Neuropsychiatric Manifestations

HIV infection presents a spectrum of neuropsychiatric sequelae that can pose diagnostic and treatment quandaries to clinicians. In patients with serious and persistent psychiatric illness, some of the early, subtle neuropsy-chiatric symptoms may be difficult to differentiate from preexisting symptoms of their psychiatric illness. HIV is neurotropic (O'Brien 1994), enters the CNS soon after infection (Resnick et al. 1988), and can acutely induce headache and meningeal signs as already noted. Long-term clinical sequelae of CNS infection range from subtle neurocognitive impairment to frank dementia, and their incidence increases with HIV illness progression. OIs and neoplasms that follow immunosuppression can also affect the CNS, resulting in mood disorders, psychosis, cognitive disorders, de lirium, and other neuropsychiatric abnormalities. In addition, prescribed and recreational psychoactive substance use may create neuropsychiatric complications, and must be considered in the differential diagnosis of patients who present with new mental status changes (McDaniel et al. 1997).

HIV-related neurocognitive disorders are diagnoses of exclusion made after other etiologies have been ruled out through a comprehensive evaluation. Common cognitive disorders in HIV infection include minor cognitive-motor disorder (MCMD) and HAD. MCMD is a mild syndrome of motor and/or cognitive dysfunction with minimal impairment in functioning (McDaniel et al. 1997) and is characterized by at least two of the following features: impaired attention or concentration, mental slowing, impaired memory, slowed movements, impaired coordination, personality change, irritability, and lability. MCMD does not necessarily progress to the more severe disorder of HAD (Masliah et al. 1996).

HAD is a subcortical dementia, and criteria for its diagnosis include acquired abnormality in two or more cognitive domains causing functional impairment; acquired abnormality in motor performance or decline in motivation or emotional control; no clouding of consciousness (delirium); and no confounding etiology. Although the exact pathophysiology of HAD remains unclear, HAD is relatively common, particularly in more advanced stages of HIV infection (McDaniel et al. 1997). Patients may also have neu-ropsychiatric impairments verifiable by testing that do not meet criteria for MCMD or HAD but that may result in functional impairment.

Psychiatric symptoms due to HIV-related medical conditions tend to occur in advanced stages of illness with significant evidence of immuno-suppression and CD4 cell counts below 200 (American Psychiatric Association 2000). Therefore, among patients with advanced HIV disease who have a preexisting severe mental illness, psychiatric changes should not be attributed to a relapse until a complete medical workup has ruled out other causes. Mental status changes due to a medical etiology can include shifts in level of consciousness characteristic of delirium, cognitive impairment, mood changes, and psychotic symptoms. The differential diagnosis (Wain-berg et al. 2000) includes not only the neuropsychiatry manifestations of HIV itself but also OIs (toxoplasmosis, cryptococcus, tuberculous meningitis), lymphoma, and delirium from metabolic derangement, substance use, or drug toxicity (McDaniel et al. 1997).

HIV/AIDS Treatment

Clinical management is intended to decrease viral load, increase CD4 cell count, provide prophylaxis against OIs as appropriate, treat OIs when present, and decrease morbidity and mortality. New knowledge about the life cycle of HIV and the advent of different classes of antiretroviral medications have altered the state-of-the-art of treatment, which now requires combination antiretroviral therapies and the prophylaxis of Ols according to guidelines based on the prevalence of each OI at various stages of immunodeficiency. Except in cases of HIV primary infection, pregnancy in an HIV-infected woman, or symptomatic HIV disease, antiretroviral therapy in asymptomatic patients known to be HIV positive is usually initiated when the CD4 cell count is between 200 and 350.

Part of instituting antiretroviral therapy involves ensuring that patients recognize their HIV infection, have access to health care, develop ongoing provider relationships, and are motivated to adhere to complicated treatments, even during an asymptomatic phase of infection. Taking a combination of at least three antiretroviral medications is currently the best way to accomplish this objective. If a patient is not ready to adhere to antiret-roviral therapy (e.g., because of chaotic life due to psychiatric instability, substance use, and/or homelessness; lack of motivation; or insufficient social supports), it is important to first address barriers to adherence. Evidence demonstrates that 95% adherence is necessary to suppress fully the replication of virus that is sensitive to the regimen being administered. Even though 80%-95% adherence decreases morbidity and mortality, long-term implications are unclear (e.g., resistant strains, neuropsychiatric sequelae). Mental health professionals often have important roles in promoting adherence.

Antiretroviral therapies are classified according to the specific step inhibited in the HIV life cycle within the CD4 lymphocyte. Individually, these agents are not very potent in inhibiting viral replication, but combining classes enables different replication steps to be "attacked," enhancing the possibility of interrupting viral reproduction. The four major classes of therapies currently available are 1) nucleoside reverse transcriptase inhibitors (NRTIs), which act by incorporating themselves into the DNA of the virus through the reverse transcriptase enzyme, resulting in DNA that is incomplete and incapable of creating new virus (didanosine, lamivudine, stavudine, zalcitabine, zidovudine [AZT], abacavir); 2) nonnucleoside reverse transcriptase inhibitors (NNRTIs), which stop HIV production by binding directly to reverse transcriptase and preventing the conversion of viral RNA to DNA (delavirdine, efavirenz, nevirapine); 3) nucleotide reverse transcriptase inhibitors, which have a mechanism of action similar to that of NRTIs (tenofovir); and 4) protease inhibitors (PIs), which affect the last stage of viral reproduction by inhibiting the viral protease enzyme from cleaving the viral protein chains into smaller infectious virions (am-prenavir, indinavir, lopinavir/ritonavir, nelfinavir, ritonavir, saquinavir).

The PIs are often potent inhibitors of one or more cytochrome P450 enzymes, which may have implications for interactions with psychiatric and other medications. A new category of antiretrovirals, called fusion inhibitors, is being developed and acts by inhibiting HIV from binding to CD4 cells.

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