The document discusses HIV infection and encephalitis. Some key points: - HIV is a retrovirus that causes AIDS and can affect the nervous system directly or indirectly through opportunistic infections. - Neurological features develop in 80% of infected individuals, manifesting as effects of HIV or infections/tumors due to immunodeficiency. - HIV encephalitis refers to cognitive impairment from cerebral HIV infection and does not include opportunistic infections from immunodeficiency. - Symptoms of HIV encephalitis include decreased cognition, psychomotor slowing, and motor symptoms like gait instability. Diagnosis involves neuropsychological testing and neuroimaging. Treatment includes antiretroviral therapy and

1. HIV INFECTION - ENCEPHALITIS
Mrs. M. Pradeepa MPT (Neuro)
Vice Principal
PPG College of Physiotherapy
Coimbatore, Tamilnadu, India

2. INTRODUCTION
• The human immunodeficiency virus (HIV) is an
enveloped retrovirus that contains 2 copies of a
single-stranded RNA genome. It causes the acquired
immunodeficiency syndrome (AIDS) that is the last
stage of HIV disease.
• AIDS was first clinically observed in 1981 in the
United States.
• Both HIV-1 and HIV-2 are believed to have
originated in non-human primates in West-central
Africa, and are believed to have transferred to
humans a process known as zoonosis in the early
20th century

3. HIV AND NERVOUS SYSTEM EFFECTS
• Direct Or Primary Effect
• HIV virus and its products
• Indirect or Secondary Effect
• Opportunistic infection
• HIV associated neoplasms

4. HIV AND CNS
• Neurological features develop in 80% of infected
individuals manifesting as either direct effects of
the HIV virus or infections, tumours and
associated vascular disorders due to
immunodeficiency.
• In a minority of patients, CNS HIV-1 infection
evolves into encephalitis during the late stages of
systemic infection, which compromises brain
function and presents clinically as acquired
immunodeficiency syndrome dementia complex
(ADC)

5. HIV AND CNS
• Potential site of involvement:
• Meninges
• Brain
• Spinal cord
• Cranial and spinal nerves
• ANS
• Muscle

6. HIV AND CNS CLINICAL SYNDROMES
• Dementia
• Infection – Encephalitis, cerebral abcess,
Meningitis
• Cerebral tumors
• Retinopathy
• Myelopathy
• Vascular disorders
• Peripheral neuropathies

7. DEFINITION
• HIV encephalitis refers to cognitive impairment
resulting from productive cerebral infection by
the human immunodeficiency virus
• It does not apply to opportunistic infections
resulting from generalized cell mediated
immunodeficiency

8. TERMINOLOGY
• Severe cognitive impairment related to HIV
encephalitis was also referred to as HIV
associated dementia (HAD) or the AIDS
dementia complex
• Currently, other terms used to describe this
illness include HIV associated neurocognitive
disorder (HAND) and HIV associated
neurocognitive impairment

9. EPIDEMIOLOGY
• Prevalence estimates for HIV associated
neurocognitive disorder range from 35 to 100%
• Upto 50% of HIV patients have clinically apparent
neurological disease.
• Upto 20% of HIV patients present for the first time
with neurological manifestations.
• Upto 90% of HIV patients have neuropathological
changes on autopsy.
• India has the second largest burden of HIV related
pathology next to sub-Saharan Africa.
• Neurological complications associated to HIV-1
infections, are very common in our clinical setting.

10. TYPES
• HIV neurocognitive impairment be divided into:
• Type I - corresponding to neurocognitive
disability resulting from active HIV encephalitis
• Type II - corresponding to mild cognitive
impairment, for which the neuropathological
substrate has not been established

11. SITES
• Although HIV encephalitis may occur anywhere
within the nervous system, there is a distinct
predilection for pathologic changes to be found
predominantly within subcortical white
matter and basal ganglia

12. PATHOPHYSIOLOGY
• HIV enters the CNS by a mechanism called “Trojan horse” that
consists of the migration of infected monocytes through the BBB.
• Infected monocytes then fuse with resident microglial cells,
perivascular macrophages and potentially adult neural precursors
• Viral replication is also seen in a restrictive manner in astrocytes
• This results in direct and indirect effects of HIV infection will lead to
neuronal dysfunction
• DE: Infected astrocytes and microglia release factors inducing
neurotoxicity such as cytokines, chemokine and reactive oxygen
species (ROS).
• IE: This may also contribute to the disruption of the BBB and result
in further entry/exit of virions and viral proteins
• In addition, HIV associated glycoproteins may interfere with
synaptic activity
• However, neurons are not productively infected by the virus

14. CLINICAL PRESENTATION
• Symptoms may develop over weeks to months
• Cognition:
• Decreased concentration
• Forgetfulness particularly daily or recent events
• Slowing of thought process
• Global dementia
• Psychomotor slowing: verbal response delayed, near
or absolute mutism, vacant stare
• Unwareness of illness or disinhibition
• Confusion, disorientation
• Organic psychosis

15. CLINICAL PRESENTATION
• Motor symptoms:
• Poor balance
• Gait instability – slow and rigid gait
• Slowness of movements
• Tremors
• Other involuntary movements – choreoathetoid
movements
• Myoclonic jerks
• Bladder and bowel incontinence

16. DIAGNOSIS
• Currently, the diagnosis is made through the neuropsychometric
performance testing, in combination with neuroimaging
• Laboratory
• Classical HIV disease biomarkers (low CD4 count, high viral load)
are no longer closely associated with neurological impairment
although markers of systemic inflammation appear to correlate with
cognitive impairment
• ELISA test, Saliva test, Viral load test, Western blot test (HIV tests)
• Radiology description
• Increased white matter signal on fluid level attenuated inversion
recovery (FLAIR) images although these are only apparent in the
more advanced stages of cognitive impairment
• Symmetric patchy periventricular regions

17. Neuroimaging of HIV – Associated
Neurocognitive Disorders

18. DIFFERENTIAL DIAGNOSIS
• Superimposed opportunistic infections or
neoplasms - the presence of subcortical
microglial nodule encephalitis with
multinucleated microglial cells is virtually
pathognomonic for HIV encephalitis

19. MANAGEMENT
• Although implementation of combined
antiretroviral therapy has reduced the
prevalence of severe neurocognitive impairment,
optimized HIV therapy is not sufficient to avert
cognitive impairment
• It is believed that in addition to combined
antiretroviral therapy, treatments that
will address inflammation and
cardiovascular risks may provide benefit

20. MANAGEMENT
• HAART (Highly active antiretroviral therapy)
management comprises two nucleoside reverse
transcriptase inhibitors (e.g. zidovudine and
didanosine) and a protease inhibitor (e.g.
ritonavir or indinavir), or a nonnucleoside
reverse transcriptase inhibitor (nevirapine).
• Opportunistic infection – treatment of specific
infection

21. THANK YOU