Brain Infection - MR Flair
Brain Infection - MR Flair
Search Pattern Assist ?Exam
Purpose
2. Recognize the effects of any phase of the inflammatory process (i.e. proinflammatory: days 1-3 and inflammatory: days 3-7, or anti inflammatory: >7 days in leptomeningeal infection.
3. Recognize the effects of the initial humoral immune response to parenchymal brain infections.
4. Recognize the effects of the inflammatory response to parenchymal brain infections.
5. Recognize the effects of the sequestration/suppurative inflammatory response to persistent active infection leading to empyema and abscess formation.
6. Recognize extra cranial sources of infection directly producing secondary CNS infections and pachymeningitis with or without cortical abscesses.
7. Recognize the effects of septic emboli causing concurrent, multicentric CNS infections.
8. Recognize the effects of infections causing arteritis and mycotic aneurysms.
9. Recognize the effects of ventriculitis and intraventricular infected sequestra.
10. Assess for infections with somewhat characteristic features (i.e. HSV1 & 2, Ramsey-Hunt (varicella Zoster) cranial neuropathy, tuberculosis, etc.).
11. Assess for features of infection in the immuno-incompetent host (i.e. HIV, AIDS, steroid therapy, transplant patients, chemotherapy).
12. Lepto- or pachymeningitis differential includes: neurosarcoidosis, CNS lymphoma/leukemia, carcinomatous meningitis.
13. Single persistent brain abscess differential includes: single met, tumefactive MS, sequestered stage hematoma, sequestered brain infarction, focal CNS tumor (especially glioma).
14. Multicentric brain abscess differential includes: brain mets, gliomatosis (GBM with extension), primary CNS lymphoma.
15. Multicentric parenchymal lesions simulating encephalitis differential includes: immune overshoot problems (ADEM, SIRS-systemic immune response syndrome, cytokine storm, paraneoplastic syndrome etc.), PRES (posterior encephalopathy syndrome vasculopathy), gliomatosis, toxic encephalopathies (drug reactions & alcohol toxicity), metabolic encephalopathies (mainly hypoxia, diabetic glucose problems, Wernicke's encephalopathy, Sodium-related encephalopathy), vasculitic arteriopathies, mitochondrial disorders (children).
16. Cranial neuropathies simulating Lyme's disease or neurosyphillus, include: CNS lymphoma/leukemia, metastatic carcinomatosis, neurosarcoidosis, Miller-Fisher hyper immune response.
Findings
MR flair
There is evidence of only hyper intense, subpial edema and/or hyperintense sulcal protein accumulation, and/or subtle edema in the inner pial layer representing the effects of the activated hyperacute humeral immune response to primary leptomeningeal infection (usually first 24 hours). [Yes/No]
There is evidence of edema involving the inner or outer pia along with the subpial space consistent with proinflammatory phase of leptomeningitis (usually 1-3 days). There is often minimal contrast leak and venous hyperemia. [Yes/No]
There is evidence of edema involving the outer arachnoid layer and the dura as well as the inner pial layer and possibly with epidural or subdural effusion/empyema implying the disease is in the inflammatory stage (days 3-7). [Yes/No]
There is evidence of complications of the leptomeningitis with extradural or subdural effusions or empyema formation or ventriculitis/infected coagulum, or inflammation of the cranial nerves. [Yes/No]
There is evidence of contrast enhancement in one or more parapharyngeal space consistent with aggressive sinusitis, which can via a venous route produce cavernous sinus thrombophlebitis or internal jugular vein thrombophlebitis (i.e. Lemierre's syndrome) leading to secondary meningitis or brain abscess. [Yes/No]
There is evidence of aggressive (coalescent) otomastoiditis with adjacent secondary meningitis and/or empyema, or abscess. [Yes/No]
There is evidence of infection involving parapharyngeal space, cavernous sinus, or central skull base with secondary meningitis and/or empyema or abscess. [Yes/No]
There is evidence of contrast enhancement in the sphenoid sinusitis secondarily spread into one or more cavernous sinuses (cavernous thrombophlebitis), and possibly the sella with potential pituitary abscess, and rarely a carotid mycotic aneurysm. Any of these can cause a secondary leptomeningitis. [Yes/No]
There is evidence of regional or multicentric parenchymal (cytogenic) edema consistent with likely viral or immune-based cerebritis/cerebellitis/rhombencephalitis. [Yes/No]
There is evidence of parenchymal (cytogenic) edema in a cortical or penetrating vein distribution consistent with phlebothrombosis and possible infected thrombophlebitis. [Yes/No]
There is evidence of focal (reasonably delimited) parenchymal edema representing likely pyogenic cerebritis, the 1st phase of brain infection, usually lasting for the initial 4 days. The second cerebritis (days 4-8) there is initial central necrosis, but there is no capsule. [Yes/No]
There is cerebritis and early abscess capsule formation evident as a hypointense (collagen) outer ring (occurring days 8-12). [Yes/No]
There is evidence of parenchymal edema in one or more gray matter locations consistent with viral encephalitis. It may also occur in the frontotemporal/limbic distribution of herpes simplex (HSV) encephalitis. [Yes/No]
There is evidence of mixed parenchymal edema involving gray and white matter consistent with HIV encephalitis or PML infection. [Yes/No]
There is evidence of subependymal edema consistent with ventriculitis and/or hydrocephalus. [Yes/No]
There is evidence of organized intraventricular debris (infected sequestra). [Yes/No]
No other significant imaging findings are present. [Yes/No]
