Neuropsychological alterations in hepatitis C infection: The role of inflammation

Abstract

About 50% of patients with hepatitis C virus (HCV) infection complain of neuropsychiatric symptoms, "brain fog", weakness, fatigue, and exhibit some degree of quality of life impairment, irrespective of the severity of liver disease. Since the first observation of HCV-related cognitive deficits, 10 studies have been published that have evaluated neuropsychiatric performance in patients with HCV infection and different degrees of hepatic impairment�� Unfortunately, these have often included patients with cirrhosis, patients who had acquired the infection through previous intravenous drug misuse, who had a history of relatively recent treatment with interferon, or were on psychoactive medication�� In addition, different neuropsychological batteries and tests that explored different cognitive domains were used, which makes the results of the studies difficult to compare�� Finally, limited information is available on the pathogenesis of HCV-related cognitive impairment�� Cerebral and/or systemic inflammation may be important players but their potential role has not been substantiated by experimental data�� The present review outlines the available evidence of the presence of cognitive impairment in patients with HCV infection, with a focus on the potential relationship with cerebral and/or systemic inflammation.

Patients with hepatitis C infection and normal liver function: an evaluation of cognitive function

“…Moreover, the HCV family (Flaviviridae) includes several viruses with known neurotropic effects, such as the West Nile virus, Saint Louis encephalitis virus, Murray Valley virus, and Japanese encephalitis virus 25. Several hypotheses have been proposed to explain the occurrence of cognitive impairment in HCV infections: The direct action of the virus in the CNS, through a ‘ Trojan horse’ effect : The infection of the CNS begins with HCV virus replication in peripheral blood mononuclear cells in the bone marrow, which subsequently serves as precursors of macrophages and microglial cells of the CNS 7. The production of tumour necrosis factor α (TNFα) and interleukin 8 (IL8) in macrophages/microglia infected with HCV may be responsible for cognitive impairment.…”

“…The direct action of the virus in the CNS, through a ‘ Trojan horse’ effect : The infection of the CNS begins with HCV virus replication in peripheral blood mononuclear cells in the bone marrow, which subsequently serves as precursors of macrophages and microglial cells of the CNS 7. The production of tumour necrosis factor α (TNFα) and interleukin 8 (IL8) in macrophages/microglia infected with HCV may be responsible for cognitive impairment.…”

Hepatitis C virus and neurological damage

“…Around 50% HCV infection patients complain of neuro psychiatric symptoms, brain fog, fatigue, and also show quality of life impairment upto some extent, regardless liver disease severity [25] . During the onset of the disease HCV patients report complications like, fatigue, malaise, maintaining attention and forgetfulness.…”

Cognitive dysfunction: an important extrahepatic manifestation of hepatitis C infection?

“…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.…”

“…The first states that HCV infection is indirectly neurotoxic by causing sustained activation and increases in systemic inflammatory cytokines which ultimately results in cognitive impairment 4. Patients with chronic HCV infection have increased production of proinflammatory cytokines such as interleukin (IL)-6, IL-4 and tumour necrosis factor α for decades.…”