This document outlines HIV-associated dementia (HAD), formerly known as AIDS dementia complex. It discusses the epidemiology, pathophysiology, risk factors, clinical features, diagnostic criteria, differential diagnosis, prognosis, workup, and management of HAD. Key points include that HAD risk is 1 in 1000 for those with HIV, incidence was previously 7% but declined with HAART and has begun increasing again. Pathogenesis involves HIV entry into the CNS via infected monocytes, cellular protein secretion, and HIV proteins damaging neurons. Diagnosis requires cognitive deficits in 2 domains impairing daily living with motor or behavioral abnormalities. Prognosis is typically rapid decline without treatment but improved survival with HAART. Management primarily involves HAART

1. Edson Mutandwa
MBBS IV

2. Presentation outline
 Introduction
 Epidemiology
 Pathophysiology
 Risk factors
 Clinical features
 Diagnostic criteria
 Differential diagnosis
 Work-up
 prognosis
 management

3. Introduction
 HIV associated dementia is one of the HIV-associated
neurocognitive disorders
 The term AIDS dementia complex was introduced by
Navia and colleagues in 1986 to describe a unique
constellation of neurobehavioral finding.

4. Epidemiology
 The risk of severe neurocognitive disorders in patients
with HIV is 1 in 1000
 The annual incidence of HIV dementia in the Western
world prior to HAART was 7%, with a cumulative risk of
5-20%.With HAART, the incidence of HIV dementia
started declining, but it has begun to increase again

5. Pathophysiology
 The mechanism by which HIV infection of the CNS leads
to neurocognitive disorders is likely multifactorial and is
the subject of intense research
 It has been proposed that HIV enters the CNS via infected
monocytes that traverse the blood-brain barrier to
replenish perivascular macrophages (Trojan horse
mechanism)

6. Pathophysiology
 Cellular proteins-secretion of chemokines,
proinflammatory cytokines, nitrous oxide, and other
neurotoxic factor
 HIV proteins (virotoxins)-Damage to neurons may occur
through the actions of specific HIV proteins, including
gp120, gp41, Tat, Nef, Vpr, and Rev
 Autoimmune disease-CNS damage may occur by
humoral immune mechanisms, as evidenced by the
presence of anti-CNS antibodies in AIDS patients with
dementia but not in those without dementia

7. Risk factors
 low weight
 Anemia
 constitutional symptoms
 low CD4+ count
 high plasma HIV-RNA load
 Female gender
 Old age (>50)

8. Clinical features
 substantial memory deficits
 negative personality
 mood changes
 impaired executive functioning
 poor attention and concentration
 mental slowing
 apathy

9. Diagnostic criteria
No other etiology of dementia and must not have the
confounding effect of substance use or psychiatric illness.
Criteria for the diagnosis of HAD included cognitive
deficits in 2 or more cognitive domains that cause
impairment in activities of daily living (ADL) and an
abnormality in either motor or neurobehavioral function

10. Diagnostic criteria
The domains included
Cognition
Language
Attention
executive function
Memory
speed of information processing
perceptual and motor skills

11. Differential diagnosis
 Alzheimer Disease
 Frontal and Temporal Lobe Dementia
 HIV-1 Associated Opportunistic Infections:
Cytomegalovirus Encephalitis
 Multiple Sclerosis
 Multiple System Atrophy
 Neurosyphilis
 Parkinson Disease
 Parkinson-Plus Syndromes
 Pick Disease

12. Prognosis
 AIDS dementia complex (ADC) has a variable
progression.
 Without treatment, the disease typically has a rapid
progression over a few months, with a mean survival rate
of 3-6 months for patients with AIDS who have untreated
ADC.
 As a result of HAART, however, the survival rate
increased from 5 months in 1993-94 to 38.5 months in the
1996-2000 period. Cognitive improvement is observed in
patients with ADC after the initiation of HAART

13. Prognosis
Poorer prognosis has been associated with the following:
 Lower educational levels
 Older age
 Lower CD4+ counts and higher HIV RNA levels
 Decreased hemoglobin level
 Reduced platelet count
 Thrush
 Low body mass index
 More constitutional symptoms
 Hepatitis C virus co-infection

14. Work-up
 Lumber puncture with CSF analysis
 neuroimaging studies (MRI)
 Electroencephalography (EEG)
 syphilis serology testing
 thyroid studies
 electrolyte levels
 drug screen
 Vitamin B-12 and folic acid levels

15. management
 highly active antiretroviral therapy (HAART) is the
cornerstone of treatment for HIV-related cognitive
disorders (aggressive therapy)
 Family counselling- psychosocial and emotional burden
on family
 Family education- patient have problems with compliance
and adherence to their medication regimen are likely to be
less inhibited . (indulge in unprotected sex)

16. Management
 caution is required when patients with ADC are treated
with psychoactive drugs because of enhanced
susceptibility to sedative properties and possible
paradoxical reactions
 These drugs can up regulate the metabolism of HAART
drugs, thus reducing its bioavailability.
 Efavirenz should be avoided in psychiatric patients
because of CNS toxicity and sucidality

17. References
 Up-to date (www.uptodate.com)
 Medscape