A 40-year-old female with past medical history of migraine and no family history of CM, presented with unilateral scotomas with a gradual onset over 7 months and progressive visual deterioration, referred as blurred vision of the right eye (RE), with a significant worsening few days before seeking medical care.\nShe was initially admitted at Ophthalmology outpatient clinic for observation. The ophthalmologic evaluation revealed a decreased visual acuity (7/10) and a visual field defect on the RE. Her left eye (LE) was completely normal (10/10, without field defect). The computerized campimetry (CC) disclosed a supero-inferior arciform defect in the RE. LE CC was normal [].\nVisual evoked potential responses showed results compatible with a right second cranial nerve dysfunction due to compressive optic neuropathy on the RE. A noncontrast enhanced computed tomography (CT) scan was performed and revealed a spontaneous hyperdense focal nodular lesion, heterogeneous, with irregular contours and a punctate area of increased attenuation coefficient related to calcification, on the right optic-carotid cistern, adjacent to the ipsilateral ON. No surrounding edema or mass effect was documented. No evidence of subarachnoid or intraventricular hemorrhage [].\nBased on the CT scan result, the patient was referred to the outpatient clinic of the Neurosurgery Department. She completed the diagnostic neuro-imaging evaluation with a CT angiography (CTA) [], a magnetic resonance imaging (MRI), and a MR angiography (MRA) of the brain.\nThe MRI showed a focal solitary well-defined rounded lesion involving the right ON in its intracranial prechiasmatic segment, sparing the chiasm. The T1-weighted noncontrasted sequence showed a spontaneously hyperintense lesion [Figures -]. In the T2-weighted MRI, the lesion exhibited a heterogeneous signal intensity and a peripheral hypointense rim [. No large vessels adjacent to the lesion were identified.\nThe MRA demonstrated a hyperintense mass due to hemosiderin. No enlarged vessels were identified [].\nThese features were considered to be consistent with an occult vascular malformation, presenting an inner hematoma (blood and blood by-products in various states of evolution) surrounded by a peripheral hemosiderin rim, suggesting the diagnosis of a CM of the intracranial segment of the right ON.\nThe patient complaints remained unchanged for one week. After this period of time, she was electively operated on, through a right pterional craniotomy. An intradural optic canal unroofing, through a drilling technique, was performed to completely expose and microsurgically remove the CM []. The CM was found over the superior surface of the ON at the entrance of the optic canal with an anterior canalicular extension.
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 .