An octogenarian female presented with left sided progressive ptosis and diminution of vision for one year. She was not a diabetic or hypertensive. There was no other significant medical, family or psycho-social history and also no history of interventions in the past. Her vitals were stable, and she was alert, conscious and oriented. Speech and higher mental functions were normal. Extra-ocular muscles showed normal range of motion bilaterally. Left corneal reflex was impaired, and right corneal reflex was intact. No facial hypoesthesia or facial deviation was present.
Imaging was done for further evaluation. Non-contrast computed tomography (NCCT) brain (Fig. 1b) showed a hyperdense mass in middle cranial fossa in left parasellar region with homogenous contrast enhancement (Fig. 1c). There was no calcification (Fig. 1a) or necrotic areas. No associated hyperostosis of the overlying bone (Fig. 1a) or perilesional oedema was present.
Further characterisation of mass was done with magnetic resonance imaging (MRI) brain which showed a well-defined extra-axial mass in left parasellar region which was hypointense on T1 (T1WI) (Fig. 2a), hyperintense on T2 (T2WI) (Fig. 1d, e) and FLAIR (fluid-attenuated inversion recovery) sequences (Fig. 1f). The mass showed intense heterogeneous post-contrast enhancement (Fig. 2b). There was no restricted diffusion within the mass on DWI (Fig. 2c) sequence or corresponding signal drop on ADC (Fig. 2d).There were blooming foci on susceptibility-weighted imaging (SWI) (Fig. 2e).
Mass was extending superiorly up to the left thalamus and ganglio-capsular region. It was also causing mass effect over the foramen of Monroe with dilatation of the lateral ventricles and surrounding periventricular seepage of cerebrospinal fluid (CSF). The lesion was extending up to the orbital apex anteriorly causing narrowing of the optic canal.
Based on CECT brain and contrast MRI of brain, differential diagnosis of a meningioma arising from sphenoid wing or a schwannoma in the left cavernous sinus was given although the imaging findings were not in favour of either of these possible differentials.
In view of encasement of left ICA and MCA by the mass and keeping in mind the possibility of sacrificing the left ICA during the surgery, a pre-operative DSA with balloon occlusion test (BOT) was requested by the neurosurgeon to look for cross-flow via anterior communicating artery in anterior circulation and posterior communicating artery in posterior circulation.
BOT was negative, and patient tolerated the procedure well.
DSA showed blush in the area supplied by M1 segment of left middle cerebral artery at 3.19 s (Fig. 3a, b) and showed progressive filling on delayed venous phase (Fig. 3a, b). This area corresponded with the location of our lesion on prior imaging. Corroborating all the imaging findings, a diagnosis of left parasellar region cavernous sinus haemangioma was concluded.
Patient was taken for surgery with the pre-op diagnosis of left parasellar haemangioma likely arising from left cavernous sinus. Intra-operatively a well-defined mass was present in the region of left cavernous sinus. The mass was reddish and highly vascular with glistening outer surface (Fig. 4A) and was engulfing the left 3rd, 4th and 6th cranial nerves along with the V1 and V2 divisions of left trigeminal nerve. Gross total resection of the mass was done, and haemostasis was achieved. The post-operative course was uneventful. Histopathology report showed dilated and congested, blood-filled vascular channels lined by bland endothelial cells consistent with the diagnosis of CSH (Fig. 4B).
Patient was discharged in satisfactory condition, and on follow-up, there was no residual neurological deficit.