Abstract: Background: This study is aim to investigate concurrent long-term psychiatric. cognitive and neurophysiological measure's of alpha-IFN neurotoxicity in the treatment of chronic viral hepatitis. Methods: Twenty patients with HCV hepatitis were enrolled while treated with alpha-IFN (3-6 MU for 6-12 months). Neurotoxicity was evaluated by psychiatric [Hamilton Depression Rating Scale (HAM-D), Hamilton Scale for Anxiety (HAM-A), Beck Depression Inventory (BDI) and State-Trait Anxiety Inventory (STAI-Y)], complete cognitive and neurophysiological assessments (EEG : spectral analysis, P300). Patients were assessed at baseline (t(0)), 2 (t(1)) and 6 months (t(2)) since the beginning of therapy. Results: Depression scores significantly increased (HAM-D: t(0)=4.4+/-2.6; t(1)=8.9+/-3.9, p<0.00; and t(2)=1.7+/-3.8, p<0.001). A concurrent increase was shown also for anxiety (HAM-A: t(0)=6.0+/-3.2; t(1)=9.6+/-4.5, p<0.005; and t(2)=9.1+/-4.5, p<0.005). Significant neurophysiological effects were also detected: increase of alpha power (p<0.05) in frontal derivations, reduction of the mean dominant frequency (p<0.005) and increase of theta power (p<0.05) in parietal derivations. In contrast, no significant cognitive changes occurred. Limitations: The study was performed on a relative small sample of patients mainly with observational intentions. Biological data (e.g. blood cytokines samples) are not available: they could have given useful information about biological mechanisms related to the alterations observed.
Mood, cognition and EEG changes during interferon alpha (alpha-IFN) treatment for chronic hepatitis C.
AMODIO, PIERO;Cavalletto L;MAPELLI, DANIELA;BERNARDINELLO, ELISABETTA;DEL PICCOLO, FRANCO;CHEMELLO, LILIANA;GATTA, ANGELO;PERINI, GIULIA
2005
Abstract
Abstract: Background: This study is aim to investigate concurrent long-term psychiatric. cognitive and neurophysiological measure's of alpha-IFN neurotoxicity in the treatment of chronic viral hepatitis. Methods: Twenty patients with HCV hepatitis were enrolled while treated with alpha-IFN (3-6 MU for 6-12 months). Neurotoxicity was evaluated by psychiatric [Hamilton Depression Rating Scale (HAM-D), Hamilton Scale for Anxiety (HAM-A), Beck Depression Inventory (BDI) and State-Trait Anxiety Inventory (STAI-Y)], complete cognitive and neurophysiological assessments (EEG : spectral analysis, P300). Patients were assessed at baseline (t(0)), 2 (t(1)) and 6 months (t(2)) since the beginning of therapy. Results: Depression scores significantly increased (HAM-D: t(0)=4.4+/-2.6; t(1)=8.9+/-3.9, p<0.00; and t(2)=1.7+/-3.8, p<0.001). A concurrent increase was shown also for anxiety (HAM-A: t(0)=6.0+/-3.2; t(1)=9.6+/-4.5, p<0.005; and t(2)=9.1+/-4.5, p<0.005). Significant neurophysiological effects were also detected: increase of alpha power (p<0.05) in frontal derivations, reduction of the mean dominant frequency (p<0.005) and increase of theta power (p<0.05) in parietal derivations. In contrast, no significant cognitive changes occurred. Limitations: The study was performed on a relative small sample of patients mainly with observational intentions. Biological data (e.g. blood cytokines samples) are not available: they could have given useful information about biological mechanisms related to the alterations observed.Pubblicazioni consigliate
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