If you’ve got the money honey, we’ve got your disease — Guns n’ Roses: Welcome to the Jungle
One of the key challenges of cognitive neuroscience is to gain an understanding of the neural mechanisms behind the various psychiatric disorders that can blight mankind. Knowledge of the how various brain mechanisms work in health, and how, and in what way, they become defective is crucial for the development of neurological treatments for such conditions. Such an approach doesn’t imply tacit acceptance of the idea that all behaviour is guided by changes in the brain, or that psychiatric problems are solely of a biological origin. Indeed it is well established that social and psychological factors can drive changes in brain function (for example purely cognitive therapies can alter the patterns of neural firing ). What understanding the neural basis of disease does allow, is the development of better methods of tackling such conditions at a neurological level, which is important because in many patients the social and psychological factors that have triggered their condition may prove to be either impractical or impossible for clinicians to alter (e.g. changing the structure of society).
Addiction is an extremely prevalent problem in modern society. Alcohol and opiate addictions alone are estimated to affect 15million Europeans, costing around 65 million Euros a year in both health and non-health related costs (2). Addiction can be defined as the persistent, compulsive dependence on a behavior or substance (3) and therefore spans not just drug dependencies, but also ‘behavioural addictions’ such as gambling, overeating, sex addiction and compulsive shopping (oniomania). Although the definition of addiction is reasonably straightforward, the process of addiction needs to be broken down into its constituent cognitive parts before it can be fully understood. Addiction, and indeed all psychiatric problems, are not unitary constructs; they reflect abnormalities in several different facets of human cognition. For example unipolar depression can involve not just low mood, but also failure to respond to pleasurable experiences (anhedonia), low energy, anxiety and loss of appetite. Breaking down such conditions into their components parts is crucial if we are to be able to understand how they develop and how they can be treated. From a clinical perspective, focusing on the array of symptoms rather than the overall condition can help identify sub-types of the condition, which in turn can allow treatments to be modified to address the particular set of symptoms presented by an individual patient.
So which cognitive processes may be at fault when an individual becomes addicted? While opinions vary on this subject, in general it can be said that addiction involves abnormalities in the following interconnected processes:
- Reward processing
- Motivation and learning
- Decision Making
- Cognitive control
By their nature addictive behaviours have, at least initially, a rewarding effect. Moreover these effects are felt both by those who later become addicted and those that do not. Clearly therefore something in the processing of rewarding events must either change during addiction, or be naturally defective in the addicted individual. Unfortunately, while there are a number of different theories concerning how reward processing is disrupted in addiction, the exact nature of the deficiency is as yet uncertain. For example do people become sensitized to a drug and thus gradually require more to be able to maintain a balanced physiological state, or are people at risk of addiction more naturally prone to negative emotions and therefore have a greater tendency to seek out rewarding stimuli despite the risk? Despite this uncertainty around the exact nature of the cognitive deficiencies in reward processing, neurological research has revealed that experience of reward (e.g. intoxication) is strongly associated with activity within circuits of the brain that make use of the neurotransmitter dopamine (neurotransmitters are the chemicals that facilitate communication between different neurons in the brain). This dopaminergic system encompasses subcortical areas directly related to processing of motivationally relevant stimuli, such as the striatum and amygdala, as well as cortical areas such as the prefrontal cortex which are involved in the prediction of future reward, the evaluation of existing rewards and decision making (4). Various addictive drugs appear to alter the balance of dopamine within this system, usually increasing it, presumably creating the feeling of high associated with drug taking. Over the long term an ‘exhaustion’ effect may occur, whereby the brain is unable to maintain its previous tonic (standard) level of dopamine because of the effect on dopamine levels of frequent performance of the addictive behaviour. This may then lead to the withdrawal state and to a situation where the addicted user becomes trapped in a cycle of repeating the addictive behaviour, not to achieve the high that the behaviour was initially associated with, but merely to maintain a acceptable tonic level of dopamine, thus avoid the ‘low’ that occurs with withdrawal from the behaviour. Other neurotransmitter systems which also innervate similar brain areas, such as the noradrenergic system, also play a part in addiction, although they have in general been less widely studied regarding their role in reward processing.
Stimuli that are not directly rewarding, but are predictive or otherwise associated with the positive effects of the addictive behaviour, act to induce cravings for the addictive behaviour. The processing of such ‘addictive cues’, in comparison to similar stimuli unassociated with the addiction, tend to provoke greater activity in a wide variety of brain areas including those involved in the actual processing of reward, alongside frontal-cortical circuits involved in the regulation of thoughts and actions, and areas involved in memory, sensory processing and the engagement of motor actions (5). This suggests that contextual factors that induce cravings can not only evoke brain activity in the reward centers of the brain, but also engage greater perceptual processing and attention, and even trigger motor activity, presumably in preparation for seeking out or performing the addictive behavior. Dysfunctions within these circuits are likely to have a knock-on effect on the processes such as learning and memory. Persistent performance of the addictive behaviour after exposure to addictive cues will lead to a strengthening of the association between the cue and the behaviour, and between both the cue and behaviour and the subsequent hedonic effects of the reward. The strengthening of such associations can lead to a behaviour that was previously under conscious control becoming habitual. The more habitual or automatic a behaviour becomes, the more effort is required to control it, and ultimately the more likely the behaviour is to be performed regardless of its utility in a particular circumstance. In short, it becomes compulsive. Indeed the ease with which a behaviour can become habitual may distinguish addicts from those who remain ‘casual users’.
In addition to the neural circuits involved in reward and learning, the frontal areas of the brain which are also activated by both the addictive behaviour itself and during craving are crucial in the process of addiction. Such areas are broadly believed to be involved in ‘cognitive control’; they act to regulate activity from the more primal, sub-cortical brain areas which are involved in motivation, emotional and learning. This effectively meaning that they provide control over thoughts and behavior. Perhaps unsurprisingly, the (partially separate) systems within the frontal cortex that are involved in decision making and in inhibiting pre-potent (i.e. habitual or natural) responses are both found to be deficient in addicted populations, thus explaining why addicts make decisions that are counter-productive to their health, even when they are fully aware of the likely consequences of their actions (8). Increasing sensitivity, or reactivity from the subcortical reward circuits, coupled with a weakening of the control exerted on them by the frontal control areas is likely to be behind the habituation of addictive behavior, and the subsequent failure to regulate that behavior. In some senses the addict (or more accurately, the frontal control areas of the addict’s brain) loses control over their instinctive behavior.
One of the most serious problems with addiction can be what is termed ‘insight’ or the ability to understand that you are ill. Lack of insight is a severe challenge for clinicians as it can be nearly impossible to effectively implement any treatment when the patient is unaware that the treatment is needed. Again frontal areas, most notably the Insula and anterior cingulate cortices, appear to be crucially involved in the lack of insight (6). The Insula is involved in monitoring internal body states (interoceptive awareness) and producing the ‘subjective experience’ relating to this. It also is involved in deriving salience from sensory information and, along with the anterior cingulate, influencing behavior accordingly (7) thus providing a crucial system for the expression of the effect of addictive cues on behaviour. Addiction-induced dysfunctions in this system may therefore lead to an inability to properly process and respond to changes in body state caused by the performance of (or withdrawal from) the addictive behavior, and may stop the individual from fully appreciating that addictive cues are provoking the cravings which are driving the addictive behaviour. Thus insight into the problematic nature of their condition is lost to the individual.
This article represents a very brief overview of the sorts of cognitive and neural structures involved in addiction. It isn’t unfortunately possible to do justice to the full scope of research into addictive behavior in a short article. What should be clear however is that drug abuse can induce changes in a multitude of different interconnected neural circuits, affecting a multitude of different cognitive functions. This effect can be somewhat different depending on the drug of abuse, but nevertheless also applies to a significant extent to non-drug addictions, implying that such neurological changes can occur without the direct influence of external chemical agents. It follows that these changes must therefore be at least partly the consequence of purely internal, cognitive shifts in the workings of the brain, which do, of course, also occur in drug based additions, thus exacerbating the natural neurochemical effects of the drug. Despite the complexity of the processes involved, increased understanding of the neurological and cognitive basis of addiction should enable, in time, more advanced and effective treatments to be designed. Future research into addiction will also hopefully enable ‘markers’ for the condition to be identified; biological or cognitive indices that predict those who are at potential risk of addiction. This in turn would improve our ability to take preventative measures to reduce the prevalence of this debilitating problem.
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