Clinical Textbook of Addictive Disorders 3rd ed - R. Frances, S. Miller, A. Mack (Guilford, 2005) WW

19. HIV/AIDS and Substance Use Disorders 413et al., 1998) have reported that substance users with HIV are at a higher risk fordementia than are individuals with other risk behaviors, but this finding has beennot found by others (Qureshi, Hanson, Jones, & Janssen, 1998; DeRonchi et al.,2002). Although the results of these studies vary, it is generally accepted that neuropsychologicalimpairments associated with substance use can vary from mild tosevere, and may be stabilized or reversed by abstinence (Selby & Azrin, 1998). Inthe AIDS patient, the impairment is progressive and, by the terminal phase of thedisease, severe. It is critical that physicians treating substance users who developAIDS be alert, because these patients may suffer from both drug- and infectionrelatedcognitive impairment. It is also important for physicians to consider thediagnosis of HIV in all substance users with cognitive impairment. They must beaware that timing of the effects of HIV on cognition is variable and not fullyunderstood.The clinical significance of the seroconversion and asymptomatic phasesare debatable, but the physician caring for people in high-risk groups shouldknow of possible CNS effects to increase the likelihood of early detection.Headaches and photophobia may be frequent in the seroconversion-relatedmononucleosis-like syndrome associated with HIV (Tindall & Cooper, 1991).Although this early syndrome is apparently common, it is frequently indistinguishablefrom other viral infections and may not be recognized. The virus canbe detected in cerebrospinal fluid shortly after infection and it has been assertedthat cognitive changes could begin during the asymptomatic phase of infectionthat usually lasts a decade or more (Bornstein et al., 1991; Lunn et al., 1991).There has been controversy over the possibility that cognitive decline canoccur before the onset of other medical symptoms. After controlling for substanceabuse, psychiatric history, use of psychoactive medications, and neurologicalproblems, HIV-positive asymptomatic patients show little difference incognitive functioning when compared with controls (Damos, John, Parker, &Levine, 1997). It is now generally accepted that caution should be exercised inassigning cognitive deficits to asymptomatic HIV-positive patients, but giventhe erratic health care utilization of substance users, which is a potential barrierto early HIV detection and intervention, professionals working with this groupshould have a low threshold for considering neurological and cognitive symptomsas possible complications of undiagnosed HIV.Early detection and monitoring of cognitive changes are critical, becausethese symptoms may be reversed and possibly prevented with antiretroviraltherapy (ART; Moore, Keruly, Gallant, & Chaisson, 1998; Price et al., 1999;Sacktor & McArthur, 1997). The impact of ART has added support to thehypothesis that, in most cases, HIV-associated dementia is the result of theeffect of the virus on the CNS rather than that of a secondary opportunisticinfection or process. Many believe that this effect is achieved by indirect mechanisms,since productive infection within the CNS is confined predominantlyto macrophages and microglia (Kolson, Lavi, Gonzalez, & Scarano, 1998;