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 27-year-old gentleman, presented with 3 months history of blurring of vision associated with headache. There was no history of loss of consciousness, seizures, or weakness in limbs. Visual examination showed acuity of 6/6 bilaterally with left temporal field defect.\nMRI of brain, T1W, T2 axial, contrast and multiplanar sequences were performed which showed evidence of lobulated mixed signal intensity lesion seen in the optic chiasm, measuring 18 × 11 mm. Multiple hemorrhagic foci of varying sizes were seen within the lesion. No obvious enhancement was seen after IV contrast material injection. On the right side, the lesion was extending anteriorly up to the optic canal and superiorly abutting the hypothalamus. The features were suggestive of CM of the optic chiasm [Figures and ].\nThe lesion was removed neuro-endoscopically through the trans-nasal trans-sphenoidal route. After reaching the sella, dura opened and the pituitary gland was displaced. Under-surface of chiasm was visualized. The lesion was seen on the surface with brownish discoloration. A small incision was made and the lesion could be removed. Post–operatively, there was a transient worsening left temporal field defect. The histopathological examination and features are consistent with organizing hematoma.