A 53-year-old woman was admitted to our institution complaining of a mild fever, severe headache, and progressive visual loss that had started 4 days before. On admission, the general condition of the patient and the results of the gross neurological examination were unremarkable. Goldmann perimetry testing showed bitemporal hemianopsia. Her visual acuity was 20/400 in the right and 20/200 in the left eye. A computed tomography scan showed a hyperdense, hemorrhagic mass measuring approximately 2.5 cm in diameter in the suprasellar region []. A magnetic resonance (MR) imaging scan [ and ] better outlined the mass: it affected both the pituitary stalk and the hypothalamus while reaching cranially the left Monro foramen and compressing the optic nerves and chiasm, a clear signal of an ongoing edema. Cerebral angiography showed no vascular malformation. The results of routine blood and serum examinations were normal. Endocrinological studies of the pituitary function were unremarkable. After 3 days, the patient underwent a gross-total resection of the lesion through an extended endoscopic, endonasal, transsphenoidal route. The resection of the lesion was combined with the opening of the third ventricle through the lamina terminalis. A careful reconstruction of the skull base was performed, with abdominal fat, nasal septal flap, and fibrin glue. After the operation, the visual symptoms improved immediately. On discharge, visual acuity was 20/50 in the right eye and 20/20 in the left eye. The patient had a transient incomplete hypopituitarism and mild diplopia which improved after few weeks. After 1 month, the neurological examination was unremarkable. Postoperative MR scan is showed in and . Histological findings confirmed the presence of a CM, showing hemosiderin, reactive fibrohistiocytic, ectatic vascular channels, and dilated cavernous spaces. On immunohistochemistry, the lesion was positive for CD34 staining, marker for endothelial lining, and was negative for elastin staining, thus ruling out an arteriovenous malformation. See showing the main steps of the endoscopic surgery.\nThe PubMed search engine () was used to perform an internet Medline literature research based on the following keywords “chiasma,” “optic,” “sovrasellar,” “CM,” “endoscopic,” and “transsphenoidal” with different combination. There were no limitations as to the timeframe, language, and publication type on the search process. We also cross-checked the references of the articles retrieved by looking for further papers of potential interest.
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.[]