Brain Pain Infections of the CNS

Transcription

1 FRIDAY, OCTOBER 28, 2016 Brain Pain Infections of the CNS Suyash Mohan MD, PDCC Assistant Professor of Radiology & Neurosurgery Division of Neuroradiology, Department of Radiology Perelman School of Medicine at University of Pennsylvania

2 Why Important? Life-threatening problems with high associated mortality ξ morbidity Increasing incidence Primarily attributed to AIDS ξ widespread use of immunosuppressants Prognosis depends on rapid identification

3 What s Important? Meningitis Ventriculitis Abscess Empyema Encephalitis Toxoplasmosis Tuberculosis Fungal Cysticercosis Neonatal infections

4 BACTERIAL INFECTIONS Meningitis: Most common CNS infection S/S include: Headache Fever Neck stiffness Photophobia Vomiting Altered consciousness Diagnosis: Clinical ξ CSF findings Role of neuroimaging: To confirm suspected meningitis To rule out meningitis mimics To evaluate for complications To rule out increased ICP before LP

5 Case: 45 yr male presented with seizures ξ fever Tubercular meningitis

6 Case: 18 yr male presented with headaches ξ fever

7 Case: 28 year-old male with mental status changes

8 Pre Post Pre Post Viral Meningitis: Symptoms improved with acyclovir

9 D/Dx of meningeal enhancement Meningeal enhancement is nonspecific, may be caused by the following 5 different etiologic subgroups: 1. Infectious 2. Carcinomatous 3. Reactive: surgery, shunt, trauma 4. Chemical: ruptured dermoid, cysticercus, intrathecal chemotherapy 5. Inflammatory: sarcoidosis, collagen vascular diseases, etc

10 Meningitis Nonspecific diffuse meningeal enhancement, FLAIR hyperintensity Cryptococcus Coccidiomycosis Tuberculosis Toxoplasmosis Listeria

11 How to differentiate between normal meningeal vessels/ cortical veins from abnormal leptomeningeal enhancement? Abnormal meningeal enhancement on MRI is: Thick Nodular/ Irregular Longer & continuous Asymmetrical Extends deep into the base of the sulci Long-segment (> 3 cm) or diffuse convexity meningeal enhancement If meningeal enhancement was present on more than three contiguous 1.5 T SE MR images Quint et al. Academic Radiology 1996: (3); Kamra et al. The British Journal of Radiology, 77 (2004),

12 How to differentiate b/w acute vs chronic meningitis? Acute: meningeal enhancement is located over the cerebral convexity Chronic: meningeal enhancement is most prominent in the basal cisterns How to differentiate b/w infective vs carcinomatous meningitis? Carcinomatous meningitis typically presents with dural enhancement

13 34 Y/M with dizziness & loss of balance. Also history of ulcerative colitis & colon cancer

14 Imaging in Meningitis Most common: normal CSF FLAIR hyperintensity Meningeal enhancement Complications: Hydrocephalus, ventriculitis Effusion, empyema, cerebritis, abscess Cerebral edema, herniation Venous thrombosis, vasospasm, infarct

15 Case: year-old male with mental status changes. PMH - Sinusitis

16 Complications Effusion vs. Empyema Cerebritis

17 Complications Hydrocephalus Ventriculitis

18 Case: 31 year-old woman with confusion and right sided weakness

19 How to differentiate between cystic tumors and abscesses? MR Spetroscopy in combination of DWI Can differentiate cystic tumors from brain abscess Suc Ac Lac AA T2 PC T1 DWI ADC PMRS

20 Brain Abscesses ξ MRS Spectra from brain abscesses reveal Acetate (1.92 ppm) Succinate (2.4 ppm) Lactate (1.3 ppm) Amino acids (0.9 ppm) Main brain metabolites like NAA, Cr ξ Cho Usually not detectable Presence of acetate ξ succinate suggests anaerobic bacterial infection Garg M et al. Radiology 2004; 230:

21 CNS TUBERCULOSIS Incidence of TB has been increasing d/t increase in AIDS ξ other immunodeficiency states CNS involvement occurs in 2 5% of all TB patients ξ in 10-15% of AIDS patients Diffuse form: Leptomeningitis Localized parenchymal forms: Tuberculoma Miliary tuberculosis Abscess

22 Tuberculoma Lip

23 Tuberculoma HPE: Central caseous necrosis, surrounded by reactive epithelial cells, Langhans giant cells, PMN cells, plasma cells ξ lymphocytes

24 MTT1 Miliary Tuberculosis

25 Tubercular abscess T2 T1 MTT1 Flair PC-MTT1 Lip DWI ADC PMRS

26 Case: 39 year-old man with confusion. PMH of NHL on treatment

27 Case: 46 year-old immunocompetent man with headache and weakness T2 PCT1 DWI ADC PMRS HPE

28 How to diagnose a fungal abscess? Intracavitary projections: Characteristic Arise from the wall Restricted diffusion in projections ξ wall No restriction rest of the abscess core Contrast enhancement only in the wall These projections are a distinguishing feature of a fungal cause on conventional MRI

29 Role of MR Perfusion Abscesses show relative decreased CBV from neoplasms, which demonstrate significantly elevated CBV Infective lesions have lower values of rcbv as compared to high grade glioma Infective lesions have higher rcbv as compared to LGG As a result of differential expression of VEGF

30 Abscess Grade II Astrocytoma Grade III Astrocytoma Glioblastoma T2 PCT1 Color map of FA CBV

31 Permeability in Infections Diffusion Perfusion CBV uncorrected CBV corrected CBF K trans v e Angiogenesis in a Tuberculoma

32 Permeability in Infections Cerebral aspergillosis: patterns variable & depend upon immunological condition 1. Edematous lesions, 2. Hemorrhagic lesions, 3. Solid enhancing lesions aspergilloma Cho T2 T1 PCT1 PMRS CBV CBF K trans v e VEGF staining in the cytoplasm of giant cells

33 PARASITIC LESIONS Toxoplasmosis Neurocysticercosis Cerebral malaria Echinococcal Schistosomiasis

34 34 year old woman post renal transplant

35 Toxoplasmosis MC opportunistic infection in HIV Frequently multifocal, predilection for BG, may hemorrhage Target sign: (30%) An enhancing nodule within and adjacent to the enhancing rim, represents an infolding of the cyst wall DWI Dark to isointense core, reflecting low viscosity ξ absence of purulent fluid, likley due to impaired immune response in immunocompromised patients

36 Cysticercosis MC and most widely disseminated parasitic infection in the world Humans become the definitive host when poorly cooked pork infected with cysticercosis is ingested Stages: 1. Vesicular stage 2. Colloidal-vesicular stage 3. Granular nodular stage 4. Nodular calcified stage

37 Cho Suc

38 Case: 48 year-old man with fever and rash

39 Herpes Simplex Encephalitis (HSE) Hemorrhage ± Contrast enhancement ± DWI is more sensitive for early detection Usually asymmetric Lesions involving bilateral anterior ξ medial temporal lobes, should be considered HSE until proven otherwise D/Dx of B/L temporal lobe lesions: 1. Herpes Encephalitis 2. Flavivirus Encephalitis 3. Limbic Encephalitis 4. Status epilepticus 5. Hypoxic ischemic injury 6. Hypoglycemia 7. Gliomatosis 8. Transient global amnesia 9. Mesial Temporal Sclerosis 10.Radiation Change

40 Flavivirus encephalitis Case fatality rate 10% to 60% Mostly disease of children Characteristic imaging findings: B/L thalamic ξ substantia nigra lesions B/L thalamic hemorrhages are considered highly specific for JE HSE vs JE: Unlike HSE, the anterior temporal lobe is usually spared ξ insular involvement is rare WD vs JE: Postero-medial thalamus is characteristically involved in JE ξ spared in WD, which involves anterolateral thalamus

41

42 2-day-old, 3 week premature, male with seizures, microcephaly & metabolic acidosis.

43 D/ Dx of subependymal & periventricular calcifications Toxoplasmosis: Basal ganglia & cortex are more commonly involved Rubella: Calcifications are evenly distributed in the necrotic brain Tuberous sclerosis: Mimics CMV Subependymal enhancing nodules in the region of the foramen of Monro & presence of hypodense cortical tubers help in differentiating the two conditions

44 What we have covered? Meningitis Ventriculitis Abscess Empyema Encephalitis Toxoplasmosis Tuberculosis Fungal Cysticercosis Neonatal infections