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Brain Infections2

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Brain Infections2

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Brain Infections2

  1. 1. Infections of the Brain and Meninges Mohamed Samir Assist. LecturerEpisode 2 “The Good, The Bad and The Infectious”
  2. 2. Infections Congenital / Neonatal Acquired • Cytomegalovirus. • Toxoplasmosis. • Rubella. • Herpes Simplex. • HIV Infection. • Enteroviruses. • Meningitis. • Pyogenic Parenchymal Infections. • Encephalitis. • TB & Fungal Infections. • Parasitic Infections.
  3. 3. Acquired: ♣ Non-Specific: 1- Meningitis. 2- Pyogenic Parenchymal Infections. 3- Encephalitis. ♣ Specific: 1- TB & Fungal Infections. 2- Parasitic Infections.
  4. 4. MeningitisMeningitis • The most common form of CNS infections. • 3 General Categories. 1- Acute Pyogenic Meningitis. 2- Lymphocytic Meningitis. 3- Chronic Meningitis.
  5. 5. M e n i n g i t i s Bacteria: Acute Pyogenic Meningitis • Neonates…. – Group B Streptococcus species (49%) – Escherichia coli (18%) • Children and infants …. – Haemophilus influenzae (40-60%) – Neisseria meningitidis (25-40%) • Adults …. – S. pneumoniae (30-50%) – N. meningitidis (10-35%) – Staphylococcus species (5-15%)
  6. 6. M e n i n g i t i s Acute Pyogenic Meningitis Routes of Infection: 1. Hematogenous spread. 2. Local extension from contiguous extracerebral infection 3. Direct implantation of bacteria into the meninges.
  7. 7. Clinical: M e n i n g i t i s Acute Pyogenic Meningitis Classic triad (85% of patients with bacterial meningitis) • Fever • Headache • Stiff neck
  8. 8. Complications: M e n i n g i t i s Acute Pyogenic Meningitis 1. Hydrocephalus. 2. Ventriculitis. 3. Subdural Effusion. 4. Empyema. 5. Infarction. 6. Parenchymal abscess.
  9. 9. • Viral (Enteroviruses 50-80%). • Mostly benign and self-limited. M e n i n g i t i s Acute Lymphocytic Meningitis
  10. 10. Imaging of Acute Meningitis
  11. 11. The most important role of CT in imaging patients with meningitis is to evaluate for: 1.Contraindications to a lumbar puncture. 2.Complications of meningitis. M e n i n g i t i s CT: Acute Meningitis
  12. 12. • NECT: M e n i n g i t i s CT:  Normal (>50% of patients).  Mild ventricular dilatation.  Cerebral edema.  Focal low-attenuating lesions.  Effacement of sulci.  Obliteration of the basal cisterns. Acute Meningitis
  13. 13. • CECT: M e n i n g i t i s CT: Acute Meningitis • Diffuse meningeal enhancement. • Cerebritis. • Abscess. • Subdural fluid collection. • Subdural empyema
  14. 14. M e n i n g i t i s CT: Acute Meningitis CT scans may reveal the cause of meningeal infection
  15. 15. Negative results on CT imaging do not exclude the presence of acute meningitis.
  16. 16. M e n i n g i t i s MRI: Acute Meningitis The most sensitive modality due to increased contrast resolution, and the absence of artifact caused by bone.
  17. 17. M e n i n g i t i s MRI: Acute Meningitis Obliterated cisterns and the distention of the subarachnoid space with widening of the interhemispheric fissure T1WI:
  18. 18. M e n i n g i t i s MRI: Acute Meningitis Cortical hyperintensities that are believed to represent edema T2WI:
  19. 19. M e n i n g i t i s MRI: Acute Meningitis •Diffuse enhancement of the subarachnoid space. T1WI+GAD:
  20. 20. M e n i n g i t i s MRI: Acute Meningitis Empyema
  21. 21. M e n i n g i t i s MRI: Acute Meningitis Cerebritis
  22. 22. Find 3 Differences
  23. 23. Parenchymal InfectionsParenchymal Infections 1. Bacterial (Pyogenic). 2. Viral.
  24. 24. Pyogenic Parenchymal InfectionsPyogenic Parenchymal Infections Cerebritis. Abscess.
  25. 25. P y o g e n i c P a r e n c h y m a l I n f e c t i o n s Pathology: Four stages have been described in abscess evolution: 1. Early cerebritis. 2. Late cerebritis. 3. Early capsule formation. 4. Late capsule formation.
  26. 26. P y o g e n i c P a r e n c h y m a l I n f e c t i o n s CT: • CT manifestations of an intracranial abscess depend on the stage of the abscess formation
  27. 27. P y o g e n i c P a r e n c h y m a l I n f e c t i o n s CT: • During early cerebritis, nonenhanced CT scans may demonstrate normal findings or may show only poorly marginated subcortical hypodense areas.
  28. 28. P y o g e n i c P a r e n c h y m a l I n f e c t i o n s CT: • Contrast-enhanced CT studies demonstrate an ill-defined contrast-enhancing area within the edematous region
  29. 29. P y o g e n i c P a r e n c h y m a l I n f e c t i o n s CT: • During the early stage of a formed abscess, the lesion coalesces, with an irregular enhancing rim that surrounds a central low-attenuating area.
  30. 30. P y o g e n i c P a r e n c h y m a l I n f e c t i o n s CT: • Scans obtained with a time delay following contrast enhancement in cerebritis may show contrast "filling in" the central low-attenuating region. A formed abscess will not "fill in" the central portion of the abscess.
  31. 31. P y o g e n i c P a r e n c h y m a l I n f e c t i o n s CT: • A relatively thin well-delineated capsule marks the final stage of a fully formed abscess. • Peripheral edema results in considerable mass effect with sulcal obliteration
  32. 32. P y o g e n i c P a r e n c h y m a l I n f e c t i o n s MRI: 1. Early cerebritis stage The early cerebritis stage presents as an ill-defined hyperintense zone that can be noted on T2-weighted imaging.
  33. 33. P y o g e n i c P a r e n c h y m a l I n f e c t i o n s MRI: 1. Early cerebritis stage • Contrast-enhanced T1-weighted studies demonstrate poorly delineated enhancing areas within the isointense-to-mildly hypointense edematous region
  34. 34. P y o g e n i c P a r e n c h y m a l I n f e c t i o n s MRI: 2. Late cerebritis stage • During the late cerebritis stage, the central necrotic area is hyperintense to brain tissue on FLAIR and T2-weighted sequences. • The thick somewhat irregularly marginated rim appears isointense to mildly hyperintense on T1- weighted images and isointense to relatively hypointense on FLAIR and T2-weighted scans. • The rim enhances intensely.
  35. 35. P y o g e n i c P a r e n c h y m a l I n f e c t i o n s MRI: 3 & 4- Early and late capsule stages • The collagenous abscess capsule is visible prior to contrast as a comparatively thin-walled isointense-to-slightly hyperintense ring that becomes hypointense on T2- weighted MRIs.
  36. 36. P y o g e n i c P a r e n c h y m a l I n f e c t i o n s MRI:
  37. 37. Diffusion-weighted MR may be useful in differentiating abscess from necrotic tumor. Diffusion-weighted echo planar images demonstrate an abscess as a high signal intensity with a corresponding reduction in the apparent diffusion coefficient. The brightness on DWI is related to the cellularity and viscosity of the contents within the abscess cavity. P y o g e n i c P a r e n c h y m a l I n f e c t i o n s MRI:
  38. 38. MR spectroscopy is useful in differentiating ringlike enhanced lesions that cannot be diagnosed correctly using enhanced MRI alone. MR spectroscopy can help to specifically differentiate tumor, radiation necrosis, or abscess by identifying their different spectral profiles. P y o g e n i c P a r e n c h y m a l I n f e c t i o n s MRI:
  39. 39. • 99m TC HMPAO labeled leukocytes. • Radiolabeled polyclonal immunoglobulins P y o g e n i c P a r e n c h y m a l I n f e c t i o n s Nuclear Medicine:
  40. 40. Find 2 Differences
  41. 41. EncephalitisEncephalitis •Diffuse non-focal brain parenchymal inflammatory disease
  42. 42. • HSV TYPE 1 & 2 • Others; equine viruses. CMV, Parvoviruses, ….. E n c e p h a l i t i s Agents: Encephalitis
  43. 43. E n c e p h a l i t i s Agents: Encephalitis • In adults, herpes simplex virus type 1 (HSV-1) accounts for 95% of all fatal cases of sporadic encephalitis and usually results from reactivation of the latent virus. • In children and neonates, herpes simplex virus type 2 (HSV-2) accounts for 80-90% of neonatal and almost all congenital infections.
  44. 44. E n c e p h a l i t i s Agents: Encephalitis • In the typical adult infected with HSV-1, the neuronal spread of the latent virus occurs from the peripheral neuron in retrograde fashion to the brain, usually through the trigeminal or olfactory tract.
  45. 45. E n c e p h a l i t i s Pathology: Encephalitis • Fulminant hemorrhagic and necrotizing meningoencephalitis. Typical gross findings include severe edema and massive tissue necrosis, with petechial hemorrhages and hemorrhagic necrosis.
  46. 46. E n c e p h a l i t i s Pathology: Encephalitis • The virus has a predilection for the limbic system, involving one or both temporal lobes, and often involving the hippocampus, parahippocampus, and amygdala. Frontal and parietal spread also can occur.
  47. 47. E n c e p h a l i t i s CT: Encephalitis • CT classically reveals hypodensity in the temporal lobes either unilaterally or bilaterally, with or without frontal lobe involvement. • Hemorrhage is usually not observed. • A gyral or patchy parenchymal pattern of enhancement is observed. Contrast enhancement generally occurs later in the disease process.
  48. 48. E n c e p h a l i t i s CT: Encephalitis
  49. 49. E n c e p h a l i t i s MRI: Encephalitis • T2-weighted MRI reveals hyperintensity corresponding to edematous changes in the temporal lobes, inferior frontal lobes, and insula, with a predilection for the medial temporal lobes.
  50. 50. E n c e p h a l i t i s MRI: Encephalitis • Foci of hemorrhage occasionally can be observed
  51. 51. E n c e p h a l i t i s MRI: Encephalitis • Restricted diffusion in herpes encephalitis exist with corresponding T2 hyperintensity reflecting edema
  52. 52. E n c e p h a l i t i s MRI: Encephalitis • MR spectroscopy using proton spectroscopic MRI has demonstrated a reduction of the N-acetylaspartate (NAA)- to-choline ratio.
  53. 53. Find ANY Difference !!!!!
  54. 54. THANK YOU

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