Nearly 3,000,000 people in the United States, and over 100,000,000
people worldwide, are infected with hepatitis C virus (HCV), with an
increasing trajectory for the foreseeable future (Alter et al., 1999). While hepatic encephalopathy
has been long recognized as a disorder associated with cerebral
structural, metabolic, and cognitive changes (e.g., Tarter et al., 1989), HCV infection itself is
increasingly associated with changes in the brain, even in the absence
of hyperammonemia. Specifically, HCV-infected individuals may have
deficits in cognitive functions such as attention, working memory, and
speed of information processing (Forton et al.,
2002; Hilsabeck et al., 2002). They
may also have abnormalities on magnetic resonance spectroscopy (MRS), a
non-invasive method to measure cerebral metabolites. The most reliably
measured compounds using a standard 1.5 Tesla MRI scanner are
N-acetylaspartate (NAA), a marker of neuronal integrity; choline and
choline-containing compounds (Cho), a measure of cell membrane turnover
and lipid changes; myo-Inositol (Ins), a possible indicator of glial
proliferation and/or osmolar changes; and creatine+phosphocreatine
(Cr), an indicator of high energy stores that is often used as a
relative standard for other metabolites. In the first studies of HCV
using MRS, Forton et al. (2001; 2002) found elevated Cho/Cr in the
frontal white matter and basal ganglia in patients with HCV. In
addition patients with two or more impaired neuropsychological test
performances had higher Cho/Cr compared to those with less than two
impaired test performances.Dr. Erin D. Bigler
served as Action Editor during the course of this review.