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CNS menifestation of HIV aids.pptx

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CNS menifestation of HIV aids.pptx

  1. 1. CNS manifestation of HIV AIDS Presented by- Dr Bhagirath ram Moderator- Dr Siddhi Ma’am Department of Radiodiagnosis SPMC Bikaner
  2. 2. 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.
  3. 3. • 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
  4. 4. 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)
  5. 5. 2) Cryptococcosis • Fungal Infection. • <50-100 cells. • 3 main form – 1)Meningitis / Meningoencephalitis- Headache, Seizures and Blurred vision. • 2) Cryptococcoma and 3) Gelatinous Pseudocysts
  6. 6. 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)
  7. 7. CMV
  8. 8. TB
  9. 9. 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.
  10. 10. 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.
  11. 11. 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.
  12. 12. 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.
  13. 13. Thank you for your attention

Editor's Notes

  • 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.

  • Bizarre Looking Progressively enlarging enhancing Lesion.
  • Prevention – Start HAART when >350cells.

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