Similar brain lesions in alcoholics and Korsakoff patients: MRI, psychometric and clinical findings

Blansjaar, Ben A.; Vielvoye, G. J.; Dijk, J. Gert van; Rijnders, Ronald J.P.

doi:10.1016/0303-8467(92)90089-l

Cited by 30 publications

(25 citation statements)

References 14 publications

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“…They are typically localized around the third ventricle in the medial parts of the thalamus and hypothalamus, involve the mamillary bodies, the pineal and periaqueductal regions of the midbrain, the floor of the fourth ventricle [17] and the midline cerebellum [8], can also involve the brainstem [18], and sometimes white matter and cortex [19]. The symmetric paraventricular lesions, hyperintense on T2-weighted images, which are so typical for Wernicke encephalopathy are related to chronic thiamine or vitamin-B1 deficiency [17,20]. Vitamin B1 is a co-factor of the enzyme transketolase and there is decreased activity of the enzyme in the thiamine-deficient state.…”

Section: Discussionmentioning

confidence: 99%

“…Histologically, the earliest finding of Wernicke encephalopathy is intracellular edema with swelling of astrocytes, oligodendrocytes, myelin sheats, and neuronal dendrites. More advanced changes are demyelination, petechial hemorrhage [17,23], and astrocytic and microglial proliferation with relative neuronal sparing [11]. In the pathology literature hemorrhages are found in only 20 % of autopsied cases [17].…”

Section: Discussionmentioning

confidence: 99%

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Wernicke encephalopathy: MR findings in two patients

et al. 1999

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Wernicke encephalopathy is a serious neurologic disorder caused by vitamin-B1 or thiamine deficiency. In the literature the characteristic symmetric paraventricular lesions of Wernicke encephalopathy are hyperintense on T2-weighted sequences spin-echo (SE) and enhance on T1-weighted SE sequences after intravenous gadolinium administration in the acute phase. We present two patients in the acute phase of Wernicke encephalopathy with special reference to the MR imaging. One of our reported cases is special because of the MR demonstration of a hemorrhagic focus in the caput of the right nucleus caudatus. The other case demonstrates no enhancement on SE T1-weighted sequences after intravenous gadolinium administration.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Wernicke encephalopathy: MR findings in two patients

et al. 1999

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“…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). Like amnesic patients with Wernicke-Korsakoff syndrome, non-amnesic alcoholics also have notable volume shrinkage of the mammillary bodies (Davila et al, 1994;Shear et al, 1996;Sullivan et al, 1999; but see Charness and DeLaPaz, 1987), anterior hippocampus (Agartz et al, 1999;Sullivan and Marsh, 2003;Sullivan et al, 1995), thalamus , and cerebellum (Sullivan et al, 2000a, b), but the volume shrinkage is substantially less than in alcoholics with WE or KS (cf, Blansjaar et al, 1992;Charness, 1993Charness, , 1999Mulholland et al, 2005;Sullivan, 2000). Because of the edematous nature of WE lesions, magnetic resonance imaging (MRI) methods sensitive to fluid changes in tissue have revealed bilaterally distributed hyperintensities in medial thalamus, mammillary bodies, and periaqueductal gray matter (eg, non-alcoholics: Chu et al, 2002;Doraiswamy et al, 1994;Unlu et al, 2006;Zhong et al, 2005) (alcoholics: Schroth et al, 1991).…”

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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“…Considering gray and white matter separately, atrophy of the gray matter affects the superior portions of the cerebellum and the thalamic nuclei in particular [19,21,22]. White matter atrophy is pronounced in the supratentorial frontal, infratentorial pontine, and cerebellar regions [18,20]. …”

Section: Atrophymentioning

confidence: 99%

“…Since glutamate release increases as a consequence of thiamine deficiency and alcohol abuse triggers an overexpression of NMDA receptors, the combination of abuse and thiamine deficiency contributes to particularly severe excitotoxic cell damage. Magnesium deficiency, hyperglycemia, and genetic vulnerability are discussed as aggravating cofactors [18,28,29]. The visible morphological changes overlap largely in both diseases.…”

Section: Wernicke Encephalopathy/wernicke-korsakoff Syndromementioning

confidence: 99%

The Whole Spectrum of Alcohol-Related Changes in the CNS: Practical MR and CT Imaging Guidelines for Daily Clinical Use

Keil

Greschus

Schneider

et al. 2015

Fortschr Röntgenstr

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Alcohol addiction is the most common drug addiction. Alcohol passes both the placenta as well as the blood-brain barrier and is in multiple ways neurotoxic. Liver diseases and other systemic alcohol-related diseases cause secondary damage to the CNS.?Especially in adolescents, even a single episode of severe alcohol intoxication (?binge drinking?) may result in life-threatening neurological consequences. Alcohol-related brain and spinal cord diseases derive from multiple causes including impairment of the cellular metabolism, often aggravated by hypovitaminosis, altered neurotransmission, myelination and synaptogenesis as well as alterations in gene expression. Modern radiological diagnostics, MRI in particular, can detect the resulting alterations in the CNS with a high sensitivity. Morphological aspects often strongly correlate with clinical symptoms of the patient. It is less commonly known that many diseases considered as ?typically alcohol-related?, such as Wernicke?s encephalopathy, are to a large extent not alcohol-induced. Visible CNS alterations are thus non-pathognomonic and demand careful evaluation of differential diagnoses. This review article elucidates the pathogenesis, clinical aspects and radiological image features of the most common alcohol-related CNS diseases and their differential diagnoses. Key Points: ??Alcohol-associated changes in the CNS are common and radiologically assessable. ??They are often subtle and allow multiple differential diagnoses besides alcohol consumption. ??Knowledge of clinical exams and lab results is crucial for diagnostic accuracy. Citation Format: ??Keil VC, Greschus S, Schneider C et?al. The Whole Spectrum of Alcohol-Related Changes in the CNS: Practical MR and CT Imaging Guidelines for Daily Clinical Use. Fortschr R?ntgenstr 2015; 187: 1073???1083

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Similar brain lesions in alcoholics and Korsakoff patients: MRI, psychometric and clinical findings

Cited by 30 publications

References 14 publications

Wernicke encephalopathy: MR findings in two patients

Wernicke encephalopathy: MR findings in two patients

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

The Whole Spectrum of Alcohol-Related Changes in the CNS: Practical MR and CT Imaging Guidelines for Daily Clinical Use

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