Addiction and Self-Harming Behaviors


Take Aways

  • Overall, these results provide strong support for the hypothesis that impaired decision-making in SDI is associated with altered reactions to rewarding and punishing events, as well as altered elicitation of emotional signals that help forecast or anticipate the consequences of future events.

  • Some studies have reported that chronic alcohol abusers show significant alterations in the processing of facial expressions

A Somatic Marker Model of Addiction

  • The main point of the somatic-marker model is that decision-making is a process guided by emotions
  • The model attributes SDI difficulty to make advantageous decisions in real-life to a defect in an emotional mechanism that rapidly signals the prospective consequences of an action, and accordingly assists in the selection of the advantageous response option.

This emotional mechanism is a somatic state, a special instance of feelings that arise in bioregulatory processes and can be enacted in the body, involving physiological modifications (“body loop”), or in brain areas involved in the representation of emotional states (“as if body loop”).

1. Induction of Somatic States
Somatic states can be induced from (1) primary inducers, and (2) secondary inducers. The main distinction between primary and secondary inducers hinges on the process by which they are experienced.

  • Primary inducers are innate or learned stimuli that induce pleasurable or aversive states. Once present in the immediate environment, they automatically and obligatorily elicit a somatic response. The actual encounter of a drug by a SDI is an example of primary inducers
  • Secondary inducers, on the other hand, are entities generated by the recall of a personal or hypothetical emotional event, i.e., “thoughts” and “memories” of the primary inducer, which elicit a somatic response. The recall or imagination of a drug experience by a SDI is one example of secondary inducers.

It has been proposed that the amygdala is a critical substrate in the neural system necessary for triggering somatic states from primary inducers.

  • This somatic state is evoked via effector structures such as the hypothalamus and autonomic brainstem nuclei that produce changes in internal milieu and visceral structures along with other effector structures such as the ventral striatum, periacqueductal gray (PAG), and other brainstem nuclei, which produce changes in facial expression and specific approach or withdrawal behaviours
  • Signals from these somatic states are relayed to the brain. Signals from activated somatic states lead to the development of somatic state patterns in brainstem nuclei (e.g., the parabrachial nuclei (PBN)), and in somatosensing cortices (e.g., insular and somatosensory I and II cortices, and cingulate cortices)After a somatic state has been triggered by a primary inducer and experienced at least once, a pattern for this somatic state is formed
  • The subsequent presentation of a stimulus that evokes memories about a specific primary inducer will then operate as a secondary inducer
  • Secondary inducers are presumed to re-activate the pattern of somatic state belonging to a specific primary inducer. For example, recalling or imagining the experience of a drug re-activates the pattern of somatic state belonging to the actual previous encounter of that drug.

However, the somatic state generated by the recall or imagination of using a drug (secondary inducer) is usually fainter than one triggered by an actual use of that drug (primary inducer).

Provided that somatic state representations in somatosensing cortices develop normally, triggering somatic states from secondary inducers becomes dependent on cortical circuitry in which the orbitofrontal and ventromedial prefrontal cortex plays a critical role. The orbitofrontal/ ventromedial prefrontal cortex is a trigger structure for somatic states from secondary inducers.

2. Operation of Somatic States
During the pondering of a decision, somatic states are triggered by primary (drug cues) or secondary inducers (thoughts about taking drugs).  Once induced, they participate in two functions  (i) In one, they provide a substrate for feeling the emotional state. (ii) In the other, they provide a substrate for biasing decisions.

 (i) Feeling the Emotional State
Evidence suggests that there may be two variant forms of feelings dependent on partially separate neural sectors. This evidence is derived from studies on pain showing dissociation between two sensory aspects of pain.

One is related to feeling the pain itself, so called “pain sensation”the other is related to discomfort and the desire to avoid the pain, so called “pain affect”.

The “liking” effects include feelings of pleasure and affective facial reactions during the pleasurable stateThe “wanting” effects include the desire and urge to obtain the drug.

 (ii) Biasing the Decision to Select a Response
In order for somatic signals to influence cognition and behaviour, they must act on appropriate neural systems…as one deliberates on several options and scenarios held in their working memory, the biasing effect of somatic states is to endorse some options and reject other ones, before any of these options is translated into actions.

Once somatic states from primary and/or secondary inducers are induced in the body, a large number of channels convey body information to the central nervous system (e.g., spinal cord, vagus nerve, humoral signals).

…early evidence suggests that the biasing action of somatic states on behaviour and cognition is mediated by the release of neurotransmitters.

  • Indeed, the cell bodies of the neurotransmitters dopamine (DA), serotonin (5-HT), noradrenaline (NA), and acetylcholine (Ach) are located in the brainstem; the axon terminals of these neurotransmitter neurons synapse on cells and/or terminals all over the cortex
  • When somatic state signals are transmitted to the cell bodies of serotonin neurons, for example, the signalling influences the pattern of serotonin release at the terminalsIn turn, changes in serotonin release modulate synaptic activities of neurons subserving behaviour and cognition within the reflective system.

This chain of neural mechanisms provides a way for somatic states to exert a biasing effect on decisions.

Thus, once somatic states are enacted in the body (bodyloop) or in the brainstem (as-if-body-loop) via direct and indirect connections between the amygdala and the VMPFC, and the neurotransmitter nuclei within the brainstem, they can then influence activity in

  • regions involved in body mapping, i.e., holding patterns of somatic states that help generate feelings
  • regions involved in the triggering of somatic states (e.g., amygdala and ventromedial prefrontal cortex), so that the threshold for triggering subsequent somatic states is increased or decreased
  • regions involved in working memory (e.g., lateral orbitofrontal, dorsolateral prefrontal, and other high order association cortices), so that a particular representation is strengthened or weakened; and finally
  • somatic state signals influence activity in regions concerned with motor responses and behavioural actions (e.g., striatum and anterior cingulate/ supplementary motor area (SMA)).

The significance of this neural arrangement is that regardless of how somatic states are triggered, i.e., impulsively (primary induction) or reflectively (secondary induction), once they are triggered, they can gain access to cortical and subcortical neurons subserving cognition. Thus, depending on their strength, they have the capacity to modify and influence cognition.

According to the somatic-maker model, which proposes that decision-making is a process guided by emotions…there should be a link between abnormalities in expressing emotions and experiencing feelings in SDI on the one hand, and severe impairments in decision-making on the other hand. This section will review evidence that supports this notion.

Decision-Making in Substance Dependent Individuals
The real life problems in judgement and decision-making often observed in substance dependent individuals (SDI) have led to initial studies aimed at testing the performance of SDI on behavioural paradigms of decision-making. Since then, a number of studies that used similar decision-making paradigms have shown impairments in decision-making performance among alcohol, cannabis, cocaine, opioids, and methamphetamines abusers.

Decision-making deficits have also been reported in populations who are at high risk for drug abuse, such as adolescents with externalising behaviour disorders. Interestingly, impaired decision-making has been observed also in individuals with Antisocial Personality Disorder (APD), a psychiatric disorder that is robustly associated with substance dependence, and which involves severe disturbances in emotion processing.

The evidence for impaired decision-making in SDI stems from studies using different decision-making paradigms, including tasks of delayed discounting, betting tasks, and probabilistic choice tasks.

In a series of studies using the IGT, Bechara et al. compared the performance of SDI to patients with damage to the orbitofrontal/ VMPFC. These studies also included physiological measures of autonomic activity before and after making a choice in the IGT. The physiological responses triggered after making the choice and seeing the outcome (i.e., gain or loss of a certain amount of money) were called

  • reward/punishment responses; and those generated before making the choice were called
  • anticipatory response, i.e., responses triggered during the time the participant was pondering from which deck to chose.

Good performance in the IGT has been shown to be linked to the development of these anticipatory emotional responses, which in this case were changes in the skin conductance response. It was suggested that these anticipatory emotional responses help guide decision-making away from disadvantageous

three sub-populations of SDI:

  • one small subpopulation of SDI that was indistinguishable from healthy participants
  • a second small subpopulation that was indistinguishable from orbitofrontal/ VMPFC lesion patients
  • a third larger sub-population of SDI that was different from the other two; these SDI exhibited signs of hypersensitivity to reward

Interestingly, these subpopulations did not differ in terms of basic neuropsychological abilities or clinical characteristics such as severity of drug use. … polydrug users selected more risky choices in the high-risk conditions of the task, and failed to generate increased SCR responses when making riskier decisions with regard to healthy participants.

The evidence thus far points to the presence of decision-making impairments in SDI as measured by different behavioural paradigms….poorer decision-making performance in SDI is associated with:

Overall, these results provide strong support for the hypothesis that impaired decision-making in SDI is associated with altered reactions to rewarding and punishing events, as well as altered elicitation of emotional signals that help forecast or anticipate the consequences of future events.

Emotion Processing in Substance Dependent Individuals

  • Some studies have reported that chronic alcohol abusers show significant alterations in the processing of facial expressions
  • One study showed that alcohol dependent individuals showed specific impairments for recognising facial expressions portraying happiness and anger
  • These alterations were characterised as overestimation of the intensity of the emotion depicted in these emotional facial expressions.

other studies showed that overestimation of the intensity of emotion in facial expressions reported by alcoholics related mainly to the facial expression of fear. The degree of this overestimation correlated with the number of previous formal detoxifications.  Alcoholics also presented with difficulties in distinguishing between the facial expressions of anger and disgust.

  • These results indicate that SDI are impaired in the recognition of facial expressions portraying different emotions, including fear, anger, disgust, and happiness. 
  • The poorer recognition of facial emotional expressions can affect SDI’s interpretation of social cues, so that they can be less able to manage and regulate emotions, and to make decisions and solve problems of an interpersonal or social nature. 
  • In this sense, their poor ability to recognise facial emotional expressions has been attributed to several aspects of their addictive behaviours, such as diminished empathy, increased levels of aggression, and a higher frequency of relapse and ensuing alcohol detoxification.  
  • In particular, poor recognition of fear expressions, which is thought to depend on the amygdala, can be associated with impaired conditioning of fear responses to drug related environments, increasing the probability of relapses.

in response to unpleasant images, SDI showed decreased activity in several neuroendocrine markers, including norepinephrine, cortisol, and adrenocorticotropic hormone levels

  • SDI showed a more flattened response pattern to both pleasant and unpleasant images
  • SDI scored as less positive the images considered by normal participants to be very pleasant and arousing
  • SDI also scored as less negative the images considered by normal participants to be highly unpleasant and arousing
  • Additionally, SDI showed a consistently higher feeling of control over the emotions elicited by both pleasant and unpleasant emotions, as reflected by higher subjective scores in the control dimension in response to the emotions elicited by both pleasant and unpleasant images.

The fact that SDI showed a flattened emotional response to affective images showing both pleasant and aversive scenes may suggest that they also have a diminished emotional response to natural reinforcers other than drugs, where the latter in fact begin to possess exaggerated rewarding effects. This notion is strongly supported by imaging studies on craving in drug addiction, which show that drug related stimuli are able to strongly activate brain regions involved in emotional evaluation and reward processing [DA receptors deficits and driver for hyper-seeking, ed].

In contrast, the same brain regions show blunted activation to other natural reinforcing stimuli such as food or sex.  Consistent with this evidence, the somatic-marker model proposes that somatic states associated with natural reinforcers may not be strong enough to bias decisions in SDI, while strong somatic states associated with the prospect of abusing drugs may override decisions towards drug use.

  • SDI present with a reduced ability to perceive and experience emotions…
  • this reduced perception and experience of emotions observed in SDI in response to pleasant and unpleasant images may be the underlying cause of their poor decision-making in real life, and their apparent “myopia” for the long-term consequences of their actions.

Structural and Functional Neural Abnormalities Associated with Substance Addiction
They found significant decrements in grey matter concentrations (ranging from 5% to 11%) in a number of neural regions considered critical for the operations of the somatic-marker circuit, including the VMPFC bilaterally, the anterior insular cortex, bilaterally, in addition to changes in some temporal cortices, and also in the right anterior cingulate cortex, which is also a target region in the somatic marker neural circuitry. Interestingly, these reductions in grey matter volume were not significantly correlated with measures of severity of drug dependence.

Although all these studies reveal structural abnormalities in neural structures known to be critical for somatic state activation (or processing emotions), the critical question that remains unanswered, is whether these abnormalities preceded the substance abuse condition, or whether these abnormalities were the consequences of the abuse of these drugs.

  • A number of studies have revealed VMPFC functional abnormalities in alcohol, cocaine, and methamphetamine abuser.
  • Other studies have observed functional abnormalities in other regions known to be critical for emotional/ somatic states processing, such as the insular/ somatosensory cortices, and the striatum
  • Furthermore, metabolic abnormalities in the anterior cingulate cortex have been associated with abnormal measures on tests of executive functions in SDI.

Neuropharmacological Changes Associated with Substance Addiction

  • In humans, there is a compelling evidence for a major role of dopamine (DA) in the increased sensitisation of the incentive motivational properties of drugs of abuse.
  • This increased sensitisation to the reinforcing effects of drugs tends to facilitate the continuous administration of drugs of abuse, even when they lose their pleasurable hedonic effects (i.e., wanting vs. liking), thus contributing to the reinstatement of drug consumption after protracted abstinence.

Recent theoretical accounts have proposed that during the sensitised state, there is an enhanced DA mediated response to the incentive motivational value of drugs in the striatum and the amygdala. This enhanced response coincides with a weakened activity within the prefrontal cortex, which reflects a weakened inhibitory control of the prefrontal cortex to the hyperactive amygdala-striatum system.  This weakens the capacity of the individual to self-regulate the drug seeking behaviour, thus leading to a persistent and compulsive use of drugs, irrespective of the long-term negative consequences.
In support of this view,

  • a number of studies using PET have shown persistent reductions of dopamine D2 receptors at the level of the striatum in SDI, including alcohol, heroin, cocaine and methamphetamine dependent
  • an association between striatal dopamine D2 postsynaptic receptor densities and the metabolic activity of the orbitofrontal cortex in cocaine and methamphetamine addicts
  • This association is proposed to reflect a higher sensitivity of the orbitofrontal cortex to dopamine modulation stemming from limbic structures involved in emotional signalling and reward processing.
  • Also, it may reflect the mechanism by which altered somatic signals may bias decision-making in SDI towards immediate reward.
  • The reductions of dopamine D2 receptor densities tend to recover in certain brain regions, such as the thalamus, but the reductions seem to be long lasting at the level of the striatum.

This suggests a possible dissociation between the recoverable locomotor sensitisation effects of abused drugs, and their longer lasting and sensitised motivational/emotional effects.

Abnormal DA functions in several neural regions known to be components of the somatic-marker circuit have been reported in studies showing decreased DA transporter density in the striatum (including nucleus accumbens) and prefrontal cortex of cocaine and methamphetamine dependent individuals.

  • These findings suggest that there are significant reductions in DA release in several neural structures, considered as key components of the somatic-marker neural circuitry, in SDI.
  • This reduced DA activity may explain the blunted response of SDI to a variety of natural reinforcers, beside drugs, which has been reported in several neuroimaging as well as subjective self-report studies.
  • This reduced DA activity may also explain the sensitised response of addicted individuals to the reinforcing effects of drugs of abuse, since they are probably the only powerful stimuli that are capable of inducing reward.

The serotonin (5HT) system has also been implicated in mediating the biasing effects of somatic-markers on cognition, including decision-making.  Nonetheless, studies of the role of 5HT in addiction have been far less extensive in comparison to DA.  Some studies have proposed that low 5HT activity contributes significantly to the dysphoric, or anhedonic state associated with abstinence from drugs of abuse. Other studies showed that low 5-HT activity is associated with decreased prefrontal activity, which is necessary for exerting inhibitory or impulse control over behaviour. Thus, low 5-HT and prefrontal activity observed in SDI may explain not only their compulsive drug use, but also several other co-morbid conditions, such as their depressed mood, and antisocial behaviour.

The Neural Correlates of Substance Craving
People still disagree on how craving should be defined.  Here craving will be defined as the accompanied emotional state that is produced by emotionally competent stimuli that are associated with the reinforcing effects of drugs of abuse. To study craving in the laboratory, a number of studies have used different strategies to induce craving. These strategies include the visual presentation of the drug, or drug related paraphernalia, through images (pictures), or videos; the auditory presentation of audio-taped scripts containing autobiographical experiences related to drug use; or the direct infusion of the drug itself. The aim of this section is to review the evidence showing an overlap between the neural structures that represent critical components of the somatic-marker neural circuitry, and neural structures activated during states of craving in substance abusers. The somatic-marker model proposes that there should be a robust response within these neural structures in response to drug cues, but a diminished response of the neural circuitry to non-drug, natural reinforcers.

Grant et al. [54] used PET to study craving in recently abstinent cocaine abusers. In the scanner, participants were shown videos of drug related paraphernalia, and cocaine self-administration. A pattern of significantly increased activation associated with craving was detected primarily in frontal (VMPFC and dorsolateral –DLPFC-), parietal, temporal, and striatal regions. The correlation analyses showed that the subjective response of craving was associated with changes in the activation of the amygdala in cocaine abusers. A follow up study by the same group [23] used auditory presentation of drug cues, i.e., a script describing sensations associated with being “high” on cocaine. The results revealed increased activation in the DLPFC, orbitofrontal cortex, amygdala and adjacent rhinal cortices. The correlation analyses showed that the subjective response of craving correlated with the degree of activity within these neural regions.

cocaine dependent individuals present with a reduced sensitivity to the rewarding properties of natural reinforcers, while at the same time, they present with an increased sensitivity to drug related stimuli. …This abnormal capacity to process the emotional value of a stimulus has a significant impact on decision-making, in that it can shift the decision-making process towards short-term horizons, i.e., the seeking of drugs. In support, several fMRI studies have shown an exaggerated brain response to drug cues.

… the affective evaluation of drug related stimuli do not decrease.  Rather it increases after prolonged abstinence, thus suggesting a persistent sensitisation effect.

… the neural substrates that mediate craving in drug addicts have actually evolved to subserve natural emotional functions, such as those related to food and sex. … drug addicts tend to trigger strong emotional responses (or somatic states) in response to drug related cues, but they trigger relatively weak somatic states in response to non-drug related, natural reinforcers.

The Neural Correlates of Abnormal Decision-Making in Substance Dependent Individuals
The neural circuitry that is critical for processing emotions (or somatic state activation) overlaps considerably with that subserving decision-making…observed that decision-making was associated with increased activation in the VMPFC, anterior cingulate, parietal/insular cortices and the amygdala, predominantly on the right side. Other regions that were also activated during the performance of decision-making tasks included the dorsolateral prefrontal cortex, thalamus and cerebellum. Later imaging studies have confirmed and extended these findings, and implicated additional neural regions, e.g., the striatum, and the nucleus accumbens, in processes that are critical for decision-making. Recent studies have also reported important gender differences in brain activations induced by complex decision-making tasks.

… a more rigid stimulus driven decision-making pattern in the methamphetamine group, as opposed to a more outcome driven pattern in the healthy participants. Imaging patterns in methamphetamine individuals while performing the two-choice prediction task showed decreased activation of the orbitofrontal, dorsolateral, insular and inferior parietal cortices; orbitofrontal activation was inversely correlated with duration of methamphetamine use.

According to this model,

  • addiction is viewed as a condition in which the person becomes unable to choose according to long-term outcomes
  • Choosing according to long-term outcomes rather than short-term ones requires that the pain signals triggered by thoughts about the future negative consequences of seeking drugs dominate those triggered by the immediate rewarding consequences of consuming the drug.

Thus, drug cues acquire properties for triggering bottom-up, automatic, and involuntary somatic states through the amygdala. Once they do, this bottom-up somatic bias can modulate top-down cognitive mechanisms, in which the ventromedial prefrontal cortex is a critical substrate. If strong enough, this bottom-up influence can interfere or “hijack” the top-down cognitive mechanisms necessary for triggering somatic states about future outcomes. In other words, drugs acquire properties of triggering bottom-up, involuntary signals through the amygdala that modulate and bias top-down goal-driven attentional resources needed for the normal operation of the reflective system, which is critical for exerting control enabling an individual to resist the temptation to seek the drug.

The idea is that poor prefrontal mechanisms of decision-making in SDI are in part related to learning in the presence of a deficiency in the neurotransmitters that modulate, unconsciously or consciously, the cognitive and emotional resources involved in decision-making. In other words,

  • poor decision-making and poor learning to control certain behaviours are due in part to this deficiency
  • Reversal of this chemical deficiency alone is not sufficient for improving decision-making.

prominent characteristics of a variety of disorders, such as pathological gambling, OCD or APD. Interestingly, these disorders are often concurrent with substance dependence, suggesting possible common underlying mechanisms. Further research is necessary to address how pre-existing genetic factors, and/or environmental influences, lead to neural functional abnormalities that may account for the development of these different disorders.


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