55 yo female with diabetes who presented with headache and fever and sinusitis (diagnosed on prior outside maxface CT). For the last several hours later had worsening symptoms and altered mental status changes.

MR flair; Post contrast T1-w axial and sagittal; MR diffusion; MR susceptibility; MR T2-w spin-echo

MR flair
1. There is evidence of extensive leptomeningitis on MR flair with findings mostly in the hyperacute humeral immune phase of infection.
2. There is prominent mucosal edema in the paranasal sinuses and within the sella and within the retroglobal orbital soft tissue plus inflammation in the nasopharyngeal soft tissues. It  is possible that the leptomeningitis is related to nasopharyngeal infection spreading into the sella and secondarily into the CSF.

MR T1-w post contrast
1. There is evidence of the contrast enhancement of the dura and pial surfaces consistent with the proinflammatory phase of the leptomeningeal infection. 
2. There is pachymeningitic basilar meningitis, plus epidural venous engorgement in the upper cervical spine, plus mucosal enhancement of the nasopharyngeal mucosa, and enhancement of a persistent nasopharyngeal canal into the sella. The combination of findings from the contrast enhanced sequences plus the MR flair sequence are consistent with post infectious changes of differing ages. Likely the nasopharyngeal infections came first. It spread to the sella via the persistent nasopharyngeal canal causing basilar pachymeningitis and later spread to the CSF causing the more hyperacute leptomeningitis. 

MR diffusion
1. The DWI demonstrates the subpial edema is a similar manner and distribution as evident on the MR flair. There is no cerebritis.
2. The ADC map demonstrates restriction in the right anterior temporal fossa, possibly an early subdural empyema, despite not being evident on the T1-w post contrast sequence.

MR susceptibility (SWI)
1. Developmental right transmantle parietal venous anomaly
2. The cortical pial vessels are not as well seen as expected raising the possibility of early arterial vasospasm.

T2-w spin-echo MR
1. Evidence of early raised intracranial pressure with optic hydrops and downward cerebellar tonsillar displacement.

1. There is evidence of nasopharyngeal and upper cervical mucosal inflammation that appears to have spread through a persistent nasopharyngeal canal into the sella. From there, it produced a secondary basilar leptomeningitis. The more recent hyperacute  leptomeningitis is likely the result of septacemia spread from the nasopharyngitis to the leptomeninges. This process likely extended over several days, which accounts for the concurrent presence of inflammatory meningitis in the region of the sella, and hyperacute humeral or early proinflammatory timeframe for the remaining leptomeningitis.

2. There is SWI of an early subdural empyema in the right temporal fossa.

3. The paranasal sinusitis, although prominent is not likely the cause for the leptomeningitis.

1. Primary leptomeningitis spread via septicemia (viral or pyogenic) producing imaging features that evolve in a predictable way. But, leptomeningitis can appear like a primary type, when it is not direct extension from an adjacent paracranial infection, but the initial infections produces a septacemia causing the delay leptomeningitis, while the initial infections produces an adjacent secondary CNS infection. The two components, as in this case, exhibit different stages of activity.

2. Whenever, there are features of leptomeningitis that have features of variable age be especially careful to search for an unusual infections source.