Reward system

From Wikipedia, the free encyclopedia

The reward system (the mesocorticolimbic circuit) is a group of neural structures responsible for incentive salience (i.e., motivation and "wanting"; desire or craving for a reward), associative learning (primarily positive reinforcement and classical conditioning), and positively-valenced emotions, particularly ones involving pleasure as a core component (e.g., joy, euphoria and ecstasy). Reward is the attractive and motivational property of a stimulus that induces appetitive behavior, also known as approach behavior, and consummatory behavior. A rewarding stimulus has been described as "any stimulus, object, event, activity, or situation that has the potential to make us approach and consume it is by definition a reward". In operant conditioning, rewarding stimuli function as positive reinforcers; however, the converse statement also holds true: positive reinforcers are rewarding.

Examples of primary rewards. From top: water, food, sex, and parental care.

 

Addiction and dependence glossary
addiction – a biopsychosocial disorder characterized by persistent use of drugs (including alcohol) despite substantial harm and adverse consequences addictive drug – psychoactive substances that with repeated use are associated with significantly higher rates of substance use disorders, due in large part to the drug's effect on brain reward systems dependence – an adaptive state associated with a withdrawal syndrome upon cessation of repeated exposure to a stimulus (e.g., drug intake) drug sensitization or reverse tolerance – the escalating effect of a drug resulting from repeated administration at a given dose drug withdrawal – symptoms that occur upon cessation of repeated drug use physical dependence – dependence that involves persistent physical–somatic withdrawal symptoms (e.g., fatigue and delirium tremens) psychological dependence – dependence that involves emotional–motivational withdrawal symptoms (e.g., dysphoria and anhedonia) reinforcing stimuli – stimuli that increase the probability of repeating behaviors paired with them rewarding stimuli – stimuli that the brain interprets as intrinsically positive and desirable or as something to approach sensitization – an amplified response to a stimulus resulting from repeated exposure to it substance use disorder – a condition in which the use of substances leads to clinically and functionally significant impairment or distress tolerance – the diminishing effect of a drug resulting from repeated administration at a given dose

The reward system motivates animals to approach stimuli or engage in behaviour that increases fitness (sex, energy-dense foods, etc.). Survival for most animal species depends upon maximizing contact with beneficial stimuli and minimizing contact with harmful stimuli. Reward cognition serves to increase the likelihood of survival and reproduction by causing associative learning, eliciting approach and consummatory behavior, and triggering positively-valenced emotions. Thus, reward is a mechanism that evolved to help increase the adaptive fitness of animals. In drug addiction, certain substances over-activate the reward circuit, leading to compulsive substance-seeking behavior resulting from synaptic plasticity in the circuit.

Primary rewards are a class of rewarding stimuli which facilitate the survival of one's self and offspring, and they include homeostatic (e.g., palatable food) and reproductive (e.g., sexual contact and parental investment) rewards. Intrinsic rewards are unconditioned rewards that are attractive and motivate behavior because they are inherently pleasurable. Extrinsic rewards (e.g., money or seeing one's favorite sports team winning a game) are conditioned rewards that are attractive and motivate behavior but are not inherently pleasurable. Extrinsic rewards derive their motivational value as a result of a learned association (i.e., conditioning) with intrinsic rewards. Extrinsic rewards may also elicit pleasure (e.g., euphoria from winning a lot of money in a lottery) after being classically conditioned with intrinsic rewards.

Definition

In neuroscience, the reward system is a collection of brain structures and neural pathways that are responsible for reward-related cognition, including associative learning (primarily classical conditioning and operant reinforcement), incentive salience (i.e., motivation and "wanting", desire, or craving for a reward), and positively-valenced emotions, particularly emotions that involve pleasure (i.e., hedonic "liking").

Terms that are commonly used to describe behavior related to the "wanting" or desire component of reward include appetitive behavior, approach behavior, preparatory behavior, instrumental behavior, anticipatory behavior, and seeking. Terms that are commonly used to describe behavior related to the "liking" or pleasure component of reward include consummatory behavior and taking behavior.

The three primary functions of rewards are their capacity to:

1. produce associative learning (i.e., classical conditioning and operant reinforcement);
2. affect decision-making and induce approach behavior (via the assignment of motivational salience to rewarding stimuli);
3. elicit positively-valenced emotions, particularly pleasure.

Neuroanatomy

Overview

The brain structures that compose the reward system are located primarily within the cortico-basal ganglia-thalamo-cortical loop; the basal ganglia portion of the loop drives activity within the reward system. Most of the pathways that connect structures within the reward system are glutamatergic interneurons, GABAergic medium spiny neurons (MSNs), and dopaminergic projection neurons, although other types of projection neurons contribute (e.g., orexinergic projection neurons). The reward system includes the ventral tegmental area, ventral striatum (i.e., the nucleus accumbens and olfactory tubercle), dorsal striatum (i.e., the caudate nucleus and putamen), substantia nigra (i.e., the pars compacta and pars reticulata), prefrontal cortex, anterior cingulate cortex, insular cortex, hippocampus, hypothalamus (particularly, the orexinergic nucleus in the lateral hypothalamus), thalamus (multiple nuclei), subthalamic nucleus, globus pallidus (both external and internal), ventral pallidum, parabrachial nucleus, amygdala, and the remainder of the extended amygdala. The dorsal raphe nucleus and cerebellum appear to modulate some forms of reward-related cognition (i.e., associative learning, motivational salience, and positive emotions) and behaviors as well. The laterodorsal tegmental nucleus (LTD), pedunculopontine nucleus (PPTg), and lateral habenula (LHb) (both directly and indirectly via the rostromedial tegmental nucleus) are also capable of inducing aversive salience and incentive salience through their projections to the ventral tegmental area (VTA). The LDT and PPTg both send glutaminergic projections to the VTA that synapse on dopaminergic neurons, both of which can produce incentive salience. The LHb sends glutaminergic projections, the majority of which synapse on GABAergic RMTg neurons that in turn drive inhibition of dopaminergic VTA neurons, although some LHb projections terminate on VTA interneurons. These LHb projections are activated both by aversive stimuli and by the absence of an expected reward, and excitation of the LHb can induce aversion.

Most of the dopamine pathways (i.e., neurons that use the neurotransmitter dopamine to communicate with other neurons) that project out of the ventral tegmental area are part of the reward system; in these pathways, dopamine acts on D1-like receptors or D2-like receptors to either stimulate (D1-like) or inhibit (D2-like) the production of cAMP. The GABAergic medium spiny neurons of the striatum are components of the reward system as well. The glutamatergic projection nuclei in the subthalamic nucleus, prefrontal cortex, hippocampus, thalamus, and amygdala connect to other parts of the reward system via glutamate pathways. The medial forebrain bundle, which is a set of many neural pathways that mediate brain stimulation reward (i.e., reward derived from direct electrochemical stimulation of the lateral hypothalamus), is also a component of the reward system.

Two theories exist with regard to the activity of the nucleus accumbens and the generation liking and wanting. The inhibition (or hyper­polar­ization) hypothesis proposes that the nucleus accumbens exerts tonic inhibitory effects on downstream structures such as the ventral pallidum, hypothalamus or ventral tegmental area, and that in inhibiting MSNs in the nucleus accumbens (NAcc), these structures are excited, "releasing" reward related behavior. While GABA receptor agonists are capable of eliciting both "liking" and "wanting" reactions in the nucleus accumbens, glutaminergic inputs from the basolateral amygdala, ventral hippocampus, and medial prefrontal cortex can drive incentive salience. Furthermore, while most studies find that NAcc neurons reduce firing in response to reward, a number of studies find the opposite response. This had led to the proposal of the disinhibition (or depolarization) hypothesis, that proposes that excitation or NAcc neurons, or at least certain subsets, drives reward related behavior.

After nearly 50 years of research on brain-stimulation reward, experts have certified that dozens of sites in the brain will maintain intracranial self-stimulation. Regions include the lateral hypothalamus and medial forebrain bundles, which are especially effective. Stimulation there activates fibers that form the ascending pathways; the ascending pathways include the mesolimbic dopamine pathway, which projects from the ventral tegmental area to the nucleus accumbens. There are several explanations as to why the mesolimbic dopamine pathway is central to circuits mediating reward. First, there is a marked increase in dopamine release from the mesolimbic pathway when animals engage in intracranial self-stimulation.^[8] Second, experiments consistently indicate that brain-stimulation reward stimulates the reinforcement of pathways that are normally activated by natural rewards, and drug reward or intracranial self-stimulation can exert more powerful activation of central reward mechanisms because they activate the reward center directly rather than through the peripheral nerves.^[8][29][30] Third, when animals are administered addictive drugs or engage in naturally rewarding behaviors, such as feeding or sexual activity, there is a marked release of dopamine within the nucleus accumbens.^[8] However, dopamine is not the only reward compound in the brain.

Key pathway

Diagram showing some of the key components of the mesocorticolimbic ("reward") circuit.

Ventral tegmental area

• The ventral tegmental area (VTA) is important in responding to stimuli and cues that indicate a reward is present. Rewarding stimuli (and all addictive drugs) act on the circuit by triggering the VTA to release dopamine signals to the nucleus accumbens, either directly or indirectly.^{[citation needed]} The VTA has two important pathways: The mesolimbic pathway projecting to limbic (striatal) regions and underpinning the motivational behaviors and processes, and the mesocortical pathway projecting to the prefrontal cortex, underpinning cognitive functions, such as learning external cues, etc. 
• Dopaminergic neurons in this region converts the amino acid tyrosine into DOPA using the enzyme tyrosine hydroxylase, which is then converted to dopamine using the enzyme dopa-decarboxylase.

Striatum (Nucleus Accumbens)

• The striatum is broadly involved in acquiring and eliciting learned behaviors in response to a rewarding cue. The VTA projects to the striatum, and activates the GABA-ergic Medium Spiny Neurons via D1 and D2 receptors within the ventral (Nucleus Accumbens) and dorsal striatum. 
• The Ventral Striatum (the Nucleus Accumbens) is broadly involved in acquiring behavior when fed into by the VTA, and eliciting behavior when fed into by the PFC. The NAc shell projects to the pallidum and the VTA, regulating limbic and autonomic functions. This modulates the reinforcing properties of stimuli, and short term aspects of reward. The NAc Core projects to the substantia nigra and is involved in the development of reward-seeking behaviors and its expression. It is involved in spatial learning, conditional response, and impulsive choice; the long term elements of reward.
• The Dorsal Striatum is involved in learning, the Dorsal Medial Striatum in goal directed learning, and the Dorsal Lateral Striatum in stimulus-response learning foundational to Pavlovian response. On repeated activation by a stimuli, the Nucleus Accumbens can activate the Dorsal Striatum via an intrastriatal loop. The transition of signals from the NAc to the DS allows reward associated cues to activate the DS without the reward itself being present. This can activate cravings and reward-seeking behaviors (and is responsible for triggering relapse during abstinence in addiction).

Prefrontal Cortex

• The VTA dopaminergic neurons project to the PFC, activating glutaminergic neurons that project to multiple other regions, including the Dorsal Striatum and NAc, ultimately allowing the PFC to mediate salience and conditional behaviors in response to stimuli.
• Notably, abstinence from addicting drugs activates the PFC, glutamatergic projection to the NAc, which leads to strong cravings, and modulates reinstatement of addiction behaviors resulting from abstinence. The PFC also interacts with the VTA through the mesocortical pathway, and helps associate environmental cues with the reward. 

Hippocampus

• The Hippocampus has multiple functions, including in the creation and storage of memories . In the reward circuit, it serves to contextual memories and associated cues. It ultimately underpins the reinstatement of reward-seeking behaviors via cues, and contextual triggers. 

Amygdala

• The AMY receives input from the VTA, and outputs to the NAc. The amygdala is important in creating powerful emotional flashbulb memories, and likely underpins the creation of strong cue-associated memories. It also is important in mediating the anxiety effects of withdrawal, and increased drug intake in addiction.

Pleasure centers

Pleasure is a component of reward, but not all rewards are pleasurable (e.g., money does not elicit pleasure unless this response is conditioned). Stimuli that are naturally pleasurable, and therefore attractive, are known as intrinsic rewards, whereas stimuli that are attractive and motivate approach behavior, but are not inherently pleasurable, are termed extrinsic rewards. Extrinsic rewards (e.g., money) are rewarding as a result of a learned association with an intrinsic reward. In other words, extrinsic rewards function as motivational magnets that elicit "wanting", but not "liking" reactions once they have been acquired.

The reward system contains pleasure centers or hedonic hotspots – i.e., brain structures that mediate pleasure or "liking" reactions from intrinsic rewards. As of October 2017, hedonic hotspots have been identified in subcompartments within the nucleus accumbens shell, ventral pallidum, parabrachial nucleus, orbitofrontal cortex (OFC), and insular cortex. The hotspot within the nucleus accumbens shell is located in the rostrodorsal quadrant of the medial shell, while the hedonic coldspot is located in a more posterior region. The posterior ventral pallidum also contains a hedonic hotspot, while the anterior ventral pallidum contains a hedonic coldspot. Microinjections of opioids, endocannabinoids, and orexin are capable of enhancing liking in these hotspots. The hedonic hotspots located in the anterior OFC and posterior insula have been demonstrated to respond to orexin and opioids, as has the overlapping hedonic coldspot in the anterior insula and posterior OFC. On the other hand, the parabrachial nucleus hotspot has only been demonstrated to respond to benzodiazepine receptor agonists.

Hedonic hotspots are functionally linked, in that activation of one hotspot results in the recruitment of the others, as indexed by the induced expression of c-Fos, an immediate early gene. Furthermore, inhibition of one hotspot results in the blunting of the effects of activating another hotspot. Therefore, the simultaneous activation of every hedonic hotspot within the reward system is believed to be necessary for generating the sensation of an intense euphoria.

Wanting and liking

Tuning of appetitive and defensive reactions in the nucleus accumbens shell. (Above) AMPA blockade requires D1 function in order to produce motivated behaviors, regardless of valence, and D2 function to produce defensive behaviors. GABA agonism, on the other hand, does not requires dopamine receptor function.(Below)The expansion of the anatomical regions that produce defensive behaviors under stress, and appetitive behaviors in the home environment produced by AMPA antagonism. This flexibility is less evident with GABA agonism.

Incentive salience is the "wanting" or "desire" attribute, which includes a motivational component, that is assigned to a rewarding stimulus by the nucleus accumbens shell (NAcc shell). The degree of dopamine neurotransmission into the NAcc shell from the mesolimbic pathway is highly correlated with the magnitude of incentive salience for rewarding stimuli.

Activation of the dorsorostral region of the nucleus accumbens correlates with increases in wanting without concurrent increases in liking. However, dopaminergic neurotransmission into the nucleus accumbens shell is responsible not only for appetitive motivational salience (i.e., incentive salience) towards rewarding stimuli, but also for aversive motivational salience, which directs behavior away from undesirable stimuli. In the dorsal striatum, activation of D1 expressing MSNs produces appetitive incentive salience, while activation of D2 expressing MSNs produces aversion. In the NAcc, such a dichotomy is not as clear cut, and activation of both D1 and D2 MSNs is sufficient to enhance motivation, likely via disinhibiting the VTA through inhibiting the ventral pallidum.

Robinson and Berridge's 1993 incentive-sensitization theory proposed that reward contains separable psychological components: wanting (incentive) and liking (pleasure). To explain increasing contact with a certain stimulus such as chocolate, there are two independent factors at work – our desire to have the chocolate (wanting) and the pleasure effect of the chocolate (liking). According to Robinson and Berridge, wanting and liking are two aspects of the same process, so rewards are usually wanted and liked to the same degree. However, wanting and liking also change independently under certain circumstances. For example, rats that do not eat after receiving dopamine (experiencing a loss of desire for food) act as though they still like food. In another example, activated self-stimulation electrodes in the lateral hypothalamus of rats increase appetite, but also cause more adverse reactions to tastes such as sugar and salt; apparently, the stimulation increases wanting but not liking. Such results demonstrate that the reward system of rats includes independent processes of wanting and liking. The wanting component is thought to be controlled by dopaminergic pathways, whereas the liking component is thought to be controlled by opiate-benzodiazepine systems.

Anti-Reward system

Koobs & LeMoal proposed that there exists a separate circuit responsible for the attenuation of reward-pursuing behavior, which they termed the anti-reward circuit. This component acts as brakes on the reward circuit, thus preventing the over pursuit of food, sex, etc. This circuit involves multiple parts of the amygdala (the bed nucleus of the stria terminalis, the central nucleus), the Nucleus Accumbens, and signal molecules including norepinephrine, corticotropin-releasing factor, and dynorphin. This circuit is also hypothesized to mediate the unpleasant components of stress, and is thus thought to be involved in addiction and withdrawal. While the reward circuit mediates the initial positive reinforcement involved in the development of addiction, it is the anti-reward circuit that later dominates via negative reinforcement that motivates the pursuit of the rewarding stimuli.

Learning

Rewarding stimuli can drive learning in both the form of classical conditioning (Pavlovian conditioning) and operant conditioning (instrumental conditioning). In classical conditioning, a reward can act as an unconditioned stimulus that, when associated with the conditioned stimulus, causes the conditioned stimulus to elicit both musculoskeletal (in the form of simple approach and avoidance behaviors) and vegetative responses. In operant conditioning, a reward may act as a reinforcer in that it increases or supports actions that lead to itself. Learned behaviors may or may not be sensitive to the value of the outcomes they lead to; behaviors that are sensitive to the contingency of an outcome on the performance of an action as well as the outcome value are goal-directed, while elicited actions that are insensitive to contingency or value are called habits. This distinction is thought to reflected two forms of learning, model free and model based. Model free learning involves the simple caching and updating of values. In contrast, model based learning involves the storage and construction of an internal model of events that allows inference and flexible prediction. Although pavlovian conditioning is generally assumed to be model-free, the incentive salience assigned to a conditioned stimulus is flexible with regard to changes in internal motivational states.

Distinct neural systems are responsible for learning associations between stimuli and outcomes, actions and outcomes, and stimuli and responses. Although classical conditioning is not limited to the reward system, the enhancement of instrumental performance by stimuli (i.e., Pavlovian-instrumental transfer) requires the nucleus accumbens. Habitual and goal directed instrumental learning are dependent upon the lateral striatum and the medial striatum, respectively.

During instrumental learning, opposing changes in the ratio of AMPA to NMDA receptors and phosphorylated ERK occurs in the D₁-type and D₂-type MSNs that constitute the direct and indirect pathways, respectively. These changes in synaptic plasticity and the accompanying learning is dependent upon activation of striatal D1 and NMDA receptors. The intracellular cascade activated by D1 receptors involves the recruitment of protein kinase A, and through resulting phosphorylation of DARPP-32, the inhibition of phosphatases that deactivate ERK. NMDA receptors activate ERK through a different but interrelated Ras-Raf-MEK-ERK pathway. Alone NMDA mediated activation of ERK is self-limited, as NMDA activation also inhibits PKA mediated inhibition of ERK deactivating phosphatases. However, when D1 and NMDA cascades are co-activated, they work synergistically, and the resultant activation of ERK regulates synaptic plasticity in the form of spine restructuring, transport of AMPA receptors, regulation of CREB, and increasing cellular excitability via inhibiting Kv4.2

Disorders

Addiction

ΔFosB (DeltaFosB) – a gene transcription factor – overexpression in the D1-type medium spiny neurons of the nucleus accumbens is the crucial common factor among virtually all forms of addiction (i.e., behavioral addictions and drug addictions) that induces addiction-related behavior and neural plasticity. In particular, ΔFosB promotes self-administration, reward sensitization, and reward cross-sensitization effects among specific addictive drugs and behaviors. Certain epigenetic modifications of histone protein tails (i.e., histone modifications) in specific regions of the brain are also known to play a crucial role in the molecular basis of addictions.

Addictive drugs and behaviors are rewarding and reinforcing (i.e., are addictive) due to their effects on the dopamine reward pathway.

The lateral hypothalamus and medial forebrain bundle has been the most-frequently-studied brain-stimulation reward site, particularly in studies of the effects of drugs on brain stimulation reward. The neurotransmitter system that has been most-clearly identified with the habit-forming actions of drugs-of-abuse is the mesolimbic dopamine system, with its efferent targets in the nucleus accumbens and its local GABAergic afferents. The reward-relevant actions of amphetamine and cocaine are in the dopaminergic synapses of the nucleus accumbens and perhaps the medial prefrontal cortex. Rats also learn to lever-press for cocaine injections into the medial prefrontal cortex, which works by increasing dopamine turnover in the nucleus accumbens. Nicotine infused directly into the nucleus accumbens also enhances local dopamine release, presumably by a presynaptic action on the dopaminergic terminals of this region. Nicotinic receptors localize to dopaminergic cell bodies and local nicotine injections increase dopaminergic cell firing that is critical for nicotinic reward. Some additional habit-forming drugs are also likely to decrease the output of medium spiny neurons as a consequence, despite activating dopaminergic projections. For opiates, the lowest-threshold site for reward effects involves actions on GABAergic neurons in the ventral tegmental area, a secondary site of opiate-rewarding actions on medium spiny output neurons of the nucleus accumbens. Thus the following form the core of currently characterised drug-reward circuitry; GABAergic afferents to the mesolimbic dopamine neurons (primary substrate of opiate reward), the mesolimbic dopamine neurons themselves (primary substrate of psychomotor stimulant reward), and GABAergic efferents to the mesolimbic dopamine neurons (a secondary site of opiate reward).

Motivation

Dysfunctional motivational salience appears in a number of psychiatric symptoms and disorders. Anhedonia, traditionally defined as a reduced capacity to feel pleasure, has been re-examined as reflecting blunted incentive salience, as most anhedonic populations exhibit intact “liking”. On the other end of the spectrum, heightened incentive salience that is narrowed for specific stimuli is characteristic of behavioral and drug addictions. In the case of fear or paranoia, dysfunction may lie in elevated aversive salience.

Neuroimaging studies across diagnoses associated with anhedonia have reported reduced activity in the OFC and ventral striatum. One meta analysis reported anhedonia was associated with reduced neural response to reward anticipation in the caudate nucleus, putamen, nucleus accumbens and medial prefrontal cortex (mPFC).

Mood disorders

Certain types of depression are associated with reduced motivation, as assessed by willingness to expend effort for reward. These abnormalities have been tentatively linked to reduced activity in areas of the striatum, and while dopaminergic abnormalities are hypothesized to play a role, most studies probing dopamine function in depression have reported inconsistent results. Although postmortem and neuroimaging studies have found abnormalities in numerous regions of the reward system, few findings are consistently replicated. Some studies have reported reduced NAcc, hippocampus, medial prefrontal cortex (mPFC), and orbitofrontal cortex (OFC) activity, as well as elevated basolateral amygdala and subgenual cingulate cortex (sgACC) activity during tasks related to reward or positive stimuli. These neuroimaging abnormalities are complemented by little post mortem research, but what little research has been done suggests reduced excitatory synapses in the mPFC. Reduced activity in the mPFC during reward related tasks appears to be localized to more dorsal regions(i.e. the pregenual cingulate cortex), while the more ventral sgACC is hyperactive in depression.

Attempts to investigate underlying neural circuitry in animal models has also yielded conflicting results. Two paradigms are commonly used to simulate depression, chronic social defeat (CSDS), and chronic mild stress (CMS), although many exist. CSDS produces reduced preference for sucrose, reduced social interactions, and increased immobility in the forced swim test. CMS similarly reduces sucrose preference, and behavioral despair as assessed by tail suspension and forced swim tests. Animals susceptible to CSDS exhibit increased phasic VTA firing, and inhibition of VTA-NAcc projections attenuates behavioral deficits induced by CSDS. However, inhibition of VTA-mPFC projections exacerbates social withdrawal. On the other hand, CMS associated reductions in sucrose preference and immobility were attenuated and exacerbated by VTA excitation and inhibition, respectively. Although these differences may be attributable to different stimulation protocols or poor translational paradigms, variable results may also lie in the heterogenous functionality of reward related regions.

Optogenetic stimulation of the mPFC as a whole produces antidepressant effects. This effect appears localized to the rodent homologue of the pgACC (the prelimbic cortex), as stimulation of the rodent homologue of the sgACC (the infralimbic cortex) produces no behavioral effects. Furthermore, deep brain stimulation in the infralimbic cortex, which is thought to have an inhibitory effect, also produces an antidepressant effect. This finding is congruent with the observation that pharmacological inhibition of the infralimbic cortex attenuates depressive behaviors.

Schizophrenia

Schizophrenia is associated with deficits in motivation, commonly grouped under other negative symptoms such as reduced spontaneous speech. The experience of “liking” is frequently reported to be intact, both behaviorally and neurally, although results may be specific to certain stimuli, such as monetary rewards. Furthermore, implicit learning and simple reward-related tasks are also intact in schizophrenia. Rather, deficits in the reward system are apparent during reward-related tasks that are cognitively complex. These deficits are associated with both abnormal striatal and OFC activity, as well as abnormalities in regions associated with cognitive functions such as the dorsolateral prefrontal cortex (DLPFC).

History

Skinner box

The first clue to the presence of a reward system in the brain came with an accident discovery by James Olds and Peter Milner in 1954. They discovered that rats would perform behaviors such as pressing a bar, to administer a brief burst of electrical stimulation to specific sites in their brains. This phenomenon is called intracranial self-stimulation or brain stimulation reward. Typically, rats will press a lever hundreds or thousands of times per hour to obtain this brain stimulation, stopping only when they are exhausted. While trying to teach rats how to solve problems and run mazes, stimulation of certain regions of the brain where the stimulation was found seemed to give pleasure to the animals. They tried the same thing with humans and the results were similar. The explanation to why animals engage in a behavior that has no value to the survival of either themselves or their species is that the brain stimulation is activating the system underlying reward.

In a fundamental discovery made in 1954, researchers James Olds and Peter Milner found that low-voltage electrical stimulation of certain regions of the brain of the rat acted as a reward in teaching the animals to run mazes and solve problems. It seemed that stimulation of those parts of the brain gave the animals pleasure, and in later work humans reported pleasurable sensations from such stimulation. When rats were tested in Skinner boxes where they could stimulate the reward system by pressing a lever, the rats pressed for hours. Research in the next two decades established that dopamine is one of the main chemicals aiding neural signaling in these regions, and dopamine was suggested to be the brain's "pleasure chemical".

Ivan Pavlov was a psychologist who used the reward system to study classical conditioning. Pavlov used the reward system by rewarding dogs with food after they had heard a bell or another stimulus. Pavlov was rewarding the dogs so that the dogs associated food, the reward, with the bell, the stimulus. Edward L. Thorndike used the reward system to study operant conditioning. He began by putting cats in a puzzle box and placing food outside of the box so that the cat wanted to escape. The cats worked to get out of the puzzle box to get to the food. Although the cats ate the food after they escaped the box, Thorndike learned that the cats attempted to escape the box without the reward of food. Thorndike used the rewards of food and freedom to stimulate the reward system of the cats. Thorndike used this to see how the cats learned to escape the box.

Other species

Animals quickly learn to press a bar to obtain an injection of opiates directly into the midbrain tegmentum or the nucleus accumbens. The same animals do not work to obtain the opiates if the dopaminergic neurons of the mesolimbic pathway are inactivated. In this perspective, animals, like humans, engage in behaviors that increase dopamine release.

Kent Berridge, a researcher in affective neuroscience, found that sweet (liked ) and bitter (disliked ) tastes produced distinct orofacial expressions, and these expressions were similarly displayed by human newborns, orangutans, and rats. This was evidence that pleasure (specifically, liking) has objective features and was essentially the same across various animal species. Most neuroscience studies have shown that the more dopamine released by the reward, the more effective the reward is. This is called the hedonic impact, which can be changed by the effort for the reward and the reward itself. Berridge discovered that blocking dopamine systems did not seem to change the positive reaction to something sweet (as measured by facial expression). In other words, the hedonic impact did not change based on the amount of sugar. This discounted the conventional assumption that dopamine mediates pleasure. Even with more-intense dopamine alterations, the data seemed to remain constant. However, a clinical study from January 2019 that assessed the effect of a dopamine precursor (levodopa), antagonist (risperidone), and a placebo on reward responses to music – including the degree of pleasure experienced during musical chills, as measured by changes in electrodermal activity as well as subjective ratings – found that the manipulation of dopamine neurotransmission bidirectionally regulates pleasure cognition (specifically, the hedonic impact of music) in human subjects. This research demonstrated that increased dopamine neurotransmission acts as a sine qua non condition for pleasurable hedonic reactions to music in humans.

Berridge developed the incentive salience hypothesis to address the wanting aspect of rewards. It explains the compulsive use of drugs by drug addicts even when the drug no longer produces euphoria, and the cravings experienced even after the individual has finished going through withdrawal. Some addicts respond to certain stimuli involving neural changes caused by drugs. This sensitization in the brain is similar to the effect of dopamine because wanting and liking reactions occur. Human and animal brains and behaviors experience similar changes regarding reward systems because these systems are so prominent.

Psychological trauma

From Wikipedia, the free encyclopedia

 

Psychological trauma

Psychological trauma is damage to a person's mind as a result of one or more events that cause overwhelming amounts of stress that exceed the person's ability to cope or integrate the emotions involved, eventually leading to serious, long-term negative consequences. Trauma is not the same as mental distress.

Given that subjective experiences differ between individuals, people will react to similar traumatic events differently. In other words, not all people who experience a potentially traumatic event will actually become psychologically traumatized. However, some people will develop post-traumatic stress disorder (PTSD) after being exposed to a major traumatic event. This discrepancy in risk rate can be attributed to protective factors some individuals may have that enable them to cope with trauma; they are related to temperamental and environmental factors from among others. Some examples are resilience characteristics and active seeking of help.

Signs and symptoms

People who go through these types of extremely traumatic experiences often have certain symptoms and problems afterwards. The severity of these symptoms depends on the person, the type of trauma involved, and the emotional support they receive from others. The range of reactions to and symptoms of trauma can be wide and varied, and differ in severity from person to person. A traumatized individual may experience one or several of them.

After a traumatic experience, a person may re-experience the trauma mentally and physically. For example, the sound of a motorcycle engine may cause intrusive thoughts or a sense of re-experiencing a traumatic experience that involved a similar sound (e.g., gunfire). Sometimes a benign stimulus (e.g., noise from a motorcycle) may get connected in the mind with the traumatic experience. This process is called traumatic coupling. In this process, the benign stimulus becomes a trauma reminders, also called a trauma trigger. These can produce uncomfortable and even painful feelings. Re-experiencing can damage people's sense of safety, self, self-efficacy, as well as their ability to regulate emotions and navigate relationships. They may turn to psychoactive substances including alcohol to try to escape or dampen the feelings. These triggers cause flashbacks, which are dissociative experiences where the person feels as though the events are recurring. Flashbacks can range from distraction to complete dissociation or loss of awareness of the current context. Re-experiencing of symptoms is a sign that the body and mind are actively struggling to cope with the traumatic experience.

Triggers and cues act as reminders of the trauma and can cause anxiety and other associated emotions. Often the person can be completely unaware of what these triggers are. In many cases this may lead a person suffering from traumatic disorders to engage in disruptive behaviors or self-destructive coping mechanisms, often without being fully aware of the nature or causes of their own actions. Panic attacks are an example of a psychosomatic response to such emotional triggers.

Consequently, intense feelings of anger may frequently surface, sometimes in inappropriate or unexpected situations, as danger may always seem to be present due to re-experiencing past events. Upsetting memories such as images, thoughts, or flashbacks may haunt the person, and nightmares may be frequent. Insomnia may occur as lurking fears and insecurity keep the person vigilant and on the lookout for danger, both day and night. Trauma doesn't only cause changes in one's daily functions, but could also lead to morphological changes. Such epigenetic changes can be passed on to the next generation, thus making genetics one of the components of psychological trauma. However, some people are born with or later develop protective factors such as genetics and sex that help lower their risk of psychological trauma.

The person may not remember what actually happened, while emotions experienced during the trauma may be re-experienced without the person understanding why. This can lead to the traumatic events being constantly experienced as if they were happening in the present, preventing the subject from gaining perspective on the experience. This can produce a pattern of prolonged periods of acute arousal punctuated by periods of physical and mental exhaustion. This can lead to mental health disorders like acute stress and anxiety disorder, traumatic grief, undifferentiated somatoform disorder, conversion disorders, brief psychotic disorder, borderline personality disorder, adjustment disorder, etc.

In time, emotional exhaustion may set in, leading to distraction, and clear thinking may be difficult or impossible. Emotional detachment, as well as dissociation or "numbing out" can frequently occur. Dissociating from the painful emotion includes numbing all emotion, and the person may seem emotionally flat, preoccupied, distant, or cold. Dissociation includes depersonalisation disorder, dissociative amnesia, dissociative fugue, dissociative identity disorder, etc. Exposure to and re-experiencing trauma can cause neurophysiological changes like slowed myelination, abnormalities in synaptic pruning, shrinking of the hippocampus, cognitive and affective impairment. This is significant in brain scan studies done regarding higher-order function assessment with children and youth who were in vulnerable environments.

Some traumatized people may feel permanently damaged when trauma symptoms do not go away and they do not believe their situation will improve. This can lead to feelings of despair, transient paranoid ideation, loss of self-esteem, profound emptiness, suicidality, and frequently, depression. If important aspects of the person's self and world understanding have been violated, the person may call their own identity into question. Often despite their best efforts, traumatized parents may have difficulty assisting their child with emotion regulation, attribution of meaning, and containment of post-traumatic fear in the wake of the child's traumatization, leading to adverse consequences for the child. In such instances, seeking counselling in appropriate mental health services is in the best interests of both the child and the parent(s).

Causes

Situational trauma

Trauma can be caused by man-made, technological and natural disasters, including war, abuse, violence, mechanized accidents (such as vehicle accidents) or medical emergencies.

An individual's response to psychological trauma can be varied based on the type of trauma, as well as socio-demographic and background factors. There are several behavioral responses commonly used towards stressors including the proactive, reactive, and passive responses. Proactive responses include attempts to address and correct a stressor before it has a noticeable effect on lifestyle. Reactive responses occur after the stress and possible trauma has occurred and is aimed more at correcting or minimizing the damage of a stressful event. A passive response is often characterized by an emotional numbness or ignorance of a stressor.

Those who are able to be proactive can often overcome stressors and are more likely to be able to cope well with unexpected situations. On the other hand, those who are more reactive will often experience more noticeable effects from an unexpected stressor. In the case of those who are passive, victims of a stressful event are more likely to suffer from long-term traumatic effects and often enact no intentional coping actions. These observations may suggest that the level of trauma associated with a victim is related to such independent coping abilities.

There is also a distinction between trauma induced by recent situations and long-term trauma which may have been buried in the unconscious from past situations such as childhood abuse. Trauma is sometimes overcome through healing; in some cases this can be achieved by recreating or revisiting the origin of the trauma under more psychologically safe circumstances, such as with a therapist. More recently, awareness of the consequences of climate change is seen as a source of trauma as individuals contemplate future events as well as experience climate change related disasters. Emotional experiences within these contexts are increasing, and collective processing and engagement with these emotions can lead to increased resilience and post traumatic growth, as well as a greater sense of belongingness. These outcomes are protective against the devastating impacts of psychological trauma. 

In psychodynamics

Psychodynamic viewpoints are controversial, but have been shown to have utility therapeutically.

French neurologist, Jean-Martin Charcot, argued in the 1890s that psychological trauma was the origin of all instances of the mental illness known as hysteria. Charcot's "traumatic hysteria" often manifested as paralysis that followed a physical trauma, typically years later after what Charcot described as a period of "incubation". Sigmund Freud, Charcot's student and the father of psychoanalysis, examined the concept of psychological trauma throughout his career. Jean Laplanche has given a general description of Freud's understanding of trauma, which varied significantly over the course of Freud's career: "An event in the subject's life, defined by its intensity, by the subject's incapacity to respond adequately to it and by the upheaval and long-lasting effects that it brings about in the psychical organization".

The French psychoanalyst Jacques Lacan claimed that what he called "The Real" had a traumatic quality external to symbolization. As an object of anxiety, Lacan maintained that The Real is "the essential object which isn't an object any longer, but this something faced with which all words cease and all categories fail, the object of anxiety par excellence".

Fred Alford, citing the work of object relations theorist Donald Winnicott, uses the concept of inner other, and internal representation of the social world, with which one converses internally and which is generated through interactions with others. He posits that the inner other is damaged by trauma but can be repaired by conversations with others such as therapists. He relates the concept of the inner other to the work of Albert Camus viewing the inner other as that which removes the absurd. Alford notes how trauma damages trust is social relations due to fear of exploitation and argues that culture and social relations can help people recover from trauma.

Stress disorders

All psychological traumas originate from stress, a physiological response to an unpleasant stimulus. Long-term stress increases the risk of poor mental health and mental disorders, which can be attributed to secretion of glucocorticoids for a long period of time. Such prolonged exposure causes many physiological dysfunctions such as the suppression of the immune system and increase in blood pressure. Not only does it affect the body physiologically, but a morphological change in the hippocampus also takes place. Studies showed that extreme stress early in life can disrupt normal development of hippocampus and impact its functions in adulthood. Studies surely show a correlation between the size of hippocampus and one's susceptibility to stress disorders. In times of war, psychological trauma has been known as shell shock or combat stress reaction. Psychological trauma may cause an acute stress reaction which may lead to posttraumatic stress disorder (PTSD). PTSD emerged as the label for this condition after the Vietnam War in which many veterans returned to their respective countries demoralized, and sometimes, addicted to psychoactive substances.

The symptoms of PTSD must persist for at least one month for diagnosis to be made. The main symptoms of PTSD consist of four main categories: trauma (i.e. intense fear), reliving (i.e. flashbacks), avoidance behavior (i.e. emotional numbing), and hypervigilance (i.e. continuous scanning of the environment for danger). Research shows that about 60% of the US population reported as having experienced at least one traumatic symptom in their lives, but only a small proportion actually develops PTSD. There is a correlation between the risk of PTSD and whether or not the act was inflicted deliberately by the offender. Psychological trauma is treated with therapy and, if indicated, psychotropic medications.

The term continuous posttraumatic stress disorder (CTSD) was introduced into the trauma literature by Gill Straker (1987). It was originally used by South African clinicians to describe the effects of exposure to frequent, high levels of violence usually associated with civil conflict and political repression. The term is also applicable to the effects of exposure to contexts in which gang violence and crime are endemic as well as to the effects of ongoing exposure to life threats in high-risk occupations such as police, fire, and emergency services.

As one of the processes of treatment, confrontation with their sources of trauma plays a crucial role. While debriefing people immediately after a critical incident has not been shown to reduce incidence of PTSD, coming alongside people experiencing trauma in a supportive way has become standard practice.

Vicarious trauma

Vicarious trauma affects workers who witness their clients' trauma. It is more likely to occur in situations where trauma related work is the norm rather than the exception. Listening with empathy to the clients generates feeling, and seeing oneself in clients' trauma may compound the risk for developing trauma symptoms. Trauma may also result if workers witness situations that happen in the course of their work (e.g. violence in the workplace, reviewing violent video tapes.) Risk increases with exposure and with the absence of help seeking protective factors and pre-preparation of preventive strategies.

Diagnosis

As "trauma" adopted a more widely defined scope, traumatology as a field developed a more interdisciplinary approach. This is in part due to the field's diverse professional representation including: psychologists, medical professionals, and lawyers. As a result, findings in this field are adapted for various applications, from individual psychiatric treatments to sociological large-scale trauma management. While the field has adopted a number of diverse methodological approaches, many pose their own limitations in practical application.

The experience and outcomes of psychological trauma can be assessed in a number of ways. Within the context of a clinical interview, the risk of imminent danger to the self or others is important to address but is not the focus of assessment. In most cases, it will not be necessary to involve contacting emergency services (e.g., medical, psychiatric, law enforcement) to ensure the individuals safety; members of the individual's social support network are much more critical.

Understanding and accepting the psychological state of an individual is paramount. There are many misconceptions of what it means for a traumatized individual to be in psychological crisis. These are times when an individual is in inordinate amounts of pain and incapable of self-comfort. If treated humanely and respectfully the individual is less likely to resort to self harm. In these situations it is best to provide a supportive, caring environment and to communicate to the individual that no matter the circumstance, the individual will be taken seriously rather than being treated as delusional. It is vital for the assessor to understand that what is going on in the traumatized person's head is valid and real. If deemed appropriate, the assessing clinician may proceed by inquiring about both the traumatic event and the outcomes experienced (e.g., post-traumatic symptoms, dissociation, substance abuse, somatic symptoms, psychotic reactions). Such inquiry occurs within the context of established rapport and is completed in an empathic, sensitive, and supportive manner. The clinician may also inquire about possible relational disturbance, such as alertness to interpersonal danger, abandonment issues, and the need for self-protection via interpersonal control. Through discussion of interpersonal relationships, the clinician is better able to assess the individual's ability to enter and sustain a clinical relationship.

During assessment, individuals may exhibit activation responses in which reminders of the traumatic event trigger sudden feelings (e.g., distress, anxiety, anger), memories, or thoughts relating to the event. Because individuals may not yet be capable of managing this distress, it is necessary to determine how the event can be discussed in such a way that will not "retraumatize" the individual. It is also important to take note of such responses, as these responses may aid the clinician in determining the intensity and severity of possible post traumatic stress as well as the ease with which responses are triggered. Further, it is important to note the presence of possible avoidance responses. Avoidance responses may involve the absence of expected activation or emotional reactivity as well as the use of avoidance mechanisms (e.g., substance use, effortful avoidance of cues associated with the event, dissociation).

In addition to monitoring activation and avoidance responses, clinicians carefully observe the individual's strengths or difficulties with affect regulation (i.e., affect tolerance and affect modulation). Such difficulties may be evidenced by mood swings, brief yet intense depressive episodes, or self-mutilation. The information gathered through observation of affect regulation will guide the clinician's decisions regarding the individual's readiness to partake in various therapeutic activities.

Though assessment of psychological trauma may be conducted in an unstructured manner, assessment may also involve the use of a structured interview. Such interviews might include the Clinician-Administered PTSD Scale, Acute Stress Disorder Interview, Structured Interview for Disorders of Extreme Stress, Structured Clinical Interview for DSM-IV Dissociative Disorders- Revised, and Brief Interview for post-traumatic Disorders.

Lastly, assessment of psychological trauma might include the use of self-administered psychological tests. Individual scores on such tests are compared to normative data in order to determine how the individual's level of functioning compares to others in a sample representative of the general population. Psychological testing might include the use of generic tests (e.g., MMPI-2, MCMI-III, SCL-90-R) to assess non-trauma-specific symptoms as well as difficulties related to personality. In addition, psychological testing might include the use of trauma-specific tests to assess post-traumatic outcomes. Such tests might include the post-traumatic Stress Diagnostic Scale, Davidson Trauma Scale, Detailed Assessment of post-traumatic Stress, Trauma Symptom Inventory, Trauma Symptom Checklist for Children, Traumatic Life Events Questionnaire, and Trauma-related Guilt Inventory.

Children are assessed through activities and therapeutic relationship, some of the activities are play genogram, sand worlds, coloring feelings, self and kinetic family drawing, symbol work, dramatic-puppet play, story telling, Briere's TSCC, etc.

Definition

The Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR) defines trauma as direct personal experience of an event that involves actual or threatened death or serious injury; threat to one's physical integrity, witnessing an event that involves the above experience, learning about unexpected or violent death, serious harm, or threat of death, or injury experienced by a family member or close associate. Memories associated with trauma are typically explicit, coherent, and difficult to forget. The person's response to aversive details of traumatic event involves intense fear, helplessness or horror. In children it is manifested as disorganized or agitative behaviors.

Trauma can be caused by a wide variety of events, but there are a few common aspects. There is frequently a violation of the person's core assumptions about the world and their human rights, putting the person in a state of extreme confusion and insecurity. This is seen when institutions depended upon for survival violate, humiliate, betray, or cause major losses or separations instead of evoking aspects like positive self worth, safe boundaries and personal freedom.

Psychologically traumatic experiences often involve physical trauma that threatens one's survival and sense of security. Typical causes and dangers of psychological trauma include harassment, embarrassment, abandonment, abusive relationships, rejection, co-dependence, physical assault, sexual abuse, partner battery, employment discrimination, police brutality, judicial corruption and misconduct, bullying, paternalism, domestic violence, indoctrination, being the victim of an alcoholic parent, the threat or the witnessing of violence (particularly in childhood), life-threatening medical conditions, and medication-induced trauma. Catastrophic natural disasters such as earthquakes and volcanic eruptions, large scale transportation accidents, house or domestic fire, motor vehicle accident, mass interpersonal violence like war, terrorist attacks or other mass victimization like sex trafficking, being taken as a hostage or being kidnapped can also cause psychological trauma. Long-term exposure to situations such as extreme poverty or other forms of abuse, such as verbal abuse, exist independently of physical trauma but still generate psychological trauma.

Some theories suggest childhood trauma can increase one's risk for mental disorders including post-traumatic stress disorder (PTSD), depression, and substance abuse. Childhood adversity is associated with neuroticism during adulthood. Parts of the brain in a growing child are developing in a sequential and hierarchical order, from least complex to most complex. The brain's neurons change in response to the constant external signals and stimulation, receiving and storing new information. This allows the brain to continually respond to its surroundings and promote survival. The five traditional signals (sight, hearing, taste, smell, and touch) contribute to the developing brain structure and its function. Infants and children begin to create internal representations of their external environment, and in particular, key attachment relationships, shortly after birth. Violent and victimizing attachment figures impact infants' and young children's internal representations. The more frequently a specific pattern of brain neurons is activated, the more permanent the internal representation associated with the pattern becomes. This causes sensitization in the brain towards the specific neural network. Because of this sensitization, the neural pattern can be activated by decreasingly less external stimuli. Childhood abuse tends to have the most complications with long-term effects out of all forms of trauma because it occurs during the most sensitive and critical stages of psychological development. It could also lead to violent behavior, possibly as extreme as serial murder. For example, Hickey's Trauma-Control Model suggests that "childhood trauma for serial murderers may serve as a triggering mechanism resulting in an individual's inability to cope with the stress of certain events."

Often psychodynamic aspects of trauma are overlooked even by health professionals: "If clinicians fail to look through a trauma lens and to conceptualize client problems as related possibly to current or past trauma, they may fail to see that trauma victims, young and old, organize much of their lives around repetitive patterns of reliving and warding off traumatic memories, reminders, and affects."

Treatment

A number of psychotherapy approaches have been designed with the treatment of trauma in mind—EMDR, progressive counting (PC), somatic experiencing, biofeedback, Internal Family Systems Therapy, and sensorimotor psychotherapy, and Emotional Freedom Technique (EFT) etc.

There is a large body of empirical support for the use of cognitive behavioral therapy for the treatment of trauma-related symptoms, including post-traumatic stress disorder. Institute of Medicine guidelines identify cognitive behavioral therapies as the most effective treatments for PTSD. Two of these cognitive behavioral therapies, prolonged exposure and cognitive processing therapy, are being disseminated nationally by the Department of Veterans Affairs for the treatment of PTSD. A 2010 Cochrane review found that trauma-focused cognitive behavioral therapy was effective for individuals with acute traumatic stress symptoms when compared to waiting list and supportive counseling. Seeking Safety is another type of cognitive behavioral therapy that focuses on learning safe coping skills for co-occurring PTSD and substance use problems. While some sources highlight Seeking Safety as effective with strong research support, others have suggested that it did not lead to improvements beyond usual treatment. Recent studies show that a combination of treatments involving dialectical behavior therapy (DBT), often used for borderline personality disorder, and exposure therapy is highly effective in treating psychological trauma. If, however, psychological trauma has caused dissociative disorders or complex PTSD, the trauma model approach (also known as phase-oriented treatment of structural dissociation) has been proven to work better than the simple cognitive approach. Studies funded by pharmaceuticals have also shown that medications such as the new anti-depressants are effective when used in combination with other psychological approaches. At present, the selective serotonin reuptake inhibitor (SSRI) antidepressants sertraline (Zoloft) and paroxetine (Paxil) are the only medications that have been approved by the Food and Drug Administration (FDA) in the United States to treat PTSD. Other options for pharmacotherapy include serotonin-norepinephrine reuptake inhibitor (SNRI) antidepressants and anti-psychotic medications, though none have been FDA approved.

Trauma therapy allows processing trauma-related memories and allows growth towards more adaptive psychological functioning. It helps to develop positive coping instead of negative coping and allows the individual to integrate upsetting-distressing material (thoughts, feelings and memories) and to resolve these internally. It also aids in the growth of personal skills like resilience, ego regulation, empathy, etc.

Processes involved in trauma therapy are:

• Psychoeducation: Information dissemination and educating in vulnerabilities and adoptable coping mechanisms.
• Emotional regulation: Identifying, countering discriminating, grounding thoughts and emotions from internal construction to an external representation.
• Cognitive processing: Transforming negative perceptions and beliefs about self, others and environment to positive ones through cognitive reconsideration or re-framing.
• Trauma processing: Systematic desensitization, response activation and counter-conditioning, titrated extinction of emotional response, deconstructing disparity (emotional vs. reality state), resolution of traumatic material (in theory, to a state in which triggers no longer produce harmful distress and the individual is able to express relief.)
• Emotional processing: Reconstructing perceptions, beliefs and erroneous expectations, habituating new life contexts for auto-activated trauma-related fears, and providing crisis cards with coded emotions and appropriate cognition. (This stage is only initiated in pre-termination phase from clinical assessment and judgement of the mental health professional.)
• Experiential processing: Visualization of achieved relief state and relaxation methods.

Trauma informed teaching practice is an educative approach for migrant children from war-torn countries have typically experienced complex trauma, and the number of such children entering Canadian schools has led some school jurisdictions to consider new classroom approaches to assist these pupils. Along with complex trauma, these students often have experienced interrupted schooling due to the migration process, and as a consequence may have limited literacy skills in their first language. One study of a Canadian secondary school classroom, as told through journal entries of a student teacher, showed how Blaustein and Kinniburgh's ARC (attachment, regulation and competency) framework was used to support newly-arrived refugee students from war zones. Tweedie et al. (2017) describe how key components of the ARC framework, such as establishing consistency in classroom routines; assisting students to identify and self-regulate emotional responses; and enabling student personal goal achievement, are practically applied in one classroom where students have experienced complex trauma. The authors encourage teachers and schools to avoid a deficit lens to view such pupils, and suggest ways schools can structure teaching and learning environments which take into account the extreme stresses these students have encountered.

A number of complementary approaches to trauma treatment have been implicated as well, including yoga and meditation. There has been recent interest in developing trauma-sensitive yoga practices, but the actual efficacy of yoga in reducing the effects of trauma needs more exploration.

Psychological pain

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Psychological_pain 

Psychological pain
Other names	Suffering, mental agony, mental pain, emotional pain, algopsychalia, psychic pain, social pain, spiritual pain, soul pain
Vincent van Gogh's 1890 painting Sorrowing old man ('At Eternity's Gate'), where a man weeps due to the unpleasant feelings of psychological pain.
Specialty	Psychiatry, psychology
Medication	Antidepressant medication, Analgesic medication

Psychological pain, mental pain, or emotional pain is an unpleasant feeling (a suffering) of a psychological, non-physical origin. A pioneer in the field of suicidology, Edwin S. Shneidman, described it as "how much you hurt as a human being. It is mental suffering; mental torment." There is no shortage in the many ways psychological pain is referred to, and using a different word usually reflects an emphasis on a particular aspect of mind life. Technical terms include algopsychalia and psychalgia, but it may also be called mental pain, emotional pain, psychic pain, social pain, spiritual or soul pain, or suffering. While these clearly are not equivalent terms, one systematic comparison of theories and models of psychological pain, psychic pain, emotional pain, and suffering concluded that each describe the same profoundly unpleasant feeling. Psychological pain is believed to be an inescapable aspect of human existence.

Other descriptions of psychological pain are "a wide range of subjective experiences characterized as an awareness of negative changes in the self and in its functions accompanied by negative feelings", "a diffuse subjective experience ... differentiated from physical pain which is often localized and associated with noxious physical stimuli", and "a lasting, unsustainable, and unpleasant feeling resulting from negative appraisal of an inability or deficiency of the self."

Cause

The adjective 'psychological' is thought to encompass the functions of beliefs, thoughts, feelings, and behaviors, which may be seen as an indication for the many sources of psychological pain. One way of grouping these different sources of pain was offered by Shneidman, who stated that psychological pain is caused by frustrated psychological needs. For example, the need for love, autonomy, affiliation, and achievement, or the need to avoid harm, shame, and embarrassment. Psychological needs were originally described by Henry Murray in 1938 as needs that motivate human behavior. Shneidman maintained that people rate the importance of each need differently, which explains why people's level of psychological pain differs when confronted with the same frustrated need. This needs perspective coincides with Patrick David Wall's description of physical pain that says that physical pain indicates a need state much more than a sensory experience.

In the fields of social psychology and personality psychology, the term social pain is used to denote psychological pain caused by harm or threat to social connection; bereavement, embarrassment, shame and hurt feelings are subtypes of social pain. From an evolutionary perspective, psychological pain forces the assessment of actual or potential social problems that might reduce the individual's fitness for survival. The way we display our psychological pain socially (for example, crying, shouting, moaning) serves the purpose of indicating that we are in need.

In personality disorders

Borderline personality disorder (BPD) has long been believed to be the one psychiatric disorder that produced the most intense emotional pain and distress in those who suffer with this condition. Studies have shown that borderline patients experience chronic and significant emotional suffering and mental agony. Borderline patients may feel overwhelmed by negative emotions, experiencing intense grief instead of sadness, shame and humiliation instead of mild embarrassment, rage instead of annoyance, and panic instead of nervousness. People with BPD are especially sensitive to feelings of rejection, isolation and perceived failure. Both clinicians and laymen alike have witnessed the desperate attempts to escape these subjective inner experiences of these patients. Borderline patients are severely impulsive and their attempts to alleviate the agony are often very destructive or self-destructive. Suicidal ideation, suicide attempts, eating disorders (anorexia nervosa, binge eating disorder, and bulimia nervosa), self-harm (cutting, overdosing, starvation, etc.), compulsive spending, gambling, sex addiction, violent and aggressive behaviour, sexual promiscuity and deviant sexual behaviours, are desperate attempts to escape this pain.

The intrapsychic pain experienced by those diagnosed with BPD has been studied and compared to normal healthy controls and to others suffering from major depression, bipolar disorder, substance use disorder, schizophrenia, other personality disorders, and a range of other conditions. The excruciatingly painful inner experience of the borderline patient is both unique and perplexing. In clinical populations, the rate of suicide of patients with borderline personality disorder is estimated to be 10%, a rate far greater than that in the general population and still considerably greater than for patients with schizophrenia and bipolar disorder. However, 60–70% of patients with borderline personality disorder make suicide attempts, so suicide attempts are far more frequent than completed suicides in patients with BPD.

The intense dysphoric states which patients diagnosed with BPD endure on a regular basis distinguishes them from those suffering from other personality disorders: major depressive disorder, bipolar disorder, and virtually all known Axis I and Axis II conditions. In a 1998 study entitled "The Pain of Being Borderline: Dysphoric States Specific to Borderline Personality Disorder", one hundred and forty six diagnosed borderline patients took a 50-item self-report measure test. The conclusions from this study suggest "that the subjective pain of borderline patients may be both more pervasive and more multifaceted than previously recognised and that the overall "amplitude" of this pain may be a particularly good marker for the borderline diagnosis".

Feelings of emptiness are a central problem for patients suffering from personality disturbances. In an attempt to avoid this feeling, these patients employ defences to preserve their fragmentary selves. In narcissistic personality disorder this can be detachment, exhibitionism, excessive self-concern, self-isolation, negation of other’s humaneness, assumption of a false self & acting out are some common defences. Feelings of emptiness may be so painful that suicide is considered.

Neural mechanisms

Research suggests that physical pain and psychological pain may share some underlying neurological mechanisms. Brain regions that were consistently found to be implicated in both types of pain are the anterior cingulate cortex and prefrontal cortex (some subregions more than others), and may extend to other regions as well. Brain regions that were also found to be involved in psychological pain include the insular cortex, posterior cingulate cortex, thalamus, parahippocampal gyrus, basal ganglia, and cerebellum. Some advocate that, because similar brain regions are involved in both physical pain and psychological pain, we should see pain as a continuum that ranges from purely physical to purely psychological. Moreover, many sources mention the fact that we use metaphors of physical pain to refer to psychological pain experiences. Further connection between physical and psychological pain has been supported through proof that acetaminophen, an analgesic, can suppress activity in the anterior cingulate cortex and the insular cortex when experiencing social exclusion, the same way that it suppresses activity when experiencing physical pain. and reduces the agitation of people with dementia. However use of paracetamol for more general psychological pain remains disputed.

Religious Perspectives

Many religious traditions, such as the Noble Eightfold Path in Buddhism, have attempted or managed to provide treatment of psychological suffering. Meditation has mental health benefits. The most common form of meditative practice as therapy is mindfulness, but breath focused exercises are also used for dealing with the stresses and anxiety related to emotional pain, reducing physiological symptoms.