Background: In advanced moyamoya disease (MMD), cerebral perfusion may depend on transdural collaterals from external carotid artery branches. Direct revascularization can provide immediate flow augmentation, but surgical bypass can jeopardize those same compensatory vessels. We describe stage two of a bilateral direct bypass in a patient with recurrent ischemic strokes, focusing on collateral-aware perioperative planning, intraoperative neuroprotection, and graft-flow verification. Case Description: We report a patient in her late fifties with bilateral MMD and multiple prior strokes who underwent staged bilateral superficial temporal artery (STA) to middle cerebral artery (MCA) bypass. Eight days after contralateral revascularization, a left-sided bypass was performed. Intraoperative navigation identified hypertrophied middle meningeal artery (MMA) branches collateralizing to the anterior cerebral artery (ACA), which were preserved to maintain perfusion to the ACA territory. Neuroprotective measures were deployed including papaverine, heparinized saline flush, mild hypothermia, and thiopentone to reduce ischemia during temporary MCA clipping. Controlled hypertension was induced to further enhance collateral flow. Patency was confirmed with Doppler ultrasonography and indocyanine green angiography, and postoperative imaging several months after the second stage confirmed bilateral bypass patency with no new infarction. Conclusion: The educational value of this case lies in distinguishing the STA donor from the MMA collateral pathway and tailoring the bone opening to protect the latter. It demonstrates how staged revascularization, meticulous collateral preservation, targeted intraoperative neuroprotection, and multimodal verification of graft flow can be integrated in the management of complex bilateral MMD and provides practical technical and perioperative lessons for cerebrovascular surgeons undertaking direct bypass in patients with critically flow-dependent collateral circulation.
Background: Microvascular decompression (MVD) is an established etiological treatment for neurovascular compression syndromes, particularly trigeminal neuralgia and hemifacial spasm. Classical techniques often rely on interposition materials; however, recurrence or persistent symptoms may be related to incomplete decompression, implant displacement, excessive material, granuloma formation, recurrent vascular compression, or arachnoid adhesions. Methods: We describe a technical modification of sling-assisted vascular transposition using an extracranial self-locking knot during MVD. In selected patients with neurovascular compression syndromes, including trigeminal neuralgia, hemifacial spasm, recurrent conflicts, or vertebrobasilar dolichoectasia, a standard retrosigmoid approach is performed. After complete release of the arachnoid and circumferential mobilization of the culprit vessel, a sling is fabricated using a suturable, non-absorbable dural substitute. First, an extracranial suture is placed through the dural analog, the mesh is fabricated beneath the vessel, and then the analog is anchored to the tentorium or the petrous dura mater depending on the desired vector. Final adjustment is achieved using an extracranial self-locking knot, which is advanced progressively until adequate decompression is obtained and then locked in position, avoiding deep intracranial knotting. Results: The technique was feasible and reproducible in our initial experience. To date, no complications attributable to the sling construct or extracranial locking mechanism have been observed. Conclusion: The extracranial self-locking knot is a simple technical modification for vascular transposition during MVD. It may facilitate reproducibility and standardization of vascular fixation, particularly in complex, recurrent, or dolichoectatic neurovascular conflicts.
Background: Middle meningeal arteriovenous fistula (MMAVF) is a rare dural arteriovenous shunt that may occur after head trauma and can be associated with acute epidural hematoma (AEDH). Although spontaneous closure has been reported, treatment decisions may be challenging when a large shunted venous pouch is present despite the absence of cortical venous reflux (CVR). Case Description: A man in his 60s sustained a moderate traumatic brain injury after falling down the stairs. Initial computed tomography (CT) revealed right AEDH, right temporal bone fracture, left acute subdural hematoma, traumatic subarachnoid hemorrhage, and pneumocephalus. CT angiography (CTA) on postinjury day 6 suggested MMAVF at the fracture site. Digital subtraction angiography revealed multiple shunt points along the petrosquamous branch of the middle meningeal artery (MMA) with drainage predominantly into a large venous pouch. No CVR was observed. Given the large shunted venous pouch and concern for potential hemorrhagic risk, endovascular embolization was performed, resulting in occlusion of the dominant shunt point and near-complete obliteration of the shunt complex. Follow-up CTA showed no obvious enhancing vascular lesion suggestive of persistent shunting. Conclusion: In selected patients with head trauma, particularly those with AEDH and a fracture line crossing the MMA territory, CTA may be considered a minimally invasive screening tool for associated vascular lesions. Even without CVR, traumatic MMAVF with multiple shunt points and a large shunted venous pouch may warrant endovascular treatment based on angioarchitecture. The distinctive angioarchitecture observed in the present case may provide insight into the pathophysiology of traumatic MMAVF.
Background: Dural-based lesions are typically suggestive of meningiomas; however, metastatic tumors such as clear cell renal cell carcinoma (RCC) may closely mimic this presentation, posing diagnostic and surgical challenges. Case Description: A 68-year-old male presented with a progressively enlarging right parietal mass. Imaging demonstrated an extra-axial lesion with calvarial involvement and intracranial extension, initially suggestive of meningioma. The patient underwent surgical resection, which revealed a highly vascular lesion with bone destruction and no clear dural plane. Histopathological and immunohistochemical analysis confirmed metastatic clear cell RCC. Conclusion: Calvarial lesions with osteolysis and extracranial extension should raise suspicion for metastatic disease. RCC metastases may mimic meningiomas radiologically but differ significantly in intraoperative behavior, particularly due to their hypervascularity. Recognizing these features is essential for appropriate surgical planning and management.
Background: Very late recurrence of glioblastoma (GBM) after prolonged progression-free survival is exceptionally rare, particularly in patients who did not receive temozolomide. Such cases offer a rare window into the biological heterogeneity and dormancy potential of an otherwise rapidly lethal tumor. Case Description: A middle-aged man underwent gross total resection of an isocitrate dehydrogenase (IDH)-wild-type GBM followed by adjuvant radiotherapy alone (45 Gy/25 fractions), temozolomide having been unavailable for financial reasons. He remained clinically and radiologically disease-free for approximately 8 years before developing progressive headache and memory impairment. Magnetic resonance (MR) imaging demonstrated a large recurrent left frontotemporal mass with extensive edema and corpus callosum involvement. Multivoxel MR spectroscopy showed a markedly elevated choline-to-creatine ratio (4.5) with reduced N-acetylaspartate, favoring recurrent high-grade glioma over radiation necrosis. Repeat biopsy confirmed recurrent GBM with a molecular profile of IDH1/IDH2 wild-type status, telomerase reverse transcriptase promoter mutation, epidermal growth factor receptor amplification, CDKN2A/B homozygous deletion, PTEN alteration, and a methylated O6-methylguanine-DNA methyltransferase promoter. Conclusion: This case illustrates that very late recurrence can occur in IDH-wild-type GBM after radiotherapy alone, despite aggressive molecular features, and supports the emerging biological model of therapy-induced tumor cell dormancy. It reinforces the need for long-term surveillance and repeat molecular profiling at recurrence to guide individualized salvage therapy.
