There are at least two distinct enhancing intra-axial lesions within the left frontal lobe.
The larger one centered within the posteromesial orbitofrontal region, probably within the rectus gyrus measuring approximately 2.5 x 2 x 1.5 cm in maximum perpendicular dimension (AP x LR x CC), which associated with its significant surrounding vasogenic oedema is causing less approximately 1 cm midline shift, deforming and displacing the traversing ACAs with flow signal void preserved.
The second smaller lesion is subcortical within the middle frontal gyrus, measuring approximately 7 x 7 x 8mm in perpendicular dimension. This is also surrounded by a significant vasogenic oedema causing mass effect, effacing the sulci.
Vasogenic edema extends through the genu and body of the corpus callosum into the contralateral hemisphere, effacing the frontal horn of the lateral ventricles bilaterally. There is no hydrocephalus at this stage.
There are also small poorly defined enhancing foci ventral to the smaller lesion. Another small subcortical focus of abnormal enhancement was also noted within the triangular portion of the right inferior frontal gyrus, which is only visible on one slice, with no significant surrounding parenchymal edema.
Diffusion characteristic of these lesions is equivocal with no definite true restriction identified. Signal characteristics on the other sequences are also nonspecific.
On MRS, the selected voxel demonstrates significant increased choline to creatinine ratio (at 3.2 and 3ppm respectively) and decreased NAA at 2ppm. This is associated with a moderate increased lactate at 1.3ppm.
No leptomeningeal enhancement was identified. Intracerebral arteries are grossly normal.
Within the left frontal sinus material of slightly increased T1 and low T2 signal is noted . No contrast enhancement is seen. There is poor definition of the posterior aspect of the sinus wall both on MR and CT. No subdural empyema is seen. No leptomeningeal enhancement.
CBV maps shows gyriform areas of elevated CBV distinct from the contrast enhancing areas.
NGT was noted.
Conclusion: Despite the MRS findings which is suggestive for tumoral lesions, e.g. high grade glioma; in this clinical setting (febrile and septic, as stated by the clinical teams) the multiplicity of the lesions, changes in the left frontal sinus and discordant findings between contrast enhanced scans and CBV maps, favours an infective process (multiple foci of cerebritis) over the neoplasm.
Further follow up will be of use .