title: Vermal atrophy of alcoholics correlate with serum thiamine levels but not with dentate iron concentrations as estimated by MRI.
abstract: Chronic alcohol consumption is frequently accompanied by cerebellar degeneration. The exact aetiology of alcoholic cerebellar degeneration is still a matter of debate. The aim of the present study was to investigate whether patients with chronic alcohol consumption exhibit a decrease in dentate nuclei intensity as measured by MRI, and if so, whether this decrease correlates with cerebellar atrophy as revealed by MR imaging or with clinical signs of cerebellar ataxia. A decrease in dentate nuclei intensity would indirectly indicate that iron accumulation, and therefore, oxidative stress may play a role in alcoholic cerebellar degeneration. MRI of 45 alcoholics and 44 age and sex-matched healthy control subjects was performed using a 3D-T1-weighted fast low angle shot (FLASH) echo sequence. Signal intensities of the dentate nuclei and cerebellar white matter were bilaterally measured. Planimetric measurements of cerebellar size were performed using a 3D-T1-weighted magnetization prepared rapid acquisition gradient echo (MPRAGE) sequence. Results demonstrated that dentate nuclei intensity was not significantly decreased in patients with chronic alcohol consumption (mean +/- SD signal intensity 65.36 +/- 13.0) if compared with control subjects (mean +/- SD signal intensity 68.95 +/- 9.4) (p = 0.15). Dentate nuclei intensity did not correlate with cerebellar size neither in control subjects nor in alcoholics. In contrast, vitamin B1 level correlated with cerebellar size in alcoholics even if the vitamin B1 concentration was within normal values (r = 0.344, p = 0.028). These results support the view that thiamine deficiency rather than direct neurotoxic effects of alcohol is the main causative factor for the development of alcoholic cerebellar degeneration.
authors.affiliation: Department of Neurology, University Duisburg-Essen, Hufelandstr. 55, 45122 Essen, Germany. matthias.maschke@uni-essen.de
authors.forename: Matthias
authors.initials: M
authors.lastname: Maschke
authors.forename: Johannes
authors.initials: J
authors.lastname: Weber
authors.forename: Udo
authors.initials: U
authors.lastname: Bonnet
authors.forename: Albena
authors.initials: A
authors.lastname: Dimitrova
authors.forename: Julia
authors.initials: J
authors.lastname: Bohrenkämper
authors.forename: Sonja
authors.initials: S
authors.lastname: Sturm
authors.forename: Bernhard W
authors.initials: BW
authors.lastname: Müller
authors.forename: Markus
authors.initials: M
authors.lastname: Gastpar
authors.forename: Hans-Christopher
authors.initials: HC
authors.lastname: Diener
authors.forename: Michael
authors.initials: M
authors.lastname: Forsting
authors.forename: Dagmar
authors.initials: D
authors.lastname: Timmann
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000428:Alcohol Drinking / Q000097:blood* / Q000473:pathology*; D001284:Atrophy / Q000473:pathology; D001923:Brain Chemistry; D016022:Case-Control Studies; D002529:Cerebellar Nuclei / Q000378:metabolism / Q000473:pathology*; D002531:Cerebellum / Q000473:pathology*; D005260:Female; D006801:Humans; D007091:Image Processing, Computer-Assisted; D007501:Iron / Q000378:metabolism; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D012720:Severity of Illness Index; D013831:Thiamine / Q000097:blood*; D014168:Transferrin / Q000378:metabolism; D005723:gamma-Glutamyltransferase / Q000097:blood
chemical_list: D014168:Transferrin; D007501:Iron; D005723:gamma-Glutamyltransferase; D013831:Thiamine