A 33-year-old female presented 3 months postpartum with a headache of moderate severity and progressive visual loss in both eyes. On examination, the patient's Glasgow coma scale (GCS) was 15/15. Visual field examination showed left homonymous incomplete hemianopia. Her visual acuity was 20/25 in the right eye and 20/30 in the left eye. Her discs and macula were healthy bilaterally. Extraocular movements were intact and pupils were reactive. The rest of her examination was unremarkable. Complete endocrine workup was normal.\nMagnetic resonance imaging (MRI) revealed a large heterogeneous, hyperintense, hemorrhagic right suprasellar extra-axial complex cystic structure measuring 31 × 30 × 90 mm on T1-weighted images. There was mass effect on the adjacent hypothalamus and third ventricle displacing them toward the left and superiorly in addition to the optic pathway. The pituitary stalk was displaced toward the left. The lesion encased the right posterior cerebral artery and displaced the right carotid artery laterally []. Computed tomography (CT) arteriography demonstrated a completely thrombosed center. The imaging findings were compatible with suprasellar CM.\nThe patient underwent right frontal craniotomy and gross total resection of her suprasellar intrachiasmatic large infiltrative hemorrhagic CM. Organizing blood clots with reactive fibrohistiocytic and inflammatory reaction admixed with some ectatic vascular channels suggestive of a vascular malformation were noted. There were small foci admixed with granulation tissue, showing some dilated cavernous spaces that would be compatible with a vascular malformation such as cavernous angioma. On immunohistochemistry, the lesion was CD163+, CD20 rare, CD3+, CD34+, CD31+, CD38+, CTK−, EMA plasma cells, GFAP−, S100 dendritic cells, SMA vascular smooth muscle.\nThe patient had an uneventful operative course. Her visual acuity improved to 20/20 in both eyes. Extraocular muscles showed mild limitation of both eyes in an upward gaze. Otherwise, she was stable with no neurological deficits. Follow-up MRI at 12 months revealed complete removal of the suprasellar hemorrhagic CM with no evidence of a residual lesion or recurrence [].
A 71-year-old male without significant medical history presented with sudden binocular diplopia and left frontal headache. Physical examination 48 h after onset of symptoms revealed a partial third cranial nerve palsy on the left side. Initial cerebral magnetic resonance imaging (MRI) demonstrated an 8 mm oval lesion in the anterior left interpeduncular cistern that was hyperintense on T1 and heterogeneous on T2-weighted images [ and ]. On the computed tomography angiography (CTA), the lesion enhanced but did not correspond to an intracranial aneurysm []. The patient was observed. Over the following week, the left third cranial nerve deficit worsened significantly. The ipsilateral pupil was fully dilated and unreactive. Complete ptosis and paralysis of the oculomotor nerve-related muscles were also observed. A second MRI showed ferromagnetic susceptibility signals on gradient echo images []. Constructive interference steady state (CISS) T2-weighted sequences better delineated the lesion and its relation to the oculomotor nerve []. The suspected diagnosis was CA of the third cranial nerve. Given the recent complete third nerve paralysis and the risk of recurrent hemorrhage, surgery was performed.\nSurgery was performed 2 months after onset of symptoms. Through a left subtemporal approach, exposure of the interpeduncular cistern revealed a raspberry-like lesion bulging from the third cranial nerve, anterolateral to the left cerebral peduncle []. A well delineated plane of dissection allowed removal of the lesion while preserving the integrity of the nerve [ and ].\nPostoperative computed tomography (CT) scan showed no complication []. Histopathological analysis showed a lesion with high vascularity and hyalinized channels lined by a single layer of endothelial cells, findings that confirmed the diagnosis of a cavernous angioma []. Six months after surgery, the patient remained with a complete oculomotor palsy.\nWe found eight surgical cases of oculomotor nerve CA [].[] Three patients presented with a pure oculomotor nerve deficit,[] two cases had mixed ophthalmic and oculomotor nerve symptomatology[] and one case had an optic nerve deficit in addition to ophthalmic and oculomotor nerve involvement.[] In two cases, despite the fact that the CA location was proven to be on the third cranial nerve intraoperatively, no oculomotor nerve deficit was found at presentation: One had only ipsilateral trigeminal symptoms[] and the other had pituitary dysfunction with ipsilateral optic nerve deficit.[]\nIn the six patients with oculomotor nerve palsy, three cases presented acutely with complete oculomotor nerve palsy in less than 24 h,[] two cases presented with a partial deficit that worsened to a complete palsy over 7-10 days[] and one patient developed slow progressive partial oculomotor palsy over a 6-month period.[] Cases with severe acute oculomotor nerve deficit at presentation had MRI findings suggesting intralesional hemorrhage such as hyper-T1 and hyper-T2 signals.[] Radiological findings of acute hemorrhage were not found in patients with a more slowly progressive symptomatology.[]\nSeven of the eight cases of oculomotor nerve CA had partial or total resection of the lesion []. Of the five cases with total resection, only one had recovery of nerve function with complete resolution of symptoms after 6 months.[] Of the remaining four patients without recovery, three did not have surgical preservation of nerve integrity.[] One case with partial oculomotor palsy developed immediate postoperative worsening after partial resection followed by subsequent improvement of nerve function.[] One case without preoperative oculomotor nerve deficit developed persistent oculomotor paralysis after partial resection.[]