Meningoencephalitis with venous sinus thrombosis with venous infarcts
Presentation
Post syncope with headache and midline spinal tenderness. Febrile, raised inflammatory markers, upper limb weakness, right lower limb weakness. Altered sensation in the lower limb. Immunocompromised. Past medical history of HIV, intra-abdominal TB, osteopenia.
Patient Data
The density of the superior sagittal sinus is unusually high for a non- contrast study and is concerning for superior sagittal sinus thrombosis. Bilateral parietal low-density lesions with generalized effacement of the convexity sulci, suspicious for venous infarcts int his setting. No hemorrhagic transformation. No extra-axial collection.
Patchy subcortical and cortical based T2/FLAIR high signal regions at the posterior aspects of the frontal lobes and the convexities of the parietal and occipital lobes, corresponding to regions of diffusion restriction. Associated susceptibility artefact within the largest of the cortical based T2 high signal regions at the right occipital lobe suggestive of hemorrhagic transformation.
Filling defect within the superior sagittal sinus extending into the right transverse sinus and sagittal sinus to the level of the jugular bulb. Left transverse sinus is nondominant. Marked pachymeningeal enhancement throughout the brain. Leptomeningeal enhancement is noted at the convexities of the posterior frontal lobes, the parietal and occipital lobes. No discrete extra-axial collections identified.
Linear susceptibility artefact is also noted at the left occipital lobe - probably sulcal. Downward transtentorial or tonsillar herniation with complete effacement of suprasellar cistern, no hydrocephalus.
Case Discussion
Extensive dural venous sinus thrombosis with with patent but nondominant left transverse/sigmoid sinuses. In this context, bilateral diffusion restricting abnormalities are presumably venous infarcts.
The pachymeningeal enhancement and leptomeningeal enhancement is concerning for infection in the context of sepsis and immunosuppression.
Downward transtentorial herniation and tonsillar herniation is presumably due to a combination of venous hypertension and cerebral edema.
Overall, meningoencephalitis with superimposed extensive venous thrombosis and venous ischemia is favored.
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