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).

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.

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).

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.

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.

There is evidence of aggressive (coalescent) otomastoiditis with adjacent secondary meningitis and/or empyema, or abscess.

There is evidence of infection involving parapharyngeal space, cavernous sinus, or central skull base with secondary meningitis and/or empyema or 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 parenchymal (cytogenic) edema in a cortical or penetrating vein distribution consistent with phlebothrombosis and possible infected thrombophlebitis.

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 is cerebritis and early abscess capsule formation evident as a  hypointense (collagen) outer ring (occurring days 8-12).

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 mixed parenchymal edema involving gray and white matter consistent with HIV encephalitis or PML infection.

There is evidence of subependymal edema consistent with ventriculitis and/or hydrocephalus.

There is evidence of organized intraventricular debris (infected sequestra).

No other significant imaging findings are present.