HIV Neurocognitive Disorders

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Continuing Education Activity

Patients with human immunodeficiency virus infection (HIV infection) have been noted to have various forms of neuropsychiatric illnesses. These include symptoms of both cognitive disorders as well as mood and anxiety symptoms. This activity reviews the epidemiology, etiology, clinical signs and symptoms, evaluation, and treatment of neurocognitive disorder secondary to HIV disease and highlights the interprofessional team's role in evaluating and treating this condition. This activity also reviews in-depth basic screening tools for the disease and evidence-based treatment guidelines. This activity also covers a section on current research studies on neurocognitive disorders secondary to HIV disease.


  • Review the impact of HIV disease on major cognitive disorders or dementia.
  • Identify the different stages of dementia or neurocognitive disorder secondary to HIV disease.
  • Outline the management options available for dementia or neurocognitive disorder secondary to HIV disease.
  • Describe the importance of improving care coordination amongst interprofessional team members to improve outcomes for patients affected by dementia secondary to HIV disease.


Patients with human immunodeficiency virus infection (HIV infection) have been noted to have various forms of neuropsychiatric illnesses. Neuropsychiatric illnesses include symptoms of both cognitive disorders as well as mood and anxiety symptoms.[1] In the past, before the advent of antiretroviral treatment, several neuropsychiatric disorders remained untreated, resulting in a large mortality rate.[2] Most of these disorders stemmed from untreated infectious diseases secondary to AIDS (acquired immunodeficiency syndrome) like toxoplasmosis and encephalitis.[3] The decline in neurocognitive disorders notably came hand in hand with the advent of HAART (highly active antiretroviral therapy). Combination treatment for HIV was developed around 1996, and since then, HIV-related neuropsychiatric disorders started to decline.[4] 


The human immunodeficiency virus (HIV) directly crosses the blood-brain barrier during the acute phase of infection. However, it is during the chronic inflammation phase that cognitive changes are seen. Monocytes, macrophages, and white matter are all affected in the brain.[5] HIV reproduces in the microglia, which are known as the brain's "immune cells." These changes are associated with clinical signs and symptoms of neurocognitive disorder seen with HIV disease.


The epidemiological study of HIV-associated dementia had started after the advent of antiretroviral (ARV) treatment after noticing that the virus causes cognitive impairments. This was a common occurrence and seen in about 40% of people dying with AIDS. Of note, the initial description was of a feature of ongoing neurocognitive impairment along with Parkinson-like features. However, with the advent of cART (combination antiretroviral therapy) and increased longevity of persons infected with HIV, the ongoing cognitive impairments continued to be present for a long period of illness.[6]

However, neurocognitive disorders have undergone a significant change; initially, in the late 1980s, the large body of neurocognitive disorders collectively was known as AIDS dementia complex given the degree of neurocognitive impairment seen.[7]

The AIDS task force of the American Association of Neurology included minor cognitive-motor disease and HIV-associated dementia, a term that came in the early 1990s. The variability of cognitive impairment was notable; hence an initial idea had been two categories.[8] A newer classification includes the Frascati Panel of 2006 for HIV-associated neurocognitive disorder, which includes asymptomatic neurocognitive impairment (ANI), mild neurocognitive disorder (MND), and HIV-associated dementia (HAD). Some neurocognitive deficits include a lack of processing, attention, concentration, memory, and abstraction.[9] There were notably three categories that are now universally accepted as the classification of HIV-associated dementia. These three categories are: 

  • Asymptomatic neurocognitive impairment (ANI) includes impairment in at least two cognitive domains, at least one standard deviation below the mean in testing, and no impairment with daily functioning.
  • Mild neurocognitive disorder (MND) in which neuropsychological testing results as above with mild interference with daily functioning.
  • HIV-associated dementia (HAD), which is impairment in two cognitive domains(the five cognitive domains includes attention/speed of information, working memory, verbal skills, executive functioning, and motor skills) and two standard deviations below neuropsychological testing.

The above definitions apply to primary HIV-associated neurocognitive disorder (HAND); however secondary cognitive limitations due to ongoing infections, encephalitis, etc., may be seen.


In the United States, approximately 50% of persons with ongoing HIV infection were noted to have a cognitive impairment when studies were first conducted around multiple sites in the country.[10] With the advent of antiretroviral therapy, the prevalence of HAND has shown a decline, especially in people who are on treatment consistently. HIV-associated dementia is currently seen in seropositive patients with CD4 counts below 200/mm3.[11][12]


HIV crosses the blood-brain barrier and infiltrates the macrophages in the central nervous system. A virus-induced fusion of macrophages leads to the formation of giant cells and astrocytes activation and damage (astrocytes are cells that provide metabolic support and detoxify neurons), ultimately leading to neuronal damage in many parts of the brain. The damage is caused by verotoxins, including HIV proteins gp41, gp120, Tat, Vpr, Nef, and Rev. The subcortical structures are most affected, like the limbic structures basal ganglia.[13] HIV infection also causes a breakdown of white matter and axonal damage.[14] Ultimately, this leads to a decline in cognition and notably a decreased volume of the brain structures like basal ganglia and caudate nucleus, causing atrophy of the brain volume.[15]


In the pre-HAART era, when the incidence of HIV-associated dementia was considerably high, brain autopsies showed meningitis with low counts of lymphocytes and perivascular lymphocytic cuffing.[16] The cells that are seen are generally CD 8 T- lymphocytes and CD 4 lymphocytes.[17]

HIV enters the brain via HIV-infected lymphocytes and macrophages. In addition to the passage of cell-free virus into the brain and release of the virus from the infected endothelial cells. The virus replicates in these cells and infects the microglia, astrocytes, oligodendrocytes, and neurons. HIV infection in the CNS can be detected and monitored by cerebrospinal fluid (CSF) viral load measurements. Another pathological feature in HIV-associated encephalitis is the presence of multinucleated giant cells, which was very prominent before the advent of antiretroviral drugs.[18] Multiple studies established a positive correlation between CSF viral load and the extent of cognitive dysfunction.

History and Physical

While obtaining a history from patients with HIV infection, some risk factors need to be noted. These include having a low CD4 count and the amount of virus in the blood.[19] HIV is a disease that causes overall immunodeficiency and puts individuals at risk for opportunistic infections. Often patients may carry comorbid Hepatitis B or Hepatitis C infection. Studies have shown that patients infected with Hepatitis C have a higher risk of developing cognitive impairment.[20] Another risk factor includes concurrent substance use disorders. One particular drug that has been associated with neurocognitive impairment is methamphetamine use. The use of intravenous drugs in patients with HIV infection leads to further cognitive impairment.[21] Data in the past showed that HIV infection and drug abuse, especially intravenous drug abuse, lead to overexpression of CD68 inflammatory markers and major histocompatibility complexes, which lead to further cognitive impairment.[22]

Another important aspect while taking history in HIV patients is to recognize the clinical features of HIV-associated neurocognitive disorder, which is characterized by insidious onset and slow progression. If the onset is less than 4 weeks, consider alternative causes. At the time of clinical evaluation and testing, the patient must not be febrile, excessively tired, or sedated. Delay in diagnosing HIV, initiation of HAART, and longer periods of low CD4 count are associated with a higher risk of cognitive impairment.[23]

The earliest symptoms and signs are impairment in concentration, memory, and executive functioning. As the disease progresses, psychomotor retardation, depressive symptoms, irritability, and subclinical motor signs are observed. These motor signs include tremors, hyperreflexia, etc. Later on, clinical features evolve to overall global dementia, myelopathy, neuropathy, and even Parkinson-like features.[24]


The main tool for evaluation is neuropsychological testing. Some neuropsychological testing domains that have shown impairment include episodic memory (learning and recall), executive functions, attention/working memory, information processing, verbal fluency, and fine motor skills.[24][25] Some other aspects of neurocognitive testing include trail making test (to test executive functioning), use of a grooved keyboard (to test for psychomotor skills), digit span test (to determine for psychomotor speed, abstraction, memory, and attention), and also use of the Stroop test (test attention and processing speed).[26]

Another form of evaluation is the use of imaging. In the pre-HIV era, imaging was significant for global brain atrophy. HIV-related encephalitis can be evaluated with FLAIR imaging, which will show focal atrophy in the basal ganglia, thalamus, corpus callosum, and frontal lobes.[27] Recently, 3D imaging has studied the patterns of brain atrophy to correlate with ongoing cognitive impairment. Specific areas included sensorimotor areas, parts of the corpus callosum, and parts of the frontal lobes.[28] Many of the new imaging studies have compared infected individuals to normal same-age controls. Hence, the correlation of cognitive decline in infected individuals and relevant brain areas is now well established.

A good screening tool is the International HIV Dementia Scale, which tests memory, motor speed, and psychomotor speed. The test includes:

  • Memory registration is tested by giving a patient four words and asking them to repeat. Then the patient is requested to retain the words.
  • Motor speed is tested by having the patient tap the first two fingers of their non-dominant hand as quickly as possible. The number of taps in five seconds is counted.
  • The psychomotor speed is measured by having the patient use their non-dominant hand to do a series of tasks, for example, having the patient clench their fist, place the palm face down and then place it perpendicularly on the table. The speed and sequence are measured.
  • The patient is asked to recall the four words practiced earlier.[29]

Another screening tool is the modified HIV scale, which tests immediate memory and delayed recall. Immediate and delayed memory is tested by asking patients to register four words and then asking them to repeat the words a few minutes later. Executive functioning is tested by copying a cube. Psychomotor speed is tested by asking the patient to write the alphabet in capital letters.[30]

One study showed that clinically three simple questions might be a good screening tool for HIV-associated Neurocognitive Disorder; these include asking whether patients experience memory loss, have difficulty paying attention, and feel slower while reasoning or doing complicated tasks.[31] However, the mainstay for evaluation is still getting a good clinical history and collaborative information around the start of cognitive decline. It is highly recommended by the Mind Exchange Program, which is established by expert clinicians around the world.[32]

Treatment / Management

Treatment with antiretroviral drugs (HAART) has shown improvement in cognitive function, including all cognitive domains. Also, the increase in CD4 count and the decrease in viral load are correlated with cognitive improvement.[33] The other indicator of treatment success includes the CNS penetration abilities of antiretroviral drugs. The drug's ability to cross the blood-brain barrier and achieve a high concentration in the cerebrovascular fluid is essential to lower the viral load. Letendre S et al. studied the CNS penetrability of ARV drugs. Individual ARV drugs were assigned a penetration rank of 0 (low), 0.5 (intermediate), or 1 (high). This ranking system was based on drug concentration in CSF, chemical properties, and CNS effectiveness in clinical studies. The CNS penetration-effectiveness (CPE) Rank was calculated by summing the individual penetration ranks for each ARV in the regimen.[34] For example, combinations of efavirenz, lamivudine, and zidovudine have high CPE. Drugs like abacavir have a lower CPE score. Lower CPE ranks correlated with higher CSF viral load.[35] A small study that included 37 people showed greater cognitive improvement with greater penetrability of the drug.[36] Another study looked at both HIV patients with cognitive impairment and patients with cognitive impairment without HIV, and it showed a worsening of cognitive scores. The theory is that ARV drugs with high penetrability can be neurotoxic too. So, it is suggested to suspect ARV drugs neurotoxicity when cognitive improvement is not seen with antiretroviral treatment.[37]

Most research articles emphasize the use of psychiatric medications as needed for mood disorders like depression. Many subtypes of antidepressants have been studied, including selective serotonin reuptake inhibitors, tricyclic antidepressants, and serotonin-norepinephrine reuptake inhibitors. All of these showed moderate symptomatic relief.[38][39] Psychostimulants may also be used for fatigue and apathy.[40] Psychotic and manic symptoms are less studied in HIV-positive patients; however, research was done on a small sample with psychosis and has shown a greater incidence of extrapyramidal symptoms.[41] Some of the mood stabilizers like lithium have concurrent neurotoxic effects. Some medications like carbamazepine can induce the same CYP enzyme system as many of the antiretroviral drugs causing drug interactions.[42][43] In theory, several drugs are considered neuroprotective, such as memantine, pentoxifylline, selegiline, nimodipine, and peptide T. However, only selegiline has shown efficacy.[44]

Differential Diagnosis

Differential diagnoses include primary neurocognitive disorder and its subtypes. Given that persons with HIV have increased longevity, the primary neurocognitive disorder may also set in. It often becomes progressively more difficult to differentiate between neurocognitive disorder secondary to HIV and primary neurocognitive disorder.[45] Another differential diagnosis is major depressive disorder, which can present with signs and symptoms of pseudodementia. Some common features also include psychomotor retardation and lack of concentration. The prevalence of Major depressive Disorder is higher in persons with HIV. Some symptoms remain in common, including apathy rather than the lack of interest in other activities. There is an increased incidence of dysphoria in both entities.[46][47]

Other differentials include substance intoxication and withdrawal, metabolic disorders, opportunistic infections (CNS toxoplasmosis, cryptococcal meningitis), brain tumors, traumatic brain injury, and even adverse effects of antiretroviral medications like efavirenz.[48]

The following conditions are important to remember in the differential diagnosis when considering possible HIV-associated dementia:

Central Nervous System Disease

  • CNS lymphoma
  • CNS toxoplasmosis
  • CNS vasculitis
  • Cryptococcal meningitis
  • Cytomegalovirus encephalitis
  • Metastatic disease
  • Neurosyphilis
  • Progressive multifocal leukoencephalopathy 
  • Tuberculous meningitis

 Substance Withdrawal or Intoxication

  • Alcohol
  • Chronic cannabis
  • Opioids

Metabolic and Endocrine Disease

  • Addison disease
  • B12 deficiency
  • Thyroid disease 

Psychiatric Illness

  • Delirium
  • Mood disorders (major depression, dysthymia)

Pertinent Studies and Ongoing Trials

The longitudinal CHARTER study is one of the most prominent clinical research studies that focus on neurocognitive deficits in persons with HIV. It investigated the incidence and predictors of neurocognitive change over 16 to 72 months (mean 35) in 436 HIV-infected participants in the CNS HIV Anti-Retroviral Therapy Effects Research cohort. The conclusion was that neurocognitive changes were complex and depended on several factors, including HIV treatment and the extent of HIV infection and comorbid infections.[49]

In a study of the Use of Nonantiretroviral Medications That May Impact Neurocognition, Three thousand three hundred women (71% with HIV) and data from almost 42,000 visits were studied. HIV infection was associated with neurocognitive adverse effects (NC-AE) medication use, which may influence the determinations of HIV-associated neurocognitive impairment. So it is advised that physicians consider the impact of NC-AE medications when evaluating patients with HIV and concurrent neurocognitive symptoms.[50]

The mind exchange working group consists of sixty-six experts from thirty countries who have published their assessment guidelines, diagnosis, and treatment of HIV-associated neurocognitive disorder.[32]


According to the MIND exchange working group, there have been no studies that discuss the prognosis of HIV-associated neurocognitive disorder (HAND), however markers of HIV disease (low CD4 count and high viral load), ongoing poor scores on neuropsychological testing, and concurrent mood disorder all point towards a poor prognosis.


Complications of HIV dementia, as mentioned above, can also include comorbid mood and anxiety disorders. Research has shown that chronic stress can lead to a weakened immune system and increase the risk of other diseases.[51] Also, given the longevity of persons living with HIV now, other forms of dementia, including primary neurocognitive illness, have become a comorbid complication.[52]

Deterrence and Patient Education

Patient education is primarily around early diagnosis and treatment of the disease. Treatment with HAART can delay and even deter the onset of dementia secondary to HIV disease. High viral loads and low CD4 cell counts are associated with a higher incidence of HIV-associated dementia.

Enhancing Healthcare Team Outcomes

The mainstay of treatment lies in early detection. All providers who encounter patients with HIV disease should be encouraged to start their patients on HAART. Patients must receive education about the onset of HIV-associated dementia, especially early signs of asymptomatic neurocognitive impairment, which may show a decrease in functioning. All providers must also be educated about the stages of dementia, especially when patients speak about the gradual loss of functioning in daily activities.

Infectious disease specialists treating these patients are encouraged to perform simple screening tests like the Mini-Mental State Exam or the Montreal Cognitive Assessments to look for neurocognitive impairment. They are also encouraged to simultaneously screen for symptoms of depression, including anhedonia, apathy, and lack of concentration. If there is any deficit seen in the screening tests, providers are highly encouraged to refer the patients for neuropsychological testing to determine areas of dysfunction.

Given that mood symptoms are prevalent in patients with HIV disease, a careful history is necessary regarding the onset of mood symptoms, and screeners such as the PHQ-9 may be used. If a patient scores in the range of moderate to severe depression, then a referral to a mental health provider should be made. Evidence has shown that treatment of concurrent mood and even psychotic symptoms has played a role in treating HIV-associated neurocognitive disorder. In case patients with HIV disease are hospitalized and show signs of cognitive dysfunction, a careful distinction must be made between delirium and cognitive decline. Longitudinal cognitive assessments and neurological exams must be made during the hospitalization.

Specialty-trained nurses can assist clinicians with early detection of this disease by conducting a cognitive screen every year and monitoring scores to recognize any sharp decline. Nurses can also help educate patients regarding the importance of compliance with HAART to prevent this disease. Clinical pharmacists can help providers identify treatment options with minimal adverse side effects and check for drug-drug interactions. A collaborative interprofessional team approach to patients with HIV can help deter neurocognitive disorders and ensure adequate management if the disease occurs. [Level 5]

Article Details

Article Author

Paroma Mitra

Article Editor:

Tariq Sharman


6/29/2021 3:52:04 PM



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