High-flow bypass for giant dolichoectatic vertebrobasilar aneurysms: illustrative cases

Richard Shaw Department of Neurosurgery, Royal Prince Alfred Hospital, Camperdown, Sydney, New South Wales, Australia; and

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Alistair Kenneth Jukes Department of Neurosurgery, Royal Prince Alfred Hospital, Camperdown, Sydney, New South Wales, Australia; and
Department of Neurosurgery, Royal Adelaide, Adelaide Women’s and Children’s Hospitals, Adelaide, South Australia, Australia

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Rodney Stewart Allan Department of Neurosurgery, Royal Prince Alfred Hospital, Camperdown, Sydney, New South Wales, Australia; and

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BACKGROUND

Giant fusiform dolichoectatic vertebrobasilar artery aneurysms are challenging lesions with a poor natural history. When there is progressive brainstem compression from these lesions, endovascular treatment can be insufficient, and bypass surgery remains a possible salvage option. High-flow bypass surgery with proximal occlusion can potentially arrest aneurysm growth, promote aneurysm thrombosis, and reduce rupture risk. The authors describe their experience in two patients with giant fusiform dolichoectatic vertebrobasilar artery aneurysms treated with high-flow bypass.

OBSERVATIONS

Both patients presented with enlarging giant dolichoectatic vertebrobasilar aneurysms causing symptomatic brainstem compression. The authors performed staged treatment involving high-flow bypass from the external carotid artery to the posterior cerebral artery using a saphenous vein graft, Hunterian proximal vertebrobasilar occlusion, and finally posterior fossa decompression with or without direct aneurysm thrombectomy and debulking. Postoperative angiography revealed successful flow reversal, aneurysm exclusion, and no brainstem stroke. Clinically, one patient had improvement in their modified Rankin Scale (mRS) score from 3 preoperatively to 1 at 12-month follow-up. The second patient had a deterioration in their mRS score from 4 to 5 at 12-month follow-up.

LESSONS

High-flow bypass strategies remain high risk but can be a viable last resort in patients with neurological deficits and enlarging giant fusiform dolichoectatic vertebrobasilar artery aneurysms.

ABBREVIATIONS

BA = basilar artery; ECA = external carotid artery; EC-IC = extracranial-to-intracranial; MRI = magnetic resonance imaging; mRS = modified Rankin Scale; PCA = posterior cerebral artery; PICA = posterior inferior cerebellar artery; SCA = superior cerebellar artery; STA = superficial temporal artery; SVG = saphenous vein graft; VA = vertebral artery

BACKGROUND

Giant fusiform dolichoectatic vertebrobasilar artery aneurysms are challenging lesions with a poor natural history. When there is progressive brainstem compression from these lesions, endovascular treatment can be insufficient, and bypass surgery remains a possible salvage option. High-flow bypass surgery with proximal occlusion can potentially arrest aneurysm growth, promote aneurysm thrombosis, and reduce rupture risk. The authors describe their experience in two patients with giant fusiform dolichoectatic vertebrobasilar artery aneurysms treated with high-flow bypass.

OBSERVATIONS

Both patients presented with enlarging giant dolichoectatic vertebrobasilar aneurysms causing symptomatic brainstem compression. The authors performed staged treatment involving high-flow bypass from the external carotid artery to the posterior cerebral artery using a saphenous vein graft, Hunterian proximal vertebrobasilar occlusion, and finally posterior fossa decompression with or without direct aneurysm thrombectomy and debulking. Postoperative angiography revealed successful flow reversal, aneurysm exclusion, and no brainstem stroke. Clinically, one patient had improvement in their modified Rankin Scale (mRS) score from 3 preoperatively to 1 at 12-month follow-up. The second patient had a deterioration in their mRS score from 4 to 5 at 12-month follow-up.

LESSONS

High-flow bypass strategies remain high risk but can be a viable last resort in patients with neurological deficits and enlarging giant fusiform dolichoectatic vertebrobasilar artery aneurysms.

ABBREVIATIONS

BA = basilar artery; ECA = external carotid artery; EC-IC = extracranial-to-intracranial; MRI = magnetic resonance imaging; mRS = modified Rankin Scale; PCA = posterior cerebral artery; PICA = posterior inferior cerebellar artery; SCA = superior cerebellar artery; STA = superficial temporal artery; SVG = saphenous vein graft; VA = vertebral artery

Giant fusiform dolichoectatic vertebrobasilar aneurysms are rare lesions accounting for less than 1% of intracranial aneurysms.1,2 They are often significantly thrombosed with intramural hemorrhage and thrombus propagation contributing to progressive enlargement and symptoms.3 Although their pathogenesis is unclear, many factors have been implicated. Common vascular risk factors, such as hypertension, as well as other forms of arterial injury, such as dissection or dysplasia, can result in matrix metalloproteinase dysfunction within the arterial wall.4 Histological examinations have revealed that internal elastic lamina fragmentation and neoangiogensis within a thickened intima can lead to subsequent intramural hemorrhage and thrombus formation.3,4 Anatomical variations such as the absence of posterior communicating arteries can also contribute to the hemodynamic stress and morphological changes that propagate this process.

Giant fusiform dolichoectatic vertebrobasilar aneurysms have a poor natural history. Steinberg et al.5 reported that 80% of patients with giant vertebrobasilar aneurysms were either dead or severely disabled within 5 years of presentation. In another series, Xu et al.6 reported that 42% of dolichoectatic vertebrobasilar aneurysms had radiological progression and that 44% had deterioration in their modified Rankin Scale (mRS) scores over a mean follow-up of 50.1 months. Treating giant fusiform dolichoectatic vertebrobasilar aneurysms is also challenging. Their size and morphology make direct clipping impossible; they are difficult to access surgically and can involve vital brainstem perforators. Earlier strategies by Drake and colleagues7,8 involved Hunterian ligation of the vertebral artery (VA) or basilar artery (BA). However, this required adequate collateral flow from the posterior communicating arteries, which are often absent. Endovascular flow diversion has also had modest outcomes compared with its success at other locations without brainstem perforators.9 In a meta-analysis, Kiyofuji et al.10 found a 47% mortality rate or significant morbidity associated with flow diversion. Periprocedural stroke occurred in 23% of cases, and long-term aneurysm occlusion occurred in only 52% of cases.

Extracranial-to-intracranial (EC-IC) bypass has been advocated as a means of preventing ischemic strokes from aneurysm thrombosis. This can be achieved by grafting the superficial temporal artery (STA) to the posterior cerebral artery (PCA) or superior cerebellar artery (SCA). It results in the delivery of approximately 30 mL/minute of blood flow with the capacity to dilate and increase over time.11 Alternatively, a high-flow bypass using an interpositional saphenous vein or radial artery can be used and likely delivers considerably more immediate blood flow. In combination with Hunterian ligation, it is possible to sufficiently reduce the risk of brainstem stroke while also preventing further aneurysm growth or hemorrhage. We present two illustrative cases from our clinical experience in the treatment of giant fusiform dolichoectatic vertebrobasilar aneurysms through high-flow bypass surgery and Hunterian ligation.

Illustrative Cases

Case 1

Clinical Presentation

An otherwise healthy 16-year-old male had initially presented 2 years earlier with symptoms of brainstem compression. He had progressive headaches, nausea, vomiting, and ataxia as well as evidence of lower cranial nerve dysfunction with dysphagia and impaired cough reflex. His preoperative mRS score was 3.

Initial magnetic resonance imaging (MRI) and angiography demonstrated a fusiform aneurysm extending from the right VA (at the level of the posterior inferior cerebellar artery [PICA] origin) to the proximal BA, with a maximal transverse diameter of 26 mm (Fig. 1). Of note, he also had small posterior communicating arteries bilaterally. His initial treatment 2 years earlier had involved a right far lateral craniotomy for clip ligation of his right VA (Hunterian ligation) as well as a PICA-PICA bypass. Over the subsequent 2 years, the right VA segment of the aneurysm had thrombosed and occluded. However, there was progressive enlargement of the BA aneurysm with further brainstem compression. A 19-mm left PICA aneurysm had also formed adjacent to the PICA-PICA anastomosis and was compressing the brainstem posteriorly (Fig. 1).

FIG. 1
FIG. 1

Case 1. Preoperative imaging. A: Initial three-dimensional (3D) digital subtraction angiography (DSA), left VA injection, when the patient was 14 years old, showing a giant fusiform aneurysm involving the right VA (arrow) and proximal basilar trunk (asterisk). B: Initial sagittal postcontrast T1-weighted MRI showing partial thrombosis within the aneurysm (arrow) with significant brainstem compression. C: Postoperative 3D DSA, left VA injection, when the patient was 14 years old, showing the persistent basilar aneurysm component (asterisk) and patency of the PICA-PICA bypass (arrow). D: Follow-up sagittal computed tomographic angiogram when the patient was 16 years old, showing persistence of the basilar aneurysm component and new left PICA aneurysm formation posteriorly adjacent to the previous bypass (arrow).

Surgical Treatment Strategy

Given his progressive and symptomatic brainstem compression from the enlarging basilar aneurysm as well as his new PICA aneurysm, the patient required a more definitive treatment strategy, which was performed in a staged fashion. Stage 1 involved a right external carotid artery (ECA)-to-PCA (P2) high-flow bypass to establish an alternative posterior circulation (see High-Flow Bypass Technique). After successful bypass was confirmed with clinical assessment and postoperative angiography (Fig. 2), stage 2 was performed 1 week later. This involved a translabyrinthine and transcochlear approach to provide direct basilar trunk access. As seen in Fig. 3, aneurysm clip occlusion of the left VA (distal to the PICA origin) was used to complete Hunterian ligation of the remaining aneurysm inflow (the right VA having been occluded 2 years prior). Aneurysm clip occlusion of the basilar trunk distal to the aneurysm was also performed, thereby trapping the aneurysm. The final-stage (stage 3) surgery involved a suboccipital craniectomy for posterior fossa decompression, resection of the left PICA aneurysmal segment, and reanastomosis to maintain patency of the previous PICA-PICA bypass.

FIG. 2
FIG. 2

Case 1. Postoperative right common carotid artery (CCA) injection, anteroposterior (A) and lateral (B) views, revealing right ECA-to-PCA (P2) high-flow bypass with SVG (black arrows). Revascularization of the proximal BA and its distal branches seen through flow reversal from the SVG (black arrows). C: Final postoperative sagittal postcontrast T1-weighted MRI after successful high-flow bypass, left PICA aneurysm resection, and posterior fossa decompression, showing improvement in the extent of brainstem compression (arrow).

FIG. 3
FIG. 3

Case 1. Left transcochlear intraoperative view showing proximal clip occlusion of the left VA (white arrow) between the lower cranial nerve rootlets. The giant dolichoectatic BA aneurysm is seen distal to the aneurysm clip (asterisk).

Initial Surgical Outcome

A postoperative angiogram confirmed high-flow bypass patency with flow reversal in the distal BA (Fig. 1). There was no residual flow seen in the vertebrobasilar aneurysm, indicating successful trapping. The patient also had successful resection of the left PICA aneurysm, and PICA-PICA reanastomosis patency was confirmed with computed tomography angiography. Postoperative MRI showed no evidence of brainstem ischemic stroke. The patient developed left facial weakness and hearing loss after the translabyrinthine/transcochlear trapping of the vertebrobasilar aneurysm. He also developed hydrocephalus requiring insertion of a ventriculoperitoneal shunt. His dysphagia and impaired cough were initially unchanged postoperatively. His preoperative mRS score of 3 remained unchanged at the time of hospital discharge.

Follow-Up

At 12-month follow-up, the patient had regained independent function (mRS score 1) and had returned to school. He underwent successful facial reanimation surgery and insertion of a cochlear implant. There was no evidence of aneurysm filling or growth at the last follow-up more than 2 years postoperatively.

Case 2

Clinical Presentation

A 52-year-old male had a history of smoking, hypertension, and hyperlipidemia. He had a ventriculoperitoneal shunt in situ due to hydrocephalus secondary to his giant aneurysm. He had also had a pontine ischemic stroke 6 years prior and required a walking aid to mobilize. At the time of presentation to our institution, he had urinary incontinence and severe gait disturbance and could no longer mobilize independently. He had a preoperative mRS score of 4.

Preoperative MRI and angiography demonstrated a giant fusiform dolichoectatic aneurysm from the intracranial origin of the left VA to the basilar tip with a maximal transverse aneurysm diameter of 40 mm (Fig. 4). The patient had bilaterally absent posterior communicating arteries.

FIG. 4
FIG. 4

Case 2. A: Preoperative sagittal postcontrast T1-weighted MRI showing the giant aneurysm with significant circumferential thrombosis (white arrow), residual central filling (black arrow), and brainstem compression (asterisk). B: Preoperative three-dimensional digital subtraction angiography (DSA), left VA injection, confirming central patency through the vertebrobasilar aneurysm. C and D: Postoperative DSA with sequential right CCA injection, anteroposterior views, showing patent ECA-to-PCA (P2) high-flow bypass with SVG (white arrows). Flow reversal seen with distal-to-proximal filling of the BA and VA (black arrows).

Surgical Treatment Strategy

Using a staged strategy, the patient underwent a right ECA-to-PCA (P2) high-flow bypass to establish an alternative posterior circulation. Clip ligation of the extracranial right VA was performed at the same operation as the high-flow bypass (through a separate retromastoid incision in the same operative position). A postoperative angiogram confirmed the patency of the bypass graft before the left extracranial VA was then occluded endovascularly with coils, thereby completing proximal Hunterian occlusion of the aneurysm. The next stage involved a suboccipital craniectomy and C1 laminectomy for posterior fossa decompression. Finally, a right subtemporal approach for internal debulking and thrombectomy of the basilar aneurysm was performed.

Initial Surgical Outcome

The patient had technically successful high-flow bypass and bilateral VA Hunterian ligation. Postoperative angiography confirmed bypass patency and flow reversal in the BA and VA (Fig. 4). Three days later, he developed an acute right temporal intracerebral and subdural hemorrhage that required a craniectomy. His previous ventriculoperitoneal shunt had also become blocked and required temporary external ventricular drainage before eventual shunt replacement.

Despite these complications, MRI performed at 1 and 3 months postoperatively showed no evidence of new brainstem stroke. However, he made a poor neurological recovery and had a postoperative mRS score of 5. He was discharged to a high-level care nursing facility.

Follow-Up

The patient demonstrated no evidence of aneurysm growth, and his bypass remained patent on all follow-up imaging. Despite this, he demonstrated no significant neurological recovery at 12 months (mRS score 5). The patient died 24 months after surgery. The cause was not investigated but was presumed to be secondary to aspiration pneumonia.

The surgical treatment strategy used in both patients is summarized in Table 1.

TABLE 1

Patient characteristics and surgical treatment

Case No.Age (yrs)/SexPresentationPast Medical HistoryAneurysm MorphologyPreop mRS ScoreAneurysm Treatment StrategyComplications12-Mo Postop mRS ScoreLast FU mRS Score
116/MHeadache, nausea, vomiting, ataxia, lower CN dysfunctionPrevious rt VA Hunterian ligation & PICA-PICA bypassGiant, fusiform aneurysm from rt VA (PICA origin) to proximal BA; 2nd large lt PICA aneurysm3Rt ECA-PCA (P2) bypass w/ SVG; TL/TC trapping of aneurysm; pst fossa decompression + PICA aneurysm resection & reanastomosisHCP, CNVII & VIII palsy, dysphagia, HAP11 (24 mos)
252/MHeadache, ataxia, urinary incontinence, blurred visionPrevious ischemic pontine stroke, HCP w/ VPS, HTN, hyperlipidemiaGiant, fusiform aneurysm from lt VA to BA apex4Rt ECA-PCA (P2) bypass w/ SVG + rt VA clip occlusion; lt VA coil occlusion; pst fossa decompression; subtemporal ultrasonic aneurysm debulkingSDH & ICH, HCP & blocked VPS, DVT/PE, HAP56 (24 mos)

CN = cranial nerve; DVT = deep vein thrombosis; HAP = hospital-acquired pneumonia; HCP = hydrocephalus; HTN = hypertension; ICH = intracerebral hematoma; PE = pulmonary embolism; PICA = posterior inferior cerebellar artery; pst = posterior; SDH = subdural hematoma; TL/TC = translabyrinthine/transcochlear; VPS = ventriculoperitoneal shunt.

High-Flow Bypass Technique

Both patients had insufficient posterior communicating artery collateral supply. Consequently, we elected to perform an ECA-to-PCA (P2) high-flow bypass to initially establish an alternative posterior circulation before proximal Hunterian ligation. Although a detailed description of this surgical technique has been published previously,12 we herein describe some key tenets of our bypass strategy.

Preoperatively, patients are started on aspirin (300 mg/day), and this is continued postoperatively. After the induction of general anesthesia, a lumbar drain is inserted to assist with cerebrospinal fluid relaxation. The patient is positioned supine with an ipsilateral shoulder roll to allow the head to be turned parallel to the floor. The proximal carotid bifurcation is exposed through a linear incision along the medial border of the sternocleidomastoid muscle, and the proximal ECA is isolated. A standard subtemporal craniotomy and approach is then performed to identify the P2 segment of the PCA medial to the tentorial edge and a suitable graft insertion site. A generous segment of the great saphenous vein is exposed and harvested from between the ankle and knee. Venous branch points are ligated with LIGACLIPs. The graft distance is carefully measured between both ECA and PCA recipient sites before final vein harvest. We do not reverse the graft or use a valvulotome because of the potential endothelial damage and increased thrombosis risk. Similarly, we do not routinely tunnel the graft between incisions and instead connect our cranial and cervical neck incisions to directly inlay the graft in a subcutaneous plane. Prior to commencing the anastomoses, mild hypertension and thiopentone burst suppression are induced. A small dose of intravenous heparin (3000 units) is administered. The distal end-to-side anastomosis from saphenous vein graft (SVG) to PCA is performed first using an 8-0 nylon suture in a continuous technique before another end-to-side anastomosis is performed to the ECA using 7-0 nylon in a similar fashion.

Neuromonitoring with electroencephalography, motor evoked potentials, and somatosensory evoked potentials is used throughout the operation. Intraoperative bypass patency is confirmed with Doppler ultrasound and indocyanine green video angiography.

Patient Informed Consent

The necessary patient informed consent was obtained in this study.

Discussion

Giant fusiform dolichoectatic vertebrobasilar artery aneurysms are associated with significant morbidity and mortality, with or without intervention. Although there are data to suggest that some patients with dolichoectatic vertebrobasilar artery aneurysms have a comparatively benign natural history,2,13 other data have indicated that larger vertebrobasilar aneurysms carry a poor prognosis without surgery.5,6 In a recent cohort study by Nakatomi et al.,14 91% of patients managed nonoperatively died compared with 57.1% of those undergoing surgical intervention. The use of EC-IC bypass is one such surgical intervention that some have adopted to treat these lesions.2,14–18 We report two cases treated with staged ECA-to-PCA high-flow bypass, proximal Hunterian ligation, and posterior fossa brainstem decompression.

Observations

In both cases, our surgical strategy resulted in the complete arrest of aneurysmal growth without any radiological evidence of brainstem stroke. Despite both cases being technically successful operations, the patient in case 1 had improvement in his clinical status from an mRS score of 3 to 1, whereas the patient in case 2 had a worsening in his mRS score and eventually died at 24-month follow-up. Similarly, Kalani et al.19 reported 11 patients with complex vertebrobasilar aneurysms undergoing STA to SCA or PCA bypass with an initial bypass success rate of 92.3%. However, good long-term outcomes were achieved in only 27% of cases, and the overall mortality rate was 45%. The discrepancy between technical and clinical outcomes could be attributable to several factors. First, the need for antiplatelet and/or anticoagulation to prevent bypass occlusion and/or sudden aneurysmal thrombosis that threatens brainstem perforators is inherently a high risk. Case 2 in our report had a postoperative intracerebral and subdural hemorrhage requiring urgent craniectomy, and this adversely impacted the patient’s outcome. This hemorrhage was likely due to the combination of temporal lobe retraction for the subtemporal approach and the need for postoperative antiplatelet/anticoagulant medications. Kalani et al.19 also reported postoperative hemorrhage in 36% of their patients. Second, patient factors are likely to play a key role. The patient in case 2 in our report was older, had more severe brainstem compression at presentation, had the complete absence of bilateral posterior communicating arteries, and had previously experienced a minor brainstem stroke. Some of these variables have previously been identified as predictors of a poorer clinical outcome.5,6,20

Despite the giant aneurysm size and significant brainstem compression in both of our patients, we were able to achieve successful bypass and proximal aneurysm occlusion without evidence of brainstem stroke. The possible explanation for this is multifactorial. First, both patients presented with a significant volume of thrombus within their aneurysms before treatment. We hypothesize that when this process occurs gradually, it may be protective for preventing further brainstem stroke, because brainstem perforators may develop some form of collateral supply. Some have also suggested that propagating thrombus with bypass and proximal occlusion may be safer than initiating new thrombosis in an aneurysm that previously had none.2

Second, we employed an SVG high-flow bypass strategy. This provides greater immediate blood flow than an STA graft without the risk of vasospasm associated with radial artery grafts. We hypothesize that the STA may be insufficient to immediately revascularize the posterior circulation in patients who cannot wait for an STA graft to gradually provide more blood flow. This may at least partially explain some of the brainstem strokes seen in other reports adopting an STA bypass strategy.2,19

We make another observation from our experience: Bypass techniques alone are insufficient to address these aneurysms. This is supported by our illustrative cases as well as the literature. First, in the initial operation in case 1 (2 years prior to bypass), Hunterian ligation of the dominant and diseased right VA was performed for flow reduction in the aneurysm. Despite this, the basilar component of the patient’s aneurysm continued to progress. It was only after clip occlusion of the left VA (in conjunction with high-flow bypass) that the aneurysm growth stopped. Other reports have similarly found that aneurysms with partial or no proximal occlusion often continue to progress.2,19 It is likely that bypass without proximal occlusion inadequately alters vertebrobasilar hemodynamics to halt aneurysm progression and that it may also contribute to bypass involution, given the absence of flow demand through the bypass.2 Furthermore, proximal occlusion enables an attempt at decompressive thrombectomy within the aneurysm to further alleviate brainstem compression, as seen in case 2.

Lessons

Our staged surgical strategy was able to successfully provide alternate posterior circulation through a high-flow bypass and permit proximal Hunterian ligation to arrest aneurysm growth without brainstem stroke. However, such a surgical strategy is obviously not without significant limitations and considerable risk. There is significant perioperative risk and morbidity associated with the operative approaches, the sequential high-risk neurovascular hemodynamic alterations, and the antiplatelet/anticoagulation requirements perioperatively. The patient in case 1 experienced morbidity of the surgical approach with facial weakness and hearing loss in order to definitively treat his aneurysm. The patient in case 2 experienced further unexpected postoperative hemorrhage that undoubtedly contributed to his poor neurological outcome despite the absence of new brainstem stroke.

Another entirely appropriate limitation of our surgical strategy is its limited indication. Both of our patients presented with progressive aneurysm enlargement and symptoms of critical brainstem compression that could not be addressed endovascularly. They also both lacked adequate posterior communicating artery collaterals, making bypass the only surgical strategy to maintain posterior circulation perfusion. Our treatment strategy is by no means complete or applicable to all cases of giant dolichoectatic vertebrobasilar aneurysms. Our strategy should also not be mistaken as disregard for nonoperative or endovascular treatment options, which should be critically considered in all cases.

Nevertheless, our cases show that high-flow bypass and proximal Hunterian ligation is a possible but high-risk salvage strategy in patients with progressive aneurysm enlargement and brainstem compression. Our current strategy attempts to adopt lessons from multiple previous reports. Although each surgical strategy alone is likely inadequate, our current technique involving high-flow bypass and proximal Hunterian ligation with additional posterior fossa and/or direct aneurysmal decompression may achieve an acceptable long-term outcome without devastating brainstem stroke in appropriately selected patients. Further efforts are required to better understand individual patient hemodynamics and identify those patients in whom the likely benefits of such an intervention outweigh the considerable risks.

Author Contributions

Conception and design: all authors. Acquisition of data: Shaw, Allan. Analysis and interpretation of data: Shaw. Drafting the article: all authors. Critically revising the article: all authors. Reviewed submitted version of manuscript: Shaw, Allan. Approved the final version of the manuscript on behalf of all authors: Shaw. Administrative/technical/material support: all authors. Study supervision: Jukes.

References

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  • FIG. 1

    Case 1. Preoperative imaging. A: Initial three-dimensional (3D) digital subtraction angiography (DSA), left VA injection, when the patient was 14 years old, showing a giant fusiform aneurysm involving the right VA (arrow) and proximal basilar trunk (asterisk). B: Initial sagittal postcontrast T1-weighted MRI showing partial thrombosis within the aneurysm (arrow) with significant brainstem compression. C: Postoperative 3D DSA, left VA injection, when the patient was 14 years old, showing the persistent basilar aneurysm component (asterisk) and patency of the PICA-PICA bypass (arrow). D: Follow-up sagittal computed tomographic angiogram when the patient was 16 years old, showing persistence of the basilar aneurysm component and new left PICA aneurysm formation posteriorly adjacent to the previous bypass (arrow).

  • FIG. 2

    Case 1. Postoperative right common carotid artery (CCA) injection, anteroposterior (A) and lateral (B) views, revealing right ECA-to-PCA (P2) high-flow bypass with SVG (black arrows). Revascularization of the proximal BA and its distal branches seen through flow reversal from the SVG (black arrows). C: Final postoperative sagittal postcontrast T1-weighted MRI after successful high-flow bypass, left PICA aneurysm resection, and posterior fossa decompression, showing improvement in the extent of brainstem compression (arrow).

  • FIG. 3

    Case 1. Left transcochlear intraoperative view showing proximal clip occlusion of the left VA (white arrow) between the lower cranial nerve rootlets. The giant dolichoectatic BA aneurysm is seen distal to the aneurysm clip (asterisk).

  • FIG. 4

    Case 2. A: Preoperative sagittal postcontrast T1-weighted MRI showing the giant aneurysm with significant circumferential thrombosis (white arrow), residual central filling (black arrow), and brainstem compression (asterisk). B: Preoperative three-dimensional digital subtraction angiography (DSA), left VA injection, confirming central patency through the vertebrobasilar aneurysm. C and D: Postoperative DSA with sequential right CCA injection, anteroposterior views, showing patent ECA-to-PCA (P2) high-flow bypass with SVG (white arrows). Flow reversal seen with distal-to-proximal filling of the BA and VA (black arrows).

  • 1

    Peluso JPP, van Rooij WJ, Sluzewski M, Beute GN. Aneurysms of the vertebrobasilar junction: incidence, clinical presentation, and outcome of endovascular treatment. AJNR Am J Neuroradiol. 2007;28(9):17471751.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 2

    Lawton MT, Abla AA, Rutledge WC, et al. Bypass surgery for the treatment of dolichoectatic basilar trunk aneurysms: a work in progress. Neurosurgery. 2016;79(1):8399.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 3

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