Unilateral blindness and complete ophthalmoplegia following middle cerebral artery aneurysm clipping: a case report.

BACKGROUND

Middle cerebral artery (MCA) aneurysms rarely cause ophthalmic complications due to their anatomical distance from ocular structures. We report an exceedingly rare case of acute unilateral blindness and complete ophthalmoplegia following MCA aneurysm clipping via a pterional/trans-sylvian approach, a complication not previously documented in the literature with concurrent optical coherence tomography (OCT) findings.

CASE PRESENTATION: A 49-year-old man with a history of hypertension presented with a severe headache. Computed tomography (CT) and angiography confirmed a subarachnoid hemorrhage (SAH) secondary to a ruptured complex aneurysm of the left MCA. Preoperative MRI also revealed significant ipsilateral sinusitis. He underwent an emergent left pterional craniotomy with a trans-sylvian approach; proximal control was achieved on the M1 segment, and the aneurysm was clipped. Notably, no dissection or manipulation of the internal carotid artery (ICA) or opticocarotid cistern was performed. Twenty-four hours postoperatively, he developed no light perception (NLP) vision, complete ophthalmoplegia, ptosis, chemosis, and reduced corneal sensation in the left eye. Fundus examination revealed diffuse retinal whitening without a cherry-red spot, and optical coherence tomography (OCT) showed inner retinal edema, suggestive of probable ophthalmic artery occlusion (OAO) or orbital infarction syndrome, inconsistent with direct MCA aneurysm effects. The right eye was normal. MRI/MRA and fluorescein angiography were not feasible due to his unstable condition. Three days later, rehemorrhage prompted reoperation, but he suffered cardiopulmonary arrest and died.

CONCLUSION

To our knowledge, this is the first reported case of OCT-documented inner retinal ischemia and complete ophthalmoplegia following a pterional/trans-sylvian clipping of an MCA aneurysm. It highlights the risk of rare, indirect ischemic injury to the orbital apex, potentially via retrograde microembolic or hemodynamic mechanisms, emphasizing the need for multidisciplinary awareness even in surgeries remote from the optic apparatus.