How the Brain Recovers in Abstinence and Recovery

If addiction is characterized by loss of control over the use of substances and behaviour and a severely diminished self control or volitional control over behaviour is recovery the regaining over control over behaviours?

 

This study (1)  looked at the recovery of grey matter (and brain function in cocaine addicts (CD).  This study used a brain imaging technique called voxel based morphometry (VBM) to assess how local grey matter (GM) volume varies with years of drug use and length of abstinence in a cross-sectional study of cocaine users (presently or formerly inpatients or outpatients at treatment centres) with various durations of abstinence (1–102 weeks) and years of use (0.3–24 years).

“Extensive evidence indicates that current and recently abstinent cocaine abusers compared to drug-naïve controls have decreased grey matter in regions such as the anterior cingulate, lateral prefrontal and insular cortex. Relatively little is known, however, about the persistence of these deficits in long-term abstinence despite the implications this has for recovery and relapse.

Lower grey matter volume associated with years of use was observed for several regions including anterior cingulate, inferior frontal gyrus and insular cortex. Conversely, higher grey matter volumes associated with abstinence duration were seen in regions that included the anterior and posterior cingulate, insular, right ventral and left dorsal prefrontal cortex. Grey matter volumes in cocaine dependent individuals crossed those of drug-naïve controls after 35 weeks of abstinence, with greater than normal volumes in users with longer abstinence.

The asymmetry between the regions showing alterations with extended years of use and prolonged abstinence suggest that recovery involves distinct neurobiological processes rather than being a reversal of disease-related changes. Specifically, the results suggest that regions critical to behavioral control may be important to prolonged, successful, abstinence.

Findings suggest a cumulative effect of cocaine use wherein the longer the period of substance use the lower the grey matter volume [22]. That these effects were observed in abstinent users is consistent with prior reports of GM deficits in alcoholism that last from 6–9 months to more than a year or, in some reports, up to at least 6 years following abstinence [42][44].

Similarly, decreased GM as a function of years of use of heroin [6], [45], [46] and cocaine [15] have previously been reported. in regions important to emotional regulation…given that emotional reactivity has been implicated as a factor modulating vulnerability to drug abuse [49], this may have been a preexisting factor that served to increase the likelihood of the development and prolongation of drug abuse.

If addiction can be characterized as a loss of self-directed volitional control [22], abstinence and its maintenance may be characterized by a reassertion of these aspects of executive function [24]

Current cocaine users demonstrate reduced GM in brain regions critical to executive function, such as the anterior cingulate, lateral prefrontal, orbitofrontal and insular cortices [6][11]. In contrast, the group of abstinent CD users reported here show elevations in GM as a function of abstinence duration that exceeds control levels after 36 weeks, on average, of abstinence. One possible explanation for this is that abstinence may require reassertion of cognitive control and behavior monitoring that is diminished during current cocaine dependence [11], [50], [51].

 

We, and others, have previously hypothesized that drug abusers may develop increased cerebellar activity to compensate for reduced prefrontal activity in tasks demanding elevated levels of cognitive control [52], [53] and that this may play a role in maintaining abstinence [24]. Reassertion of behavioral control may produce a practice-related expansion [54] in GM regions such as the anterior insula, anterior cingulate, cerebellum, and dorsolateral prefrontal cortex and is consistent with our previous reports of elevated activity levels, compared to controls, in long-term abstinent substance users [24], [55].

 

It should be noted that we also observed regions displaying increased GM with abstinence in bilateral cingulate gyri that did not overlap with those showing decreased GM with years of use. This suggests that the brain is capable of compensating in response to changes in demands, such as the maintenance of abstinence [54], [76].”

It would have been interesting to correlate the findings of this type of research with more information on the treatment undertaken, e.g. was it a 12 step facilitation treatment, to assess the nature of this behaviour-based neuro-plasticity. We need more research into translating the elements of “how it works” into the areas of the brain to observe where it works. In other words how do new attitudes and behaviours shape the brain literally. How does the brain recover volume, connectivity, functionality via behavioural change?

The brain areas which regain volume are implicated also in emotion regulation. It is interesting that the authors point to a possibility that the decreased brain volume in certain areas regulating emotion may also be a pre-existing condition, or in other words, a vulnerability to later addiction risk.

It may be that in recovery some of us learn to master or at least attempt to manage and control emotions in a way we could not previously.

For us this is an essential part of the pathomechanism of addictive  behaviours,  this emotion processing and regulation deficit; a deficit we learn to overcome in recovery. An unmanageability that we learn to manage in recovery.

In our next blog we will look at how these emotional factors drive the addiction cycle to it’s chronic endpoint.

We will look at how emotional dysregulation around forgiveness has contributed to a need to continually distance ourselves chemically from the incidents that needed our forgiveness. It will also look at how forgiveness itself is a emotional regulation strategy in itself, just like “letting go” is. We learn so many emotion regulation strategies in recovery and these appear essential to long term recovery.

References

1. Connolly, C. G., Bell, R. P., Foxe, J. J., & Garavan, H. (2013). Dissociated Grey Matter Changes with Prolonged Addiction and Extended Abstinence in Cocaine Users. PLoS ONE, 8(3), e59645. doi:10.1371/journal.pone.0059645

 

 

What recovers in Recovery? – Cognitive Control over emotions?

 In recent blogs we have called for an increase in research into the neurobiology of recovery to add to the extensive research already published on the neurobiology of the addiction cycle.
There has been extensive research into the neurobiology of addiction, most of this has focused on reward and motivation networks of the brain.  In effect this suggests there is a pathological wanting in addicts, an excessive motivation towards drug taking over all other rewarding activities.
This view does not fully consider that this pathological wanting is in itself a product of dysregulated stress systems in the brain, many the product of neglect, abuse and maltreatment in childhood. These stress factors are also reflective of the role of emotional distress in the addiction cycle . This distress is we feel a product of the emotion processing and regulation deficits commonly seen in all addictive behaviours such as alcohol and substance addiction, eating and gambling disorders and sex addiction etc (and often reflective of childhood maltreatment).
In fact , this emotion processing and  regulation deficit is also apparent in certain children of alcoholics and may be a vulnerability to later alcoholism as these children demonstrate a deficit in impulsivity (common to alcoholics and addicts) and a decision making profile based on choosing now over later (short term gains based) and which recruits more subcortical and motor expressive (compulsive) parts of the brain rather than cortical and reflective/evaluative parts of the brain.
This means they make decisions to alleviate the distress of decisions (as undifferentiated emotions appear to be distressing) not via evaluative processes). This has obvious consequence for decision making over a life span.
This emotion dysregulation is also seen in active addicts and alcoholics and at the endpoint of addiction there is a fairly complete reliance of this compulsive decision making profile, which begs the question, does the decision making deficits seen in at risk children simply get worse in the addiction cycle via the neuro toxic effects of substance abuse?
This emotion (and stress) dysregulation also potentiates reward (makes things more rewarding) so alcohol is seen as more stimulating than for non risk children. This vulnerability may lead to the need  to regulate, especially negative, emotions ( and low self esteem ) via the stimulating and highly rewarding effects of alcohol make perpetuate the addiction cycle to it’s chronic endpoint where chronic emotional distress acts as a compulsive stimulus to the responding of chronic alcohol and drug use.
This emotion dysregulation also seems to play a huge part in relapse – so it begs the question does this emotion regulation improve in time via recovery, particularly long term recovery?
In the next two blogs we look at how the emotion regulation areas of the brain become reinforced, strengthened by the process of recovery or in other words we appear to develop the brain capacity for controlling and regulating our emotions more adaptively and this reduces the stress/distress which often prompts relapse.
Personally, I can wholeheartedly say, that the one main aspect I have developed in my recovery has been the awareness and skills in regulating/controlling emotions. Via recovery I have learnt to identify, label, describe by verbalising and sharing with others how I feel. This processes and regulates the emotions that used to cause me so much distress.
I have also developed a more acute awareness of the the emotional expression and needs of yours. These were previously aspects of my life which were completely lacking and frustrating/confusing as a result.
By emotionally engaging in with the world, by becoming more emotionally literate, I can converse with the world in a way that was previously beyond my capabilities.
The research we look at in the next two blogs asks the question – is cognitive control over emotions, lacking in active addiction, one of the main brain functions that improve in recovery?
A core aspect of alcohol dependence is poor regulation of behavior and emotion.
Alcohol dependent individuals show an inability to manage the appropriate experience and expression of emotion (e.g., extremes in emotional responsiveness to social situations, negative affect, mood swings) (1,2). Dysfunctional emotion regulation has been considered a primary trigger for relapse (1,3) and has been associated with prefrontal dysfunction.
While current alcohol dependence is associated with exaggerated bottom-up (sub-cortical) and compromised top-down (prefrontal cortex) neural network functioning, there is evidence suggesting that abstinent individuals may have overcome these dysfunctional patterns of network functioning (4) .
Neuro-imaging studies showing chronic alcohol abuse to be associated with stress neuroadaptations in the medial prefrontal and anterior cingulate regions of the brain (5 ), which are strongly implicated in the self-regulation of emotion and behavioral self-control (6).
One study (2) looking at how emotional dysregulation related to relapse, showed compared with social drinkers, alcohol-dependent patients reported significant differences in emotional awareness and impulse control during week 1 of treatment. Significant improvements in awareness and clarity of emotion were observed following 5 weeks of protracted abstinence.
Another study (7) which did not look specifically at emotional regulation but rather on the recovering of prefrontal areas of the brain known to be involved also in the inhibition of  impulsive behaviour and emotional regulation showed that differences between the short- and long-abstinence groups in the patterns of functional recruitment suggest different cognitive control demands at different stages in abstinence.

In one study, the long-term abstinent group (n=9) had not consumed cocaine for on average 69 weeks, the short-term abstinent (SA) group (n=9) had an average 0f 2.4 weeks.

Relative to controls, abstinent cocaine abusers have been shown to have reduced metabolism in left anterior cingulate cortex (ACC) and right dorsolateral prefrontal cortex (DLPFC), and greater activation in right ACC.
In this study  the abstinent groups of cocaine addicts showed more elevated activity in the DLPFC ; a finding that has also been observed in abstinent marijuana users (8).
The elevation of frontal activity also appears to undergo a shift from the left to right hemisphere over the course of abstinence.  The right is used more in processing (labelling/identifying) of emotion.
Furthermore, the left inferior frontal gyrus (IFG) has recently been shown to be important for response inhibition (9) and in a task similar to that described here, older adults have been shown to rely more on left PFC (10). Activity observed in these regions is therefore likely to be response inhibition related.
The reliance of the SA group on this region suggests that early in abstinence users may adopt an alternative cognitive strategy in that they may recruit the LIFG in a manner akin to children and older adults to achieve behavioral results similar to the other groups.
In longer,  prolonged abstinence a pattern topographically typical of normal, healthy controls may emerge.
In short-term abstinence there was an increased inhibition-related dorsolateral and inferior frontal activity indicative of the need for increased inhibitory control over behaviour,  while long-term abstinence showed increased error-related ACC activity indicative of heightened behavioral monitoring.
The results suggest that the improvements in prefrontal systems that underlie cognitive control functions may be an important characteristic of successful long-term abstinence.
Another study (11) noted the loss of grey matter in alcoholism that last from 6–9 months to more than a year or, in some reports, up to at least 6 years following abstinence (12 -14).
It has been suggested cocaine abuse blunts responses in regions important to emotional regulation (15)
Given that emotional reactivity has been implicated as a factor in vulnerability to drug abuse (16)  this may be a preexisting factor that  increased the likelihood of the development and prolonging of drug abuse
If addiction can be characterized as a loss of self-directed volitional control (17),  then abstinence (recovery) and its maintenance may be characterized by a reassertion of these aspects of executive function (18)  as cocaine use has been shown to reduce grey matter in brain regions critical to executive function, such as the anterior cingulate, lateral prefrontal, orbitofrontal and insular cortices (19-24) .
The group of abstinent cocaine addicts (11) reported here show elevations in  (increased) grey matter in abstinence exceeded those of the healthy control in this study after 36 weeks, on average, of abstinence .
One possible explanation for this is that abstinence may require reassertion of cognitive control and behavior monitoring that is diminished during current cocaine dependence.
Reassertion of behavioral control may produce a expansion (25)  in grey matter  in regions such as the anterior insula, anterior cingulate, cerebellum, and dorsolateral prefrontal cortex .
All brain regions implicated in the processing and regulating of emotion. 
References
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