HATIP 2007
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Screening for HIV dementia

By Theo Smart (continues from part 1)

Healthcare staff should be particularly on the alert in those patients about to go on ART, since cognitive impairment could interfere with HIV control. According to a recent editorial by Brew and González-Scarono in Neurology, “at the very least [it] can lead to poor adherence and at worst to disability and death. In fact, poor adherence alone is important, as there is a direct relationship between inadequate levels of antiretroviral drugs and the development of resistance. Failure to recognize cognitive impairment will not only impair individual therapy but will harm the efforts to control HIV in a community, as cognitively impaired patients are less inhibited and are more likely to engage in HIV-related risk behaviour. This may be compounded if the transmitted strains are also resistant to HAART.”

However, at the primary health care level, staff may see a variety of neurological complaints that may have nothing to do with HIV. To help healthcare workers first recognize and manage these conditions, a very clear and easy to use resource manual “Where there is no neurologist,” by Dr Birbeck, has just been made available online at the World Federation of Neurology’s website

(see http://www.wfneurology.org/link_ebooks.htm.)

As for HIV dementia, despite the Ethiopian study experience, the IHDS appears to be a fairly simple tool that, translated into the local language, could be used by non-neurologist personnel to screen for overt HIV dementia in developing countries. In the Ugandan study, the sensitivity of the IHDS for HIV dementia was 80% and specificity was 57% (using a cut off of  ≤ 10) (Nakasujja).

International HIV dementia scale (from Sacktor 2003)

Memory-Registration – Give four words to recall (dog, hat, bean, red) translated into the local language (in Luganda: kopo, engatto, doodo, myufo) – 1 second to say each. Then ask the patient all four words after you have said them. Repeat words if the patient does not recall them all immediately. Tell the patient you will ask for recall of the words again a bit later.

1.  Motor Speed: Have the patient tap the first two fingers of the non-dominant hand as widely and as quickly as possible.

  •  4 = ³ 15 in 5 seconds
  •  3 = 11-14 in 5 seconds
  • 2 = 7-10 in 5 seconds
  • 1 = 3-6 in 5 seconds
  • 0 = 0-2 in 5 seconds

2.  Psychomotor Speed: Have the patient perform the following movements with the non-dominant hand as quickly as possible:

 1) Clench hand in fist on flat surface. 2) Put hand flat on surface with palm down. 3) Put hand perpendicular to flat surface on the side of the 5th digit. Demonstrate and have patient perform twice for practice.

  • 4 = 4 sequences in 10 seconds
  • 3 = 3 sequences in 10 seconds
  • 2 = 2 sequences in 10 seconds
  • 1 = 1 sequence in 10 seconds
  • 0 = unable to perform

3.  Memory-Recall: Ask the patient to recall the four words. For words not recalled, prompt with a semantic clue as follows: animal (dog); piece of clothing (hat); vegetable (bean); color (red).

  • Give 1 point for each word spontaneously recalled.
  • Give 0.5 points for each correct answer after prompting
  • Maximum – 4 points.

Total International HIV Dementia Scale Score

This is the sum of the scores on items 1-3. The maximum possible score is 12 points.  A patient with a score of <10 should be evaluated further for possible dementia.

Further assessments and diagnosis of dementia

According to the South African Handbook of HIV Medicine, at the referral level, assessment generally starts by taking a patient’s thorough history, and performing a careful physical exam to find any underlying illness and whether any special investigations are needed. “Staging the patient is a crucial step in determining the likely aetiology of a neurological problem.”

Dr Hall also emphasized that the neurological disorders caused by HIV become more common as CD4 cell count fall and with higher plasma or CSF viral loads. A neurological assessment should find the characteristic clinical picture (as describe above).

The International Neurological Study (ACTG 5199 – see below) has assembled a battery of neurological tests thatmay help trained (and equipped) neurologists assess the functional parameters that are impaired in HIV-D (downloadable as pdf and powerpoint files from the NeuroAIDS conference site http://nerve.neurology.unc.edu/ana/archive.htm). However, in light of the Ethiopian study, which used some of the same performance tests, it is probably advisable for neurologists to establish norms for each indicator among the general population in their local setting.

Diagnosis also requires that viral, bacterial and fungal opportunistic infections of the CNS must be ruled out (this will be discussed in a future HATIP). Although it can be helpful to perform CSF and radiological evaluations (particularly to rule out OIs and neoplasms), the neuroimaging abnormalities typically observed with HIV-D are not always specific to the condition.

“Typically these individuals will have changes on CSF evaluation and on neuroimaging, but there are really no specific or diagnostic features on either of those two investigations that reliably tell you, this is HIV-associated dementia and nothing else. And perhaps this is why it’s such a complicated condition to diagnose,” said Dr Miller.

However, he noted that neuroimaging characteristically shows cerebral atrophy. “Some of the features that are associated with HIV dementia on MRI picture are a very enlarged ventricular system, which is a reflection of the brain cell atrophy that occurs, and very high signal intensities at the junction of the gray and white matter are very typical of changes that are seen in people who have this problem.”

Treatment of HIV dementia

The first and most obvious treatment for HIV-related CNS disease is ART — and improvements on treatment may be dramatic (Robertson 2004). This appears to correlate with viral activity in the CNS. For example, a recent autopsy study showed a significant drop in brain tissue viral load in patients treated with ART in the previous three months, and many other studies show sustained improvement in neuropsychological function after several months of ART in both adults and children (Hall 2006).

And recently, Dr Sacktor presented data at the NeuroAIDS conference showing clear improvement in cognitive performance after three months on ART in a study of 23 Ugandan patients (96% of whom had some neurological impairment at baseline). IHDS scores went up from a baseline of 8.0 to 10 at three months and to 12 after six months.

However, Dr Hall stressed that a few large studies now show that significant neurological deficits are still common in treated populations, with an overall current prevalence of 30%, a prevalence 37% in those with CD4 cell counts below 200, and with progressive deficits reported in some treated subjects (Sacktor 2002, McArthur 2003, Albert).

In the first study, an analysis of the Adult AIDS Clinical Trials Group (AACTG), A5001 (“AACTG Longitudinal Linked Randomized Trials (ALLRT) Protocol” which involved 1498 subjects all on ART, 43% were found to be neurologically impaired at baseline (this correlated with a nadir CD4 cell below 200).  More than half of these were unimpaired after 52 weeks on therapy, while 19% who were unimpaired at baseline became impaired (Median 93 weeks).

In another study, ACTG 362, of 643 subjects on ART who were followed prospectively for neurological problems. 57 participants had neurological impairment at baseline, 47% of these remained impaired at week 48, while 6% of the unimpaired developed neurological disorders over the course of the study.

According to Dr Hall, ART may not always stop CNS progression because most “antiretrovirals have poor penetrance across the blood-brain barrier.” Since the virus remains compartmentalized in the brain, there may be continuing replication in the CNS (in fact, virological failure in the CSF appears to be common) and could cause continuing neurological decline.

Several antiretrovirals, including the nucleoside analogues: AZT, d4T, 3TC and abacavir, and the non-nucleoside analogue reverse transcriptase inhibitors: efavirenz and nevirapine, have been suggested as having better CSF penetration, though it is not clear how this reflects on levels within the actual brain tissue — or even whether this is indeed necessary for clinical response.

“Many people have tried to link this to actual drug penetration into the brain or into central nervous system compartments and look at drug levels. But as yet, I think we can’t obviously say that any of that data is meaningful. There’s much we don’t know about the penetration of antiretrovirals through the blood-brain barrier and the blood CSF barrier and even though actual measurements of certain antiviral drugs looks low in CSF, one nevertheless sees a very good clinical outcome,” said Dr Miller.

Nevertheless, Dr Hall stressed that it is “probably reasonable to add these [CNS penetrant antiretrovirals] in neurologically impaired patients.”

The International Neurological Study

And of course, with the exception of Dr Sacktor’s small study, most of those data again come from developed countries. To address this in a wider number of resource-limited settings, the US National Institutes of Mental Health (NIMH) and NIAID AIDS Clinical Trials Group is conducting a multicentre international study, to explore the effects of antiretroviral therapy on cognitive functioning in resource-limited settings. ACTG 5199: The International Neurological Study (Robertson, Kumwenda, Supparatpinyo) will enroll a maximum of 880 subjects at 11 sites including Blantyre and Lilongwe, Malawi; Harare, Zimbabwe; Johannesburg and Durban, South Africa; Pune and Chennai, India; Rio de Janeiro and Porte Alegre, Brazil; Lima, Peru and Chiang Mai, Thailand. More information is available online at http://nerve.neurology.unc.edu/ana.

 

Other potential therapies for HIV dementia

Several other adjunctive medications have also been proposed for HIV-D and are being evaluated in clinical trials. For example, calcium channel blockers have been proposed. However, an American trial of one such drug, nimodipine, ACTG 162, was stopped in 1995 after no benefits were seen (Navia).

Dr Miller noted that most recently the old anti-convulsive valproic acid has been suggested as worth investigating due to its affect on dopamine transporters and changes in various transporter proteins involved with that neurotransmitter. However, valproic acid has also been shown to stimulate HIV replication from latently infected cells.

Finally, at the recent NeuroAIDS conference, a couple of presentations suggested a potential role for minocycline, an off-patent antibiotic, a derivative of tetracycline, which readily crosses the blood-brain barrier (Sacktor 2006, Zink). The drug is safe and well tolerated in trials with up to four years of follow-up, and has been on the market for 30 years, used for acne and rheumatoid arthritis. Data from the SIV macaque model suggest that it has an anti-inflammatory and neuro-protective affects, and may even directly inhibit viral replication in the brain (Zink 2005).

Dr Sacktor is primary investigator for a multicentre trial of minocycline for HIV-infected patients with neurological disease. Minocycline is also moving into clinical trials in Uganda.

Development of this particular adjunctive therapy (if it works) might be particularly useful in Africa, because in addition to being cheap, safe and off-patent, according to a presentation by Dr Christine Zink, it may also reduce peripheral neuropathies, and has activity against malaria and other common infections such as chlamydia.

References

Albert SM, NEAD Study Group et al. Medication management skill in HIV: I. Evidence for adaptation of medication management strategies in people with cognitive impairment. II. Evidence for a pervasive lay model of medication efficacy. AIDS Behav 7(3): 329-338, 2003.

Baldewicz TT et al. Changes in neuropsychological functioning with progression of HIV-1 infection: results of an 8-year longitudinal investigation. AIDS Behav 8: 345-355, 2004.

Becker JT et al. Prevalence of cognitive disorders differs as a function of age in HIV virus infection. AIDS 18: S11-S18, 2004.

Belec L et al. Low prevalence of neuropsychiatric clinical manifestations in central African patients with acquire immune deficiency syndrome. Trans R Soc Trop Med Hyg 83:844-846, 1989.

Birbeck G et al. A study of HIV-dementia among hospice patients in Lusaka, Zambia. Presented at Assessment of NeuroAIDS in Africa, Blantyre, Malawi, 2004.

Birbeck GL. Barriers to care for patients with neurologic disease in rural Zambia. Archives of Neurology;57(3):414-417, 2000

Birbeck GL, Munsat T. Neurological services in sub-Saharan Africa: a case study among Zambian primary healthcare workers. Journal of Neurological Sciences 200(1-2): 75-78, 2002.

Brana C et al. A soluble factor produced by macrophages mediates the neurotoxic effects of HIV-1 tat in vitro. AIDS 13(12):1443-1452, 1999.

Brew BJ and González-Scarano F. HIV-associated dementia. An inconvenient truth. Neurology 68:324-325, 2007.

Cherner M et al. Effects of HIV-1 infection and aging on neurobehavioral functioning: preliminary findings. AIDS 18: S27-S34, 2004.

Clifford DB, Evans S. Ethiopian NeuroAIDS assessment. Presented at Assessment of NeuroAIDS in Africa, Tanzania, 2006.

Dore GJ et al. Changes to AIDS dementia complex in the era of highly active antiretroviral therapy. AIDS 13(10):1249-1253, 1999.

Dore GJ et al. Impact of highly active antiretroviral therapy on individual AIDS-defining illness incidence and survival in Australia. Journal of Acquired Immune Deficiency Syndromes 29(4):388-395, 2002.

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Gonzalez E et al. HIV-1 infection and AIDS dementia are influenced by a mutant MCP-1 allele linked to increased monocyte infiltration of tissues and MCP-1 levels. Proc Natl Acad Sci U S A;99(21):13795-13800, 2002.

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Hall C. Human immunodeficiency virus infection: nervous system involvement. Presented at Assessment of NeuroAIDS in Africa, Blantyre, Malawi, 2004.

Howlett WP et al. Neurological disorders in AIDS and HIV disease in the northern zone of Tanzania. AIDS 3:289-296, 1989.

Ives NJ et al. The changing pattern of AIDS-defining illnesses with the introduction of highly active antiretroviral therapy (HAART) in a London clinic. Journal of Infectious Diseases 42(2):134-139, 2001.

Maj M et al. WHO neuropsychiatric AIDS study, cross-sectional phase II neuropsychological and neurological findings. Arch Gen Psyc 51(1):51-61, 1994.

Mayeya J et al. Zambia mental health country profile. International Review of Psychiatry  16(1–2), 63–72, 2004.

Mbewe E et al. Clinical and demographic features of treated first-episode psychotic disorders: a Zambian study. Schizophr Res. 86(1-3):202-7, 2006.

McArthur JC et al. Dementia in AIDS patients: incidence and risk factors. Multicenter AIDS cohort study. Neurology 43(11):2245-2252.

McArthur JC et al. Human immunodeficiency virus-associated dementia: an evolving disease. Journal of NeuroVirology, 2003.

Miller S. Neurological complications of HIV infection. Presented at the Botswana International HIV Conference, Gaborone, 2006.

Nakasujja N et al. Human immunodeficiency virus neurological complications: an overview of the Ugandan experience. J Neurovirol; 11 Suppl 3:26-9, 2005.

Nath A, Sacktor N. Influence of highly active antiretroviral therapy on persistence of HIV in the central nervous system. Curr Opin Neurol. 19(4):358-61, 2006.

Navia BA et al. A phase I/II trial of nimodipine for HIV-related neurologic complications. Neurology;51(1):221-8, 1998.

Olley BO et al. Persistence of psychiatric disorders in a cohort of HIV/AIDS patients in South Africa: a 6-month follow-up study. J Psychosom Res 61(4):479-84, 2006.

Olley BO et al. Post-traumatic stress disorder among recently diagnosed patients with HIV/AIDS in South Africa. AIDS Care;17(5):550-7, 2005.

Perriens JH et al. Neurological complications of HIV-1-seropositive internal medicine inpatients in Kinshasa, Zaire. JAIDS. 2:333-340, 1992.

Price RW. HIV-1 infection of the central nervous system (CNS) and the AIDS dementia complex (ADC): Introduction & some issues for Africa. Presented at Assessment of NeuroAIDS in Africa. Blantyre, Malawi, 2004.

Robertson K et al.  Assessment of neuroAIDS in Africa. J Neurovirol; 11 Suppl 1:7-16, 2005.

Robertson KR et al.   Highly active antiretroviral therapy improves neurocognitive functioning. JAIDS,   36(1):562-566, 2004.

Sacktor NC et al. The International HIV Dementia Scale. Neurology 60;1:A186-187, 2003.

Sacktor NC et al. The International HIV Dementia Scale: a new rapid screening test for HIV dementia. AIDS;19(13):1367-74, 2005.

Sacktor NC et al. Antiretroviral therapy improves cognitive impairment in HIV+ individuals in sub-Saharan Africa. Neurology 67(2):311-4, 2006.

Sacktor NC. The epidemiology of human immunodeficiency virus-associated neurological disease in the era of highly active antiretroviral therapy. Journal of NeuroVirology 8(2) Supplement 1, pgs 115 – 121, 2002.

Sacktor NC. Assessment of HIV dementia in Uganda. Results from the Academic Alliance Cohort. Presented at Assessment of NeuroAIDS in Africa, Tanzania, 2006.

Sacktor NC et al. HIV-associated cognitive impairment before and after the advent of combination therapy. Journal of Neurovirology 8(2):136-142, 2002.

Sacktor NC et al. HIV-associated neurologic disease incidence changes: Multicenter AIDS Cohort Study, 1990-1998. Neurology 56(2):257-260, 2001.

Sevigny JJ et al. An evaluation of neurocognitive status and markers of immune activation as predictors of time to death in advanced HIV infection. Arch Neurol. 64(1):97-102, 2007.

Shiu C et al. HIV-1 gp120 as well as alcohol affect blood-brain barrier permeability and stress fiber formation: involvement of reactive oxygen species. Alcohol Clin Exp Res.;31(1):130-7, 2007.


Stern Y et al. Factors associated with incident human immunodeficiency virus-dementia. Archives of Neurology 58(3):473-479, 2001.

Taore M et al. Neuro  AIDS  in  Mali:  Present and  future research activities. Presented at Assessment of NeuroAIDS in Africa, Tanzania, 2006.

Tozzi V et al. Neurocognitive impairment and survival in HIV-positive patients treated with HAART: results from an urban observational cohort. Eleventh Conference on Retroviruses and Opportunistic Infections, San Francisco, abstract 507, 2004.

Valcour VG et al. Cognitive impairment in older HIV-1-seropositive individuals: prevalence and potential mechanisms. AIDS 18: 379-386, 2004a.

Valcour V et al. Higher frequency of dementia in older HIV-1 individuals: the Hawaii Aging with HIV-1 Cohort. Neurology 63: 822-827, 2004b.

Wang GJ et al. Decreased brain dopaminergic transporters in HIV-associated dementia patients. Brain 127(11): 2452-8, 2004.

Wong MH et al. Frequency of and risk factors for HIV dementia in an HIV clinic in sub-Saharan Africa. Neurology 68:350-355, 2007.

Wilt SG et al. In vitro evidence for a dual role of tumor necrosis factor-alpha in human immunodeficiency virus type 1 Encephalopathy. Ann Neurol 37(3):381-394, 1995.

Zink MC et al. Neuroprotective and anti-human immunodeficiency virus activity of minocycline. JAMA ;293(16):2003-11, 2005.

Zink MC. Impact of minocycline on SIV CNS and PNS Disease. Presented at Assessment of NeuroAIDS in Africa, Tanzania, 2006.

Resources

The World Federation of Neurology:  http://www.wfneurology.org/

Also presentations from the Assessment of NeuroAIDS conference are available online at: http://nerve.neurology.unc.edu/ana/archive.htm].

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About HATIP

A regular electronic newsletter for health care workers and community-based organisations on HIV treatment in resource-limited settings.

Its publication is supported by the UK government's Department for International Development (DfID), the Diana, Princess of Wales Memorial Fund and the Stop TB Department of the World Health Organization.

Other supporters include Positive Action GlaxoSmithKline (founding sponsor); Abbott Fund; Abbott Molecular; Cavidi; Elton John AIDS Foundation; Merck & Co., Inc.; Pfizer Ltd; F Hoffmann La Roche; Schering Plough; and Tibotec, a division of Janssen Cilag.

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