Cortical Gray Matter Loss in Treatment‐Naïve Alcohol Dependent Individuals

Fein, George; Sclafani, Victoria Di; Cardenas, V. A.; Goldmann, H.; Tolou‐Shams, Marina; Meyerhoff, Dieter J.

doi:10.1111/j.1530-0277.2002.tb02574.x

Cited by 164 publications

(157 citation statements)

References 45 publications

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“…Although there is a substantial literature regarding its incidence on structural brain damage (eg Fein et al, 2002;Hommer et al, 2001;Pfefferbaum et al, 1992) and neuropsychological function (Parsons and Nixon, 1998;Oscar-Berman et al, 1997) in detoxified alcohol-dependents, no study has explored its consequences in alcoholdependents with preserved psychosocial functioning.…”

Section: Introductionmentioning

confidence: 99%

Brain Morphometry and Cognitive Performance in Detoxified Alcohol-Dependents with Preserved Psychosocial Functioning

Chanraud

Martelli

Delain

et al. 2006

Neuropsychopharmacol

373

295

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The extent of structural brain damage and related cognitive deficits has been little described in alcohol-dependent individuals with preserved social functioning. Thus, we investigated the relationship between regional alterations, executive performance, and drinking history. Volumes of gray and white matter were assessed using magnetic resonance imaging voxel-based morphometry in healthy men and in detoxified alcohol-dependent men with good psychosocial functioning. Their executive performance was assessed using neuropsychological tests. Regression analyses were carried out in the regions in which volume differences were detected. Decreases in gray matter were detected bilaterally in alcohol-dependents in the dorsolateral frontal cortex (up to 20% lower), and to a lesser extent in the temporal cortex, insula, thalamus, and cerebellum. Decreases in white matter volume were widespread, being up to 10% in corpus callosum. The degradation of neuropsychological performance correlated with gray matter volume decreases in the frontal lobe, insula, hippocampus, thalami and cerebellum, and with white matter decrease in the brainstem. An early age at first drinking was associated with decreased gray matter volumes in the cerebellum, brainstem (pons), and frontal regions. Regional alteration in gray and white matter volume was associated with impairment of executive function despite preserved social and somatic functioning in detoxified patients. Besides involving frontal regions, these findings are consistent with a cerebello-thalamo-cortical model of impaired executive functions in alcohol-dependent individuals.

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Section: Introductionmentioning

confidence: 99%

Brain Morphometry and Cognitive Performance in Detoxified Alcohol-Dependents with Preserved Psychosocial Functioning

Chanraud

Martelli

Delain

et al. 2006

Neuropsychopharmacol

373

295

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“…Treatment-naïve alcoholics represent the vast majority of individuals with AUD. Compared to treatment-seeking alcoholics, treatment-naïve alcoholics have been reported to demonstrate a different drinking trajectory and less severe levels of lifetime alcohol consumption (Fein and Landman, 2005), as well as lower magnitudes of alcohol-induced cerebral morphological abnormalities (Fein et al, 2002). Therefore, morphological findings obtained for treatment-seeking alcoholics may not necessarily generalize to treatment-naïve individuals.…”

Section: Introductionmentioning

confidence: 99%

Non-treatment-seeking heavy drinkers: Effects of chronic cigarette smoking on brain structure

Durazzo

Cardenas

Studholme

et al. 2007

Drug and Alcohol Dependence

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We previously reported [Cardenas, V.A., Studholme, C., Meyerhoff, D.J., Song, E., Weiner, M.W., 2005. Chronic active heavy drinking and family history of problem drinking modulate regional brain tissue volumes. Psychiatry Res. 138, 115−130] that non-treatment-seeking, active heavy drinkers (HD) demonstrated smaller regional neocortical gray matter volumes compared to light drinking controls; however, the potential effects of chronic cigarette smoking on regional brain volumes were not addressed. The goal of this retrospective analysis was to determine if chronic smoking affected brain structure in the non-treatment-seeking heavy drinking sample from our earlier report (i.e., Cardenas et al., 2005). Regional volumetric comparisons were made among age-matched smoking HD (n = 17), non-smoking HD (n = 16), and non-smoking light drinkers (nsLD; n = 20) from our original sample. Quantitative volumetric measures of neocortical gray matter (GM), white matter (WM), subcortical structures, and cerebral spinal fluid (CSF) were derived from high-resolution magnetic resonance imaging. Smoking HD demonstrated smaller volumes than nsLD in the frontal, parietal, temporal GM, and for total neocortical GM. Smoking HD also demonstrated smaller temporal and total GM volumes than non-smoking HD. Non-smoking HD and nsLD did not differ significantly on GM volumes. Further, the three groups did not differ on lobar WM, subcortical structures or regional CSF volumes. These retrospective analyses indicate neocortical GM volume reductions in non-treatment-seeking smoking HD, but not in non-smoking HD, which are consistent with our studies in recently detoxified treatment-seeking alcohol-dependent samples.

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“…The effects of thiamine deficiency on brain morphology have been well documented in patients with chronic alcoholism, which itself produces widespread shrinkage of brain tissue (Cardenas et al, 2005;Fein et al, 2002;Jernigan et al, 1991;Pfefferbaum et al, 1992) and attendant deficits in motor and cognitive function that can persist even after months of abstinence along with adequate nutrition (eg, Eckardt et al, 1998;Fein et al, 1990;Parsons, 1993;Sullivan et al, 2000c). Although alcohol-related brain abnormalities are partially reversible with prolonged sobriety (Carlen et al, 1978;Gazdzinski et al, 2005;Mann et al, 1999;O'Neill et al, 2001;Parks et al, 2002;Pfefferbaum et al, 1995Pfefferbaum et al, , 1998Schroth et al, 1988), cortical gray and white matter may sustain long-term volume shrinkage and even loss (Jernigan et al, 1991;Pfefferbaum et al, 1992), especially in the prefrontal cortex (De Bellis et al, 2005) of older alcoholics (Cardenas et al, 2005;Pfefferbaum et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

Development and Resolution of Brain Lesions Caused by Pyrithiamine- and Dietary-Induced Thiamine Deficiency and Alcohol Exposure in the Alcohol-Preferring Rat: A Longitudinal Magnetic Resonance Imaging and Spectroscopy Study

Pfefferbaum

Adalsteinsson

Bell

et al. 2006

Neuropsychopharmacol

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Wernicke's encephalopathy (WE) is characterized by lesions in thalamus, hypothalamus (including mammillary nuclei), and inferior colliculi, results in serious disabilities, has an etiology of thiamine deficiency, is treatable with thiamine, and occurs most commonly with alcoholism. Despite decades of study, whether alcohol exposure exacerbates the neuropathology or retards its resolution remains controversial. To examine patterns of brain damage and recovery resulting from thiamine deprivation with and without alcohol exposure, we conducted in vivo magnetic resonance imaging (MRI) and magnetic resonance spectroscopy (MRS) at 3 T in alcohol-preferring (P) rats, which had voluntarily consumed large amounts of alcohol before thiamine manipulation. A total of 18 adult male P rats (nine alcohol-exposed) received a thiamine-deficient diet for 2 weeks: 10 (five alcohol-exposed) received intraperitoneal (i.p.) pyrithiamine (PT) and eight (four alcohol-exposed) received i.p. thiamine supplementation. Neurological signs developed by day 14. Rats were scanned before thiamine depletion and 18 and 35 days after thiamine repletion. Two-dimensional J-resolved MRS single-voxel spectra with water reference were collected in a voxel subtending the thalamus; metabolite quantification was corrected for voxel tissue content. MRI identified significant enlargement of dorsal ventricles and increase in signal intensities in thalamus, inferior colliculi, and mammillary nuclei of PT compared with thiamine-treated (TT) groups from MRI 1-2, followed by significant normalization from MRI 2-3 in thalamus and colliculi, but not mammillary nuclei and lateral ventricles. Voxel-by-voxel analysis revealed additional hyperintense signal clusters in the dorsal and ventral hippocampus and enlargement of the fourth ventricle. MRS showed a significant decline and then partial recovery in thalamic N-acetylaspartate, a marker of neuronal integrity, in PT compared with TT rats, with no change detected in creatine, choline, or glutamate. PT rats with prior alcohol exposure exhibited attenuated recovery in the thalamus and arrested growth of the corpus callosum; further, two of the five alcohol-exposed PT rats died prematurely. Parenchymal and ventricular changes with thiamine manipulation concur with human radiological signs of WE. The enduring macrostructural and neurochemical abnormalities involving critical nodes of Papez circuit carry liabilities for development of amnesia and incomplete recovery from other cognitive and motor functions subserved by the affected neural systems.

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Cortical Gray Matter Loss in Treatment‐Naïve Alcohol Dependent Individuals

Cited by 164 publications

References 45 publications

Brain Morphometry and Cognitive Performance in Detoxified Alcohol-Dependents with Preserved Psychosocial Functioning

Brain Morphometry and Cognitive Performance in Detoxified Alcohol-Dependents with Preserved Psychosocial Functioning

Non-treatment-seeking heavy drinkers: Effects of chronic cigarette smoking on brain structure

Development and Resolution of Brain Lesions Caused by Pyrithiamine- and Dietary-Induced Thiamine Deficiency and Alcohol Exposure in the Alcohol-Preferring Rat: A Longitudinal Magnetic Resonance Imaging and Spectroscopy Study

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