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CNS infections

Imaging evaluation of spectrum of infective pathologies of CNS including encephalitis,meningitis,abscesses,congenital pathologies and hiv associated conditions etc.

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CNS infections

  1. 1. CNS INFECTIONS BY - DR. SAHIL CHAUDHRY MODERATOR - DR.PRAVEEN JOHN AJIMS MANGALORE
  2. 2. CLASSIFICATION • Congenital/Neonatal Infections of the Brain – Cytomegalovirus – HIV Infection – Herpes Simplex – Toxoplasmosis – Rubella • Meningitis • Pyogenic Parenchymal Infections – Cerebritis & Abscess • Encephalitis – Herpes Simplex Encephalitis – Japanese Encephalitis – HIV Encephalitis • Tuberculosis • Fungal Infections • Parasitic Infections – Neurocysticercosis
  3. 3. Congenital CNS Infections • Congenital infections are typically caused by the so- called TORCH agents: – TOxoplasmosis – Rubella – Cytomegalovirus – Herpes Simplex Virus • Other important agents are Human Immunodeficiency Virus & Syphilis • These infections have severe effects on the developing brain and can result in Developmental Brain Anomalies
  4. 4. Cytomegalovirus Infection • Congenital infection caused by transplacental transmission of human herpes virus • Best diagnostic clue – Microcephaly (Prior to 18 wks ) – Cerebral calcification (40-70%) • Periventricular (sub ependymal) – Cortical gyral abnormalities like Agyria ~ pachygyria ~ diffuse polymicrogyria ~ focal cortical dysplasia (18-24 wks ) – Cerebellar hypoplasia – Myelin delay or destruction (Third trimester ) • Location: – Dystrophic periventricular Ca++ has predilection for germinal matrix zones • Gestational age at time of infection determines pattern of CNS injury
  5. 5. Cytomegalovirus Infection - NECT • 4-month-old patient with congenital CMV infection show multiple foci of dystrophic intraparenchymal calcifications, especially in the periventricular distribution. • Cortical abnormalities are also seen in the right frontal cortex (arrows). • Ventricular dilatation and WM volume loss.
  6. 6. Cytomegalovirus Infection - NSG Findings • Periventricular echogenicity and focal calcification • Ring-like regions of periventricular lucency may precede Ca++ • Periventricular pseudocysts and ventricular adhesions • Cerebellar hypoplasia
  7. 7. Cytomegalovirus Infection - MRI • TIWI – Periventricular subependymal foci of Tl shortening due to Ca ++ – Ventricular dilatation and periventricular WM volume loss – Cerebellar hypoplasia • T2WI – Cortical gyral abnormalities - Ranging from agyria to focal cortical dysplasia – Myelination delay or destruction – Periventricular pseudocysts – Focal WM lesions with increased T2 (gliosis) predominately in parietal deep WM – Late T2 signal changes affect white matter between juxta-cortical and periventricular layers
  8. 8. • FLAIR: – Focal,patchy, or confluent regions of increased signal due to gliosis • T2* GRE: – Periventricular decreased signal due to Ca++ • MRS: – Decreased NAA/Cr ratio due to loss of neuronal elements, Increased myoinositol (gliosis)
  9. 9. Cytomegalovirus Infection
  10. 10. Congenital HIV Infection • Best diagnostic clue: Basal ganglia Ca++, volume loss • NECT – Atrophy (57-86%), frontal> BG > diffuse – BG Ca++ (30-85%) > frontal white matter (WM) > cerebellum • CECT: – May show faint enhancement of BG prior to appearance of Ca++
  11. 11. Congenital HIV Infection - MRI • T1WI: – Atrophy • T2WI: – High signal in frontal subcortical WM if progressive encephalopathy • T2* GRE: – May accentuate Ca++ • T1 C+: – Faint BG enhancement initially • MRA: – Fusiform vasculopathy (late) • MRS: – Decreased NAA, Increased Cho/Cr, presence of amino acids
  12. 12. Congenital HIV Infection - MRI • Axial (FLAIR) imaging (A, B) in a 4-year-old child infected with in utero HIV shows marked brain parenchymal volume loss with ill- defined areas of FLAIR hyperintensities in the white matter of bilateral cerebral hemispheres (arrows).
  13. 13. Coronal oblique catheter angiogram shows fusiform dilation of the ICA, proximal MCA consistent with HIV vasculopathy Axial NECT shows bilateral and symmetrical calcificadons in the basal ganglia, mostly in the globi pallidi
  14. 14. Congenital HIV Infection – D/D • Cytomegalovirus – Periventricular Ca++ • Microcephaly – Neuronal migration anomalies, cortical dysplasias – Congenital toxoplasmosis – Scattered Ca++ – Hydrocephalus
  15. 15. Congenital Herpes Simplex Virus Infection • Best diagnostic clue: Ca++ in GM, hypodensities in WM, cysts, cortical enhancement • NECT – Severe atrophy – Ca++ in basal ganglia (BG), thalami, cortex, subcortical WM • Occasional bleeds - same locations – Hydrocephalus, cysts • CECT: – Enhancement of cortex
  16. 16. • T1WI – Atrophy, low signal in WM, cysts, hydrocephalus, bleeds – Dysplastic cortex • T2WI – High signal in WM - cyst formation – Cerebellar high signal in 50% of patients • Tl C+ – Patchy enhancement - in cortex – Meningeal enhancement • MRS – May show increased Cho during acute period, Decreased NAA – Chronic stage - all metabolites low
  17. 17. • Neonatal HSV 2. (A, B) – Axial CT head images in a newborn with seizures show multifocal areas of hypoattenuation in the cerebral hemispheres, especially in left frontal and bilateral parietal lobes. • (C) Axial T2-weighted and (D) diffusion-weighted images show – Multifocal areas of T2 hyperintensity and restricted diffusion in both cerebral hemispheres and involving both the cortex and underlying white matter. • This patient had HSV 2 virus on cerebrospinal fluid examination.
  18. 18. Congenital Toxoplasmosis • Caused by Toxoplasma gondii, an intracellular parasite that infects birds and mammals. • Human infection occurs through consumption of undercooked, infected meat or by ingestion of infectious oocysts. • Parasites are disseminated hematogenously to the placenta and the fetus. • Tansmission rate from the mother to the fetus increases with each trimester, the severity of infection decreases with each trimester. • Within the cranium there is diffuse inflammation of the meninges, with varying sized granulomatous lesions.
  19. 19. • Inflammation of the ependyma (ependymitis) causes obstruction of the cerebral aqueduct leading to hydrocephalus. • Unlike CMV infection, there is no malformation of cortical development seen with toxoplasmosis • Clinically significant abnormalities occur when the fetus is infected before 26 weeks of gestational age.
  20. 20. Congenital Toxoplasmosis • Multiple discrete intraparenchymal and periventricular calcifications. • Calcifications are seen in the basal nuclei, periventricular regions, or cerebral parenchyma.
  21. 21. Congenital Toxoplasmosis • 11-week-old patient with congenital toxoplasmosis show massive hydrocephalus caused by aqueductal stenosis. • There are calcifications in bilateral basal nuclei (arrows) and calcification of the ependyma (arrowhead). • In infants with severe infection, there is marked destruction with hydrocephalus, porencephaly, and extensive basal ganglia calcifications. • In cases with mild infection (typically after the 30th week of gestation) there is mild ventricular enlargement and few intracranial calcifications.
  22. 22. Congenital Rubella • Axial T2-weighted MR imaging (A, B) in a 2-year-old patient with congenital rubella infection shows multifocal areas of T2 hyperintensities in the white matter of bilateral cerebral hemispheres (arrows) with delayed brain myelination patterns are also seen • On imaging, there can be intracranial calcification in basal ganglia, periventricular region & cortex.
  23. 23. MENINGITIS
  24. 24. Meningitis • Inflammatory infiltration of the pia mater, arachnoid, and CSF • Commonly related to hematogenous dissemination from a distant infection • Can be divided into acute pyogenic (bacterial), lymphocytic (viral), & Chronic (TB) Meningitis. • Best diagnostic clue: – Positive CSF by lumbar puncture Morphology – Smooth, intense leptomeningeal enhancement typical – TB, fungal meningitis are often basilar and confluent; may be nodular • • Imaging may be normal early.
  25. 25. Meningitis • NECT – Normal study is most common – Mild ventricular enlargement – Subarachnoid space enlargement – Basal cisterns effaced • CECT – Enhancing exudate in sulci, cisterns may be seen – Low density areas related to perfusion alterations • CTA: Arterial narrowing, occlusion
  26. 26. Meningitis • Tl WI: – Exudate is isointense • T2WI: – Exudate is hyperintense • FLAIR: – Hyperintense signal in sulci, cisterns • Tl C+: – Exudate typically enhances • MRA: – Arterial narrowing, occlusion
  27. 27. A, Gyriform hyperintensities are seen bilaterally and along the interhemispheric fissure on this T2-weighted image. B, Gadolinium-enhanced MRI study shows enhancement along the cerebral sulci bilaterally.
  28. 28. Meningitis • (A) Axial FLAIR image through the brain shows increased signal along the left parietal cerebral sulci (arrowheads) in a patient with meningoencephalitis. • (B) Corresponding axial T1WI shows localized pial enhancement along the parietal sulci and overlying meninges (arrowheads).
  29. 29. Pachymeningitis in a patient with bacterial meningitis , T1+C shows also subdural empyemas on the left side
  30. 30. Subdural empyema with strand in a patient with bacterial meningitis , CT+C shows a bilateral subdural effusion with cortical surface enhancement (empyema) , note that the attenuation of the effusion is higher than that of the cerebrospinal fluid
  31. 31. Pyogenic Parenchymal Infections
  32. 32. Cerebral Abscess • Focal pyogenic infection of the brain parenchyma, typically bacterial; fungal or parasitic less common • Four pathologic stages: • Early cerebritis, • late cerebritis, • early capsule, • late capsule
  33. 33. • Best diagnostic clue – Imaging varies with stage of abscess development – Early capsule: Well-defined, thin-walled with enhancing rim – Ring-enhancing lesion with High signal (restricted diffusion) can be seen on DWI, low ADC – T2 hypointense abscess rim with surrounding edema • Location – Typically supratentorial, but may occur infratentorial (up to 14%) – Frontal and parietal lobes most common, gray-white junction (hematogenous)
  34. 34. Cerebral Abscess - CT • NECT – Early cerebritis: Ill-defined hypodense subcortical lesion with mass effect; may be normal early – Late cerebritis: Central low density area; peripheral edema, increase in mass effect – Early capsule: Hypodense mass with moderate vasogenic edema and mass effect – Late capsule: Edema, and mass effect may diminish
  35. 35. • CECT – Early cerebritis: +/- Mild patchy enhancement – Late cerebritis: Irregular peripheral rim enhancement – Early capsule: Low density center with thin, distinct enhancing capsule • Deep part of capsule is thinnest; thickest near cortex – Late capsule: Cavity shrinkage, thickened capsule • May be multiloculated and have "daughter“ abscesses
  36. 36. Cerebral Abscess - MRI • T1WI – Early cerebritis: Poorly marginated, mixed hypointense/isointense mass – Late cerebritis: Hypointense center, isointense/mildly hyperintense rim – Early capsule: Shows Rim which is isointense to hyperintense to WM; center hyperintense to CSF – Late capsule: Cavity shrinks, capsule thickens • T2WI – Early cerebritis: Ill-defined hyperintense mass – Late cerebritis: Hyperintense center, hypointense rim; hyperintense edema – Early capsule: Hypointense rim • Related to collagen, hemorrhage, or paramagnetic free radicals – Late capsule: Edema and diminution of mass effect
  37. 37. • DWI – Increased signal intensity in cerebritis and abscess – ADC map: Markedly decreased signal centrally within abscess • Tl C+ – Early cerebritis: Patchy enhancement – Late cerebritis: Intense but irregular rim enhancement – Early capsule: Well-defined, thin-walled enhancing rim – Late capsule: Cavity collapses, thickened enhancement of capsule • Capsule is thinnest on the ventricular side
  38. 38. MRS: Central necrotic area may show presence of acetate, lactate, alanine, succinate, pyruvate, and amino acids Resolving abscess: Hyperintense on T2WI, FLAIR; hypointense rim when it resolves Small ring/punctate enhancing focus may persist for months
  39. 39. Cerebral Abscess • Progression from cerebritis to abscess. (A, B) Axial diffusion-weighted sequence and T1 postcontrast image demonstrate areas of restricted diffusion in the left temporal lobe and the posterior right cerebral hemisphere that demonstrate some poorly defined enhancement. • (C) Follow-up axial T1 postcontrast sequence 7 days later demonstrates progression to rim enhancement typical of abscess formation.
  40. 40. Cerebral Abscess
  41. 41. ENCEPHALITIS
  42. 42. Herpes Simplex Encephalitis (HSE) • Typically reactivation in immunocompetent patients • Best diagnostic clue – Abnormal signal and enhancement of medial temporal and inferior frontal lobes – Involvement of cingulate gyrus and contralateral temporal lobe highly suggestive • Atypical patterns seen in infants, children – May affect cerebral hemispheres primarily
  43. 43. Herpes Simplex Encephalitis (HSE) • NECT – CT often normal early – Low attenuation, mild mass effect in medial temporal lobes, insula – Hemorrhage is typically a late feature – Predilection for limbic system – Basal ganglia is spared – Earliest CT findings is usually at 3 days after symptom onset • CECT: – Patchy or gyriform enhancement of temporal lobes, a late feature
  44. 44. Herpes Simplex Encephalitis (HSE) • TlWI – Decreased signal in gray and white matter due to loss of gray-white junction, mass effect – May see subacute hemorrhage as increased signal within edematous brain – Atrophy and encephalomalacia, in chronic cases • T2WI, PD/Intermediate & FLAIR : – Increased signal in gray, subcortical white matter – Typically bilateral, but asymmetric • T2* GRE: – If hemorrhagic, hypointensity "blooms“ within edematous brain
  45. 45. • DWI: – May be hyperintense (restricted diffusion) • Tl C+ – May see mild, patchy enhancement early – Gyriform enhancement usually seen 1 week after initial symptoms – Meningeal enhancement is occasionally seen – Enhancement is seen in temporal lobes, insular cortex, subfrontal area and cingulate gyrus • MR findings may be seen within 2 days of symptoms
  46. 46. Herpes Simplex Encephalitis (HSE)
  47. 47. DDX- ACUTE INFARCT,GIOLAMATOSIS CEREBRI,HHV 6 ,LIMBIC ENCEPHALITIS
  48. 48. • VZV-MENINGITS WITH CEREBELLITIS • EBV-BG THALAMI BRAIN STEM SPLENIUM • WEST NILE VIRUS-SIMILAR TO EBV • SSPE-ATROPHY WITH INV. CORTEX ,SCWM,BG •
  49. 49. Japanese Encephalitis • Japanese encephalitis (JE) is a flaviviral encephalitis that is a major health problem in Asia, where it is a leading cause of viral encephalitis with 30,000 to 50,000 cases reported annually. • Case fatality rates are reported as up to 60%. • Lesions are typically T2 hyperintense and T1 hypointense on MR imaging, and are seen involving the thalami and brainstem, in particular the substantia nigra, basal ganglia, cerebral cortex, corpus striatum, and cerebellum. • The most consistent finding in JE is bilateral thalamic lesions with or without hemorrhagic changes on MR imaging.
  50. 50. Japanese Encephalitis • (A, B) T2-weighted image demonstrates abnormal signal involving the midbrain (A) and bilateral thalami (B).
  51. 51. ENCEPHALITIS LETHARGICA
  52. 52. BICKERSTAFF ENCEPHALITIS VZV CMV
  53. 53. RASMUSSEN ENCEPHALITIS
  54. 54. Tuberculosis • Typically causes tuberculous meningitis (TBM) and/or localized CNS infection, tuberculoma • Best diagnostic clue – Basilar meningitis + extracerebral TB (pulmonary) – Meningitis + parenchymal lesions is highly suggestive • Location – TBM: Basal meningitis – Tuberculomas: Typically parenchymal, supratentorial (often parietal lobes) • Infratentoriallesions are less common, can involve brainstem (up to 8%) • Dural tuberculomas may occur
  55. 55. Tuberculosis - CT • NECT – TBM: May be normal early (10-15%) • Isodense to hyperdense exudate effaces CSF spaces, fills basal cisterns, sulci – Tuberculoma • Hypodense to hyperdense round or lobulated nodule/mass with moderate to marked edema • Ca++ uncommon (approximately 20%) • CECT – TBM: Intense basilar meningeal enhancement – Tuberculoma: Solid or ring-enhancing • "Target sign": Central Ca++ or enhancement surrounded by enhancing rim (not pathognomonic for TB)
  56. 56. Tuberculosis - MRI • T1WI – TBM: Exudate isointense or hyperintense to CSF – Tuberculoma • Noncaseating granuloma: Appear Hypointense to brain • Caseating granuloma with solid center: Appear Hypointense or isointense to brain • Caseating granuloma with necrotic center: Appear Hypointense or isointense to brain with central hypointensity • Caseating granulomas may have hyperintense rim (paramagnetic material)
  57. 57. • T2WI – TBM: Exudate appears isointense or hyperintense to CSF; may see low signal nodules (rare) – Tuberculoma • Noncaseating granuloma: Hyperintense to brain • Caseating granuloma with solid center: Iso- to hypointense with hypointense rim (hypointensity due to free radicals, solid caseation or increased cellular density) • Caseating granuloma with necrotic center: Has Central hyperintensity with hypointense rim • Hypointense rim + surrounding edema common
  58. 58. • TI C+ – TBM: Marked meningeal enhancement, basilar prominence; may be nodular • Punctate/linear basal ganglia enhancement = vasculitis – Tuberculomas • Noncaseating granuloma: Nodular, with homogeneous enhancement • Caseating granuloma with solid center: Have Peripheral rim enhancement • Caseating granuloma with necrotic center: Peripheral rim-enhancement, central low signal
  59. 59. Tuberculosis - MRI • FLAIR – TBM: Increased intensity in basal cisterns, sulci related to proteinaceous exudate – Tuberculoma: Similar to T2 characteristics • DWI – May show hyperintense center of tuberculoma • MRS – TB abscess has prominent lipid, lactate but no amino acid resonances
  60. 60. CT+C in a patient with tuberculous meningitis demonstrating marked enhancement in the basal cistern and meninges with dilatation of the ventricles
  61. 61. CT+C of a child with tuberculous meningitis demonstrating acute hydrocephalus and meningeal enhancement
  62. 62. CT+C reveals avid enhancement in the basilar cisterns
  63. 63. T1+C shows basal exudates and hydrocephalous
  64. 64. TB meningitis with tuberculoma
  65. 65. Extensive infarcts of the right basal ganglia and internal capsule after the appearance of vasculitis in the thalamoperforating arteries in a child treated for tuberculous meningitis
  66. 66. T2 of a biopsy-proven right parietal tuberculoma , note the low signal intensity rim of the lesion and the surrounding hyperintense vasogenic edema
  67. 67. T1+C in a child with a tuberculous abscess in the left parietal region , note the enhancing thick-walled abscess
  68. 68. Multiple enhancing tuberculomas in both cerebellar hemispheres
  69. 69. Multiple ring enhancing tuberculomas
  70. 70. Fungal Diseases • Blastomycosis: Rare, sporadic, caused by B dermatitidis, generally affecting lungs/skin • Coccidioidomycosis: Sporadic, relatively common, caused by C Immitis, generally affecting lungs • Histoplasmosis: Common, due to inhalation of H Capsulatum (found in animal/bird feces) • Candidiasis: Relatively common, opportunistic affects immunosuppressed patients • Best diagnostic clue: – Meningeal enhancement, multiple enhancing non-specific appearing lesions in brain and/or spinal cord in immunosuppressed patient • Location: – Meninges, brain, spinal cord, vertebral bodies + discs
  71. 71. Fungal Diseases - CT • NECT – Areas of low density ~ lacunar infarctions (infarcts may be larger) – Diffuse brain edema, herniations, Hemorrhages – Hydrocephalus – Vertebral body destruction • CECT – Multiple foci of non-specific enhancement – Some are ring-like
  72. 72. Fungal Diseases - MRI • T1WI: – Ill-defined areas of decreased signal intensity • T2WI , PD/Intermediate & FLAIR: – Focal or diffuse areas of increased signal – Spine: Increased Signal in vertebrae, disc and spinal cord • T2* GRE: – May accentuate Ca++ or presence of blood products • DWI: – Slightly bright on trace images but no restricted diffusion on ADC map
  73. 73. Fungal Diseases - MRI • Tl C+ – Meningeal enhancement • Thick meningeal enhancement  thick acute exudates or meningeal fibrosis – Areas of non-specific appearing enhancement, may be ring-like, solitary-to-miliary • May be seen in spinal cord – Enhancement of disc, vertebrae and epidural space  discitis/osteomyelitis • MRA: – Vessel irregularities (vasculitis), occlusions, mycotic aneurysms • MRS: – Mildly increased Cho, decreased NAA, increased lactate
  74. 74. Fungal Diseases
  75. 75. BLACK TURBINATE SIGN – ASPERGILLOSIS ,RHINOCEREBRAL MUCORMYCOSIS
  76. 76. Neurocysticercosis • Intracranial parasitic infection caused by the pork tapeworm, Taenia solium • Four pathologic stages: Vesicular, colloidal vesicular, granular nodular, nodular calcified • Best diagnostic clue: – Cyst with "dot" inside • Location – Convexity subarachnoid spaces most common – May involve cisterns> parenchyma> ventricles – Parenchymal cysts often hemispheric, at gray-white junction – Intraventricular cysts are often isolated • Fourth ventricle is most common – Basal cistern cysts may be racemose (grape-like) – Rare CNS locations: Sella, orbit, spinal cord
  77. 77. Neurocysticercosis - CT • NECT – Vesicular stage (viable larva): Smooth, thin-walled cyst, isodense to CSF, no edema • Hyperdense "dot" within cyst = proto scolex – Colloidal vesicular stage (degenerating larva): Hyperdense cyst fluid with surrounding edema – Granular nodular (healing) stage: Mild edema – Nodular calcified (healed) stage: Small, Ca++ nodule
  78. 78. • CECT – Vesicular stage: No (or mild) wall enhancement – Colloidal vesicular stage: Thicker ring-enhancing fibrous capsule – Granular nodular stage: Involuting enhancing nodule – Nodular calcified stage: Shrunken, calcified nodule – Subarachnoid lesions: Multiple isodense cysts without scolex
  79. 79. Neurocysticercosis - MRI • T1WI & T2WI – Vesicular stage: Cystic lesion isointense to CSF • May see discrete, eccentric scolex • No surrounding edema – Colloidal vesicular stage: Cyst is mild to moderate hyperintense to CSF • Surrounding edema, mild to marked – Granular nodular stage: Thickened, retracted cyst wall; edema decreases – Nodular calcified stage: Shrunken, Ca++ lesion
  80. 80. • FLAIR – Vesicular stage: Cystic lesion isointense to CSF • May see discrete, eccentric scolex (hyperintense to CSF); no edema – Colloidal vesicular stage: Cyst is hyperintense to CSF • Surrounding edema, mild to marked – Useful to detect intraventricular cysts (hyperintense) • T2* GRE: Useful to demonstrate calcified scolex • DWI: Cystic lesion typically isointense to CSF
  81. 81. Neurocysticercosis - MRI • TI C+ – Vesicular stage: No enhancement typical, may see mild enhancement • May see discrete, eccentric scolex enhancement – Colloidal vesicular stage: Thick cyst wall enhances • Enhancing marginal nodule (scolex) – Granular nodular stage: Thickened, retracted cyst wall; may have nodular or ring-enhancement – Nodular calcified stage: Small calcified lesion, rare minimal enhancement
  82. 82. • In children, may see "encephalitic cysticercosis" with multiple small enhancing lesions and diffuse edema • Intraventricular cysts may cause ventriculitis and/or hydrocephalus • Cisternal NCC may appear racemose (multilobulated, grape-like), typically lacks scolex
  83. 83. Neurocysticercosis • Two large left frontal lobe cysticerci lack identifiable scolices and demonstrate adjacent edema representing colloidal vesicular stage. Multiple smaller cysticerci with internal scolices and lack of associated edema are in the vesicular stage. Scolices can be best seen in these cysticerci on postcontrast images (C and D).
  84. 84. CT without contrast CT+C
  85. 85. CT without contrast shows calcifications
  86. 86. RACEMOSE NCC
  87. 87. Intraventricular NCC resulting in acute hydronephrosis
  88. 88. GIANT NCC WITH TRAPPED VENTRICLE
  89. 89. Lyme Disease -Caused by the spirochete Borrelia burgdorfrei -Can cause white matter disease with a nonspecific imaging appearance of T2 prolongation predominantly in the subcortical white matter -Associated enhancement of multiple cranial nerves or meningeal enhancement may suggest the diagnosis
  90. 90. Sagittal (A and B) and axial (C) FLAIR show arcuate and confluent subcortical white matter involvement and callososeptal interface involvement remarkably similar to that in MS but without involvement of the periventricular white matter
  91. 91. Facial neuritis , a 48 year old woman with headache and peripheral right facial palsy , prominent enhancement of seventh cranial nerve on postinfusion axial T1 (A) and coronal spoiled gradient-recalled sequences (B)
  92. 92. T1+C (A and B) with enhancing bilateral third and fifth cranial nerves , seventh cranial nerve
  93. 93. HYATID T1 T2
  94. 94. LISTERIA RHOMBENCE -PHALITIS
  95. 95. CEREBRAL SHISTOSOMIASIS PSEUDOTUMOUR WITH ARBORISING PATTERN
  96. 96. Approach To Ring Enhancing Parenchymal Lesions
  97. 97. • Abscess : – Typically T2 hypointense rim and DWI + – Multiple lesions may occur related to septic emboli • Tuberculosis: – Tuberculomas often occur with meningitis – Typically not cystic • Neoplasm – Primary or metastatic (primary often known) – Thick, irregular margin enhancement typical – May have cyst and mural nodule (I.e., pilocytic astrocytoma, hemangioblastoma)
  98. 98. Arachnoid cyst Solitary lesion with CSF density/intensity No enhancement Amebic encephalitis: T1WI: Centrally hypointense mass T2WI: Hyperintense lesions, +/- hemorrhage May have hypointense rim Tl C+: Heterogeneous or ring-enhancement
  99. 99. METS/EM BOLI
  100. 100. ABSCESS
  101. 101. PILO
  102. 102. MS/TD
  103. 103. GBM
  104. 104. Mets
  105. 105. Demyelination
  106. 106. Radionecrosis
  107. 107. Enhancing subacute hemorrhagic stroke
  108. 108. CNS IMAGING IN AIDS
  109. 109. CNS disease in HIV / AIDS
  110. 110. • Up to 90% of those infected by the HIV will have CNS involvement • CNS infection by HIV may occur concurrently or shortly after acute systemic HIV infection • During this acute stage, structural neuroimaging studies are usually normal even if the infected individual has clinical signs of CNS involvement
  111. 111. • HIV infection of the CNS produces a progressive cognitive-motor disorder often called the AIDS Dementia Complex (ADC). • As the HIV-induced brain injuries progress, cortical atrophy and WM disease due to HIV oligodendroglial damage occurs - HIV leukoencephalopathy. MR and/or CT detect these changes as atrophy and white matter disease.
  112. 112. HIV Encephalitis • Best diagnostic clue: Combination of atrophy and symmetric, periventricular or diffuse white matter (WM) disease • Location: – Bilateral periventricular and centrum semiovale WM, basal ganglia, cerebellum, brainstem
  113. 113. HIV Encephalitis - CT • NECT – Children: Atrophy and WM diffuse hypodensity • In utero HIV infection: Characteristic bilateral and symmetrical calcifications in basal ganglia and frontal WM with eventual contrast-enhancement – Adults: Normal or mild atrophy and WM hypodensity • CECT: – Usually no contrast-enhancement
  114. 114. HIV Encephalitis - MRI • T1WI: – WM abnormality may not be evident • T2WI – 2 imaging patterns • Focal abnormalities of high signal intensity • Diffuse moderate-high signal WM changes • FLAIR – Same imaging patterns as T2WI – Allows early detection of small « 2 cm) lesions in cortical/subcortical and deep WM locations
  115. 115. • Tl C+: – No enhancement in involved regions • MRS – AIDS patients with CD4 < 200/mm3, neurologic evidence of AIDS dementia complex, and atrophy • Subcortical region shows Decrease N-acetyl aspartate (neuronal loss) and Increased choline in WM (astrocytosis or microglial proliferation) – Cognitively normal and clinically asymptomatic patients • Subcortical region shows only increased choline
  116. 116. HIV Encephalitis
  117. 117. White Matter T2 hyperintensities without mass effect or enhancement. Usually begins in the Frontal lobes.
  118. 118. Cortical atrophy with WM changes in advanced HIV encephalopathy
  119. 119. • MRS may provide means for early diagnosis and evaluation of treatment in HIV. NAA Co mI high Cho,mI low NAA
  120. 120. • Opportunistic infections Toxoplasmosis CMV, Herpes Cryptococcosis, other fungal PML Mycobacteria, neurosyphilis • Malignancies Lymphomas Kaposi sarcoma
  121. 121. TOXOPLASMOSIS • MC cause of intracranial mass lesion in AIDS. • Focal/multiple ring and /or nodular enhancing lesions . • Predilection for CM junctions and Basal Ganglia. • “Asymmetric target sign” • MRS shows decr/ absent NAA,Cho,Cr peaks and a tall Lipid-Lactate peak.
  122. 122. TOXOPLASMOSIS
  123. 123. Progressive multifocal leukoencephalopathy • PML is a central demyelinating disease resulting from the reactivation of a latent infection of oligodendrocytes by JC polyomavirus. • Incidence : 4-5% of AIDS patients. • Clinically, limb weakness is commonest presentation, visual field defects, speech abnormalities, ataxia and dementia may be seen.
  124. 124. PML imaging findings • Lesions can occur in any part of brain but are commonest in parieto-occipital regions. • MRI shows multifocal, asymmetric bilateral white matter lesions that are of high signal on T2W and low signal on T1W images. • Extension to the subcortical U-fibres gives the lesions a characteristic ‘scalloped’ appearance.
  125. 125. PML Imaging findings • CT reveals asymmetric focal zones of low attenuation that involve the periventricular and subcortical white matter. • This appearance is a differential diagnostic feature compared with the typically more symmetric areas of low attention seen in patients with HIV encephalopathy. • They don’t enhance and haemorrhage is unusual.
  126. 126. PML
  127. 127. CMV Encephalitis - Ependymal and subependymal irregular T2 hyperintensities and enhancement.
  128. 128. CRYPTOCOCCOSIS • MC fungal infection in AIDS • Cryptococcoma , miliary nodules,meningitis • Symmetric perivascular spread in BG and midbrain (Dilated Virchow Robin spaces) + choroid plexus granulomas, relatively specific for cryptococcosis.
  129. 129. CNS TB
  130. 130. Herpes simplex ventriculitis
  131. 131. GELATINOUS PSEUDOCYSTS IN DILATED VR SPACES WITH SOAP BUBBLE MORPHOLOGY
  132. 132. LYMPHOMA • 2nd MC cause of IC mass lesion after toxoplasmosis. • Primary CNS lymphoma- B cell NHL • Lesions can mimic toxoplasmosis • Predilection for BG, Thalamus, PV WM, CORPUS CALLOSUM • NCCT- hyper dense, periventricular with fluffy enhancement. • infiltrative + crossing midline
  133. 133. Imaging findings • lower signal intensity than grey matter on T2W MRI. This reflects the dense cellularity of lymphoma. • Lesions have relatively little mass effect and oedema for their size. • Heamorrhage is unusual and calcifications seen only after treatment. • Enhancement is typical in a smooth or nodular ring surrounding a zone of central necrosis.
  134. 134. Multifocal Primary Cerebral lymphoma BG WITH SUBEPENDYMAL SPREAD
  135. 135. Primary Cerebral lymphoma
  136. 136. Lymphoma Vs Toxoplasmosis • Single enhancing mass lesions in AIDS is more likely to be Lymphoma. • Sub ependymal spread is a feature of lymphoma. • Thallium-201 SPECT and FDG-PET show greater uptake in lymphoma than toxoplasmosis. • DWI has limited value.
  137. 137. Toxoplasma Vs Lymphoma • MR Spectroscopy toxoplasma low or absent NAA, Cho, Cr high Lipid (+Lactate) lymphoma low NAA, Cr high Cho high Lipid, lactate
  138. 138. INCREASED rCBV IN LYMPHOMA
  139. 139. DECREASED rCBV IN TOXOPLASMA GRANULOMA
  140. 140. Mild to moderate atrophy, white matter lesions, cortical and subcortical infarctions, gummas, leptomeningeal enhancement, and arteritis have all been reported NEUROSYPHILIS
  141. 141. Aspergillosis in an HIV-infected patient who presented with rapidly progressive proptosis. Axial postcontrast T1-weighted imageshows a peripherally enhancing low- signal intensity mass within the left orbit that is causing proptosis.Intracranial extension is present,as evidenced by dural enhancement in themiddle cranial fossa (arrow). Opacification and enhancement of the left ethmoid air cells is seen. In addition, enhancement is seen within the periorbital soft tissue and in the left temporalis muscle
  142. 142. Neuro Immune Reconstitution Inflammatory Syndrome • Two types –UNMASKING AND PARADOXICAL • PML MCC • NATALIZUMAB FOR MS • RISK FACTORS –CD4 AND THERAPY INTERVAL
  143. 143. References: • Diagnostic Neuroradiology, Osborn. • Central Nervous System Infections, Neuroimaging Clinics, November 2012 • Central Nervous System Infection, Neuroimaging Clinics, November 2010 • CT & MRI of Whole Body, John Haaga.

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