Stephen J Ferrando and Constantine G Lyketsos

Since the beginning of the HIV epidemic, the neuro-cognitive manifestations of the infection have been widely recognized. HIV infection is associated with a range of cognitive and behavioral symptoms that become more frequent and severe as the immune system declines and symptomatic illness and AIDS ensue. In order to approach the neuropsychiatric evaluation and treatment of the HIV patient, it is critical that the clinician develop a working understanding of central nervous system (CNS) manifestations of HIV disease, including HIV-associated neurocognitive disorders.

The clinical and neuropathological manifestations of the AIDS dementia complex (ADC) were described in two classical papers by Navia and colleagues in 1986 (Navia et al., 1986a, 1986b). These authors described what came to be known as the ADC triad of cognitive, motor, and behavioral symptoms that occurred in nearly one-fourth of AIDS patients and was often progressive to severe dementia. In autopsy specimens of patients with the disorder, the authors described characteristic changes in the white matter and subcortical structures, including diffuse white matter pallor and rarefaction, and lymphocyte and macrophage infiltration (signs of inflammation). In most cases, these changes correlated well with the clinical manifestations of the disorder. See Chapter 19 for a thorough review of the neuropathology of HIV.

In response to work in this area during the first 10 years of the epidemic, the American Academy of Neurology (AAN) published in 1991 diagnostic criteria for two HIV-associated CNS disorders: HIV-associated minor cognitive motor disorder (MCMD) and HIV-associated dementia (HAD, known previously as ADC) (American Academy of Neurology AIDS Task Force, 1991). These criteria contained the classical triad of clinical symptoms and stipulated that the symptoms must cause everyday functional impairment in order to make a diagnosis. In the years prior to the advent of highly active combination antiretroviral therapy (HAART), the criteria were modified and validated in longitudinal studies (Dana Consortium on Therapy for HIV Dementia and Related Cognitive

Disorders, 1996). These disorders were found to predict shorter survival, even after statistically controlling for other HIV illness markers (Sacktor et al., 1996; Wilkie et al., 1998).

The landscape changed with the advent and widespread use of HAART in the mid-1990s. The incidence of HAD has declined (Sacktor et al., 2001a), but, since patients live longer, these disorders may have a stable or increasing prevalence. Further, milder forms of impairment persist in a substantial proportion of patients (Ferrando et al., 1998; Starace et al., 2002), with higher levels of immune functioning (Dore et al., 1999), and the course is highly variable, including fluctuation over time, progression, or even regression of the symptoms. Motor manifestations, while continuing to occur in some cases, are less frequent. Finally, comorbid and differential diagnostic considerations for the cause of these disturbances have shifted away from opportunistic infections toward entities such as substance abuse, hepatitis C coinfection, and the neu-ropsychiatric and metabolic side effects of antiretro-viral medications. To account for these shifts, the diagnostic criteria for HIV-associated neurocognitive disorders are undergoing revision.

This chapter provides an overview ofthe diagnostic criteria, differential diagnosis, assessment, and treatment of the HIV-associated neurocognitive disorders. See Chapters 7 and 19 for review of neuropsycholo-gical assessment and HIV neuropathology.

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