Disruption of Frontocerebellar Circuitry and Function in Alcoholism

Sullivan, Edith V.; Harding, Anthony John; Pentney, Roberta J.; Dlugos, Cynthia A.; Martin, Peter; Parks, Mitchell H.; Desmond, John E.; Chen, Shen-Hsing Annabel; Pryor, Michelle R.; Rosa, Eve De; Pfefferbaum, Adolf

doi:10.1097/01.alc.0000052584.05305.98

Cited by 133 publications

(113 citation statements)

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“…The DLPFC, ACC, and insula are fundamentally involved in decision making, problem solving, impulse control, regulation of mood and affect, craving, and evaluation and anticipation of stimulus salience and hedonics (Baler and Volkow, 2006;Paulus, 2007;Redish et al, 2008;Sinha and Li, 2007). The cerebellum is associated with aspects of learning and memory, working memory, executive skills, and reward processing (Anderson et al, 2006;Martin-Solch et al, 2001;Paul et al, 2009;Sullivan, 2003;Sullivan et al, 2003), and the corona radiata provides reciprocal connections linking frontal, parietal, and temporal neocortical regions and subcortical structures (Aralasmak et al, 2006;Makris et al, 1999;Schmahmann et al, 2007). Neurobiological abnormalities in these regions are linked to cognitive, emotional, and behavior disturbances that may confer risk for the relapse/remit cycle commonly observed in all substance-use disorders (Crews and Boettinger, 2009;Kalivas and O'Brien, 2008;Kalivas and Volkow, 2005).…”

Section: Discussionmentioning

confidence: 99%

“…Although the cerebellum and corona radiata are not considered to be core components of the brain reward system, there is a clear rationale for their inclusion as constituents of the reward system. The cerebellum is involved in aspects of learning and memory, working memory, executive skills, and reward processing (Anderson et al, 2006;Martin-Solch et al, 2001;Olbrich et al, 2006;Paul et al, 2009;Sullivan, 2003;Sullivan et al, 2003). The corona radiata is comprised of projection bundles (e.g., corticothalamic, corticostriatal, corticopontine) and reciprocal fi bers that link frontal, parietal, and temporal neocortical regions and subcortical nuclei involved in executive skills, impulse control, emotional regulation, and reward processing (Aralasmak et al, 2006;Cummings, 1995Cummings, , 1998Makris et al, 1999;Mega and Cummings, 1994;Saint-Cyr, 2003;Schmahmann et al, 2007).…”

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confidence: 99%

“…The corona radiata is comprised of projection bundles (e.g., corticothalamic, corticostriatal, corticopontine) and reciprocal fi bers that link frontal, parietal, and temporal neocortical regions and subcortical nuclei involved in executive skills, impulse control, emotional regulation, and reward processing (Aralasmak et al, 2006;Cummings, 1995Cummings, , 1998Makris et al, 1999;Mega and Cummings, 1994;Saint-Cyr, 2003;Schmahmann et al, 2007). AUDs are associated with morphological and metabolite abnormalities of the cerebellum, particularly the vermis, as well as in the reciprocal connections between the cerebellum and frontal lobes (Bendszus et al, 2001;Martin et al, 1995;Parks et al, 2002;Sullivan, 2000;Sullivan and Pfefferbaum, 2005;Sullivan et al, 2003). Additionally, numerous studies have reported regional whitematter morphological and metabolite abnormalities in AUDs, particularly in the frontal white matter that includes the corona radiata (Durazzo and Meyerhoff, 2007;Pfefferbaum and Sullivan, 2005;Sullivan, 2000).…”

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confidence: 99%

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Metabolite Levels in the Brain Reward Pathway Discriminate Those Who Remain Abstinent From Those Who Resume Hazardous Alcohol Consumption After Treatment for Alcohol Dependence

Durazzo¹,

Pathak²,

Gaździński³

et al. 2010

J. Stud. Alcohol Drugs

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ABSTRACT. Objective:This study compared baseline metabolite levels in components of the brain reward system among individuals who remained abstinent and those who resumed hazardous alcohol consumption after treatment for alcohol dependence. Method: Fiftyone treatment-seeking alcohol-dependent individuals (abstinent for approximately 7 days [SD = 3]) and 26 light-drinking nonsmoking controls completed 1.5-T proton magnetic resonance spectroscopic imaging, yielding regional concentrations of N-acetylaspartate, cholinecontaining compounds, creatine-containing compounds, and myoinositol. Metabolite levels were obtained in the following component of the brain reward system: dorsolateral prefrontal cortex, anterior cingulate cortex, insula, superior corona radiata, and cerebellar vermis. Alcohol-dependent participants were followed over a 12-month period after baseline study (i.e., at 7 days of abstinence [SD = 3]) and were classifi ed as abstainers (no alcohol consumption; n = 18) and resumers (any alcohol consumption; n = 33) at follow-up. Baseline metabolite levels in abstainers and resumers and light-drinking nonsmoking controls were compared in the above regions of interest. Results: Resumers demonstrated signifi cantly lower baseline N-acetylaspartate concentrations than light-drinking nonsmoking controls and abstainers in all regions of interest. Resumers also exhibited lower creatine-containing-compound concentrations than abstainers in the dorsolateral prefrontal cortex, superior corona radiata, and cerebellar vermis. Abstainers did not differ from light-drinking nonsmoking controls on baseline metabolite concentrations in any region of interest. Conclusions: The signifi cantly decreased N-acetylaspartate and creatine-containing-compound concentrations in resumers suggest compromised neuronal integrity and abnormalities in cellular bioenergetics in major neocortical components and white-matter interconnectivity of the brain reward pathway. The lack of metabolite differences between abstainers and light-drinking nonsmoking controls suggests premorbid factors potentially contributed to the baseline brain metabolite abnormalities observed in resumers. A LCOHOL-USE DISORDERS (AUDs; i.e., alcohol dependence and abuse) are characterized by a chronically relapsing/remitting course over the lifetime (Dawson et al., 2007;Jin et al., 1998;Miller et al., 2001;Zywiak et al., 2006). The resumption of hazardous levels of alcohol consumption after treatment is common (Donovan, 1996;Maisto and Connors, 2006;Miller et al., 2001;Monahan and Finney, 1996), and appears to be mediated by a complex interplay among genetic, neurobiological, neurocognitive, psychological/psychiatric, and sociodemographic factors (Adinoff et al., 2005;Baler and Volkow, 2006;Bottlender and Soyka, 2005;Bradizza et al., 2006;Glenn and Parsons, 1991;Goodman, 2008;Heinz et al., 2003;Jin et al., 1998;Koob, 2003;Moos and Moos, 2006;Parsons et al., 1990;Sher et al., 2005;Weiss and Porrino, 2002;Zywiak et al., 2006). A considerable amount of research has inve...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Metabolite Levels in the Brain Reward Pathway Discriminate Those Who Remain Abstinent From Those Who Resume Hazardous Alcohol Consumption After Treatment for Alcohol Dependence

Durazzo¹,

Pathak²,

Gaździński³

et al. 2010

J. Stud. Alcohol Drugs

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“…In addition, animal models have recently revealed alcohol-related dendritic regression within Purkinje neurons (Dlugos & Pentney, 2002) that appears to be reversible following ethanol withdrawal (Dlugos & Pentney, 1997). The processes involved in dendritic regression and subsequent reconstruction are highly complex, and their effects on neuronal processing downstream are completely unknown (Sullivan et al, 2003).…”

Section: Eyeblink Classical Associative Learning: Neuronal Circuit Anmentioning

confidence: 99%

Trace Eyeblink Conditioning in Abstinent Alcoholic Individuals: Effects of Complex Task Demands and Prior Conditioning.

McGlinchey¹,

Fortier²,

Capozzi³

et al. 2005

Neuropsychology

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Chronic misuse of alcohol affects an integrated neural circuit supporting the formation of associative memories acquired during eyeblink classical conditioning (R. McGlinchey-Berroth et al., 1995). The authors of this study investigated single-cue trace conditioning in amnesic and nonamnesic abstinent alcoholic individuals who either were or were not trained in a single-cue delay conditioning task. Overall, untrained alcoholic participants were severely impaired in acquisition, and alcoholic participants previously trained in single-cue delay conditioning performed similarly to untrained control participants. Individual performance in acquisition varied significantly within task but was relatively stable between the trace and delay tasks; there were nonamnesic and amnesic alcoholic participants who acquired responses at a normal rate in both delay and trace conditioning. The similarity of performances in delay and trace conditioning suggests a common source of impairment across both tasks.

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“…A loss of synapses, resulting from alcohol abuse, can cause some of the abnormal movements often seen in alcohol abusers, such as unsteady gait, tremors and lack of coordination. In addition, other deficits have been associated with alcohol use and abuse, including impairments in the following cognitive functions: memory, verbal learning, abstract thinking, problemsolving, perceptual analysis and synthesis, speed of information and efficiency, as well as perceptual motor skills [24,[47][48][49][50][51][52][53] . Also, research found that when compared to cocaine, alcohol had more negative effects on attention and executive functioning [22] .…”

Section: Introductionmentioning

confidence: 99%