here I present CNS manifestation of HIV AIDS, Including opportunistic infections and aids defining malignancies.

1. CNS manifestation of HIV
AIDS
Presented by- Dr Bhagirath ram
Moderator- Dr Siddhi Ma’am
Department of Radiodiagnosis SPMC Bikaner

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

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)

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

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)

43. CMV

46. TB

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.

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.

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.

75. Thank you for your attention