title: Cerebral glucose utilisation in hepatitis C virus infection-associated encephalopathy.
abstract: Patients with hepatitis C virus (HCV) infection frequently show neuropsychiatric symptoms. This study aims to help clarify the neurochemical mechanisms behind these symptoms and to add further proof to the hypothesis that HCV may affect brain function. Therefore, 15 patients who reported increasing chronic fatigue, mood alterations, and/or cognitive decline since their HCV infection underwent neurologic and neuropsychological examination, magnetic resonance imaging, (18)F-fluoro-deoxy-glucose positron emission tomography of the brain, and single photon emission tomography of striatal dopamine and midbrain serotonin transporter (SERT) availability. None of the patients had liver cirrhosis. Patients' data were compared with data of age-matched controls. In addition, regression analysis was performed between cognitive deficits, and mood and fatigue scores as dependent variables, and cerebral glucose metabolism, dopamine, or SERT availability as predictors. Patients showed significant cognitive deficits, significantly decreased striatal dopamine and midbrain SERT availability, and significantly reduced glucose metabolism in the limbic association cortex, and in the frontal, parietal, and superior temporal cortices, all of which correlated with dopamine transporter availability and psychometric results. Thus, the study provides further evidence of central nervous system affection in HCV-afflicted patients with neuropsychiatric symptoms. Data indicate alteration of dopaminergic neurotransmission as a possible mechanism of cognitive decline.
authors.affiliation: Department of Neurology, Medical School Hannover, Hannover, Germany.
authors.forename: Meike
authors.initials: M
authors.lastname: Heeren
authors.forename: Karin
authors.initials: K
authors.lastname: Weissenborn
authors.forename: Dimitrios
authors.initials: D
authors.lastname: Arvanitis
authors.forename: Martin
authors.initials: M
authors.lastname: Bokemeyer
authors.forename: Annemarie
authors.initials: A
authors.lastname: Goldbecker
authors.forename: Argyro
authors.initials: A
authors.lastname: Tountopoulou
authors.forename: Thomas
authors.initials: T
authors.lastname: Peschel
authors.forename: Julian
authors.initials: J
authors.lastname: Grosskreutz
authors.forename: Hartmut
authors.initials: H
authors.lastname: Hecker
authors.forename: Ralph
authors.initials: R
authors.lastname: Buchert
authors.forename: Georg
authors.initials: G
authors.lastname: Berding
mesh_terms: D001921:Brain / Q000378:metabolism*; D001928:Brain Diseases, Metabolic / Q000000981:diagnostic imaging / Q000209:etiology / Q000378:metabolism* / Q000523:psychology; D003071:Cognition / Q000502:physiology; D004298:Dopamine / Q000378:metabolism; D005260:Female; D019788:Fluorodeoxyglucose F18; D005947:Glucose / Q000378:metabolism*; D006526:Hepatitis C / Q000150:complications* / Q000000981:diagnostic imaging / Q000378:metabolism; D006801:Humans; D008182:Luria-Nebraska Neuropsychological Battery; D008568:Memory / Q000502:physiology; D049268:Positron-Emission Tomography; D019275:Radiopharmaceuticals; D050486:Serotonin Plasma Membrane Transport Proteins / Q000378:metabolism; D015899:Tomography, Emission-Computed, Single-Photon
chemical_list: D019275:Radiopharmaceuticals; C493230:SLC6A4 protein, human; D050486:Serotonin Plasma Membrane Transport Proteins; D019788:Fluorodeoxyglucose F18; D005947:Glucose; D004298:Dopamine