This document discusses the neurological manifestations of HIV infection. It notes that neurological complications occur in over 40% of people living with HIV/AIDS. The complications can be directly due to HIV itself, such as HIV-associated neurocognitive disorders, or due to opportunistic infections like tuberculosis or toxoplasmosis. Assessment of HIV-associated neurocognitive disorders involves evaluating cognition, motor skills, and neuropsychological performance. Management involves antiretroviral therapy and other treatments to reduce neurological impairment.
2. HIV ENTRY – TROJAN HORSE THEORY
Presenting feature of HIV/
AIDS in 10-20%
Neurologic complications
are present in more than
40% of PLHA
Autopsy - prevalence of
neuro-pathologic
abnormalities in 80%
3. NEUROLOGICAL COMPLICATIONS OF
HIV/AIDS
HIV itself
• HAND
• HIV neuropathy
• Aseptic meningitis
• HIV myelopathy
• HIV myopathy
OI
• TB
• Toxoplasma
• Cryptococcus
• PML
• CMV
Lymphoma
ART related
4. CHANGING PARADIGM
1981-1994 – OI, ADC
1995-2006 - HAART,
Decline of CNS
complications
2007-2012 - DSPN, HAND,
CHAIN
‘’The most severe HAND diagnosis (HAD) was rare, but milder forms
of impairment remained common, even among those receiving
CART’’ - CHARTER’ 2010
‘’The association of sustained impairment with worse current
immune status (low CD4 cell count) suggests that restoring immuno-
competence increases the likelihood of neuro-cognitive recovery.’’ -
ALLRT ‘2007
5. ASSESSMENT OF HAND
Cognition
• Modified HIV Dementia Scale
Memory registration
Motor speed
Memory recall
construction
Motor
• Timed Gait
• Paper based tapping test
Neuropsychology
• Trails Making Test A & B
• Figural Visual Scanning Task
• Digit-Symbol Task (WAIS-R)
6. Spectrum of Cognitive Impairment
HAND impairment >=2 of everyday
domains function Stages of ADC
1.Language 1.Mental
2.Attention acuity
3.Execution 2.Efficiency
4.Memory in work
5.Motor skill 3.Social
6.Information functioning
processing
ANI >=1 SD below no/mild
expected
MND >=1 SD below moderate
expected
ADC >=2 SD below severe
expected
7. PATHOGENESIS AND CO-FACTORS
Low NAA in frontal cortex
Fronto-striatal pathway High level of Glx in basal CSF viral load
injury ganglia
CD4
WM abnormality with Activated Kynurenine
increased volume of gray pathway
matter Metabolic causes
QUIN correlated with
Atorphy of posterior greater cell loss in Elevated BMI
cerebellar vermis. Neuronal striatum and limbic Poor nutrition
loss of granular/ perkinje cortex
cell layer of cerebellum. Increased QUIN in CSF
Depression
Decreased thickness of and correlation with
corpus callosum. HAND svereity Cocaine abuse
Expansion of ventricular QUIN elevates CCR5 Co-infection
size expression and viral (HCV, VZV)
replication
11. STROKE IN HIV
EPIDEMIOLOGY ETIOLOGY
Prevalence: 6 - 34%
– 9.1 for infarction Meningitis- 28%
– 12.7 for ICH Vasculitis – 20%
Young patients: 33.4 Vasculopathy – 20%
yrs v/s 64.0 yrs in HIV
Coagulopathy - 19%
negative
Cardioembolic -14%
42% of HIV+ stroke
were first HIV dx
12. HIV MYELOPATHY
In 55% patients dying of
AIDS
In advanced immuno-
suppression
Cervical> thoracic
Sensory-motor deficits
Brisk DTRs
Associated Vit B12
deficiency
Lipid-laden macrophages
Others: HTLV,VZV,CMV,
spinal Lymphoma
13. HIV PERIPHERAL NEUROPATHY
Distal sensory
polyneuropathy(DSPN)
MC neuropathy in HIV/AIDS
33% patients of HIV/AIDS
Present in 88% in autopsy
With low CD4 count
Stocking-glove sensory loss
Mononeuritis multiplex
Inflammatory demyeliting
polyradiculopathy
14. HIV myopathy ART induced
Peripheral neuropathy
Polymyositis CVA
Nemaline (rod body) Psychiatric
myopathy manifestations
Vacuolar myopathy Myopathy
IBM IRIS