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• W1997492152 abstract "There are generally three criteria that must be achieved before establishing a causal relationship between two conditions such as infection with the hepatitis C virus (HCV) and the subsequent development of cognitive impairment: (1) there must be evidence of temporal precedence, where the ‘cause’ happened before the ‘effect’; (2) there should be covariation between the conditions, demonstrated as a relationship response between the presence or absence of either factor; and (3) the absence of other plausible alternatives to explain the relationship. The report by Abrantes et al1 presents us with an opportunity to take stock and consider the evidence in favour of a direct association between infection with HCV and the subsequent development of cognitive impairment. Although the neurological features of hepatic encephalopathy are well described in patients with viral liver cirrhosis, recent reports have highlighted changes in cognitive performance in HCV-infected patients that emerge long before any evidence of significant hepatic dysfunction.2 These cognitive symptoms appear ‘specific’ to HCV infection and are not as evident in patients infected with hepatitis B virus.3 In a recent review on the topic by Senzolo et al,4 the majority of reports supported an increased prevalence of cognitive impairment in patients with HCV infection which appeared to be independent of a history of substance abuse, coexistent depression or hepatic encephalopathy. Deficits in measures of immediate and sustained attention, higher executive function, verbal learning ability, verbal recall and working memory were reported in isolation or in combination in eight out of 10 studies. Unfortunately, methodological flaws in many of these studies limit any conclusions we can draw with regard to the existence of HCV-specific cognitive impairment. All studies to date have followed a cross-sectional study design. ‘One-off’ neuropsychological testing is prone to performance bias and can be very unreliable, especially in a group of patients of different ages, educational and social backgrounds as reflected in the overall HCV-infected population. Longitudinal follow-up over an appropriate time frame with multiple assessment points is more robust methodologically in establishing persistent cognitive impairment, and only then is it possible to start looking for covariant relationships. The use of domain-specific neuropsychological tests is essential and, given the small numbers of patients enrolled in these trials, ideally a consensus on the neuropsychological instruments used across studies would increase the homogeneity and facilitate comparisons. These test results should be scored against large and local normative databases rather than simply compared with small internal control groups. Careful exclusion of patients with minimal hepatic encephalopathy, clarification of liver fibrosis/cirrhosis status and controlling for patients treated with interferon are important when presenting an argument that cognitive impairment is HCV-specific. This detailed phenotyping also enables physicians to extrapolate clinically relevant conclusions for specific populations." @default.
• W1997492152 created "2016-06-24" @default.
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• W1997492152 date "2013-07-09" @default.
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• W1997492152 title "Cognitive dysfunction: an important extrahepatic manifestation of hepatitis C infection?" @default.
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• W1997492152 doi "https://doi.org/10.1136/postgradmedj-2012-131337" @default.
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