BACKGROUND
Tuberculum sellae meningiomas frequently extend into the optic canals, which leads to a progressive longitudinal visual loss. Therefore, in addition to tumor removal, unroofing and exploration inside the optic canal are important procedures.
OBJECTIVE
To perform endoscopic endonasal tumor removal with optic canal decompression for small primary or recurrent meningiomas associated with a progressive visual loss at the inferior-medial optic canal, which corresponded to a blind corner in the ipsilateral pterional/subfrontal approach.
METHODS
We retrospectively reviewed 2 cases of primary meningiomas that arose in the inferior-medial optic canal and 4 recurrent cases from the remnant inside the medial optic canal that had previously undergone craniotomy for tuberculum sellae meningiomas, and were treated by the endoscopic endonasal approach.
RESULTS
All tumors were detectable and could be removed without manipulation of the affected optic nerve. The average maximum diameter of the tumor was 8.4 mm (range: 5-12 mm). Two patients who had a long history of progressive visual disturbance and papillary atrophy did not recover from severe visual disturbances postoperatively. However, others showed considerable improvement, maintaining postoperative visual function during follow-up. There were no postoperative complications.
CONCLUSION
Endoscopic endonasal approach has several advantages for meningiomas in the medial optic canal and associated with progressive visual disturbance. In surgery of tuberculum sellae meningiomas, optic canal decompression and exploration inside the optic canal are important procedures to avoid symptomatic recurrence, which may be facilitated by the endoscopic endonasal approach. Papillary atrophy and duration of visual deterioration are predictive factors for postoperative visual outcomes.
We report a case of bypass surgery for a cerebrovascular ischemic event caused by giant cell arteritis (GCA). A 70-year-old female with transient right hemiparesis was admitted to our hospital. Diffusion-weighted imaging showed acute infarction of the left subcortical watershed areas. Magnetic resonance angiography (MRA) showed severe stenosis at the left cavernous portion of the intracranial internal carotid artery. Despite intravenous anticoagulation therapy, her right hemiparesis worsened. An emergent left superficial temporal artery-middle cerebral artery (STA-MCA) bypass was performed. The intima of the STA was markedly hypertrophic. We identified abnormal tissue and part of the STA was sent for pathological examination. After bypass surgery, the neurological findings transiently improved; however, exacerbation of the right hemiparesis and aphasia occurred on the second postoperative day. Increasing acute cerebral infarction was identified on magnetic resonance imaging, and MRA showed that the bypass was occluded. An occipital artery (OA)-MCA anastomosis was added, but the bypass occluded again. The postoperative pathologic diagnosis was GCA in both the STA and OA. Strokes associated with GCA are rare and difficult to distinguish from atherothrombotic cerebral infarction. When a donor blood vessel abnormality is observed during bypass surgery, rapid pathological diagnosis is recommended to avoid bypass failure.
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