abstinence and recovery

Recovering Cognitive Control Over Emotions In Recovery.

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. 
1. Berking M, Margraf M, Ebert D, Wupperman P, Hofmann SG, Junghanns K. Deficits in emotion-regulation skills predict alcohol use during and after cognitive-behavioral therapy for alcohol dependence. J Consult Clin Psychol. 2011;79:307–318.
2.  Fox HC, Hong KA, Sinha R. Difficulties in emotion regulation and impulse control in recently abstinent alcoholics compared with social drinkers. Alcohol Clin Exp Res. 2008;33:388–394.
3..Cooper ML, Frone MR, Russell M, Mudar P. Drinking to regulate positive and negative emotions: A motivational model of alcohol use. J Pers Soc Psychol. 1995;69:990
4. Camchong, J., Stenger, A., & Fein, G. (2013). Resting‐State Synchrony in Long‐Term Abstinent Alcoholics. Alcoholism: Clinical and Experimental Research37(1), 75-85.
5. Sinha, R., & Li, C. S. (2007). Imaging stress- and cue-induced drug and alcohol craving: Association with relapse and clinical
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6. Beauregard, M., Lévesque, J., & Bourgouin, P. (2001). Neural correlates of conscious self-regulation of emotion. Journal of
Neuroscience, 21(18), RC165
7. Connolly, C. G., Foxe, J. J., Nierenberg, J., Shpaner, M., & Garavan, H. (2012). The neurobiology of cognitive control in successful cocaine abstinence. Drug and alcohol dependence121(1), 45-53.
8.  Tapert SF, Schweinsburg AD, Drummond SP, Paulus MP, Brown SA, Yang TT, Frank LR. Functional MRI of inhibitory processing in abstinent adolescent marijuana users.Psychopharmacology (Berl.) 2007;194:173–183.[PMC free article]
9. Swick D, Ashley V, Turken AU. Left inferior frontal gyrus is critical for response inhibition. BMC Neurosci. 2008;9:102.[PMC free article]
10. Garavan H, Hester R, Murphy K, Fassbender C, Kelly C. Individual differences in the functional neuroanatomy of inhibitory control. Brain Res. 2006;1105:130–142
11. 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 one8(3), e59645.
12. Chanraud S, Pitel A-L, Rohlfing T, Pfefferbaum A, Sullivan EV (2010) Dual Tasking and Working Memory in Alcoholism: Relation to Frontocerebellar Circuitry. Neuropsychopharmacol 35: 1868–1878 doi:10.1038/npp.2010.56.
13.  Wobrock T, Falkai P, Schneider-Axmann T, Frommann N, Woelwer W, et al. (2009) Effects of abstinence on brain morphology in alcoholism. Eur Arch Psy Clin N 259: 143–150 doi:10.1007/s00406-008-0846-3.
14.  Makris N, Oscar-Berman M, Jaffin SK, Hodge SM, Kennedy DN, et al. (2008) Decreased volume of the brain reward system in alcoholism. Biol Psychiatry 64: 192–202 doi:10.1016/j.biopsych.2008.01.018.
15, Bolla K, Ernst M, Kiehl K, Mouratidis M, Eldreth D, et al. (2004) Prefrontal cortical dysfunction in abstinent cocaine abusers. J Neuropsychiatry Clin Neurosci 16: 456–464 doi:10.1176/appi.neuropsych.16.4.456.
16.  Piazza PV, Maccari S, Deminière JM, Le Moal M, Mormède P, et al. (1991) Corticosterone levels determine individual vulnerability to amphetamine self-administration. Proc Natl Acad Sci USA 88: 2088–2092. doi: 10.1073/pnas.88.6.2088
17.  Goldstein RZ, Volkow ND (2002) Drug addiction and its underlying neurobiological basis: neuroimaging evidence for the involvement of the frontal cortex. Am J Psychiatry 159: 1642–1652. doi: 10.1176/appi.ajp.159.10.1642
18. Connolly CG, Foxe JJ, Nierenberg J, Shpaner M, Garavan H (2012) The neurobiology of cognitive control in successful cocaine abstinence. Drug Alcohol Depend 121: 45–53 doi:10.1016/j.drugalcdep.2011.08.007.
19.  Liu X, Matochik JA, Cadet JL, London ED (1998) Smaller volume of prefrontal lobe in polysubstance abusers: a magnetic resonance imaging study. Neuropsychopharmacol 18: 243–252 doi:10.1016/S0893-133X(97)00143-7.
20.  Bartzokis G, Beckson M, Lu P, Nuechterlein K, Edwards N, et al. (2001) Age-related changes in frontal and temporal lobe volumes in men – A magnetic resonance imaging study. Arch Gen Psychiatry 58: 461–465. doi: 10.1001/archpsyc.58.5.461
21. Franklin TR, Acton PD, Maldjian JA, Gray JD, Croft JR, et al. (2002) Decreased gray matter concentration in the insular, orbitofrontal, cingulate, and temporal cortices of cocaine patients. Biol Psychiatry 51: 134–142. doi: 10.1016/s0006-3223(01)01269-0
22.  Matochik JA, London ED, Eldreth DA, Cadet J-L, Bolla KI (2003) Frontal cortical tissue composition in abstinent cocaine abusers: a magnetic resonance imaging study. NeuroImage 19: 1095–1102. doi: 10.1016/s1053-8119(03)00244-1
23.  Lim KO, Wozniak JR, Mueller BA, Franc DT, Specker SM, et al. (2008) Brain macrostructural and microstructural abnormalities in cocaine dependence. Drug Alcohol Depend 92: 164–172 doi:10.1016/j.drugalcdep.2007.07.019.
24.  Ersche KD, Barnes A, Jones PS, Morein-Zamir S, Robbins TW, et al. (2011) Abnormal structure of frontostriatal brain systems is associated with aspects of impulsivity and compulsivity in cocaine dependence. Brain 134: 2013–2024 doi:10.1093/brain/awr138.
25.  Ilg R, Wohlschlaeger AM, Gaser C, Liebau Y, Dauner R, et al. (2008) Gray matter increase induced by practice correlates with task-specific activation: A combined functional and morphometric magnetic resonance Imaging study. J Neurosci 28: 4210–4215 doi:10.1523/JNEUROSCI.5722-07.2008.

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