CNS INFECTIONS IMAGING PART 1.......pptx

CNS INFECTIONS IMAGING PART 1.pptx

1. IMAGING IN CNS INFECTIONS PART I MODERATOR – DR. PRASANTHI MDRD.DNB PRESENTOR – DR. SWETHA

2. CNS INFECTIONS ACQUIRED – BACTERIAL TUBERCULAR VIRAL PARASITIC FUNGAL CONGENITAL – TORCH INFECTIONS

3. ACQUIRED PYOGENIC INFECTIONS MODES OF SPREAD 1. HEMATOGENOUS SPREAD – From remote systemic infections 2. GEOGRPAHIC EXTENSION – From sinusitis, Otomastoiditis 3. DIRECT EXTENSION – Penetrating injuries, skull fractures and post surgical

4. CAUSATIVE AGENTS 1. NEONATAL MENINGITIS – Most common is group B beta hemolytic streptococci 2. CHILDHOOD – N. Meningitis Hemophilus.influenza 3. ADULTS – Strep. Pneumoniae N. Meningitidis

5. SPECTRUM OF INFECTIONS 1. MENINGITIS 2. ABSCESS 3. VENTRICULITIS 4. EMPYEMA

6. MENINGITIS Meningitis is an acute or chronic inflammatory infiltrate of meninges and CSF. Pachymeningitis involves the dura and arachnoid Leptomeningitis affects the pia and subarachnoid spaces The "gold standard " for the diagnosis of bacterial meningitis is CSF analysis. Remember : Imaging is neither sensitive nor specific for the detection of meningitis.

7. ON CT MILD VENTRICULAR ENLARGEMENT WITH periventricular seepage Blurred ventricular margins Evaluate for sinusitis and otomastoiditis ON CECT PACHYMENINGITIS – Focal dural enhancement – dura arachinoid enhancement LEPTOMENINGITIS – Leptomeningeal enhancement extending into sulci and cisterns – pial cisternal enhancement M/C/S – CONVEXITIES ( BACTERIAL) BASAL CISTERNS ( TUBERCULOSIS )

8. ON MRI PURULENT EXUDATES ( Dirty CSF ) T1WI – Isointense T2WI – Iso to hyperintense DWI – Diffusion restriction is seen T1C+ - Pial cisternal and dura arachinoid enhancement

9. DD”S FOR HYPERINTENSE CSF ON FLAIR 1. BLOOD – Subarachinoid hemorrhage 2. PUS – Meningitis 3. CSF METASTASIS 4. High inspired O2 5. Susceptibilty artefact 6. Prominent vessels – MOYA MOYA and PIAL ANGIOMA 7. Gd in CSF – Renal failure

10. Complications The complications of meningitis can be remembered using the mnemonic HACTIVE : H : hydrocephalus A : abscess C :  cerebritis  / cranial nerve lesion T : thrombosis I : infarct V : ventriculitis  E : extra-axial collection: empyema and hygroma

11. BRAIN ABSCESS 1. EARLY CEREBRITIS 2. LATE CEREBRITIS 3. EARLY ENCAPSULATION 4. LATE ENCAPSULATION

12. EARLY CEREBRITIS Focal suppurative encephalitis without necrosis 1 to 3 days of initial infection ON IMAGING CT – Illdefined hypodense mass without enhancement MRI T1WI – Hypointense T2WI – Hyperintense T1C+ - Mild / NO enhancement DD- Stroke and Neoplasm

13. LATE CEREBRITIS Focal suppurative encephalitis with central necrosis Necrotic foci appears as poorly organised mass ON IMAGING CT – Round /ovoid hypodense mass CECT – Thin irregular rim enhancement MRI T2 / FLAIR – Hyperintense center with irregular hypointense rim T1C+ - Moderate rim enhancement DWI – Diffusion restriction is present

14. EARLY ENCAPSULATION Coalescent core with well defined wall of fibroblasts Well encapsulated ON IMAGING DUAL RIM SIGN – Hypointense periphery and hyperintense inner rim Central core – T2 hyperintense with Diffusion restriction Adjacent vasogenic edema

15. LATE ENCAPSULATION Wall thickens and shrinks – CRENULATED APPEARANCE Decreased inflammation and edema Enhancing focus may persist for months

16. VENTRICULITIS AKA – EPENDYMITIS OR PYOCEPHALUS ROUTES OF SPREAD 1. Intraventricular rupture of brain abscess Deeply seated Multiloculated Close to the ventricular wall 2. Choroid plexitis 3. VP Shunting

17. ON IMAGING VENTRICULOMEGALY DEPENDENT DEBRIS – Pus filled level in occipital horns ENHANCING VENTRICULAR WALL ON CECT/ CEMRI DEBRIS – Hyperintense to CSF on T1WI Hypointense to CSF on T2WI FLAIR OR T2WI – Halo of periventricular hyperintensity DWI – Stricking Diffusion restriction in layered debris

18. EMPYEMAS EXTRAXIAL INFECTIONS OF THE CNS IS RARE ROUTES OF SPREAD 1. FRONTAL SINUSITIS WITH WALL OSTEOMYELITIS Potts puffy tumour Epidural and subdural empyemas 2. POST TRAUMATIC AND POST SURGICAL

19. EPIDURAL EMPYEMA Small focal Biconvex or lentiform Can cross the midline M/C/S – Frontoparietal convexity Associated with potts puffy tumour Thin hypointense line between collection and brain is dura SUBDURAL EMPYEMA Small to large Can involves the interhemisphere fissure

20. ON IMAGING T2/FLAIR Hyperintense with Enhancing encapsulated wall Strong diffusion restriction DD 1. Subdural effusions – Bilateral, NO DR , 2. Subdural Hygromas – No enhancement and DR 3. Chronic subdural hematoma – Blooming noted

21. TUBERCULOSIS IN CNS ETIOPATHGENSEIS M. TB in the blood circulation forms small foci called RICH FOCUS in subpial and subependymal surfaces Furthur rupture of these foci into the subarachinoid space forms spectrum of tubercular brain infections

22. Spectrum of infections 1. TUBERCULOUS MENINGITIS 2. TUBERCULOMAS 3. TUBERCULOUS ABSCESS

23. TUBERCULOUS MENINGITIS Usually seen in combination with tuberculomas 70 to 80 percent of CNS Tuberculosis CEMRI is the procedure of choice NCCT Normal in early stages Non specific hydrocephalus Blurred ventricular margins Mildly hyperdense CSF exudates with predominance to basal cisterns

24. CECT THICK, INTENSE PIA- SUBARACHINOID ENHANCEMENT – Basal cistern predominance

25. EXUDATES 1. Isointense on T1WI 2. Hyperintensity of sulci and basal cisterns on T2WI 3. Linear nodular pial- subarachinoid enhancement 4. May extend into perivascular spaces 5. Flow voids in major arteries appear irregular and reduced – Due to PANARTERITIS Often lead to Penetrating artery infarcts 6. CRANIAL NERVE INVOLVEMENT – they appear thickened and enhanced

26. DD 1. PYOGENIC MENINGITIS – Involves cerebral convexities 2. CARCINOMATOUS MENINGITIS 3. NEUROSARCOIDOSIS basal cistern involvement is seen but pituitary, infundibulum and hypothalamus is also involved

27. TUBERCULOMA AKA Tubercular granuloma It is a focal parenchymal infection with central caseous necrosis most common site frontal and parietal lobes Majority cases – Small (2.5cm) , milliary nodules Giant tuberculomas ( 4- 6cm )

28. ON IMAGING NCCT – Round/lobulated iso to slightly hyperdense mass with perilesional vasogenic edema Healed granuloma CECT Punctate, solid or ring enhancement depending on the stage of the disease Can also seen as focal dural enhancing mass

29. MRI T1WI Iso to hypointense T2WI Most of the cases hypointense Central caseous necrosis if present – T2 Hyperintensity T1C+ - Rim enhancement is seen DWI – No restriction if central liquefied may restrict MRS – Large lipid peak with absence of another metabolities like aminoacids and succinate

30. DD 1.NEUROCYSTICERCOSIS GM-WM junction is involved Multiple lesions in different stages 2. PYOGENIC ABSCESS Diffusion restriction is seen 3. NEOPLASM Lack elevated choline

31. TUBERCULAR ABSCESS Central necrotic liquefied debris NO PUS Most commonly seen in immunocomprimised patients Can be found anywhere in the brain and brain stem

32. ON IMAGING NCCT Hypodense with mass effect and vasogenic edema CECT Peripheral rim enhancement is seen MRI > 3cm( larger than tuberculomas ) Multiloculated T2/FLAIR Hyperintense DWI – Diffusion restriction

33. HERPES SIMPLEX ENCEPHALITIS HSV 1 – OROLABIAL HERPES HSV2 – GENITAL HERPES From orolabial and ocular herpes to trigeminal ganglion and remains dormant later lead to reinfection or reactivation

34. LOCATION 1. Anteromedial temporal lobe 2. Insular cortex 3. Cingulate gyrus 4. Basi frontalcortex

35. ON IMAGING NCCT – Bilateral Asymmetrical involvement of temporal lobes, insular cortex and cingulate gyrus CECT - early cases stages enhancement Late cases stages gyriform enhancement Only Cortex is involved in most cases with white matter sparing Sometimes edema may extent into white matter

36. On MRI T1 WI hypointense cortex T2 WI hyperintensity with mass effect T1C + gyriform enhancement GRE- blooming foci indicates petechial hemorrhages Chronic cases encephalomalacia DWI - early cases diffusion restriction is seen

37. DDS 1. Diffusely infiltrating gliomas 2 acute cerebral ischemia 3. HHV encephalitis 4. Limbic encephalitis 5. Neurosarcoidosis

38. Hhv 6 encephalitis In population 90 percent individuals are seropositive for HHV 6 Rick factors are Stem cell transplantation and solid organ transplantation leads to HHV Encephalitis On imaging Bilateral symmetrical medial temporal lobe involvement with no extra limbic involvement

39. VARICELLA ZOSTER ENCEPHALITIS Multiple ischemic infarcts in pediatric population- cortex, basal ganglia and deep white matter T2 hyperintensity with diffusion restriction VZV Vasculopathy – Ischaemic or Hemorrhagic Infarcts Subarachanoid haemorrhage Aneurysms Arterial ectasia

40. Meningitis and encephalitis is seen Acute cerebellitis with leptomeningeal enhancement Multifocal leukoencephalopathy CRANIAL NERVE INVLOVEMENT CNVIII- RAMSAY HUNT SYNDROME

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