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.[]
A 40-year-old female patient came to our attention with complains of sudden headache and vision loss. Examination revealed bitemporal hemianopia, diminished visual acuity in both eyes and nuchal rigidity. MRI showed multiple CMs, one of which localized in the optic chiasm, revealing recent bleeding \n[]. The patient had undergone four previous craniotomies at another institution for removal of bleeding CMs in different locations without sequelae. The senior author (JAMC) decided to perform emergent surgical exploration through a right pterional craniotomy, removing the clot and the lesion. Histopathological examination was reported as a CM. On the follow-up, the vision improved and the patient is capable of reading and driving, but 11 years after the surgery a right homonymous hemianopsia persists.