Abstract
BackgroundGray matter volume studies have been limited to few brain regions of interest, and white matter and glucose metabolism have received limited research attention in Korsakoff's syndrome (KS). Because of the lack of brain biomarkers, KS was found to be underdiagnosed in postmortem studies.Methodology/Principal FindingsNine consecutively selected patients with KS and 22 matched controls underwent both structural magnetic resonance imaging and 18F-fluorodeoxyglucose positron emission tomography examinations. Using a whole-brain analysis, the between-group comparisons of gray matter and white matter density and relative glucose uptake between patients with KS and controls showed the involvement of both the frontocerebellar and the Papez circuits, including morphological abnormalities in their nodes and connection tracts and probably resulting hypometabolism. The direct comparison of the regional distribution and degree of gray matter hypodensity and hypometabolism within the KS group indicated very consistent gray matter distribution of both abnormalities, with a single area of significant difference in the middle cingulate cortex showing greater hypometabolism than hypodensity. Finally, the analysis of the variability in the individual patterns of brain abnormalities within our sample of KS patients revealed that the middle cingulate cortex was the only brain region showing significant GM hypodensity and hypometabolism in each of our 9 KS patients.Conclusions/SignificanceThese results indicate widespread brain abnormalities in KS including both gray and white matter damage mainly involving two brain networks, namely, the fronto-cerebellar circuit and the Papez circuit. Furthermore, our findings suggest that the middle cingulate cortex may play a key role in the pathophysiology of KS and could be considered as a potential in vivo brain biomarker.
Highlights
Korsakoff’s syndrome (KS) is marked by global amnesia, which develops either insidiously or in the wake of Wernicke’s encephalopathy and whose most common etiology is the combination of thiamine deficiency and alcoholism [1]
Between-Group Comparisons As illustrated in Figure 1A, the analysis revealed significantly (p,0.001) lower gray matter (GM) density in the KS group than controls bilaterally in the cerebellum, lingual gyrus, fusiform gyrus, dorsomedian thalamus, hypothalamus, median and superior orbitofrontal cortex, superior and middle frontal cortex, supplementary motor area, anterior and middle cingulate cortex, cuneus, precuneus and paracentral lobule, left superior temporal gyrus, Heschl’s gyrus, insula, supramarginal gyrus, and right postcentral and precentral gyri
This study revealed widespread morphological and metabolism abnormalities in KS patients, but two networks appeared to be impaired, namely the frontocerebellar and Papez circuits
Summary
Korsakoff’s syndrome (KS) is marked by global amnesia, which develops either insidiously or in the wake of Wernicke’s encephalopathy and whose most common etiology is the combination of thiamine deficiency and alcoholism [1]. Postmortem studies of alcoholic Korsakoff patients have shown pathological abnormalities involving periventricular and periaqueductal gray matter, walls of the third ventricle, floor of the fourth ventricle and cerebellum [6]. Damage has been found in the hippocampus [7], certain nuclei of the thalamus [8,9], hypothalamus [10] and more the mammillary bodies [11,12], cerebral cortex [13], brainstem nuclei [14] and locus coeruleus [15]. Gray matter volume studies have been limited to few brain regions of interest, and white matter and glucose metabolism have received limited research attention in Korsakoff’s syndrome (KS). Because of the lack of brain biomarkers, KS was found to be underdiagnosed in postmortem studies
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