Orbital involvement (fig 5, 6, 7, 11, 14, 15, 16, 18 and 21) was noted in 60% of cases, presenting as proptosis, optic nerve, and extraocular muscle involvement in the form of heterogeneous enhancing soft tissue in the intra as well as extraconal compartment of orbit  appearing hypointense on T1, hyperintense on T2/FLAIR showing few foci of diffusion restriction on DWI with corresponding low ADC values and few foci of blooming on SWI with corresponding hyperintensity on phase sequence. There are multiple patchy areas of heterogenous post contrast enhancement. Optic neuritis and optic atrophy were each found in 10% of cases, with optic neuritis appearing as abnormal enhancing thickening seen along optic nerve which is showing diffusion restriction on DWI with corresponding low ADC values.

T2/STIR weighted hyperintensity seen involving intraocular, intraorbital and intra canalicular segments of optic nerve with its mild thinning without post contrast enhancement consistent with optic atrophy.

Intracranial extension occurred in 50% of the cases, indicated by cerebral abscess formation and cavernous sinus invasion. Cerebral abscess (fig 1,2,4,8 and 9)were identified as  well defined altered signal intensity peripherally enhancing collections involving predominantly frontal and temporal lobes, brainstem and cerebellum showing mixed signal intensity with predominant T2 hypointense component at patchy areas of T2 hyperintensities within. There is hypointense rim and its showing multiple large areas of diffusion restriction in the contents of the collection which was seen extending into cavernous sinus subsequently leading to cavernous sinus invasion and thrombosis.

Meningeal enhancement (fig 4, 10, 13 and 20) was observed in 40% of cases, appearing as diffuse or nodular enhancement along the meninges on contrast-enhanced T1-weighted images, often corroborated by diffusion-weighted imaging (DWI) to exclude abscess or ischemia.

Vascular complications, such as internal carotid artery thrombosis (fig 3,12,17 and 22)and cavernous sinus thrombosis (fig 4), were identified in 30% of patients. These were most effectively visualized Gradient ECHO MR sequences (VIBE sequence) which demonstrated loss of flow voids, vessel irregularity, and filling defects.

Osteomyelitis was present in approximately 30% of cases, with MRI showing T1-weighted hypo intensity and T2-weighted hyperintensity of the affected bone marrow. Post-contrast T1-weighted imaging demonstrated diffuse enhancement, often extending to adjacent soft tissues, indicative of bone and periosteal involvement.