AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Background

Physicians frequently encounter neurologic and psychiatric complications in patients with human immunodeficiency virus (HIV) infection. This is not surprising since the HIV virus enters the central nervous system (CNS) early in the course of the infection. Prior to the advent of highly active antiretroviral therapy (HAART), dementia was a common source of morbidity and mortality, usually observed in the late stages of AIDS, and was seen in up to 50% of patients prior to their death.¹ In 1986, the term AIDS dementia complex (ADC) was introduced to describe a unique constellation of neurobehavioral findings. ADC is now considered a single entity with a broad and varied spectrum of clinical manifestations and severity.

Globally, 33.2 million people were estimated to be living with HIV/AIDS in 2007.² Of those people, only 2 million have access to HAART because they live in developed countries.

In the United States, 1 million people are estimated to live with HIV.¹ With the changing face of AIDS and HIV infection, a geographical difference in how ADC presents is now clear. HAART has brought dramatic changes in the lives of patients and divided the disease into "have" and "have nots." On one hand, in developed countries like the United States, having an HIV-infected patient present for the first time with a full-blown ADC picture is rare; on the other hand, in countries like Africa where HAART is not available, this scenario is still the norm.

Pathophysiology

The HIV virus enters the CNS by infecting macrophages and monocytes that then cross the blood brain barrier, carrying the virus with them. Immunohistochemistry studies show that the virus is most densely located in the basal ganglia, subcortical regions, and frontal cortex. Pathological changes at autopsy are also predominantly subcortical, involving the deep gray (ie, basal ganglia, thalamus) and white matter regions. Infected macrophages or microglial cells then elaborate proinflammatory diffusable cellular neurotoxins, including tumor necrosis factor-alpha (TNF-alpha), cytokines, interleukins, chemokines, nitric oxide, and excitatory amino acids. These neurotoxic agents create an inflammatory environment by activating uninfected microglia and then proceed to injure surrounding astrocytes and neurons. HIV does not directly infect the neuron, but the neuron is damaged by the effects of various proinflammatory neurotoxins.

Using immunohistochemical techniques, many HIV viral products have been implicated in HIV dementia. The basal ganglia show the highest immunostaining by the HIV p24 antigen. Some studies show that gp41 expression in the basal ganglia and frontal lobes correlates significantly with the severity of dementia. Other viral proteins, including tat and gp120, are present in abundance in the brains of patients with HIV dementia. gp120 causes neuronal death in vitro and is accompanied by the opening of calcium channels in the neuronal membrane.

A lot of research and interest has been generated in the role of p53 (tumor suppressor transcription factor), which appears to have multiple roles in the pathogenesis of the disease. HIV proteins tat and gp120 cause microglia to release factors that promote neuronal p53 activation. All 3 cell types in the brain (microglia, astrocytes, and neurons) accumulate p53, causing cell cycle arrest; in neurons, this ultimately induces apoptosis and cell death by oxidative injury and DNA damage.

In summary, both viral (eg, gp120, gp41, tat) and host cell products (eg, TNF-alpha, cytokines, interleukins, quinolates, nitric oxide, platelet-activating factors) can either amplify or directly contribute to neuronal injury. However, the presence of macrophages and microglia correlate better with clinical dementia than with the amount of HIV-infected cells in the brain, as determined by gp41-positive cells.

See Medscape's HIV Pathogenesis Resource Center.

Frequency

United States

The annual incidence of HIV dementia in the Western world prior to HAART was 7%, with a cumulative risk of 5-20%.³ With HAART, the incidence of HIV dementia started declining initially, but has begun increasing again. The prevalence of the disorder is now increasing; the cumulative incidence is 25-38% and the prevalence is around 37%.³ Milder forms of ADC affect an additional 30-40% of patients. In 4-15% of patients, ADC is the presenting clinical manifestation of HIV disease.³ The multicenter AIDS cohort study found a rate of HIV dementia of less than 1% in asymptomatic seropositive patients.⁴

Mortality/Morbidity

ADC causes a significant increase in the overall morbidity due to AIDS.

• The increase in morbidity results from a combination of factors, including the increased number of hospitalizations, increased duration of hospital stays, and decreased life expectancy compared with AIDS patients who do not have dementia. In the pre-HAART era, AIDS patients who had untreated ADC had an average life span of 6 months, which was significantly less than that for AIDS patients without dementia. This has now increased to 38 months for ADC patients in the Western hemisphere who have been on a stable regimen of HAART.³
• The overall psychosocial and emotional burden on the family and friends of such patients is tremendous, far beyond that of a cognitively intact patient with AIDS.
• Patients with cognitive difficulties have problems with compliance and adherence to their medication regimen. Because of their neuropsychiatric problems, these patients are likely to be less inhibited and are more prone to HIV-related risk behavior like unprotected intercourse, and they therefore pose a greater risk of transmission of the virus.  

Race

HIV has a high incidence and prevalence in the African-American community, which is reflected in the race distribution of ADC.

Sex

Some data suggest that female sex may be a risk factor of HIV dementia.⁵ Some studies have found that women with HIV may have a more rapid progression of neurologic symptoms and signs.^{6, 3}

Age

The Multicenter AIDS Cohort Study reported that older age was associated with more rapid progression to dementia and death.⁷ Becker et al reported that the prevalence of cognitive disorders in those who are HIV positive and older than 50 years was significantly greater than in younger patients.⁸

CLINICAL

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

History

Patients with AIDS dementia complex (ADC) present with a triad of cognitive, motor function, and behavioral symptoms. Patients often present with a combination of motor and behavioral symptoms. Alternatively, patients with ADC can initially present solely with psychiatric symptoms such as depression, mania, or psychosis.

• Types of ADC
  
  
  • ADC is broadly divided into 2 clinical categories, (1) the more severe form (ie, HIV-associated dementia complex, HIV-associated myelopathy) and (2) the less severe form (ie, HIV-associated minor cognitive/motor disorders consistent with HIV-associated neurocognitive disorder).
  • The major difference between HIV-associated dementia complex and HIV-associated minor cognitive/motor disorder is the degree of impairment in activities of daily living. In patients with HIV-associated dementia complex, social or occupational functioning is severely impaired, whereas in patients with HIV-associated minor cognitive/motor disorder, functioning in the most demanding activities of daily living is mildly impaired.
• HIV-associated minor cognitive/motor disorder consistent with HIV-associated neurocognitive disorder
  
  
  • In the less severe form, patients with HIV-associated minor cognitive/motor disorder initially report poor short-term memory and concentration, behavioral problems, or personality changes.
  • Patients with mild HIV dementia commonly present with psychiatric symptoms of depression and anxiety. Therefore, screening all patients with HIV infection who present with depression for early HIV dementia is imperative.
  • Behavioral changes also include apathy, lethargy, loss of sexual drive, and diminished emotional responsiveness. Others may notice social withdrawal, irritability, emotional lability, and inflexibility. HIV dementia may manifest with acute-onset psychotic symptoms including delusions and hallucinations, and these patients are at a higher risk for suicidal and homicidal ideation. The initial interview should include screening for possible suicidal and homicidal ideation.
  • Early motor symptoms include an unsteady gait, leg weakness, clumsiness, slowing of fine motor movements, and tremor. In some patients, smooth eye pursuits or saccadic movements may be impaired.
• HIV-associated dementia complex, HIV-associated myelopathy
  
  
  • HIV-associated myelopathy predominantly manifests with motor symptoms, including paraparesis, lower-extremity spasticity, ataxia, and extensor-plantar responses in the absence of abnormalities in spinal cord imaging findings.
  • In the more severe form, patients with HIV-associated dementia complex have progressive cognitive and motor difficulties.
  • In the late stages of the disease, patients develop an akinetic mute or vegetative state in which they lie awake but do not respond to their surroundings. They also may have quadriparesis or paraparesis, myoclonus, and incontinence.

Physical

The examination includes a full Mental Status Examination (MSE), a general neurologic examination, and a general physical examination.

• Some patients with HIV can become depressed, suicidal, and homicidal. Therefore, a thorough psychiatric assessment should also be performed at each visit.
• In the early stage, findings from the MSE and the general neurologic examination are normal. MSE findings are abnormal if the patient exhibits inattention, impaired concentration (eg, digit span, serial 7's), memory loss (eg, recalling 3 objects at 5 min), slowed verbal responses, and a blunted affect.
• In the more severe form of HIV-associated dementia complex, the neurologic examination shows frontal release signs, slowed rapid movements, antisaccadic eye movements, incoordination, abnormal gait, hyperreflexia, hypertonia, extensor-plantar response weakness, and peripheral neuropathy. Cortical signs, including apraxia, aphasia, and agnosia, typically are absent.
• In the late stages of the disease, patients also may have quadriparesis or paraparesis, myoclonus, and incontinence.

Causes

• Several risk factors for ADC have been identified, including low weight, anemia, constitutional symptoms, low CD4 count, and high plasma HIV-RNA load.
• The prevalence of ADC increases 3-fold with a CD4 count of less than 200/µL and increases 7-fold with a CD4 count of less than 100/µL.
• Patients with concomitant hepatitis C virus (HCV) have a worse cognitive status than those without. See Medscape's Hepatitis C Resource Center.
• A recent report implicated apolipoprotein E4 as a risk factor for the development of dementia.

DIFFERENTIALS

Section 4 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Other Problems to be Considered

CNS infections (eg, tuberculosis, toxoplasmosis, cryptococcal meningitis, neurosyphilis, cytomegalovirus encephalitis)
Systemic infections
Progressive multifocal leukoencephalopathy
Cerebral lymphoma
Toxic-metabolic states (eg, alcoholism, vitamin B-12 deficiency, thyroid disorders, adverse medication effects, drug interaction, recreational drug use)

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Lab Studies

• Draw peripheral blood for syphilis serology testing, vitamin B-12 and folate levels, thyroid studies, routine electrolyte levels, BUN/creatinine determination, and a drug screen to effectively exclude other metabolic and infectious etiologies.
• TB testing/screening

Imaging Studies

• In the early stages, neuroimaging study findings may be entirely normal.
• CT scanning of the brain can reveal brain atrophy, ventricular enlargement, and increased white matter signal in later stages.
• MRI is the first-choice neuroimaging modality. An MRI of the brain must be performed to exclude other CNS causes of dementia, including toxoplasmosis, progressive multifocal leukoencephalopathy, and cerebral lymphoma. In the late stages of AIDS dementia complex (ADC), MRI findings typically show diffuse nonenhancing white matter, hyperintensity, cerebral atrophy, and ventricular enlargement. The degree of cerebral atrophy correlates with the symptoms and progression of ADC.
• Positron emission tomography (PET) scanning and functional nuclear MRI reveal decreased metabolism in the thalamus and basal ganglia in the early stages of ADC. PET scanning can be particularly useful in very difficult cases to help exclude CNS lymphoma, which shows increased uptake, whereas the lesions of AIDS dementia do not.
• Proton magnetic resonance spectroscopy (MRS) is a functional imaging technique that measures brain metabolites. In persons with ADC, neuronal injury is confirmed by finding lower N-acetyl aspartate (NA) levels (a marker of neuronal metabolism) in the frontal white matter. In the basal ganglia and white matter, where gliosis and inflammatory changes are noted, the level of choline-containing metabolites, which is a marker of glial metabolism, is increased. In the future, proton MRS could be used to follow the effectiveness of CNS-targeted therapies for ADC.
• Chang et al recently showed that even in the asymptomatic stage, metabolite changes are seen by MRS in the basal ganglia and frontal white matter. In the absence of clinically recognizable symptoms, elevated glial marker, myoinositol to creatinine ratio (MI/Cr), is seen in the white matter, indicating early HIV brain disease. Patients with ADC have elevated MI/Cr and choline to creatinine ratio (Cho/Cr) in basal ganglia and white matter, relative to the asymptomatic group. However, compared with controls, patients with ADC have decreased NA/Cr ratio, which is a neuronal marker. The decreased NA/Cr ratio in ADC is more profound in younger subjects. This indicates that in older individuals, the metabolic changes seen may be a combination of age and HIV infection.⁹

Other Tests

• Electroencephalogram
• • Patients with subclinical seizures may present with symptoms that mimic dementia. Consider performing an EEG to help exclude this type of pseudodementia.
  • EEG findings may be normal in early dementia or may demonstrate diffuse slowing. However, this finding is nonspecific and is present in persons with dementia from any cause (even metabolic); therefore, it does not help in making an etiologic diagnosis.
• Neuropsychological testing
• • This type of testing can be used for early screening of asymptomatic high-risk patients (eg, those with high viral load and low CD4 count) and for follow-up evaluations of patients with ADC.
  • In the early stages of the disease, MSE findings may be entirely normal. In such cases, neuropsychological testing is especially useful and can help detect mild early cognitive abnormalities. Performing this test can help quantify and determine the specific pattern of the cognitive abnormality.
  • Specialists use several neuropsychiatric screening techniques; the most widely accepted is the HIV dementia scale. The scale consists of 4 subsets that target memory (eg, recall, registration), psychomotor speed, constructional ability, and concentration. A total of 12 points can be earned, and a score of fewer than 6 points is considered abnormal. The test takes 10 minutes to administer and can be given by a nonneurologist. These tests are useful diagnostic adjuncts, but the results cannot solely determine the presence of ADC.
• Combination screening: The Memorial Sloan-Kettering rating scale is used for clinical staging of ADC from 0 (normal) to 4 (end stage). It combines functional ability results with the findings from neuropsychological testing. Currently, it is used mostly as a research instrument.

Procedures

Lumbar puncture and cerebrospinal fluid (CSF)

• CSF studies, including cryptococcal antigen, CSF Venereal Disease Research Laboratory test, fluorescent treponemal antibody-absorption test, and cytomegalovirus titers help exclude CNS infection.
• Patients with ADC usually have a mild elevation of CSF protein levels and, in the cell count, increased total immunoglobulin fraction and intrathecal synthesis of anti-HIV immunoglobulin G, with the detection of oligoclonal bands in as many as 35% of cases.
• These CSF abnormalities are nonspecific and are often present in neurologically asymptomatic patients with HIV.
• HIV-1 virus is present in CSF in the absence of neurologic abnormalities. CSF HIV RNA levels do not correlate with neuropsychological impairment; rather, plasma levels are a better correlation.
• CSF markers are helpful in early dementia, when the diagnosis may be confusing. CSF markers, including neopterin, quinolinic acid, certain cytokines (eg, TNF-alpha, interleukin 1, interleukin 6), and antibodies to gp120 (eg, HIV viral envelope protein), correlate with the severity of dementia, but are only research tools and therefore not widely available. CSF beta-2 microglobulin, an immune activation marker, is a more specific CSF marker and has a positive predictive value of 88% if levels are higher than 3.8 mg/dL. CSF beta-2 microglobulin levels were twice as high in patients who cognitively improved with HAART than in those who did not, indicating that CNS inflammation plays a major role in reversible neurocognitive deficits.
• Some studies have shown the association of plasma TNF-alpha and CSF macrophage chemoattractant protein 1 (MCP-1) with ADC.¹⁰
• Patients with HIV dementia have elevated levels of certain matrix metalloproteins in the CSF, but the clinical significance of these metalloproteins is unclear.

Histologic Findings

Gross brain specimens show white matter pallor and microglial nodules. Microscopically, ADC is typically associated with a triad of multinucleate giant cells, microglial nodules, and perivenular inflammation. Severe ADC is characterized microscopically by microgranulomatous foci of multinucleate giant cells, initially in the white matter and later in the gray matter. Reactive gliosis is also observed, in which an increase occurs in both the number and size of astrocytes, associated with infiltration by monocytes.

TREATMENT

Section 6 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Medical Care

The standard of care for a patient with AIDS is to use 3 or more antiretroviral agents. Triple therapy has been shown to improve neurologic outcome when compared with dual or single treatment regimens. The routine use of HAART has changed the epidemiology of HIV dementia in the Western hemisphere. HAART regimen can reverse some of the neurologic deficits of HIV-D, showing improvements in motor and psychomotor speed. This improvement was independent of CNS penetration. Multiple studies have shown that patients on HAART show either partial reversals of neuropsychological deficits and significant improvement, which is sustained, whereas patients not on HAART steadily decline.¹¹

Several cohort studies have shown that treatment with multiple antiretroviral agents is superior to either no treatment or monotherapy in patients with AIDS dementia complex (ADC).³ This finding is based on clinical follow-up of patients with neuropsychological testing. The Strategies for Management of Anti-Retroviral Therapy (SMART) study showed that it is better to follow HIV plasma viral load and consistently keep it suppressed than to adjust therapy based on peripheral CD4 counts.¹²

More than a dozen antiretroviral medications are used to treat HIV. Most of them have poor CSF-to-plasma drug ratios, indicating poor CNS penetration. Exceptions include stavudine, abacavir, nevirapine, and zidovudine (ZDV), which is also known as azidothymidine. However, whether this translates into poor drug levels in CNS tissue, and whether drug penetrance is clinically important remains unclear. Because stavudine and abacavir have good CNS penetration, including one of these when administering triple therapy is logical. One study showed that patients with multiple CNS penetrance who were treated with HAART were not different from those treated with single penetrance regimens.⁴ However, in the absence of more data, no general recommendation exists to change patient’s therapy of HAART to higher penetrance based on their cognitive status. 

• Monotherapy
• • ZDV is the most-studied antiretroviral medication. Since its initial introduction in 1987, several studies have consistently shown that ZDV reduces the rate of HIV dementia from greater than 53% to 10%. It improves radiologic, neuropsychologic, and clinical findings in patients with ADC.
  • Didanosine has also been studied as monotherapy in children with ADC and has shown to result in significant clinical improvement.
• Combination antiretroviral therapy
• • Several studies have shown that treatment with highly active antiretroviral therapy (HAART) is superior to ZDV monotherapy or no therapy in protecting against ADC. Interestingly, HAART prevents the progression of cognitive decline independent of the drugs' CSF penetration properties. No differences in cognitive testing results are noted when single versus multiple CSF-penetrating drugs are used. Moreover, adding ZDV, which is the drug with the best CSF penetrance, does not improve the clinical efficacy of the HAART combinations.
  • ADC is clearly an indication for HAART, regardless of the combination of antiretroviral agents used.
• Investigational therapy
• • Researchers are studying several experimental therapies (eg, memantine, nimodipine, delavirdine, peptide T, lexipafant).
  • These therapies are either neuroprotective agents or they attempt to block the release of neurotoxic agents by macrophages or platelets. Several of these protocols are undergoing clinical trials.

Consultations

• Psychiatrist
• • Patients with ADC commonly exhibit agitation, anxiety, fatigue, depression, and other psychiatric manifestations. Mania and psychosis have been described as presenting symptoms or complications of ADC.
  • Consultation with a psychiatrist may be required to discuss appropriate use of antidepressants, antipsychotics, or stimulants.
  • Psychotherapy may be helpful for patients with mild-to-moderate dementia to help them to understand, mourn, and adapt to this new impairment in functioning.
• Rehabilitation therapist
• • The care of patients with ADC is best accomplished with a team approach.
  • Both the physical and occupational therapist play a vital role in trying to maximize the functional capacity of the patient.

Diet

• Nutritional therapies
• • Nutritional therapies may be considered as potential interventions in the follow-up care for patients with cognitive motor symptoms associated with HIV infection.
  • Oxidative free-radical scavengers, such as vitamin E, the experimental antioxidant OPC-4117, and the trace mineral and antioxidant selenium, may prove therapeutically useful.

MEDICATION

Section 7 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

HIV infection is significant in the pathogenesis of ADC. Initiate antiretroviral therapy for untreated patients, and intensify therapy for patients currently on antiretroviral therapy.

Drug Category: Antiretrovirals

Inhibitors of reverse transcriptase; thus, cause chain termination when incorporated into a growing viral strand.

FOLLOW-UP

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Further Inpatient Care

• Once the diagnostic workup is completed, patients can receive follow-up care in an outpatient setting. Patients with advanced dementia may need supportive inpatient care.

Further Outpatient Care

• Systemic virologic suppression is associated with cognitive improvement, which may reflect a decrease in the CNS viral load.
• Neuropsychological testing is a more sensitive method of following cognitive changes than a simple neurologic examination. Serial testing should be performed at regular intervals to monitor for improvement in scores and responses to therapy.
• Radiologic follow-up with serial neuroimaging (ie, MRI) at regular intervals is a useful follow-up tool. These test results show decreased brain atrophy and improvement in white matter changes if the patient is responding to antiretroviral therapy.
• Nutritional therapies may be considered as potential interventions for the cognitive motor symptoms associated with HIV infection. Oxidative free-radical scavengers, such as vitamin E, the experimental antioxidant OPC-4117, and the trace mineral and antioxidant selenium, may prove therapeutically useful.

In/Out Patient Meds

• Antiretroviral medications should be continued indefinitely in most cases.

Deterrence/Prevention

• Aggressive early treatment of patients with HIV disease with antiviral medications and early suppression of viral replication results in successful control of infection and prevents most of the devastating consequences of HIV dementia. Several studies have shown that early and aggressive treatment of HIV infection decreases the rate of dementia from greater than 50% to 10%.
• See Medscape's HIV Transmission and Prevention Resource Center.
• See Medscape CME courses Expanded HIV Testing in Primary Care and Opt-out HIV Testing as a Public Health Tool.

Complications

• Adverse effects from medications and drug interactions are the most common complications.

Prognosis

• ADC has a variable progression. Typically, without treatment, the disease has a rapid progression over a few months, with a mean survival rate of 3-6 months. The survival rate has increased from 5 months in 1993-94 to 38.5 months in the 1996-2000 period.³ The prevalence is increasing, but presentation is now milder. Predictors of rapid neurologic progression prior to HAART were psychomotor slowing, injection drug use, and low CD4 counts. Co-infection with hepatitis C is another marker of worse prognosis. Cognitive improvement is observed in patients with ADC after the initiation of HAART. Sevigny et al have shown a significant and independent association of HIV-associated dementia with time to death. HIV-associated dementia is a significant risk factor for death. Poor medication adherence may be a factor. Plasma and CSF MCP-1 levels were also associated with time to death.¹⁰
• Include cognitive screening tests in routine examination of patients, especially with those at high risk such as those who are older or who have high plasma HIV RNA levels, low CD4 counts or HCV, and poor baseline cognitive status.
• The development of dementia is usually delayed until severe immunodeficiency develops. This finding is interesting because HIV invades the brain early in its course. ADC may remain static or may fluctuate. ADC may improve with medical therapy, or it may worsen abruptly with severe metabolic disorders (eg, hypoxemia, pneumonia) and then improve with the resolution of the metabolic disorders. Some studies report that older age, a lower CD4 cell count, decreased hemoglobin level, reduced platelet count, and thrush are related to rapid disease progression. One study showed that injection drug use and the presence of psychomotor slowing are associated with rapid progression of the dementia.

Patient Education

• Educate the patient at an early stage, and discuss future medicolegal implications of dementia. A patient should be strongly encouraged to prepare a living will or to assign power of attorney.
• Educate patients and families about the persistent dangers of the transmission of HIV. The following Web sites can be referenced for further information.
• • Centers for Disease Control and Prevention - HIV and Its Transmission
  • National Institutes of Health - HIV Infection and AIDS: An Overview
  • UCSF Center for HIV Information - HIV Transmission and Prevention in Adolescents
• Education of family members, friends, and caregivers of a patient with HIV dementia is of great importance. HIV dementia is a multifaceted problem, and caregivers should know about the complications, including psychiatric complications. Often, friends and family need counseling and support to deal with this chronic and difficult condition.
• For excellent patient education resources, visit eMedicine's Dementia Center, Immune System Center, and Sexually Transmitted Diseases Center. Also, see eMedicine's patient education articles Dementia Due to HIV Infection, Dementia Overview, and HIV/AIDS.

MISCELLANEOUS

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Medical/Legal Pitfalls

• Failure to exclude all other infectious etiologies because dementia due to HIV disease is a diagnosis of exclusion.

ACKNOWLEDGMENTS

Section 10 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author Brenda Jones, MD to the development and writing of this article.

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

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Article Last Updated: Apr 4, 2008