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CNS menifestation of HIV aids.pptx
1. CNS manifestation of HIV
AIDS
Presented by- Dr Bhagirath ram
Moderator- Dr Siddhi Ma’am
Department of Radiodiagnosis SPMC Bikaner
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3. HIV Encephalitis
• HIV infects astrocytes but does not directly infect neurons.
• The CNS-resident astroglia and microglia become activated,
proliferate, and change to have an inflammatory expression signature.
• These activated cells, along with monocyte-derived perivascular
macrophages, are the main contributors to neuroinflammation in HIV
infection.
• Neurons can be injured indirectly by viral proteins and neurotoxins.
4. • HIV encephalitis (HIVE) and HIV leukoencephalopathy (HIVL) are the
direct result of HIV infection of the brain.
• Opportunistic infections are absent early although coinfections or
multiple infections are common later in the disease course.
• HIV-associated neurocognitive disorders (HANDs) are the most
frequent neurologic manifestations of HIVE and HIVL.
• The term "acquired immunodeficiency dementia complex" refers
specifically to HIV-associated dementia
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18. Opportunistic infections
•1. Toxoplasmosis
• Overall MCC of mass lesion – TOXO
• Parasitic infection caused by ingestion – tachyzoites- goes in CNS becoming
bradyzoites.
• MC location – Basal ganglia, Thalamus, white matter
• Multifocal>Solitory
• Presentation- focal neurological findings (Mild hemiparesis)superimposed
on symptoms of Global encephalopathy (Headache, Confusion and
lethargy)
• Nodular ring enhancing masses on T1C+ (Eccentric Target sign)
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25. 2) Cryptococcosis
• Fungal Infection.
• <50-100 cells.
• 3 main form – 1)Meningitis / Meningoencephalitis- Headache, Seizures and
Blurred vision.
• 2) Cryptococcoma and 3) Gelatinous Pseudocysts
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30. PML
• Due to JC virus
• 2 Forms -1)cPML and 2)iPML
• Causing progressive Demyelinating Encephalopathy.
• 3 Phases- I)Primary-Clinically Inapparent Infection.
II) Latent Peripheral Infection- Kidney, BM, Lymphoid Tissue.
III) Reactivation and dissemination to blood –CNS
Causing Multifocal asymmetric Demyelination with a predilection for frontal and preoccipital white
matter.
Small lesions Coalesce into large confluent lesions in white matter.
Presentaion- altered mental status, Headache, lethargy, Motor Deficits, Aphasias, Gait difficulties.
MC affected site-Supratentorial Lobar white matter
2nd MC site- Post. Fossa white Matter (Middle Cerebellar Paducles)
51. CNS –IRIS /Neuro-Iris
• T-cell mediated encephalitis.
• Dysregulated Immune response and pathogen driven Disease.
• Unmasking IRIS- Unmasking undiagnosed Pathogen.
• Paradoxical IRIS- Against Ags.
• MCC- PML>TB>fungal.
• Highest risk – Low CD4 and Less Time interval in initiating Tx.
• <50 Cells
• PML IRIS- After HAART increased PML lesion.
• TB IRIS- Meningitis, Tuberculomas and Radiculopathies.
• Presentation- Clinical Deterioration of Newly treated HIV Positive Despite
Raising CD4 Counts and decreased Viral load.
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66. Neoplasms in HIV/AIDS
• Two Organisms causing –
EBV HHV-8
*HL *KS
*NHL *PEL
*MCC
ADMs (AIDS Defining Malignancies) – NHL,KS,Ca Cx.
• NHL – DLBCL
• MC Cerebral Mass Lesion in AIDS- TOXO>NHL.
67. PCNSL
• Solitary> Multiple
• MC 90% supratentorial.
• Prefrontal in BGs and Deep white Matter – Abutting Lateral Ventricle
• Crossing Carpus collosum.
• Central necrosis and Hemorrage.
DDX- Toxo – Multiple Eccentric target Sign( Eccentrically Located
Nodule with a ring enhancement Mass)
PET and Spect -Lymphoma – Hot But Toxo not.
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71. KS –HHV8
• MC sarcoma in immunosuppressed Pts
• 2nd MC – Leiomyosarcoma
• 3rd MC – Angiosarcoma and fibrohystiocytic lesions
KS – Mc Ca in untreated HIV pts.
- MC site is Skin>mucus Membrane >LN> Viscera
-Face> Genitals> mucous Membrene
Cranial KS- LC than PCSNL ( Localized Scalp thickening)
T1- Isointense with Muscle
T2- Hyperintense
T1 C+ and CECT- Enhance strongly.
1)Brain pathology in HIV/AIDS varies with patient age and disease acuity. In early stages, the brain appears grossly normal. Advanced HIVE results in generalized brain volume loss ("atrophy") with enlarged ventricles and subarachnoid spaces.
2) CT Findings. NECT scans may be normal in the early stages. Mild to moderate atrophy with patchy or confluent white matter hypodensity develops as the disease progresses (14- 2). HIVE does not enhance on CECT.
T2 /FLAIR – Widespread Pattern of confluent and Linear Hyperintensities.
In Acute Stage Punctate Perivascular Hyperintensities seen.
