Cisternal, Falciform, and Optic Canal Decompression Influencing Optic Nerve Biomechanics: A Microsurgical Anatomic Study.

BACKGROUND: Questions remain regarding optic nerve (ON) physiology, mechanical compliance, and microvasculature, particularly surgical outcomes and atypical visual field defects associated with sellar/parasellar pathology (eg, tumors and aneurysms). OBJECTIVE: To study the microsurgical/histological anatomy of each ON segment and corresponding microvasculature, calculate area of optic-carotid space at each decompression stage, and measure ON tension before/after compression. METHODS: Five cadaveric heads (10 sides) underwent sequential dissection: (1) intradural (arachnoidal) ON dissection; (2) falciform ligament opening; (3) anterior clinoidectomy, optic canal decompression, and ON sheath release. At each step, we pulled the nerve superiorly/laterally with a force meter and measured maximal mobility/mechanical tension in each position. RESULTS: Cisternal ON microvasculature was more superficial and less dense vs the orbital segment. ON tension was significantly lower with higher mobility when manipulated superiorly vs lateromedially. Optic-carotid space significantly increased in size at each decompression stage and with ON mobilization both superiorly and laterally, but the increase was statistically significant in favor of upward mobilization. At decompression step, upward pull provided more space with less tension vs side pull. For upward pull, each step of decompression provided added space as did side pull. CONCLUSION: Opening the optic canal, falciform ligament, and arachnoid membrane decompresses the ON for safer manipulation and provided a wider optic-carotid surgical corridor to access sellar/parasellar pathology. When tailoring decompression, the ON should be manipulated superiorly rather than lateromedially, which may guide surgical technique, help prevent intraoperative visual deterioration, facilitate postoperative visual improvement, and help understand preoperative visual field deficits based on mechanical factors.

Matricidal cavernous aneurysms: a multicenter case series.

BACKGROUND: Cavernous carotid artery aneurysms (CCAs) represent a unique subset of intracranial aneurysms due to their distinct natural history and the anatomy of the cavernous sinus. Enlarging CCAs can cause elastic compression of the parent internal carotid artery (ICA). We suggest defining aneurysms that cause luminal stenosis of their parent vessels as 'matricidal aneurysms.'Though many patients are asymptomatic, presenting symptoms of CCAs include ophthalmoplegia with resulting diplopia, vision changes, pain, ptosis, facial numbness, and cavernous-carotid fistula. Less commonly, patients with CCAs can present with epistaxis, subarachnoid hemorrhage, and-in cases of matricidal aneurysms-ischemia due to stenosis. The proper management of stenosis caused by a matricidal CCA is not well established and may not be intuitive. METHODS: We present a multicenter retrospective case series of patients with matricidal CCAs. RESULTS: Forty patients with matricidal aneurysms presented with both asymptomatic and symptomatic stenosis. These patients were either treated with conservative medical management, coiling, flow diversion, or endovascular sacrifice of the parent artery. Planned treatment modalities were not executed in 11 cases (28% treatment failure rate). Presenting symptoms, patient outcomes, and follow-up data are presented for all cases. CONCLUSION: Matricidal aneurysms require careful consideration and planning. The restricted anatomy of the cavernous sinus can make successful execution of endovascular interventions more difficult. Direct elastic compression of the parent artery does not respond to angioplasty and stenting in the same way atherosclerotic stenosis does. Because of this, planning for the possibility of parent vessel sacrifice is important.