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.

Cerebral microglia activation in hepatitis C virus infection correlates to cognitive dysfunction

“…HCV PCR‐positive and HCV PCR‐negative patients did not show any significant differences. Our results are supported by previous studies but are in contrast to the results by Byrnes et al . .…”

“…Interestingly, these symptoms are independent from the grade of liver disease and virus replication rate . Even HCV PCR‐negative patients suffer from neuropsychiatric symptoms and have been shown to score similarly to HCV PCR‐positive patients with neuropsychiatric symptoms in neuropsychological tests . The cause of HCV infection associated neuropsychiatric symptoms is unclear.…”

Hepatitis C virus and neurological damage

“…The results have shown significant decrease in striatal and midbrain dopamine availability and decrease metabolism in limbic, parietal, frontal, and temporal cortices. These findings further confirmed significant role for defective dopaminergic transmission in causing cognitive impairment in the HCV [64] . The HCV infection has also been linked with myopathy and a few cases of noninflammatory and inflammatory myopathies were reported.…”

HCV encephalopathy – an artefact due to medical care?

“…Importantly though, no clear correlation between detectable viremia and mental impairment has been found. Studies including Anti‐HCV‐positive non‐viremic patients show similar rates and intensity of mental impairment in these subjects as in HCV‐positive viremic patients .…”