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.

1. NEUROLOGICAL
MANIFESTATIONS OF
HIV INFECTION
AN UPDATE
Dr. Dibbendhu Khanra

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

8. MANAGING HAND
 CART
 CPE score
 MME score
 Thalidomite
 Memantine
 Nimodipine
 Selegiline
 Minocycline
 Lexipafant
 PDGF-BB

9. HIV AND CEREBRAL SOL
TOXO
PCNSL
TB
CRYPTO

10. PML V/S HIVE
PML
HIVE
MS

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