DES 9 janvier P. David. Clinic of Neuroradiology Erasme Hospital Université Libre de Bruxelles Belgium

Transcription

1 DES 9 janvier 2015 P. David Clinic of Neuroradiology Erasme Hospital Université Libre de Bruxelles Belgium

2 CNS Infections Early recognition in children, infants Longterm effects on the brain :devastating Manifestations of CNS infections on imaging studies : similar in children and adults. Epidemiology and causative agents : different

3 Congenital infections Infections of fns # older children and adults CNS while it is developing. «The age of the fetus at the time of the insult is more important than the nature of the insult» Infections during the first two trimesters will result in congenital malformations Third trimester : destructive lesions

4 Congenital infections Two main pathways for the transmission of infection to the fetus Bacteria: cervix to amniotic fluid Toxoplasmosis,syphilis,rubella,cytomegalovirus and other viruses:transmitted via the transplacental route.

5 Congenital infections Cytomegalovirus Most common serious viral congenital infection in developped countries 1 % of all births 10 % symptoms (J,HSM, Petechiae: common clinical signs) 10 % neurologic or developmental abnormalities in the first year of life Unfortunately,severe permanent neurological conditions : IC calcifications, microcephaly, impaired hearing, chorioretinitis, seizures..

6 CMV : mechanism of CNS injury Germinal matrix Primary vascular target Microcephaly,Polymicrogyria, Hypoplastic cerebellum,delayed myelination,diminished white matter,ca++

7 CMV : imaging finding The timing of the injury will determine the severity of the abnormalities

8 CMV : first half of second trimester Lissencephaly Hypoplastic cerebellum Delayed myelination Marked ventriculomegaly Significant periventricular calcifications

9 CMV: second half of second trimester More typical polymicrogyria Less ventricular dilatation Less consistent cerebellar hypoplasia

10 End of gestation Normal gyral pattern Mild ventricular prominence Damage to the white matter Scattered Calcifications: non specific

11 Cmv Boniver CCHR second half of second trimester Bo,M

12 Bo,m

13 Transfontanel US : «lenticulostriate vasculopathy» (trisomy 13, 21, anoxic/toxic injury) Ra,f

14 End of gestation Be,s

15 Be,s

16 Developmental delay or seizures Periventricular calcifications Cortical malformations Myelination delay Cerebellar hypoplasia Think about congenital CMV!

17 Toxoplasmosis Protozoan:Toxoplasma gondii (rodents,birds, mammals) Oocysts in uncooked meat 1/1000 live births

18 Toxoplasmosis:principal CNS findings Chorioretinitis Abnormal cerebrospinal fluid Hydrocephalus Seizures Whether involvement is generalized or primarily limited to CNS : the prognosis is quite poor

19 Toxoplasmosis Findings on CNS imaging studies may be similar to those in CMV infections. Calcifications (basal ganglia, periventricular region, cerebral cortex) Microcephaly Hydrocephalus

20 Toxoplasmosis, CMV A spectrum is seen from Relatively Mild disease (few PVC, mild atrophy) To severe disease (near total destruction of the cortex and brain; diffuse cerebral calcifications)

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24 Neonatal Herpes Simplex encephalitis involvement of CNS (Maternal type II herpetic lesions) May result in: Mental retardation Severe neurologic deficits The Outcome is usually poor.

25 Imaging findings Patchy, widespread areas of abnormal signal Primarily in the white matter Cortical gray matter Loss of brain substance occur rapidly,often as early as the second week.

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27 Rubella : imaging findings Time of the in-utero infection When early infected : congenital anomaly Late : non specific area of edema or loss of brain tissue.

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30 Aquired immunodeficiency syndrom Rarely neonatal period Median : 8 months

31 Infectious diseases Consider primary location Meninges : meningitis Sub-or epidural spaces : empyemas Brain : cerebritis and abscess ventriculitis pyogenic infections encephalitis viral infections

32 CNS infections Specific features? Herpes Tuberculosis Listeria rhombo-encephalitis

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36 CNS infections Imaging procedures CT and MRI - HRCT of skull base - T1Wi, T2Wi, GE - (magnetization transfer) Gd T1Wi and FLAIR - MRA - Diffusion - MR spectroscopy Angiography

37 Meningitis Most common form of CNS infection in children Imaging is not performed routinely Clinical diagnosis unclear Neurologic deterioration Persistant seizures or focal neurological deficits Patients recovery slow

38 Infectious brain diseases Meningitis : MRI > CT Role of MRI!!! --->complications! Hydrocephalus Venous sinus thrombosis Cerebral infarction (venous,arterial) Effusions Cerebritis,Abscess Ventriculitis Empyema

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40 Meningite nn Infarct nx base Dumoulin,melanie Cathy chr Du,me

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42 Vandenbroeck Cathy chr Méningite à E.Coli / Cata Vdb

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47 Van berlamont Thrombose sls +infarc parasagit

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49 1 month old Born at term Secondary neurologic deterioration Meningitis E Coli Shunting MRI

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52 Parmentier Méningite NN à Proteus>>abcés>>tt >>ok

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55 Pyogenic parenchymal infections Abcess is a continually evolving lesion. Four stages: Early cerebritis (3-5 days) Late cerebritis (5 days-2weeks) Early capsule (2 weeks) Late capsule (2 weeks-month )

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58 Brain abscess : symptoms Neonates:signs of increased intracranial pressure (Citrobacter, Proteus) Older:Headache,Vomiting,Epilepsy, Vision impairment,impairment of consciousness Fever is often absent!..

59 Abscess : CT and MRI findings «Capsule is thin-regular and shows an uniform enhancement» The rim is: Hypersignal on T1Wi Hyposignal on T2Wi Abscess and Neonates:Large size,thin capsule,typically in the periventricular white matter.

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62 Tuberculous meningitis Differs in clinical presentation and radiographic appearance from the pyogenic meningitis Irritability anorexia, Sometimes, fever Drowsiness, neck stifness, cranial neuropathy, vomiting convulsions coma, irregular pulse and respiration! Headache only 20 % of patients

63 Tuberculous meningitis If tuberculous meningitis is not promptly recognized and treated : the results to the brain are devastating. If untreated : rapid progress to death (3 weeks)

64 Théramene TBC,Tuberculome thal dt,meningite base

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67 Viral infections: CNS Herpes Simplex Varicella Zoster Human deficiency virus Subacute Sclerosing Panencephalitis Poliovirus Auto-immune diseases:cns Rasmussen Adem

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72 Aquired immunodeficiency syndrome Rarely neonatal period Median : 8 months Encephalopathy : prominence of the subarachnoid spaces and ventricles (atrophy) Calcifications of the basal ganglia and subcortical white matter Intracranial neoplasm and infection rare in HIV infected children

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74 Progressive multifocal leukoencephalopathy Most common infection in pediatric AIDS Appearance identical to that in adults

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76 Rasmussen Encephalitis One of the leading cause of intractable seizures Seizures > Motor deficit > Hemiplegia Auto-immune mechanism Progressive atrophy / Prolonged T2 Area

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78 ADEM Monophasic disease Immune-mediated response Occuring after a viral infection or vaccination spontaneously

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80 Fungal Infections Candida Aspergillosis Coccidoidosis Other

81 Candida chez gd préma Dd hh ss épendimaire Ismail a changé de nom: Boutchcoula,randa

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83 infarcissement chez un immunodéprimé( leucémie):penser àaspergillus Urban

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85 Parasitic Infections Cysticercosis Miscellaneous

86 Neurocysticercosis Taenia solium Is the most common parasitic infection world wide! Is the main etiology in the world for epilepsy!

87 Neurocysticercosis 1. Vesicular stage Small cyst + mural nodule No edema/no contrast enhancement 2. Colloidal vesicular stage When larvum dies ---> inflammatory response > edema, ring enhancement

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89 Neurocysticercosis 3. Granular nodular stage ---> thick capsule, scolex calcifies ---> edema - contrast enhancement 4. Nodular calcified stage ---> calcified nodule

90 Hydatid cyst (echinococcosis)