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G Fein

Publications and source records attributed to G Fein.

At least 19 recordsLinked to original sources
PubMed2004

Impairment on a simulated gambling task in long-term abstinent alcoholics.

BACKGROUND: Recent research indicates that currently active or recently detoxified substance abusers make more disadvantageous decisions on a simulated gambling task (SGT). This study expands on the current literature by using the SGT to examine decision making in long-term abstinent alcoholics (mean of 6.6 years' abstinence) who do not have antisocial personality disorder or a history of conduct disorder. METHODS: A total of 102 subjects (58 controls and 44 abstinent alcoholics) were tested on the SGT, in which subjects choose cards from 4 different decks that vary in terms of the magnitude of the immediate win (large or small) and the magnitude of long-term loss (large or small). The association of SGT performance with alcohol use variables, with the number of externalizing symptoms, and with personality measures of social deviance was examined. RESULTS: Compared with controls, long-term abstinent alcohol-dependent subjects had more externalizing symptoms, had personality profiles associated with a proneness to social deviance, and made more disadvantageous decisions on the SGT. The magnitude of disadvantageous decision making was associated with the duration of peak alcohol use but was associated with only one measure (low socialization) of socially deviant personality traits. CONCLUSIONS: The results suggest that alcoholics can achieve long-term abstinence despite persistent deficits in decision making and abnormal personality profiles. The decision-making deficits either may be the result of long-term alcoholism or may reflect a factor predisposing to alcoholism that persists with abstinence. The possibility is raised that alcoholics who cannot achieve long-term abstinence are even more impaired on their decision making and have more abnormal personality profiles than the abstinent alcoholics studied here.

Adult↗
PubMed2002

Cortical gray matter loss in treatment-naïve alcohol dependent individuals.

BACKGROUND: Most studies of the impact of alcohol dependence on the brain have examined individuals in treatment. Such samples represent a small proportion of alcoholics in the general population. Such samples may embody a bias (Berkson's fallacy) if the association between variables (for example, alcoholism and cortical gray matter loss) differs between the population of alcoholics in treatment and alcoholics in the general population. Our objective was to determine if treatment-naïve alcoholics show structural brain changes versus controls and to compare our findings with reports evaluating alcoholic samples drawn from treatment populations. METHODS: Structural MRI was used to assess whole brain and regional volumes of cortical gray matter and white matter in 24 young to middle-aged treatment-naïve alcohol-dependent males versus 17 controls. RESULTS: Cortical gray matter volumes in alcohol-dependent individuals were negatively associated with age and lifetime duration of alcohol use (which were highly confounded). These subjects showed reduced whole brain (p < 0.05), prefrontal (p < 0.01), and parietal (p < 0.05) cortical gray matter compared with controls. White matter and temporal cortex, tissues that usually show volume reductions in samples drawn from treatment, did not differ between treatment-naïve alcoholics and controls (all p > 0.40). CONCLUSIONS: Our findings are consistent with the hypothesis that structural brain changes in treatment-naïve alcoholics are less severe than those reported in clinical samples of alcoholics, perhaps due to less concomitant psychopathology and a reduced severity of alcoholism in treatment-naïve alcoholics. However, caution must be taken when comparing our findings with results from clinical samples, as we did not directly compare treatment-naïve alcoholics with treated alcoholics and our treatment-naïve sample tended to be younger than the (clinical) samples reported in the literature. Nevertheless, we suggest that most of the reports of the central nervous system consequences of alcoholism may not accurately describe the majority of alcoholic-dependent individuals.

Adult↗
PubMed2001

Reliability of tissue volumes and their spatial distribution for segmented magnetic resonance images.

Before using MRI tissue segmentation in clinical studies as a dependent variable or as a means to correct functional data for differential tissue contribution, we must first establish the volume reliability and spatial distribution reproducibility of the segmentation method. Although several reports of volume reliability can be found in the literature, there are no articles assessing the reproducibility of the spatial distribution of tissue. In this report, we examine the validity, volume reliability, and spatial distribution reproducibility for our K-means cluster segmentation. Validation was examined by classifying gray matter, white matter, and CSF on images constructed using an MRI simulator and digital brain phantom, with percentage volume differences of less than 5% and spatial distribution overlaps greater than 0.94 (1.0 is perfect). We also segmented repeat scan MRIs from 10 healthy subjects, with intraclass correlation coefficients greater than 0.92 for cortical gray matter, white matter, sulcal CSF, and ventricular CSF. The original scans were also coregistered to the repeat scan of the same subject, and the spatial overlap for each tissue was then computed. Our overlaps ranged from 0.75 to 0.86 for these tissues. Our results support the use of K-means cluster segmentation, and the use of segmented structural MRIs to guide the analysis of functional and other images.

Adult↗
PubMed2001

Effects of chronic alcohol consumption on the broad phospholipid signal in human brain: an in vivo 31P MRS study.

BACKGROUND: Phosphorus magnetic resonance spectroscopy (31P MRS) allows for the measurement of phospholipids and their breakdown products in the human brain. Fairly mobile membrane phospholipids give rise to a broad signal that co-resonates with metabolic phosphodiesters. Chronic alcohol exposure increases the rigidity of isolated brain membranes and, thus, may affect the amount and transverse relaxation times (T2) of MRS-detectable phospholipids. We tested the hypothesis that subjects who were heavy drinkers have stiffer membranes than controls who were light drinkers, as reflected in a smaller broad signal component and a shorter T2 of the broad signal in 31P MR spectra of the brain. METHODS: Thirteen alcohol-dependent heavy drinkers (mean age 44 years) were studied by localized 31P MRS in the centrum semiovale and compared with 17 nondependent light drinkers of similar age. The broad component signal was separated from the metabolite signal by convolution difference, which is based on the large difference in line widths of these two signals. Longitudinal and T2 relaxation times were measured using standard methods. RESULTS: The broad component integral was 13% lower in the brain of heavy drinkers compared with light drinkers (p < 0.001) and remained significantly smaller after corrections for both longitudinal and transverse relaxations (p < 0.01). The T2 distribution of the broad component consistently showed two resolvable components in both groups. The fast relaxing component had the same T2 in both groups (T2 = 1.9 msec). The slower relaxing component T2 was 0.6 msec shorter in heavy drinkers compared with light drinkers (p = 0.08). CONCLUSIONS: These results, observed in the absence of white matter volume loss, are consistent with biochemical alterations and higher rigidity of white matter phospholipids associated with long-term chronic alcohol abuse. The observed smaller broad signal component in these relatively young heavy drinkers is a sensitive measure of white matter phospholipid damage.

Adult↗
PubMed2001

Effects of abstinence from alcohol on the broad phospholipid signal in human brain: an in vivo 31P magnetic resonance spectroscopy study.

BACKGROUND: In vivo phosphorus magnetic resonance spectroscopy (31P MRS) at a magnetic field strength of 1.5 T allows measurement of fairly mobile membrane phospholipids in the human brain. We previously showed that subjects who are heavy drinkers had a smaller signal and a shorter transverse relaxation time (T2) of white matter phospholipids than light drinkers, which suggested lower concentrations and molecular mobility of phospholipids in heavy drinkers. The purpose of the present study was to measure if such chronic alcohol-induced white matter tissue changes are persistent in long-term abstinent alcoholics. METHODS: Fourteen abstinent alcoholics (mean age 45 years, seven men and seven women) were studied by localized 31P MRS in the centrum semiovale and were compared with 13 male, alcohol-dependent, heavy drinkers and 23 nondependent light drinkers (17 men, 6 women) of similar age. Methods for measurements of the broad membrane phospholipid signal and its relaxation time were described previously. RESULTS: Phospholipid concentrations and relaxation times in alcoholics abstinent for an average of 31 months were not significantly different from those measured in light drinkers. The contribution of fast and slowly relaxing signal components to the broad phospholipid signal, however, was still different in abstinent alcoholics compared with light drinkers. No effects of sex or of family history of alcoholism were noted on any of our spectroscopic measures within the light-drinking or abstinent groups. CONCLUSIONS: Most of our results suggest at least partial recovery of chronic alcohol-induced white matter phospholipid damage with long-term abstinence. They offer myelination changes and/or dendritic rearborization as a possible mechanism for the commonly observed white matter volume gain with prolonged abstinence. But the results also suggest a persistent abnormality in the nature and/or physical properties of white matter phospholipids in long-term abstinent alcoholics.

Adult↗
PubMed2000

Hippocampal and cortical atrophy predict dementia in subcortical ischemic vascular disease.

BACKGROUND: The cause of dementia in subcortical ischemic vascular disease (SIVD) is controversial. OBJECTIVES: To determine whether cognitive impairment in SIVD 1) correlates with measures of ischemic brain injury or brain atrophy, and/or 2) is due to concomitant AD. METHODS: Volumetric MRI of the brain was performed in 1) elderly subjects with lacunes (L) and a spectrum of cognitive impairment-normal cognition (NC+L, n = 32), mild cognitive impairment (CI+L, n = 26), and dementia (D+L, n = 29); 2) a comparison group with probable AD (n = 28); and 3) a control group with normal cognition and no lacunes (NC). The authors examined the relationship between the severity of cognitive impairment and 1) volume, number, and location of lacunes; 2) volume of white matter signal hyperintensities (WMSH); and 3) measures of brain atrophy (i. e., hippocampal, cortical gray matter, and CSF volumes). RESULTS: Among the three lacune groups, severity of cognitive impairment correlated with atrophy of the hippocampus and cortical gray matter, but not with any lacune measure. Although hippocampal atrophy was the best predictor of severity of cognitive impairment, there was evidence for a second, partially independent, atrophic process associated with ventricular dilation, cortical gray matter atrophy, and increase in WMSH. Eight autopsied SIVD cases showed variable severity of ischemic and neurofibrillary degeneration in the hippocampus, but no significant AD pathology in neocortex. The probable AD group gave evidence of only one atrophic process, reflected in the severity of hippocampal atrophy. Comparison of regional neocortical gray matter volumes showed sparing of the primary motor and visual cortices in the probable AD group, but relatively uniform atrophy in the D+L group. CONCLUSIONS: Dementia in SIVD, as in AD, correlates best with hippocampal and cortical atrophy, rather than any measure of lacunes. In SIVD, unlike AD, there is evidence for partial independence between these two atrophic processes. Hippocampal atrophy may result from a mixture of ischemic and degenerative pathologies. The cause of diffuse cortical atrophy is not known, but may be partially indexed by the severity of WMSH.

Aged↗
PubMed2000

Subcortical ischemic vascular dementia: assessment with quantitative MR imaging and 1H MR spectroscopy.

BACKGROUND AND PURPOSE: Subcortical ischemic vascular dementia is associated with cortical hypometabolism and hypoperfusion, and this reduced cortical metabolism or blood flow can be detected with functional imaging such as positron emission tomography. The aim of this study was to characterize, by means of MR imaging and 1H MR spectroscopy, the structural and metabolic brain changes that occur among patients with subcortical ischemic vascular dementia compared with those of elderly control volunteers and patients with Alzheimer's disease. METHODS: Patients with dementia and lacunes (n = 11), cognitive impairment and lacunes (n = 14), and dementia without lacunes (n = 18) and healthy age-matched control volunteers (n = 20) underwent MR imaging and 1H MR spectroscopy. 1H MR spectroscopy data were coanalyzed with coregistered segmented MR images to account for atrophy and tissue composition. RESULTS: Compared with healthy control volunteers, patients with dementia and lacunes had 11.74% lower N-acetylaspartate/creatine ratios (NAA/Cr) (P = .007) and 10.25% lower N-acetylaspartate measurements (NAA) in the cerebral cortex (P = .03). In white matter, patients with dementia and lacunes showed a 10.56% NAA/Cr reduction (P = .01) and a 12.64% NAA reduction (P = .04) compared with control subjects. NAA in the frontal cortex was negatively correlated with the volume of white matter signal hyperintensity among patients with cognitive impairment and lacunes (P = .002). Patients with dementia, but not patients with dementia and lacunes, showed a 10.33% NAA/Cr decrease (P = .02) in the hippocampus compared with healthy control volunteers. CONCLUSION: Patients with dementia and lacunes have reduced NAA and NAA/Cr in both cortical and white matter regions. Cortical changes may result from cortical ischemia/infarction, retrograde or trans-synaptic injury (or both) secondary to subcortical neuronal loss, or concurrent Alzheimer's pathologic abnormalities. Cortical derangement may contribute to dementia among patients with subcortical infarction.

Aged↗
PubMed2000

Ethanol in human brain by magnetic resonance spectroscopy: correlation with blood and breath levels, relaxation, and magnetization transfer.

BACKGROUND: Proton magnetic resonance spectroscopy (1H MRS) allows measurement of alcohol in the human brain after alcohol consumption. However, the quantity of alcohol that can be detected in the brain by 1H MRS pulse sequences has been controversial, with values ranging from about 24% to 94% of the temporally concordant blood alcohol concentrations. The quantitation of brain alcohol is critically affected by the kinetics of alcohol uptake and elimination, by the relaxation times of the protons that give rise to the brain alcohol signal, and by the specifics of both pulse sequence timing and radio frequency pulse applications. METHODS: We investigated these factors in 20 light-drinking subjects after oral administration of approximately 0.85 g/kg body weight of alcohol by localized 1H MRS and measurements of blood and breath alcohol concentrations obtained at the same time. Specifically, we measured transverse and longitudinal relaxation times of brain alcohol and its signal saturation on application of on- or off-resonance radio frequency pulses. All 1H MRS measurements were performed at a time after brain and blood alcohol concentrations had equilibrated. RESULTS: 1H MRS measures of brain alcohol were correlated highly with both breath and blood alcohol concentrations after equilibration in brain tissue. The measured 1H MRS relaxation times of brain alcohol were shorter than given in previous reports that were limited by smaller subject numbers, improper use of 1H MRS methods, and estimates rather than measurements. The brain alcohol signal decreased by about 30% on application of on- or off-resonance saturation pulses. CONCLUSIONS: 1H MRS allows direct measurement of brain alcohol, formerly only possible indirectly through inferences from breath alcohol levels. Quantitation of brain alcohol levels need to take into account measured relaxation times and alcohol signal attenuation due to presence and timing of standard radio frequency MRS pulses. Saturation experiments give evidence for the existence of more than one compartment of brain alcohol characterized by different molecular environments. They suggest that a fraction of brain alcohol is invisible to 1H MRS.

Adult↗
PubMed1999

Sensory gating in chronic posttraumatic stress disorder: reduced auditory P50 suppression in combat veterans.

BACKGROUND: Posttraumatic stress disorder (PTSD) may be associated with a general impairment of cognitive function that extends beyond the processing of trauma-specific stimuli. Suppression of the auditory P50 response to repeated stimuli occurs in normal subjects and reflects the central nervous system's ability to screen out repetitive stimuli, a phenomenon referred to as sensory gating. This study examines P50 sensory gating to nonstartle auditory stimuli in PTSD subjects and normal controls. METHODS: P50 generation and gating were studied using a conditioning/testing paradigm in 15 male subjects with PTSD and 12 male controls. P50 test/conditioning (T/C) ratios were estimated using the Singular Value Decomposition method. RESULTS: The amplitude of the P50 response to the conditioning stimulus did not differ in subjects with PTSD compared to normal controls. The P50 T/C ratio is increased in PTSD subjects (mean = .408, SD = .275) as compared to the controls (mean = .213, SD = .126, two tailed t, p = .024). CONCLUSIONS: This study provides evidence that PTSD is associated with impaired gating to nonstartle trauma-neutral auditory stimuli.

Auditory Threshold↗
PubMed1999

Elevated subcortical choline metabolites in cognitively and clinically asymptomatic HIV+ patients.

OBJECTIVE: To determine whether the concentrations of the neuronal marker N-acetylaspartate (NAA) and the choline-containing metabolites (Cho) are altered in the subcortical brain of HIV+ patients who are cognitively normal and clinically asymptomatic, and to determine whether these alterations are greater in the presence of cognitive impairments and clinical symptoms. BACKGROUND: Pathologic studies suggest that subcortical gray matter carries a heavy HIV load, and neuropsychological test results are consistent with involvement of subcortical and frontostriatal brain systems in HIV disease. Noninvasive proton magnetic resonance spectroscopy (1H MRS) suggests neuronal preservation and macrophage infiltration in the subcortical brain of clinically symptomatic and cognitively impaired HIV+ individuals. Improved 1H MRS methods may allow the early detection of metabolite alterations in the subcortical brain of asymptomatic HIV+ individuals. METHODS: Two-dimensional 1H MRS imaging was performed on 30 HIV- control subjects and 70 HIV+ patients with varying severities of systemic disease and neuropsychological impairments, but without cerebral opportunistic infections. RESULTS: Subcortical Cho was elevated in HIV+ patients compared with control subjects regardless of the presence or absence of cognitive impairment or clinical symptoms. Subcortical NAA was lower than control NAA only in severely cognitively impaired HIV+ subjects. Subcortical NAA correlated with performance on a variety of neuropsychological tests but not with Centers for Disease Control clinical stage, whereas high-thalamic Cho was associated with low CD4 lymphocyte counts. CONCLUSIONS: 1H MRS imaging detects higher Cho in subcortical brain early in HIV disease, when individuals are clinically and neuropsychologically asymptomatic, whereas lower NAA is only found in subcortical brain in individuals with severe neuropsychological impairments. Quantitative 1H MRS imaging may play a role in the objective assessment of the presence, magnitude, and progression of brain involvement in HIV infection.

Adult↗
PubMed1999

Intact visual word priming in cocaine dependent subjects with and without cognitive deficit.

1. The effects of semantic and repetition priming on reaction time were assessed in 27 recently abstinent cocaine and cocaine/alcohol dependent volunteers and 12 controls without substance abuse history. 2. The 27 cocaine dependent subjects were further divided into cognitively intact (N = 13) and moderate-to-severe cognitively impaired (N = 14) groups on the basis of neuropsychological testing. 3. Both cognitively intact and cognitively impaired cocaine dependent groups showed motor-response facilitation by semantic and repetition priming not significantly different from that of non-abusing controls. 4. It is proposed that both semantic and perceptually mediated visual word priming are implicit cognitive processes resilient to the sequelae of cocaine dependence which impact upon explicit cognitive systems.

Adult↗
PubMed1999

Differential association of HIV-related neuropsychological impairment with semantic versus repetition priming.

There is evidence that the facilitating effects of stimulus repetition (repetition or identity priming) are mediated by visuoperceptual functions local to extrastriate cortex. Semantic or verbal-associative priming, on the other hand, is believed to be a function of more anterior brain systems. The present study finds evidence for disrupted semantic priming with intact repetition priming in a cognitively impaired HIV+ sample. These results are consistent with recent brain-imaging evidence for a subcortical and white-matter locus for HIV associated neuropathology resulting in effects on subcortical-frontal systems.

Adult↗
PubMed1999

Magnetization transfer ratio of white matter hyperintensities in subcortical ischemic vascular dementia.

BACKGROUND AND PURPOSE: In subjects with subcortical ischemic vascular dementia (SIVD), tissue vacuolization, myelin pallor, and demyelination have been found on pathologic examination of white matter signal hyperintensities (WMSH). Magnetization transfer ratio (MTR) values provide a potential measure of compromised white matter integrity. The purpose of this study was to determine if there were differences in MTR of WMSH between subjects with SIVD and cognitively normal healthy control subjects. METHODS: Fifteen subjects with SIVD and 16 control subjects of comparable age and sex were studied. MTR images were coregistered to MR images segmented into tissue classes (gray matter, white matter, CSF, WMSH, and lacunar infarcts). MTR of WMSH was compared across groups and examined by WMSH location, size, and total burden. RESULTS: WMSH burden was greater in SIVD patients than in control subjects (2.4% vs 0.67%). MTR of WMSH did not differ between groups, but MTR of periventricular WMSH was lower in SIVD patients than in control subjects (37.6% vs 39.4%). Even after accounting for covariant effects of lesion burden, there was still a trend toward reduced periventricular WMSH MTR in the group with dementia. There was no correlation between WMSH MTR and WMSH lesion size. CONCLUSION: These findings are consistent with observations that pathologic changes in vascular dementia are most severe in the periventricular white matter and suggest that insight into the pathophysiology of SIVD might be gleaned from studies of the periventricular region.

Aged↗
PubMed1998

Hippocampal neuronal dysfunction in schizophrenia as measured by proton magnetic resonance spectroscopy.

BACKGROUND: Previous neuropathological and neuroimaging studies have documented neuronal loss in the hippocampal region in schizophrenia. N-acetylaspartate (NAA) is a neuronal/axonal marker that may be utilized to assess neuronal loss or dysfunction by proton magnetic resonance spectroscopy (1H MRS). This study measured NAA, choline, and creatine in the hippocampal region of patients with schizophrenia using in vivo proton magnetic resonance spectroscopic imaging (1H MRSI). METHODS: 1H MRSI was performed on the right and left hippocampal regions in 30 chronic schizophrenic patients and 18 control subjects. Concentration estimates of NAA, creatine, and choline were determined. RESULTS: Relative to the control group, the patients with schizophrenia demonstrated significantly lower NAA in both the right and left hippocampal regions. No group differences in choline were noted; however, there was a trend for creatine to be higher on the left than the right hippocampus in the schizophrenic group. There was also no association between NAA and duration of illness or medication dosage. CONCLUSIONS: This preliminary study provides support for neuronal dysfunction and/or decreased neuronal density in the hippocampal region. The absence of choline signal elevation does not support accelerated turnover of membrane phospholipids, which might be expected if there were ongoing neuronal atrophy or neuronal necrosis.

Adult↗
PubMed1998

Very late pain-related activity identified with topographically mapped frequency domain analysis of evoked potentials.

OBJECTIVE: To identify low-frequency activity in the pain-evoked potential at very late latencies, consistent with C-fiber transmission velocities. METHODS: Brief (1 ms) painful (intracutaneous) and two levels of non-painful (mild and strong) electrical pulses were applied to the index and middle fingers of the left hand. Evoked potentials (EPs) were recorded from 30 electrodes covering the entire scalp. Data from the 3 stimulus conditions (approximately 60 trials per condition per subject) were compared using the frequency domain technique of complex demodulation applied to single trial data. Subjects were 14 normal right-handed male human volunteers, aged 19-36 years. RESULTS: Using descriptive probability mapping, pain versus strong non-pain differences were found in grand average data as well as in 8 of 14 subjects, consisting of greater low-frequency power at latencies from 700 to 1100 ms at electrodes near the contralateral central sulcus and at the vertex. CONCLUSIONS: There are topographically focal, pain versus non-pain differences in the 700-1100 ms latency range that can be seen using frequency-domain analytic techniques. These differences were not seen with traditional time domain analyses. They may be due to a C-fiber-related mechanism or to very late activity triggered by faster fibers.

Adult↗
PubMed1998

Premorbid brain size is a determinant of functional reserve in abstinent crack-cocaine and crack-cocaine-alcohol-dependent adults.

Studies of Alzheimer's disease patients show that individuals with larger premorbid brains have a later onset of disease, or a lessened severity of cognitive impairment, or both. This may be due to a "functional reserve" associated with the greater number of neurons and synapses available in larger brains. We used magnetic resonance imaging and the MicroCog Assessment of Cognitive Functioning to examine the association between intracranial volume (premorbid brain size) and neuropsychological function in abstinent crack-cocaine and crack-cocaine-alcohol dependent individuals. There were no significant differences between the crack-only and the crack-alcohol dependent participants in neuropsychological performance or in intracranial volume. The abstinent cocaine-dependent individuals (both crack-only and crack-alcohol) were significantly impaired in many neuropsychological domains. Intracranial volume accounted for a significant proportion of the variance in neuropsychological performance. This result is consistent with the finding in the Alzheimer's literature that larger brains can maintain function to a greater degree, or for a longer period of time, in the face of cerebral disease or insult. Functional reserve may be a heretofore little recognized protective mechanism of the brain that has consequences for the severity of expression of cerebral disease or insult throughout life.

Adult↗
PubMed1998

Alzheimer disease: quantitative H-1 MR spectroscopic imaging of frontoparietal brain.

PURPOSE: To replicate previous hydrogen-1 magnetic resonance (MR) spectroscopic imaging findings of metabolic abnormalities in patients with Alzheimer disease (AD), to verify that metabolic abnormalities are not an artifact of structural variations measured at MR imaging, to determine whether metabolic changes correlate with dementia severity, and to test whether MR imaging and MR spectroscopic imaging findings together improve ability to differentiate AD. MATERIALS AND METHODS: MR spectroscopic imaging and MR imaging were performed in 28 patients with AD and 22 healthy elderly subjects. Spectroscopic imaging data were coregistered with MR imaging segmentation data to obtain volume-corrected metabolite concentrations. RESULTS: Consistent with previous results, N-acetyl aspartate (NAA) levels were statistically significantly reduced in frontal and posterior mesial cortex of AD patients, presumably due to neuronal loss. NAA level reductions were independent of structural variations measured at MR imaging and, in parietal mesial cortex, were correlated mildly with dementia severity. Spectroscopic imaging findings of NAA level combined with MR imaging measures did not improve discrimination power for AD relative to that of MR imaging alone. CONCLUSION: Reduced NAA levels in frontoparietal brain are of limited use for diagnosis of AD. However, they are not an artifact of structural variations and thus may provide useful information for the understanding of the pathologic processes underlying AD.

Aged↗