Diagnostic Difficulties

Dopaminergic or Positive Reinforcement Theories of Addiction

As we have already suggested we feel that two main modifications need to be considered in relation to existing ‘conditioning’ theories of addiction : –

1. In neurobiological accounts of addiction there is no such thing as a positive or a negative reinforcement model of addiction or, in other words, a dopaminergic or stress-based theory of addiction and that these two main models can be combined easily to highlight how stress augments dopminergic cue reactivity, as well as craving and relapse.

2. That accurate theories of addiction need to address the distress at the heart of addiction. The addiction cycle progress from use to abuse to addictive behaviours or from cognitive control of the prefrontal cortex, and goal directed to dorsal striatal compulsive habit-like responding with the amgydala paying a crucial role in this switch between action outcome and stimulus response regions. This transition can also be explained by impaired stress and emotional regulation which first enhances  initial drug and alcohol use, then prompts further abuse to then acting as a emotional habit bias in which emotional distress acts as a stimulus response which automatically promotes the urge to relapse or use in the face of this distress.   Hence distress becomes the driving force behind decision making.

A more inclusive theory of addiction may need to show how premorbid vulnerability in emotional and stress regulatory systems feeds into and provokes the neurobiological transition to addiction and that one system feeds into the other in a reciprocal manner.  There is no intrinsic difference between the neurobiological and the psychological (especially affective and executive function) and resultant behaviour.

First we discuss the positive reinforcement model which is a  ‘conditioning’ model, before reviewing some of it’s inherent limitations.

Positive reinforcement model of addiction

The positive reinforcement model acknowledges that although physiological withdrawal from the effects of substance abuse may play an important role in relapse following short term abstinence, it fails to account for relapse after longer term abstinence. Furthermore, it also doesn’t explain the pathological “wanting” that remains present even in those who have been abstinent for many years. According to one prominent positive reinforcement model, the Incentive Sensitisation (IS) Model (1), addiction is the result of neural sensitisation of reward circuits (centred in the ventral striatum (VS)) by the neurotransmitter dopamine. Positive reinforcement mechanisms lead to a non-associative learning process, referred to as sensitization, in which repeated confrontation with a substance-related cue (which acts as a reinforcer) results in the progressive amplification of a response (substance seeking). This ‘sensitisation’ or hypersensitivity may be independent of negative withdrawal symptoms or an individual’s general negative emotional state and leads to compulsive substance-seeking and substance-taking. These mechanisms of positive reinforcement leave addicts vulnerable to relapse when confronted by substance-related cues which trigger a pathological “wanting”, as progressively distinct from initial reward-linked “liking”.

In short, IS produces a bias of attentional processing towards substance-associated stimuli and a pathological wanting of alcohol or substances. Sensitisation and attentional bias has been demonstrated in various studies (2,35). Later extensions of IS theory (4) pose that this pathological wanting is accompanied by increasingly impaired executive control over behaviour. This arises due to the chronic effects of substance abuse on the prefrontal cortex, with deleterious consequences for cognitive control of pathological wanting.

An extension of the positive reinforcement model was proposed by Everitt and Robbins (5), who posit a transition in control over substance seeking behaviour at neural level from the prefrontal cortex to the striatum. This transition corresponds with the progression from compulsive “wanting” of substance of the ventral striatum (VS) (as postulated by the IS model) to out of control “must do!” behaviour of the dorsal striatum (DS), mediated, at least in part, by dopaminergic innervations. These brain changes in neural pathways and synapses (neuroplasticity) are induced by the chronic administration of substances.

Although these dopaminergic mechanisms are crucial to the positive reinforcement theory, they do not fully capture the compulsive drive to seek and use substances. This drive, Everitt and Robbins suggest, appears to be analogous with obsessive compulsive disorder (OCD) and possibly maintained by the same underlying process of negative reinforcement.

Furthermore, dopaminergic networks have been implicated by theoretical models which suggest learning and memory (6) may also be “hijacked”.  This suggests that, in addition to the reward pathway, the role of dopaminergic pathways in the development of addiction also involves other neural circuits implicated in memory and attention.

References

1.  Robinson, T.E., & Berridge, K.C. (1993). The neural basis of drug craving: An incentive-sensitization theory of addiction. Brain Research, 18, 247-291

2  Leyton M. Conditioned and sensitized responses to stimulant drugs in humans. Prog. Neuropsychopharmacol. Biol. Psychiatry. 2007;31:1601–1613.

3.  Franken, I. H. (2003). Drug craving and addiction: integrating psychological and neuropsychopharmacological approaches. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 27(4), 563-579

4.  Robinson, T. E., & Berridge, K. C. (2008). The incentive sensitization theory of addiction: some current issues. Philosophical Transactions of the Royal Society B: Biological Sciences, 363(1507), 3137-3146

5. Everitt, B. J., & Robbins, T. W. (2005). Neural systems of reinforcement for drug addiction: From actions to habits to compulsion. Nature Neuroscience, 8, 1481–1489

6.   Hyman, S. E. (2007). Addiction: a disease of learning and memory. Focus, 5 (2), 220.

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