A 26-year-old man was admitted for recurrent headaches, loss of vision in his left eye, and elevated blood pressure. His loss of sight had been gradual, manifesting for over six months before hospitalization. He also exhibited episodes of inadequate behavior with some aggression. The patient was conscious at admission, and no other meningeal or focal neurological symptoms were found. The patient consented to publication of his protected health information.\nHis right and left eyes had logarithm of the minimum angle of resolution visual acuities of 1.0 and 0.2, respectively. T1-weighted magnetic resonance imaging (MRI) showed a hyperintense signal mass lesion occupying his chiasm and left ON (Figure ). These findings led to a diagnosis of high-grade glioma of the chiasm and left ON, or CM.\nSurgery was performed with the patient in the supine position, with his head slightly elevated and turned to the right side about 30 degrees. A left frontolateral craniotomy was performed to optimize the approach to the chiasm and left ON. Fenestration of the basal cistern and aspiration of cerebrospinal fluid yielded a relaxed brain with satisfactory gravity retraction. The left optic canal was unroofed, and several blood clots at different stages of resorption were evacuated through the longitudinal dissection of the ON. Minimal coagulation currents were applied to occlude the feeding vessels with their sharp sections. Resection was estimated to be gross total (Video ).\nThere were no surgical complications, and MRI performed six months later showed no signs of CM recurrence (Figure ). The patient was discharged after seven days, and his vision returned to normal three months later. He is still in touch with us and has reported no signs of visual deterioration or recurrent bleeding.\nThe microscopic structure of the resected CM with heterochromous thromboses is shown in Figure .
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.[]