Imaging of intracranial infections including COVID 19 pk2 ppt, pdf

This is nice presentation covers most of imporant intrancranial ( Brain) infection with many ct mri images . This presentation also includes cns (brain) manifestation of COVID-19 latest hot topic. This is very helpful for radiologist or radiology resident. Thanks.

1. IMAGING OF INTRACRANIAL INFECTIONS Pradeep Kumar

2. Congenital / neonatal infections Meningitis Pyogenic parenchymal infections Encephalitis Tubercular and fungal infections Parasitic infections

3. Congenital/neonatal infections Causative agents- TORCH agents- Toxoplasma , Rubella, CMV, HSV HIV , varicella , enteroviruses and Syphilis Routes Transplacental – toxoplasmosis, most viruses Ascending cervical infections – bacteria During birth – HSV II Can result in Developmental malformations Encephaloclastic lesions (brain destruction) Dystrophic calcifications

4. Imaging modalities CT- plain and contrast MRI- T1 , T2 axial saggital and coronal ,T2/ FLAIR- for vasogenic edema DWI/ADC- For restriction and T2 GRE and SWI for haemorrhage and calcification

5. CMV Most common congenital CNS infection (DNA; Herpes virus) Can also cause SNHL, cardiac anomalies, hepatosplenomegaly Predilection for periventricular subependymal germinal matrix Widespread periventricular tissue necrosis and subsequent dystrophic calcification. Other sites- cerebral white matter, cortex, cerebellum and brainstem

6. Imaging US/CT/MRI – encephaloclastic lesions, periventricular ca++, subependymal paraventicular cyst, ventriculomegaly MRI- delayed myelination, encephalomalacia, migrational disorder (lissencephaly, polymicrogyria, pachygyria)

7. TOXOPLASMOSIS T. gondii , obligate intracellular parasite Multifocal, scattered lesions (basal ganglia, cortical and subcortical region, periventricular location ) Macrocephaly **with hydrocephalus and ependymitis . No migrational disorder** Triad (imaging) hydrocephalus (due to ependymitis -leads to periaqueductal necrosis- aqueductal stenosis) b/l chorioretinitis intracranial calcifications

8. Axial unenhanced CT image reveals a peripherally calcified lesion (arrow) in the right caudate head that is a sequela of previous toxoplasmosis infection. The low-attenuation mass lesion with surrounding edema in the region of the left basal ganglia is from a new focus of toxoplasmosis.

9. RUBELLA Inhibits proliferation of immature undifferentiated progenitor cells in germinal matrix. Before 12 wks- fetal demise, stillbirth/severe birth defect Congenital rubella syndrome- 1 st trimester infection CNS – microcephaly , cortical /basal ganglia calcification Others Cataracts, glaucoma, chorioretinitis Cardiac anomalies Deafness CNS Imaging – similar to other viral infections, nonspecific

10. Axial NECT in congenital Rubella infection showing extensive calcifications in basal ganglia, cerebral white matter and cortex

11. Congenital Herpes simplex HSV -2 Findings 2-4 wks after birth Diffuse brain involvement CT -focal/diffuse white matter lucency , relative hyperdense cortex - hemorrhagic infarcts / thrombosis -diffuse atrophy & multicystic encephalomalacia later MRI - diffuse white matter edema, hemorrhagic infarcts/thrombosis , parenchymal or meningeal enhancement after contrast administration

12. Zika virus infections Pathology :Fetal germinal matrix Imaging CT : 1.cerebral calcification(GM-WM is most common site) 2. cerebral, cerebellar and brainstem volume loss 3. ventriculomegaly and microcephaly 4. polymicrogyria, lissencephaly and pachygyria 5. occipital and periventricular cysts MRI( SWI ) : depict parenchymal Calcifications Cortical migration defect ventriculomegaly

13. Perinatal (congenital) HIV Perinatal transmission – m.c. route Only 1/3 rd of infected mother can transmit. CNS symptoms – HIV encephalitis NECT – Diffuse cerebral atrophy (nearly 90% cases) - Basal ganglia calcifications (1/3 rd cases) - Hemorrhage (thrombocytopenia)

14. Meningitis Infective or inflamatory process of dura mater, leptomeninges (pia and arachnoid) and CSF within subarachnoid space. Pachymeningitis (dura + arachnoid) Meningoencephalitis (+ underlying parenchymal inflamation ) Types of meningitis: Acute pyogenic meningitis Acute lymphocytic meningitis(Viral) Chronic meningitis ( any infectious agent including fungi and parasites)

15. Role of CT in meningitis to identify contraindications  of a lumbar puncture to identify complications  . CT scans may reveal the cause of meningeal infection. Otorhinologic structures and congenital and posttraumatic calvarial defects can also be evaluated CT cisternography may depict CSF leaks, which may be the source of infection in cases of recurrent meningitis

16. Nonenhanced CT scan findings may be normal (>50% of patients)   effacement of basilar & convexity cisterns by inflammatory exudates and brain swelling may demonstrate mild ventricular dilatation and effacement of sulci cerebral edema and focal low-attenuating lesions. Sequelae from meningitis like periventricular and meningeal calcifications

17. Contrast-enhanced CT scans Meningeal & ependymal enhancement Help in detecting complications of meningitis, such as subdural empyema Venous thrombosis, infarction Cerebritis/abscess Ventriculitis.

18. Role of neuroimaging studies : typically used to monitor complications. Complications Hydrocephalus Ventriculitis / ependimitis Subdural effusion/ empyema Cerebritis /abscess Infarcts ( vasculitis /vasospasm) Dural sinus thrombosis/venous infarcts Cerebral edema

19. Acute lymphocytic meningitis (viral) Benign & self limited Viral in origin Enterovirus (50-80%) – echovirus, coxakie viurs and non paralytic polio virus, mumps, EBV, arbovirus Imaging usually normal unless coexisting encephalitis Brain swelling and meningeal enhancement in some cases.

20. Chronic meningitis Tubercular(most common), coccidiodomycosis , cryptococcus Hematogenous spread from the pulmonary tuberculosis is the common mechanism. Predominantly basilar exudates Sequelae- Pachymeningitis, ischemia/infarcts, atrophy, calcifications.

21. Imaging NECT- shows “en plaque” dural thickening and popcorn like calcifications particularly around basal cisterns. - meningeal enhancement - atrophy, infarction MRI -contrast enhanced T1W Image shows characteristic basal meningeal enhancement

22. Pyogenic parenchymal infections Cerebritis/cerebral abscess Complications of cerebral abscess

23. Cerebritis/cerebral abscess Focal cerebritis ( focal usually pyogenic infection without capsule or pus formation ) is the earliest stage of pyogenic brain infection from which the abscess evolves . Sources- Direct extension from adjacent structures (in about half of cases) Haematogenous Penetrating trauma

24. Early cerebritis(3-5days)- Initial phase of abscess. Focal infection Uncapsulated mass of congested vessels with perivascular PMNs infiltration and edema develops. Late cerebritis(7-10 days) - central necrotic core forms ,surrounded by outer ill-defined ring of inflammatory cells, macrophage, granulation tissue and fibroblast. Pathological stages

25. Early Capsule(10-14 days)- central core of liquified necrotic debris surrounded by well delineated capsule composed of collagen and reticulin, initially thin and incomplete ,more collagen deposited, becomes thicker. Gliosis begins at periphery. Late Capsule(>14 days)- capsule is complete & has 3 layers- 1.inner inflammatory layer of macrophage and granulation tissue 2.middle collagenous layer 3.Outer gliotic layer Late capsule stage lasts for several weeks to months. Cavity gradually shrinks and abscess heals.

26. Early cerebritis- normal or may show poorly marginated subcortical hypodense area with ill-defined enhancement in CT. MRI- poorly marginated subcortical hyperintense area in T2WI. - ill-defined contrast enhanced area within hypointense edema onT1 Images.

27. Late cerebritis- central low density with irregular enhancing rim, surrounding vasogenic edema

28. Early capsule- Thin(<5mm),well-delineated, distinct capsule that enhances strongly, uniformly and continuosly , surrounding edema present, thinner medial/ventricular margin . Rim is iso-hyperintense on T1 & iso- hypointense on T2WI

29. Late capsule- size of abscess gradually shrinks, edema diminishes. Rim enhancement persists for months. Hypointense rim in T2 images late capsule stage abscess : (Left) Axial T2WI MR shows a hyperintense mass with a hypointense rim at the gray-white junction , surrounding vasogenic edema. (Right) Axial T1 C+ MR shows a thick wall of enhancement

30. Ring enhancing lesions D/D D/D Features Metastasis GW junction; multiple Abscess Restriction of diffusion in DWI d/t high viscocity of central necrosis Smooth hypointense rim in T2WI Glioma (GBM) Thick irregular wall Elevated perfusion inhigh grade glioma in perfusion MRI Infarct ( subacute ) Usually gyral enh ; Costusion ( subacute to chronic) Demyelination (MS) the ring is incomplete and open towards the cortex Radiation necrosis Low perfusion in perfusion MRI Others Toxoplasmosis; Primary CNS lymphoma in AIDS

31. Encephalitis Diffuse, nonfocal brain parenchymal inflammatory disease due to spectrum of agents Viral Non viral Auto immune encephalitides – ADEM(post infective/vaccination)

32. Herpes simplex encephalitis Most common viral encephalitis HSV 1 usually activation of latent infection in trigeminal ganglion Fulminant, necrotising , hemorrhagic; considerable mass effect . Mortality upto 55%. Predilection for limbic system- inferomedial temporal lobe, orbital surface of frontal lobe , insular cortex, cingulate gyrus Sequential bilaterality – highly suggestive

33. Imaging CT – often normal in early disease. In adults, CT classically reveals hypodensity in the temporal lobes with or without frontal lobe involvement, usually with mass effect . Hemorrhage appear slightly later. CECT – ill defined patchy or gyriform enhancement In chronic stage – large low density areas with associated local atrophy in the affected region.

34. Togavirus (Japanese Encephalitis) Deep-seated structures characteristically involved: subcortical white matter (top arrow), thalami (middle arrow), and substantia nigra (bottom arrow)

35. Acute disseminated encephalomyelitis (ADEM) Monophasic demyelinating disorder that occur after vaccination or viral illness. Fulminant course, results in encephalopathy and focal neurological deficits, and usually resolve without long term sequelae. MRI – multiple large irregular T2 hyperintense lesions in subcortical white matter, cerebellum and brain stem.

36. D/D

37. CNS tuberculosis CT: non caseating granuloma –hyper/ isodese with homogenous enhancement, caseating granulomas enhance peripherally , target sign

38. MRI: non caseating granuloma- iso/hypointense on T1 & hyperintense on T2 with homogenous C++ Caseating solid granuloma- hypointense on T1 & strikingly hypointense on T2 Granulomas with central liquefaction- hypo on T1 & on T2 hyper with peripheral hypointense rim

39. Parasitic infections NCC Echinococcosis Amebiasis Paragonimiasis Spargonimiasis Malaria

40. Neurocysticercosis Larval form of T. solium – cysticercus cellulosae Most common CNS parasite location Subarachnoid space Brain parenchyma- corticomedullary junction Intraventricular in 20-50% cases Dying larva incite host inflamatory reaction & calcifies later

41. Pathological stages and Imaging Vesicular : Cyst with “dot” ( scolex ), no edema, no enhancement. (MRI - cyst is isointense to CSF and scolex is isointense to white matter) Colloidal vesicular : Ring enhancement, edema striking Cyst contents hyperintense on T1- and T2-weighted images ( proteinaceous fluid), cyst wall is thick and hypointense ) Granular nodular : Faint rim enhancement, edema decreased Nodular calcified: CT Ca++, MR “black dots”

42. D/D Subarachnoid NCC : TB meningitis (thick basilar exudate) Parenchymal NCC : Abscess ( restricts strongly in DWI) Intraventricular NCC : colloid cyst(solid) Ependymal cyst(cystic but not scolex) Choroid plexus cyst

43. Echinococcosis Larval stage- hydatid cyst Cerebral hydatid- seen in only 2% cases Imaging Single thin walled spherical CSF density cyst Large cystic lesion lying subcortically in middle cerebral territory of parietal area (can reach large size often over 6 cm in diameter). No edema or enhancement or adjacent calcification. Enhancement and perilesional edema are seen only if the cyst is superinfected.

44. Prion infection Creutzfeldt–Jakob disease (CJD) The typical MRI appearance of CJD is cortical ribboning , which describes ribbonlike FLAIR hyperintensity and restricted diffusion of the cerebral cortex. The basal ganglia and thalami are also involved. There is often sparing of the motor cortex. The pulvinar sign describes bright DWI and FLAIR signal within the pulvinar nucleus of the thalamus. The hockey stick sign describes bright DWI and FLAIR signal within the dorsomedial thalamus and pulvinar.

45. COVID-19 COVID-19–associated acute necrotizing hemorrhagic encephalopathy , a rare encephalopathy that has been associated with other viral infections but has yet to be demonstrated as a result of COVID-19 infection. Acute necrotizing encephalopathy (ANE) is a rare complication of influenza and other viral infections and has been related to intracranial cytokine storms, which result in blood- brainbarrier breakdown, but without direct viral invasion or parainfectious demyelination. Severe COVID-19 might have a cytokine storm syndrome Cortical signal abnormalities, particular attention was paid to presence of subtle hemorrhagic changes or leptomeningeal enhancement . Additionally, acute cerebrovascular disease, venous thrombosis , and chronic parenchymal changes were also seen in very few case.

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