Brain Proton Magnetic Resonance Spectroscopy Studies in Recently Abstinent Alcoholics*

Martin, Peter; Gibbs, S. Julian; Nimmerrichter, A.; Riddle, William R.; Welch, Larry W.; Willcott, M. Robert

doi:10.1111/j.1530-0277.1995.tb00992.x

Cited by 91 publications

(51 citation statements)

References 45 publications

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“…In alcoholism uncomplicated by WE, MRS provides evidence for abnormally low peaks of N-acetylaspartate (NAA), a marker for mature viable neurons, or choline (Cho), an index of membrane turnover, in frontal, parietal, or cerebellar regions within a month of withdrawal (Durazzo et al, 2004;Fein et al, 1994;Jagannathan et al, 1996;Schweinsburg et al, 2003Schweinsburg et al, , 2001Seitz et al, 1999) followed by improvement in NAA or Cho, suggesting neuronal recovery (Bendszus et al, 2001;Ende et al, 2005;Martin et al, 1995;Parks et al, 2002). In WE, whether preceded by alcoholism or other precipitating condition, an early deficit in NAA can improve, more so in the thalamus than cerebellum (Murata et al, 2001), a recovery pattern noted earlier by Victor et al (1971Victor et al ( , 1989.…”

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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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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“…Conversely, the longitudinal NAA increases observed in nsALC suggest greater recovery of neuronal structural elements or metabolism, while Cho increases may indicate normalization of parenchymal cell membrane synthesis/turnover or recovery of para-hippocampal cortex and myelin (Harding et al, 1997;Martin et al, 1995). Previous studies in abstinent alcoholics did not evaluate smoking effects, although the samples presumably included a significant number of smokers; these studies generally demonstrated little or no NAA recovery in major lobes and cerebellum over the first month of abstinence Parks et al, 2002), but see (Bendszus et al, 2001).…”

Section: Mtl Metabolite Concentrationsmentioning

confidence: 99%

“…MRI volumetric studies, however, cannot distinguish between injury to neuronal or glial cells, and they are not sensitive to tissue density changes reported in recovering alcoholics (Trabert et al, 1995). Proton magnetic resonance spectroscopy ( 1 H MRS) may distinguish between neuronal and glial injury and may be sensitive to changes in brain tissue density (Martin et al, 1995). We used 1 H-MRS at short echo time to measure four major metabolites (Ross and Bluml, 2001): N-acetyl-aspartate (NAA), an accepted marker of neuronal viability, is observed only in mature neurons and their processes; decreased NAA may reflect neuronal loss, atrophied dendrites and axons, and/or derangements of neurometabolism; cholinecontaining compounds (Cho) are believed to be involved in cell membrane breakdown and synthesis; creatine-containing metabolites (Cr) consist of creatine and phosphocreatine, which are involved in cell bioenergetics, and myo-inositol (m-Ino) is a putative marker of astrocytes and may also function as an osmolyte (Schweinsburg et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Chronic cigarette smoking modulates injury and short-term recovery of the medial temporal lobe in alcoholics

Gaździński

Durazzo

Yeh

et al. 2008

Psychiatry Research: Neuroimaging

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Memory function is largely mediated by medial temporal lobe (MTL), and its compromise has been observed in alcohol dependence and chronic cigarette smoking. The effects of heavy alcohol consumption and chronic smoking on hippocampal volumes and MTL metabolites and their recovery during abstinence from alcohol have not been assessed. Male alcoholics in treatment (ALC) [13 smokers (sALC) and 11 non-smokers (nsALC)] underwent quantitative magnetic resonance imaging and short-echo proton magnetic resonance spectroscopic imaging at one week and one month of sobriety. Outcome measures were compared to 14 age-matched, non-smoking light-drinkers and were related to visuospatial learning and memory. Over one month of abstinence, N-acetylaspartate, a neuronal marker, and membrane-associated choline-containing metabolites normalized in the MTL of nsALC, but remained low in the MTL of sALC. Metabolite concentration changes in both groups were associated with improvements in visuospatial memory. Hippocampal volumes increased in both groups during abstinence, but increasing volumes correlated with visuospatial memory improvements only in nsALC. In summary, chronic cigarette smoking in alcohol-dependent men appears to have adverse effects on MTL metabolite recovery during short-term sobriety. These data may also have implications for other conditions with established MTL involvement and significant smoking co-morbidity, such as schizophrenia-spectrum and mood disorders.

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“…It should be noted that the alcoholics in the present study were abstinent from alcohol for at least several months. As normalization of metabolite levels can occur with extended sobriety (Mann et al, 2001;Martin et al, 1995;Seitz et al, 1999;but see, O'Neill et al, 2001a), the metabolite values of the alcoholic group in the present study may reflect recovery. The volumetric MRS imaging (MRSI) approach permitted the measurement of neocortical regions not achievable with the large single-voxel approach.…”

Section: Discussionmentioning

confidence: 82%

Cortical NAA Deficits in HIV Infection without Dementia: Influence of Alcoholism Comorbidity

Pfefferbaum

Adalsteinsson

Sullivan

2005

Neuropsychopharmacol

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Alcoholism comorbidity is highly prevalent in individuals infected with human immunodeficiency virus (HIV). Each condition is known to affect brain structure, function, and metabolism, but the combined effects on the brain have only recently been considered. Single-voxel, proton MR spectroscopy (MRS) has yielded sensitive measures of early brain deterioration in the progression of HIV, but has limited coverage of neocortex, whereas MRS imaging (MRSI) can simultaneously interrogate large regions of cortex. Included were 15 men with HIV þ alcoholism, nine men with HIV alone, eight men with alcoholism alone (abstinent for 3-17 months), and 23 controls. The two HIV groups were matched in T-cell count and were not demented; the two alcoholism groups were relatively matched in lifetime alcohol consumption. We used MRSI with a variable-density spiral sequence to quantify major proton metabolitesFN-acetylaspartate (NAA), creatine (Cr), and choline (Cho)Fin the superior parietal-occipital cortex. Metabolites were expressed in absolute units and as the NAA/Cr ratio. Significant group effects were present for NAA and Cr. Only the HIV þ alcoholism group was significantly affected, exhibiting a 0.8 SD deficit in NAA and a 1.0 SD deficit in Cr. The deficits were not related to highly active antiretroviral therapy (HAART) status. Neither HIV infection nor alcoholism independently resulted in parietal-occipital cortical metabolite abnormalities, yet each disease carried a liability that put affected individuals at a heightened risk of neuronal compromise when the diseases were compounded. Further, the use of absolute measures revealed deficits in NAA and Cr that would have gone undetected if these metabolites were expressed as a ratio.

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Brain Proton Magnetic Resonance Spectroscopy Studies in Recently Abstinent Alcoholics*

Cited by 91 publications

References 45 publications

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

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

Chronic cigarette smoking modulates injury and short-term recovery of the medial temporal lobe in alcoholics

Cortical NAA Deficits in HIV Infection without Dementia: Influence of Alcoholism Comorbidity

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