Neurocognitive and Psychiatric Factors to Predict Alcohol Consumption
Neurocognitive and Psychiatric Factors to Predict Alcohol Consumption
Aims: Resumption of hazardous drinking after treatment is common in alcohol use disorders (AUD). This study examined the ability of multimodality magnetic resonance, neurocognitive, psychiatric and demographic, to predict alcohol consumption after treatment for AUD.
Methods: Seventy treatment-seeking participants completed 1.5T magnetic resonance studies, yielding regional gray matter (GM) and white matter (WM) surrogate markers of neuronal integrity (N-acetylaspartate: NAA) and cell membrane turnover/synthesis (choline: Cho), assessment of major psychiatric disorders and comprehensive neurocognitive assessment after ~1 month of abstinence. Participants were followed up 6-12 months after treatment and classified as Abstainers (no alcohol consumption; n = 26) and Resumers (any alcohol consumption; n = 44). Abstainers and Resumers were contrasted on various outcome measures, and those that significantly differed between groups were entered as factors in a logistical regression model to predict drinking status at follow-up.
Results: The following variables were independent predictors of resumption of drinking: temporal GM NAA, frontal WM NAA, frontal GM Cho, processing speed and comorbid unipolar mood disorder. With each standard deviation unit decrease in temporal GM NAA, frontal WM NAA, frontal GM Cho and processing speed, the odds of resumption of drinking were increased 3.1, 3.3, 6.4 and 14.2 times, respectively. Diagnosis of a unipolar mood disorder was associated with 14.5-fold increased odds of resumed drinking.
Conclusions: The findings suggest that Resumers, relative to Abstainers, demonstrated greater abnormalities in anterior frontal-subcortical circuits involved in mood and behavioral regulation, and development and maintenance of alcohol use disorders, The magnetic resonance-derived variables used in this study may provide additional information regarding the prediction and neurobiological correlates of resumption of hazardous drinking.
Within ~12 months of completion of treatment for an alcohol use disorder (AUD) (i.e. alcohol dependence or abuse), ~50-80% of individuals will resume consuming alcohol at hazardous levels (Monahan and Finney, 1996; Miller et al., 2001). Resumption of alcohol consumption in those with an AUD appears to be mediated by a combination (and possibly an interaction) of biological, neurocognitive, psychological/ psychiatric and sociodemographic factors (Parsons et al., 1990; Glenn and Parsons, 1991; Jin et al., 1998; Weiss and Porrino, 2002; Heinz et al., 2003; Adinoff et al., 2005; Bottlender and Soyka, 2005; Bradizza et al., 2006). A considerable amount of research investigating the factors associated with resumed alcohol consumption following treatment has focused on psychological/psychiatric variables (e.g. coping styles, comorbid mood, personality or substance abuse disorders), and sociodemographic (e.g. age, education, marital status) and behavioral (e.g. drinking severity and chronicity, previous treatment attempts) factors. In general, poor coping skills, low self-esteem/self-efficacy, social isolation, comorbid mood or personality disorders, greater severity of drinking history and depressive symptomatology have been associated with relapse [see Parsons et al. (1990), Glenn and Parsons (1991), Miller (1991), Miller et al. (1996b), Noone et al. (1999), Boening et al. (2001), Teichner et al. (2001), Bradizza et al. (2006), Krampe et al. (2006), Moos and Moos (2006), Walter et al. (2006) and Kodl et al. (2008)].
Fewer studies have addressed the neurobiological and neurocognitive correlates of resumption of drinking in adult AUD. In treatment seeking AUD, higher brain activation in the putamen, anterior cingulate and medial prefrontal cortex at ~2 months of abstinence was associated with the level of alcohol consumption in those who resumed drinking subsequent to treatment (Grusser et al., 2004). Higher levels of brain activation in the thalamus and striatum in response to affectively positive (versus neutral) cues were inversely related to drinking days and overall alcohol intake in those who relapsed after treatment (Heinz et al., 2007). In a group of treated AUD abstinent for ~18 days, lower frontal cerebral blood flow was observed in individuals who relapsed relative to those who remained abstinent for ~2 months following treatment (Noel et al., 2002). Greater suppression of the hypothalamus-pituitary-adrenal axis during pharmacological or behavioral challenge has been observed in relapsed versus abstinent alcoholics following treatment (Adinoff et al., 2005). Erythrocyte count, hemoglobin concentration and hematocrit in 1-month-abstinent treatment-seeking alcoholics were higher among participants who maintained sobriety compared to those who relapsed over 2-12 months following treatment (Pfefferbaum et al., 2004).
Studies investigating the utility of neurocognitive variables to predict relapse in adult AUD have yielded mixed findings. At admission to treatment, better performance on the Wechsler Adult Intelligence Scale, Block Design was observed in those who abstained versus those who relapsed within 6 months (Donovan et al., 1984). In short-term abstinent AUD, poorer performance on a global measure of learning and memory, problem solving, abstraction and perceptual motor task following detoxification was associated with relapse (Parsons, 1987; Parsons et al., 1990; Glenn and Parsons, 1991). Poorer performance on a composite measure of auditory-verbal and visuospatial learning and memory following detoxification tended to predict lower probability of long-term abstinence (Bartels et al., 2007). In treatment-seeking AUD, the interaction of coping skills and neurocognition was predictive of alcohol consumption following treatment. Specifically, those who concurrently demonstrated higher neurocognitive abilities and poor coping responses had a greater percentage of alcohol-drinking days during relapse (Tapert et al., 2004). Other studies have found neurocognitive functioning to have minimal or no value in predicting relapse in adult AUD [see Glenn and Parsons (1991), Miller (1991), Jin et al. (1998)].
Overall, the neuroimaging and neurocognitive studies of relapse in AUD suggest dysfunction in spatially overlapping brain systems involved in the initiation and maintenance of AUD/substance use disorders, as well as in decision making, impulse control, judgment, planning and reasoning skills (Koob, 2003; Lubman et al., 2004; Bowirrat and Oscar-Berman, 2005; Baler and Volkow, 2006). This is consistent with the vast number of neuroimaging and neurocognitive studies that indicate AUD is associated with abnormalities in the GM and WM of the frontal, temporal and parietal lobes, as well as subcortical nuclei (Oscar-Berman, 2000; Pfefferbaum and Sullivan, 2005; Durazzo and Meyerhoff, 2007).
To the best of our knowledge, no reports have simultaneously examined the ability of proton magnetic resonance (MR)-derived measures of brain metabolites and morphology, as well as neurocognitive, psychiatric, demographic and behavioral factors to predict resumption of alcohol consumption after treatment for adult AUD. Thus, the primary goal of the current work was to determine the extent to which our quantitative neuroimaging, neurocognitive, clinical laboratory and psychiatric/behavioral outcome measures obtained in treatment-seeking adult alcoholics with ~1 month of abstinence predict drinking status 6-12 months subsequent to outpatient treatment for AUD. We hypothesized that individuals who resumed drinking after treatment demonstrate lower levels of markers of neuronal integrity and cell membrane turnover/synthesis in the frontal, parietal and temporal lobes, poorer executive skills, and greater anxiety and depressive symptomatology relative to those who remained abstinent.
Abstract and Introduction
Abstract
Aims: Resumption of hazardous drinking after treatment is common in alcohol use disorders (AUD). This study examined the ability of multimodality magnetic resonance, neurocognitive, psychiatric and demographic, to predict alcohol consumption after treatment for AUD.
Methods: Seventy treatment-seeking participants completed 1.5T magnetic resonance studies, yielding regional gray matter (GM) and white matter (WM) surrogate markers of neuronal integrity (N-acetylaspartate: NAA) and cell membrane turnover/synthesis (choline: Cho), assessment of major psychiatric disorders and comprehensive neurocognitive assessment after ~1 month of abstinence. Participants were followed up 6-12 months after treatment and classified as Abstainers (no alcohol consumption; n = 26) and Resumers (any alcohol consumption; n = 44). Abstainers and Resumers were contrasted on various outcome measures, and those that significantly differed between groups were entered as factors in a logistical regression model to predict drinking status at follow-up.
Results: The following variables were independent predictors of resumption of drinking: temporal GM NAA, frontal WM NAA, frontal GM Cho, processing speed and comorbid unipolar mood disorder. With each standard deviation unit decrease in temporal GM NAA, frontal WM NAA, frontal GM Cho and processing speed, the odds of resumption of drinking were increased 3.1, 3.3, 6.4 and 14.2 times, respectively. Diagnosis of a unipolar mood disorder was associated with 14.5-fold increased odds of resumed drinking.
Conclusions: The findings suggest that Resumers, relative to Abstainers, demonstrated greater abnormalities in anterior frontal-subcortical circuits involved in mood and behavioral regulation, and development and maintenance of alcohol use disorders, The magnetic resonance-derived variables used in this study may provide additional information regarding the prediction and neurobiological correlates of resumption of hazardous drinking.
Introduction
Within ~12 months of completion of treatment for an alcohol use disorder (AUD) (i.e. alcohol dependence or abuse), ~50-80% of individuals will resume consuming alcohol at hazardous levels (Monahan and Finney, 1996; Miller et al., 2001). Resumption of alcohol consumption in those with an AUD appears to be mediated by a combination (and possibly an interaction) of biological, neurocognitive, psychological/ psychiatric and sociodemographic factors (Parsons et al., 1990; Glenn and Parsons, 1991; Jin et al., 1998; Weiss and Porrino, 2002; Heinz et al., 2003; Adinoff et al., 2005; Bottlender and Soyka, 2005; Bradizza et al., 2006). A considerable amount of research investigating the factors associated with resumed alcohol consumption following treatment has focused on psychological/psychiatric variables (e.g. coping styles, comorbid mood, personality or substance abuse disorders), and sociodemographic (e.g. age, education, marital status) and behavioral (e.g. drinking severity and chronicity, previous treatment attempts) factors. In general, poor coping skills, low self-esteem/self-efficacy, social isolation, comorbid mood or personality disorders, greater severity of drinking history and depressive symptomatology have been associated with relapse [see Parsons et al. (1990), Glenn and Parsons (1991), Miller (1991), Miller et al. (1996b), Noone et al. (1999), Boening et al. (2001), Teichner et al. (2001), Bradizza et al. (2006), Krampe et al. (2006), Moos and Moos (2006), Walter et al. (2006) and Kodl et al. (2008)].
Fewer studies have addressed the neurobiological and neurocognitive correlates of resumption of drinking in adult AUD. In treatment seeking AUD, higher brain activation in the putamen, anterior cingulate and medial prefrontal cortex at ~2 months of abstinence was associated with the level of alcohol consumption in those who resumed drinking subsequent to treatment (Grusser et al., 2004). Higher levels of brain activation in the thalamus and striatum in response to affectively positive (versus neutral) cues were inversely related to drinking days and overall alcohol intake in those who relapsed after treatment (Heinz et al., 2007). In a group of treated AUD abstinent for ~18 days, lower frontal cerebral blood flow was observed in individuals who relapsed relative to those who remained abstinent for ~2 months following treatment (Noel et al., 2002). Greater suppression of the hypothalamus-pituitary-adrenal axis during pharmacological or behavioral challenge has been observed in relapsed versus abstinent alcoholics following treatment (Adinoff et al., 2005). Erythrocyte count, hemoglobin concentration and hematocrit in 1-month-abstinent treatment-seeking alcoholics were higher among participants who maintained sobriety compared to those who relapsed over 2-12 months following treatment (Pfefferbaum et al., 2004).
Studies investigating the utility of neurocognitive variables to predict relapse in adult AUD have yielded mixed findings. At admission to treatment, better performance on the Wechsler Adult Intelligence Scale, Block Design was observed in those who abstained versus those who relapsed within 6 months (Donovan et al., 1984). In short-term abstinent AUD, poorer performance on a global measure of learning and memory, problem solving, abstraction and perceptual motor task following detoxification was associated with relapse (Parsons, 1987; Parsons et al., 1990; Glenn and Parsons, 1991). Poorer performance on a composite measure of auditory-verbal and visuospatial learning and memory following detoxification tended to predict lower probability of long-term abstinence (Bartels et al., 2007). In treatment-seeking AUD, the interaction of coping skills and neurocognition was predictive of alcohol consumption following treatment. Specifically, those who concurrently demonstrated higher neurocognitive abilities and poor coping responses had a greater percentage of alcohol-drinking days during relapse (Tapert et al., 2004). Other studies have found neurocognitive functioning to have minimal or no value in predicting relapse in adult AUD [see Glenn and Parsons (1991), Miller (1991), Jin et al. (1998)].
Overall, the neuroimaging and neurocognitive studies of relapse in AUD suggest dysfunction in spatially overlapping brain systems involved in the initiation and maintenance of AUD/substance use disorders, as well as in decision making, impulse control, judgment, planning and reasoning skills (Koob, 2003; Lubman et al., 2004; Bowirrat and Oscar-Berman, 2005; Baler and Volkow, 2006). This is consistent with the vast number of neuroimaging and neurocognitive studies that indicate AUD is associated with abnormalities in the GM and WM of the frontal, temporal and parietal lobes, as well as subcortical nuclei (Oscar-Berman, 2000; Pfefferbaum and Sullivan, 2005; Durazzo and Meyerhoff, 2007).
To the best of our knowledge, no reports have simultaneously examined the ability of proton magnetic resonance (MR)-derived measures of brain metabolites and morphology, as well as neurocognitive, psychiatric, demographic and behavioral factors to predict resumption of alcohol consumption after treatment for adult AUD. Thus, the primary goal of the current work was to determine the extent to which our quantitative neuroimaging, neurocognitive, clinical laboratory and psychiatric/behavioral outcome measures obtained in treatment-seeking adult alcoholics with ~1 month of abstinence predict drinking status 6-12 months subsequent to outpatient treatment for AUD. We hypothesized that individuals who resumed drinking after treatment demonstrate lower levels of markers of neuronal integrity and cell membrane turnover/synthesis in the frontal, parietal and temporal lobes, poorer executive skills, and greater anxiety and depressive symptomatology relative to those who remained abstinent.