There is evidence of minimal contrast leak consistent with hyperacute leptomeningitis consistent with the initial humeral immune response (< 24 hours).

There is evidence of clearly apparent contrast leak (not defining specific structures) consistent with the acute proinflammatory phase of primary leptomeningitis (< 3 days).

There is evidence of recognizable contrast enhancement of the dura and/or inner and outer pial layers, and/or significant contrast leak into the sulci consistent with the inflammatory response to leptomeningeal infection.

There is evidence of recognizable contrast enhancement of the dura or pial layers with possible epidural or subdural empyemas or acute pachymeningits surrounding cranial nerves (neuritis), or other structures within the basilar cisterns (like the pituitary stalk).

There is evidence of contrast enhancement  in one or more paranasal sinuses plus extraaxial effusion consistent with aggressive sinusitis with potential adjacent empyema/abscess and secondary meningitis (dura enhances in the initial phase).

There is evidence of contrast enhancement  in one or more otomastoid air cells plus extraaxial effusion consistent with coalescent otomastoiditis associated with secondary meningitis, potentially complicated by empyema, venous occlusion leading to brain abscess.

There is evidence of contrast enhancement  in one or more parapharyngeal space consistent with aggressive cellulitis, 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.

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.

There is evidence of regional or multicentric parenchymal (cytogenic) edema consistent with likely viral or immune-based cerebritis/cerebellitis/rhombencephalitis.

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. There may be hyperintense T1-w signal on the noncontrast sequence, likely represent early cytogenic injury with intracellular protein.

There is cerebritis and early abscess capsule formation evident as a hypointense (collagen) outer ring (occurring days 8-12). Mature abscess formation is > 12 days and the collagen and fibrotic capsules (thus, 2 outer rings). The abscess ultimately is sequestered in a dense fibrotic capsule and hopefully resolves over time.

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.

There is evidence of thrombosis or wall enhancement of infected cortical veins, penetrating veins, or dural sinuses consistent with either phlebothrombosis or thrombophlebitis and possible infected thrombophlebitis.

There is evidence of multicentric nodular enhancement in a distribution of terminal arteries consistent with septic embolization.

There is evidence of abnormal contrast enhancement of the ependymal surface consistent with ventriculitis.

There is evidence of pial hyperemia with possible AV fistula or dural sinus thrombosis producing elevated venous pressure.

There is evidence of raised intracranial pressure (i.e. optic hydrops, partially empty sella, and/or downward tonsillar displacement).

There is evidence of dural sinus or cortical vein CVT, which can occur in leptomeningitis.

No other significant imaging findings are present.