatric disorders such as schizophrenia and obsessive-compulsive disorder. A Scientific Workaround However, using fMRI to test participants in terms of primary reinforcers such as food or drink presents some difficulties for scientists because the fMRI machines require participants to lay as still as possible.
They have found a way around this limitation by devising studies that activate taste and smell senses. For example, eating one cookie makes you desire another, and another, until after a certain number of cookies they are no longer appealing. One study gave participants a large meal, and afterwards used the smells of foods eaten during the meal during an fMRI study. The response of the OFC during the presence of the smells became increasingly reduced, pointing to evidence that the OFC is involved in the motivation to keep doing something.
Other researchers have moved away from using food as a primary reinforcer in studies, turning instead to the use of financial rewards. Money is not a primary reinforcer because it does not meet a physiological need; however, it is a strong motivator of behavior.
Since the late s, a series of experiments using money as a reward has shown activation in the following brain areas: For more information on the anatomy of the brain, see the basics of brain structure. Amygdala Damage, Emotions and Motivation As noted in the following article on Emotionsstudies done on those with brain injuries to the amygdala, a sub cortical structure of the limbic system, exhibit dysfunctional emotional processing.
Similarly, studies on motivation — specifically conditioned learning — show that some patients with damage to the amygdala have impairments in conditioned learning concerning both positive and negative reinforcers. Researchers today are investigating this link between the amygdala and motivation — and how damage to this deep brain structure simultaneously causes emotional impairments.