Publication Abstract Display
Type: Published Abstract
Title: Motor disinhibition is more common among neuropsychologically impaired HCV+ persons than comparable HIV+ individuals or methamphetamine abusers.
Authors: Moore DJ, Vigil O, Vaida F, Grant I, Caligiuri M, the HNRC Group
Year: 2009
Publication: Journal of NeuroVirology
Volume: 15 Issue: S1 Pages: 63
Abstract:Background: Hepatitis C Virus (HCV), human immunodeficiency virus (HIV) and Methamphetamine Abuse/Dependence (METH + ) produce motor impairments. We hypothesized that impairments on certain neuropsychological tests would be associated with motor disinhibition and that these associations may point to a common underlying pathophysiology. Method: Force steadiness (FS), the ability to maintain steady levels of isometric hand muscle force, was used as a measure of motor disinhibition in the following groups: HCV+ (n = 35), METH+ (n = 20), HIV+ (n = 35), HCV + /METH+ (n = 12), HCV + /HIV+ (n = 8), METH + /HIV+ (n = 23), HCV + /METH + /HIV+ (n = 14). We examined the association with three cognitive domains likely to show variation across the various risk groups: Speed of Information Processing (SIP), Motor Skills (MS), and Executive Functions (EF). Results: Examining persons who were and were not SIP impaired showed that only HCV+ individuals had worse motor disinhibition scores as compared to non-SIP impaired HCV+ individuals. Comparing those who were and were not MS impaired revealed worse motor disinhibition in the HCV+ group and the METH + /HCV+ and METH + /HIV+ groups, but not METH+ or HIV+ groups. No differences were found among individuals who were or were not impaired on EF. Conclusion: HCV may exert a stronger motor disinhibition effect among SIP and MS impaired individuals than HIV or METH whereas a "double-hit" is needed to observe a motor disinhibition effect in METH or HIV. Findings suggest that motor disinhibition is more common among HCV individuals than HIV and METH, and that the cognitive and motor impairments observed in HCV may share a common pathophysiology.

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