How can I tell if I am starting to get AIDS-related dementia? (COGNITIVE DYSFUNCTION, 2010) (NEUROPSYCHIATRIC DISORDERS, 2010)
Nov 15, 2010
Hi Dr. Bob, I have been on a HAART regimen since 2006 (Lexiva/Norvir/Epzicom), my CD4 count is above 700, my viral load is undetectable, and yet I seem to be getting all of the symptoms of early-stage dementia (I went through the list of early-stage ARD symptoms on this site and 90% of them apply to me). I am also taking a cocktail of anti-depression/anti-anxiety medications. My doctors do not think I have ARD, but are of the opinion that my symptoms are caused by the significant number of medications I am taking. I have read about the Mental Status Exam. Should I speak with my doctor about taking an exam like this? I am worried, my memory is poor, and my ability to do my job (which requires strong cognitive abilities) well is becoming a problem. Please offer me some advice on what I can do. Thanks.
Response from Dr. Frascino
HIV-related cognitive dysfunction is much more common than many folks (including some HIV docs) realize. I'll post below some information about HIV-related cognitive impairment and other neuropsychiatric disorders. You could show this information to your HIV specialist and discuss next steps for evaluation and management.
Is It All in Your Head?
By Marshall Forstein, M.D.
People living with HIV, not surprisingly, commonly experience concerns, and even disorders, that affect their mental health. The same is true for people at high risk of infection.
While anyone who engages in unprotected sex or shares needles is at risk to contract HIV, people with pre-existing psychiatric disorders (including addictive substance use) are at increased risk for behaviors that transmit HIV.
In addition, HIV-positive people are at increased risk for mood, anxiety, substance use, and cognitive disorders.
HIV and the Brain
HIV invades the central nervous system (CNS -- the brain and spine) at the time of initial infection. During the acute period of infection, in addition to symptoms of an acute viral infection throughout the body, a substantial proportion of people experience the impact of HIV in the central nervous system, such as confusion, disorientation, slowness of thinking, and changes in mood.
Most of the time, however, the infection of the CNS goes unnoticed. Whether or not a particular individual develops symptoms of CNS disturbance depends on a variety of factors including, but not limited to: the particular strain of HIV, viral load, immunological response, inflammatory response in the body and brain, and current medical or psychiatric problems.
HIV and Emotions
Aside from the initial impact of HIV in the brain and body, there is an ongoing emotional adjustment to becoming positive. Incorporating an HIV-positive status into one's identity may include managing information about one's health with both health care providers and other relationships, and adjusting to medical care and lifestyle changes to reduce risks to health.
There is a great range of reactions and accommodations to becoming positive and adjusting one's view of the self and of one's relationship to the world. These emotional and psychological reactions may change throughout a changing course of illness.
Emotional support is often very helpful, particularly from experienced therapists or members of HIV-positive support groups who are negotiating this process of integrating the reality of being HIV-positive into their future.
The interaction of HIV on the body, brain, and mind is complex. Symptoms that seem to arise in one area often impact all the others.
Whatever the symptom, a thorough evaluation and assessment must be done to ensure the correct diagnosis and treatment. This is most comprehensively accomplished using a bio-psycho-social-cultural-spiritual model.
For example, a complaint of fatigue or lack of energy may be a symptom of depression, but may also be explained by a disturbance in sleep, endocrine function (such as adrenal insufficiency,1, 2 low thyroid, or low testosterone in both males and females3), anemia due to HIV or medications, or poor pulmonary function due to lack of exercise or some lung infection. Alternatively, low energy or fatigue may be a reaction to an existential crisis around fear of dying, losing relationships, being rejected, or a manifestation of guilt or shame about sexuality, drug use, or other concerns.
To assess a particular symptom or set of symptoms requires medical providers to take time not only to evaluate the physical aspects of having HIV, but the emotional aspects caused by living with a chronic condition that is uncertain, may progress, and cause premature functional impairment.
In other words, every biological aspect of living with HIV is accompanied by a psychological response. People with HIV can use positive coping strategies to diminish the impact of changes in physical or mental well-being. Quality of life, and the maintenance of overall function, should be the focus of treatment for anyone living with HIV. A coordinated, collaborative approach among all providers is essential to maximize the individual's capacity to function at the highest possible level for as long as possible.
While living longer with HIV is now the norm rather than the exception, there are adjustments in function and lifestyle that must be anticipated, and discussed openly between patient and provider.
Over the past decade, evidence has mounted that HIV in the central nervous system (CNS) causes variable degrees of inflammation that manifests itself in a variety of ways, including
mood disorders (depression and mania), anxiety, sleep disturbances, and cognitive impairment See Table I for early and late signs of cognitive deficits.
Surviving longer with HIV, independent of viral load and CD4 count, increases the likelihood of some impairments of cognitive function. People at greatest risk for cognitive changes are those whose CD4 counts dropped to below about 200-300 before responding to HIV meds, and those with the highest viral loads in both the cerebral spinal fluid that bathes the brain and in the blood.
The chances of developing cognitive impairments increase with
advancing age,4 co-infection with hepatitis C, the use of toxic substances such as methamphetamine, cognitive changes early in the course of infection, and depression.5 Changes in personality are also common in people with mild cognitive impairments, and the inability to function as well as expected can cause significant fear, depression, and anxiety. Advancing cognitive impairment may lead to impulsivity, poor adherence to both medications and protective sexual behaviors, and hopelessness, including suicidal thoughts and attempts.
Cognitive disorders may be due to primary HIV in the brain, or secondary dysfunction due to metabolic, endocrine, infectious, or neoplastic effects on the CNS. Medications, herbal remedies, excessive vitamins, and substances of abuse are also frequently associated with cognitive impairment.6, 7 HIV antiretrovirals (ARVs) may also cause neuropsychological impairment, and head trauma may also contribute to CNS dysfunction.
Classification of primary HIV cognitive impairment is based on criteria having to do with the presence or absence of symptoms and the degree of functional impairment. HIV Associated Neurocognitive Disorder (HAND) (see Table II) classifies impairment under three categories:
asymptomatic neurocognitive impairment (ANI) with evidence upon neuropsychological testing of cognitive deficits; mild neurocognitive disorder (MND) with some functional limitations due to the cognitive domains affected; and the often progressive and disabling HIV-associated dementia (HAD) that always requires significant impairment for diagnosis.8 As ARVs have been more widely prescribed, the incidence of HAD has declined from the number of cases seen before these medications arrived,9 but as HIV-positive people live longer, there are increasing rates of MND and ANI being diagnosed.
In spite of the fact that ARVs may slow the development of illness, and have almost eliminated the appearance of diseases that were so common before ARVs, there is evidence that the impact of HIV in the brain may cause mild to moderate cognitive impairment as people live longer and age with HIV.5 The prevalence rates of primary HIV mild neurocognitive disorder may range from 20-60%.
The most common symptoms include:
short-term memory loss, problems with attention, concentration, multitasking, and word finding, and motor slowing. No single rapid screening tool currently has been validated to diagnose MND, but there are a couple of screening tests that have been shown to correlate with the more advanced form of cognitive impairment, HAD. Providers can ask a few questions of every HIV-positive patient to get a sense of cognitive concerns. (See Table III.) The treatment of cognitive disorders in HIV includes ARVs,10 psychostimulants, and cognitive rehabilitative strategies for compensating for deficits and enhancing mental function. (See Table IV.)
As people live longer with HAD and MND, the range of symptoms may vary more than previously thought.11 There are many co-morbid conditions that can contribute to CNS dysfunction that require a comprehensive medical workup. (See Table V.)
In an aging HIV-positive population, there are also increased risks for other types of non-HIV-related cognitive disorders that may synergistically cause cognitive impairment, such as hypertension, cerebrovascular disease, depression, and diabetes.
Depression is the most common psychiatric problem in the HIV-positive population, affecting as many as 50% of primary care HIV patients. HIV-negative gay men have been reported to have rates of depression 2-3 times that of heterosexual men, and gay men with HIV appear to have higher rates than HIV-negative gay men. Women have higher rates of depression than men in both the general and HIV populations, and untreated depression in HIV is associated with increased risk of dying.
The treatment of depression in HIV-positive people has been shown to be most effective when combining antidepressant medications and psychotherapy. While acute anxiety, shock, fear, and sadness are common initial reactions to discovering HIV-positivity, depression is not a normal reaction to illness, and should be treated aggressively to prevent decreased adherence to medications and protective sexual practices.
Depression must be distinguished from sadness, grief, fear, and existential concerns such as a fear of dying or losing one's health. Since so many people with HIV may have some of the symptoms of depression due to the medical illness, it is important to look at the more emotional and less biological aspects of depression, such as loss of interest in self or others, a sense of hopelessness, and guilt for behaviors or thoughts that are unacceptable to the person.
For example, a mother who is fatigued and cannot muster the energy to play with her children, but wants to, may not be depressed compared to a mother who becomes hopeless and disinterested in doing so.
When diagnosed in a patient with co-existing substance use, depression and the substance use disorder must both be treated in a comprehensive model.
Substance Use and Abuse
There is growing evidence in the research that certain legal substances, as well as drugs of abuse, vary in their toxicity in the CNS. Alcohol, nicotine, and excessive vitamins like B6 are all legal but potentially toxic to brain function.
Episodic binge drinking is likely more toxic to brain function compared to small amounts of alcohol on a daily basis, but any alcohol with certain medications may be detrimental to brain function and may affect blood levels of medications.
Illicit drugs have varying degrees of toxicity. Additionally, the brain is more vulnerable to the effects of such drugs depending on the presence of a co-existing psychiatric disorder or previous delirium. Some illicit drugs, more than others, have direct effects on nerve development in the CNS.
Methamphetamine appears to be the most neurotoxic of all illicit substances, even in small doses, causing loss of actual nerve tissue and function in the brain. Methamphetamine is not only rapidly addictive, but also very resistant to treatment and has very high relapse rates. To date, no medication is clearly beneficial in the treatment of methamphetamine addiction. Behavioral treatments have been shown to help in some situations, but the relapse rates are very high relative to the treatment for other addictive behaviors. The long-term cure for methamphetamine addiction may be as low as 10%.
HIV infection rates are significantly increased in methamphetamine users and secondary transmission is high, as judgment and impulse control are impaired with methamphetamine use.
For an informative summary on methamphetamine effects and treatment, see www.ncjrs.gov/ondcppubs/publications/drugfact/methconf/appen-b3.html.
Other illicit drugs such as marijuana, cocaine, ecstasy, GHB, and ketamine may also have neurotoxic effects, and may disrupt or deplete neurotransmitters that are essential for a well-functioning brain.
Mental health issues are best addressed in the context of a professional relationship with a provider who is non-judgmental, open, and able to formulate a psychological understanding of behavior and the resistance to change.
Primary care and mental health providers must stay collaborative and vigilant for changes in mental status, and for interactions between medications, especially in the context of recreational substances. There are phases to the psychological adjustment of becoming HIV-positive, even when there is awareness that one has put oneself at risk for infection. Research shows that sero-conversions most often occur in the context of sexual encounters under the influence of substances. Occasional use, as well as addiction, can reduce the capacity for using condoms. Depression, cognitive impairment, intoxication, and impulsive personality traits can reduce executive function of the frontal lobes that control rational thinking and behavior.
Additionally, there is growing evidence that previous sexual abuse and trauma are highly correlated with risky behaviors. The psychological impact of sexual or emotional trauma can reduce an individual's capacity to insist on condom use, or to refrain from undesired sexual or drug use behaviors.
Couples in which one partner is positive and one negative may experience a variety of emotional responses. Fear of infecting a partner, or being infected, can precipitate a loss of intimacy, a change in sexual function, or an increase in pre-existing psychiatric symptoms.
Psychosocial support has been shown to be very important to sustaining adherence to antiretroviral medications and dealing with side effects.
Attention should also be paid to the impact of bodily changes due to HIV or its treatment. Body image can impact a sense of self-worth, cause one to be stigmatized, and can affect one's sense of sexual attractiveness and desirability.
With the promise of a longer life now possible with good medication adherence, HIV-positive people are often interested in starting or maintaining sexual relationships, and often feel hesitant, or afraid of being rejected. Many HIV-related problems (such as neuropathy, metabolic syndrome, and renal or liver disease) can cause sexual dysfunction in both men and women.
Additionally, many of the medications used for cardiovascular disease or hypertension (beta blockers), as well as many psychiatric meds (antidepressants and antipsychotics) can cause sexual side effects.
Most importantly, providers must create a safe environment in which expressing concerns about sexuality is welcomed.
Goals of Treatment
The most important mental health issues facing people who are HIV-positive today include maintaining excellent adherence to antiretroviral medications, avoiding toxic substances that impair brain function, preventing co-infection with other strains of HIV (to prevent resistance to medications that are suppressing viral replication), being treated for underlying psychiatric symptoms and disorders, and dealing with subtle changes in brain function over time. All of the above factors affect each other. Preserving brain function is at least as important as preserving liver, lung, and cardiac function. Living longer with greater quality of life should be the focus of treatment. Finding purpose and community can provide the impetus for self-care and hope.
Marshall Forstein, M.D., is Director of Training for the Division of Adult Psychiatry at The Cambridge Hospital, and an Associate Professor of Psychiatry at Harvard Medical School. He teaches medical students and is a core faculty member in the Division of Palliative Care at Harvard Medical School. Dr. Forstein has been a principal investigator on an HIV Education and Training Grant through the federal Center for Mental Health Services, and teaches and has published on the neuropsychiatry and psychosocial aspects of HIV/AIDS. He is a Distinguished Fellow of the American Psychiatric Association and is currently serving on the Residency Review Committee for Psychiatry of The Accreditation Council for Graduate Medical Education.
Mayo J, Callazos J, Martinez E, Ibarra S: Adrenal function in the human immunodeficiency virus-infected patient. Arch Intern Med 2002, 162:1095-1098 Chen F, Day SL, Metcalfe RA, et al.: Characteristics of autoimmune thyroid disease occurring as a late complication of immune reconstitution in patients with advanced human immunodeficiency virus (HIV) disease. Medicine (Baltimore) 2005, 84:98-106. Mylonakis E, Koutkia P, Grinspoon S: Diagnosis and treatment of androgen deficiency in human immunodeficiency virus-infected men and women. Clin Infect Dis 2001, 33:857-864. Becker JT et al. Prevalence of cognitive disorders differs as a function of age in HIV virus infection. AIDS 18 (suppl. 1): S11-S18, 2004. Cherner M et al. Effects of HIV-1 infection and aging on neurobehavioral functioning: preliminary findings. AIDS 18 (suppl. 1): S27-S34, 2004. Clifford DB, Evans S, Yang Y, et al.: Impact of efavirenz on neuropsychological performance and symptoms in HIV infected individuals. Ann Intern Med 2005, 143:714-721. Cespedes, M S, Aberg, J A, Neuropsychiatric Complications of Antiretroviral Therapy, Drug Safety; 2006, Vol. 29 Issue 10, p865-874 Antinori A, Arendt G, Becker JT, Brew BJ , et al. Updated research nosology for HIV-associated neurocognitive disorders, Neurology 2007; 69; 1789-1799 Dore GJ, Correll PK, Li Y, Kaldor JM, Cooper DA, Brew BJ. Changes to AIDS dementia complex in the era of highly active antiretroviral therapy. AIDS 1999; 13:1249-1253 Letendre SL, McCutchan JA, Childers ME, Woods SP, Lazzaretto D, Heaton RK, et al. Enhancing antiretroviral therapy for human deficiency virus cognitive disorders. Ann Neurol 2004; 56:416-423. Brew BJ. Evidence for a change in AIDS dementia complex in the era of highly active antiretroviral therapy and the possibility of new forms of AIDS dementia complex. AIDS 2004; 18 suppl 1:S75-S78.
Table I Neuropsychological Deficits in Early HIV Illness
Decreased attention/concentration Psychomotor slowing Reduced speed of information processing Executive dysfunction (abstraction, divided attention, shifting cognitive sets) Working memory impairment (example: remembering 4 words over 5-10 minutes while doing another task)
Neuropsychological Deficits in Late HIV IIllness
Memory impairment (short term, later long term) Language problems (finding words, miss naming common objects Visuospatial difficulties (example: drawing a clock Apraxias (neurological condition characterized by loss of the ability to perform activities that a person is physically able and willing to do)
Table II. Revised Research Criteria for HIV-Associated Neurocognitive Disorders (Hand) (Modified From HIV Neurobehavioral Research Center Criteria 24) HIV-Associated Asymptomatic Neurocognitive Impairment (ANI)*
Acquired impairment in cognitive functioning, involving at least two ability domains, documented by performance of at least 1.0 SD below the mean for age-education-appropriate norms on standardized neuropsychological tests. The neuropsychological assessment must survey at least the following abilities: verbal/language; attention/working memory; abstraction/executive; memory (learning; recall); speed of information processing; sensory-perceptual, motor skills. The cognitive impairment does not interfere with everyday functioning. The cognitive impairment does not meet criteria for delirium or dementia. There is no evidence of another preexisting cause for the ANI. *If there is a prior diagnosis of ANI, but currently the individual does not meet criteria, the diagnosis of ANI in remission can be made. If the individual with suspected ANI also satisfies criteria for a major depressive episode or substance dependence, the diagnosis of ANI should be deferred to a subsequent examination conducted at a time when the major depression has remitted or at least 1 month after cessation of substance use.
HIV-1-Associated Mild Neurocognitive Disorder (MND)*
Acquired impairment in cognitive functioning, involving at least two ability domains, documented by performance of at least 1.0 SD below the mean for age-education-appropriate norms on standardized neuropsychological tests. The neuropsychological assessment must survey at least the following abilities: verbal/language; attention/working memory; abstraction/executive; memory (learning; recall); speed of information processing; sensory-perceptual, motor skills. Typically, this would correspond to an MSK scale stage of 0.5 to 1.0. The cognitive impairment produces at least mild interference in daily functioning (at least one of the following): a) Self-report of reduced mental acuity, inefficiency in work, homemaking, or social functioning. b) Observation by knowledgeable others that the individual has undergone at least mild decline in mental acuity with resultant inefficiency in work, homemaking, or social functioning. The cognitive impairment does not meet criteria for delirium or dementia. There is no evidence of another preexisting cause for the MND. *If there is a prior diagnosis of MND, but currently the individual does not meet criteria, the diagnosis of MND in remission can be made. If the individual with suspected MND also satisfies criteria for a severe episode of major depression with significant functional limitations or psychotic features, or substance dependence, the diagnosis of MND should be deferred to a subsequent examination conducted at a time when the major depression has remitted or at least 1 month after cessation of substance use.
HIV-1-Associated Dementia (HAD)*
Marked acquired impairment in cognitive functioning, involving at least two ability domains; typically the impairment is in multiple domains, especially in learning of new information, slowed information processing, and defective attention/concentration. The cognitive impairment must be ascertained by neuropsychological testing with at least two domains 2 SD or greater than demographically corrected means. (Note that where neuropsychological testing is not available, standard neurological evaluation and simple bedside testing may be used, but this should be done as indicated in algorithm; see below). Typically, this would correspond to an MSK scale stage of 2.0 or greater. The cognitive impairment produces marked interference with day-to-day functioning (work, home life, social activities). The pattern of cognitive impairment does not meet criteria for delirium (e.g., clouding of consciousness is not a prominent feature); or, if delirium is present, criteria for dementia need to have been met on a prior examination when delirium was not present. There is no evidence of another, preexisting cause for the dementia (e.g., other CNS infection, CNS neoplasm, cerebrovascular disease, preexisting neurologic disease, or severe substance abuse compatible with CNS disorder). *If there is a prior diagnosis of HAD, but currently the individual does not meet criteria, the diagnosis of HAD in remission can be made. If the individual with suspected HAD also satisfies criteria for a severe episode of major depression with significant functional limitations or psychotic features, or substance dependence, the diagnosis of HAD should be deferred to a subsequent examination conducted at a time when the major depression has remitted or at least 1 month has elapsed following cessation of substance use. Note that the consensus was that even when major depression and HAD occurred together, there is little evidence that pseudodementia exists and the cognitive deficits do not generally improve with treatment of depression.
Table III. Cognitive Functional Status Sub-Scale of MOS-HIV Scale of Wu et al. Four questions, past 4 weeks:
Difficulty reasoning/problem solving? Forget things (location; appointment)? Trouble with keeping attention for long? Difficulty with activities using concentration/thinking? These questions do not diagnose HIV cognitive impairment, but a positive finding on them may suggest further cognitive workup.
Table IV. Treatment of HIV Cognitive Disorders Antiretrovirals Reduce peripheral VL Impact on CNS Psychostimulants Methylphenidate Dexedroamphetamine modafinil Cognitive rehabilitation
Table V. Cognitive Dysfunction in HIV Hepatitis C Methamphetamine and other drugs Depression Substances of abuse Pain medications Sleep deprivation
Cognitive Dysfunction: An Update From the 1st International Workshop on HIV & Aging By Nelson Vergel
October 21, 2010
This is part of a series of articles summarizing presentations from the 1st International Workshop on HIV & Aging, which took place in Baltimore, Md., from Oct. 4 to Oct. 5, 2010. Jump to the table of contents to see the other articles in this series.
The CHARTER cohort in the United States is a huge study that includes HIV-positive people who are an average of 43 years of age. Findings discussed at this conference revealed that almost half of those CHARTER participants had some sort of mild cognitive function. In a conference call with the study investigators, I asked how this finding compares with a similar HIV-negative population. They said that mild cognitive declines would be expected in 10 percent to 20 percent of HIV-negative people, which would mean that HIV almost doubles the rate. It seems that CD4 nadir was one of the strongest predictors of cognitive decline.
Avindra Nath, M.D., reviewed data on how HIV can possibly affect neurons even in the presence of complete HIV viral control after HAART initiation. Nath's discussion focused on Tat, which is short for "transactivator of transcription"; it's a regulatory gene within HIV that accelerates the production of more HIV virus. In fact, Tat is crucial to HIV, because HIV completely fails to replicate itself without it.
Tat protein is also toxic, so the large amounts of Tat released into the blood by HIV-infected cells are no help for the body. It can be absorbed by cells that are not infected with HIV, and can cause cell death (via a process called apoptosis) in uninfected "bystander" T cells, which can assist a person's progression toward AIDS.
In addition, Tat increases immune activation, which enables immune cells to more easily get inside of neurons and affect their functioning. Immune activation causes a state of "high alert" in which the immune system struggles to produce responses that could control HIV or other proteins that are identified as "foreign." There is a broad consensus among researchers that this chronic state of immune activation contributes to the virus's ability to cause certain health issues, including cognitive dysfunction. However, while there are some hypotheses about how HIV (or certain proteins) causes chronic immune activation, the precise mechanisms are still under investigation.
Following Nath's discussion, Marcus Kaul, Ph.D., presented data on a genome-wide analysis of HIV from the NeuroAIDS study. A protein produced by HIV called gp120 has been linked to disruptions in metabolism, inflammation and a condition known as HIV-Associated Neurocognitive Disorder (HAND). Kaul also presented data on the increase in neurofilaments in HIV-positive people, as well as increased amyloid plaque deposition in neurons, which grows as HIV infection progresses. He mentioned that Tat and gp120 prevent the "clean up" of these amyloid plaques. This plaque buildup is also worsened by the immune activation that has been found in samples of cerebrospinal fluid of HIV-positive people regardless of whether they have an undetectable viral load. Luckily, this accumulation of plaque in neurons is not similar to that seen in Alzheimer's patients, so it may not lead to the same dramatic decreases in cognitive function.
Although antiretroviral therapy can significantly increase resting cerebral blood flow (rCBF) in HIV-positive people, it does not return to normal, according to results of small cross-sectional and longitudinal studies. Using imaging techniques, these studies found that "functional brain demands in HIV-positive subjects were equivalent to those of HIV-negative subjects who were 15-20 years older."
At this conference, a study from 2006 was also mentioned, in which scientists at the National Institutes of Health found that HIV infection breaks down barriers in the intestine that normally prevent intestinal bacteria from entering the bloodstream. The blood of HIV-infected people was found to contain markedly elevated levels of lipopolysaccharide (LPS), a component of certain bacteria that is normally confined to the intestine but "leaks" out due to HIV infection. LPS may also be associated in immune activation and cognitive decline. Studies using prebiotics (nutrients that help friendly bacteria grow in the gut) and anti-inflammatory compounds have been proposed to determine if these approaches can stem the LPS leakage and improve LPS-related immune activation.
In a separate presentation, Scott Letendre, M.D., spoke about a microtubule-associated protein called Tau. High levels of phosphorylated Tau (pTau) have been associated with aging-related cognitive problems (such as dementia and Alzheimer's) in HIV-negative people. Unfortunately, pTau levels appear to be considerably higher in HIV-positive people compared to HIV-negative people of the same age, according to Letendre. In fact, it is estimated that HIV increases pTau to levels that are comparable to HIV-negative people who are 20 years older. pTau levels also appear to continue to rise in HIV-positive people on HAART even though their CD4 count is increasing.
Letendre spoke about a study in which a test called the Memory for Intentions Screening Test was administered to HIV-positive people. The test assesses a person's "prospective memory," or their ability to remember to do something they intend to do in the future. This study found that HIV-positive people had worse prospective memory than normal for their age -- but that their overall neurocognitive performance was no worse than average.
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