Cerebral arterial vasospasm complicating supratentorial meningioma resection: illustrative cases

Andrew C Pickles Stritch School of Medicine

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John T Tsiang Department of Neurological Surgery, and

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Alexandria A Pecoraro Department of Neurology, Loyola University Chicago, Maywood, Illinois

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Nathan C Pecoraro Department of Neurological Surgery, and

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Ronak H Jani Department of Neurological Surgery, and

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Brandon J Bond Department of Neurological Surgery, and
Department of Neurology, Loyola University Chicago, Maywood, Illinois

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Anand V Germanwala Department of Neurological Surgery, and

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Joseph C Serrone Department of Neurological Surgery, and

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Vikram C Prabhu Department of Neurological Surgery, and

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BACKGROUND

Cerebral arterial vasospasm is a rare complication after supratentorial meningioma resection. The pathophysiology of this condition may be similar to vasospasm after aneurysmal subarachnoid hemorrhage, and treatment options may be similar.

OBSERVATIONS

The authors present two cases of cerebral vasospasm after supratentorial meningioma resection and perform a systematic literature review of similar cases.

LESSONS

Cerebral arterial vasospasm after supratentorial meningioma resection may be associated with significant morbidity due to cerebral ischemia if not addressed in a timely manner. Treatment paradigms may be adopted from the management of arterial vasospasm associated with subarachnoid hemorrhage.

ABBREVIATIONS

ACA = anterior cerebral artery; AChA = anterior choroidal artery; CAV = cerebral arterial vasospasm; CT = computed tomography; DCA = diagnostic cerebral angiography; HHH = hypertensive hypervolemic hemodilutional; ICA = internal carotid artery; MCA = middle cerebral artery; MRI = magnetic resonance imaging; SAH = subarachnoid hemorrhage; WHO = World Health Organization

BACKGROUND

Cerebral arterial vasospasm is a rare complication after supratentorial meningioma resection. The pathophysiology of this condition may be similar to vasospasm after aneurysmal subarachnoid hemorrhage, and treatment options may be similar.

OBSERVATIONS

The authors present two cases of cerebral vasospasm after supratentorial meningioma resection and perform a systematic literature review of similar cases.

LESSONS

Cerebral arterial vasospasm after supratentorial meningioma resection may be associated with significant morbidity due to cerebral ischemia if not addressed in a timely manner. Treatment paradigms may be adopted from the management of arterial vasospasm associated with subarachnoid hemorrhage.

ABBREVIATIONS

ACA = anterior cerebral artery; AChA = anterior choroidal artery; CAV = cerebral arterial vasospasm; CT = computed tomography; DCA = diagnostic cerebral angiography; HHH = hypertensive hypervolemic hemodilutional; ICA = internal carotid artery; MCA = middle cerebral artery; MRI = magnetic resonance imaging; SAH = subarachnoid hemorrhage; WHO = World Health Organization

Meningiomas are the most frequently diagnosed primary tumor of the central nervous system.1,2 Resection of meningiomas is the first-line treatment, with the extent of removal being inversely related to the rate of recurrence.3 Preservation of the arachnoid plane around a meningioma facilitates a more complete resection with avoidance of injury to the adjacent cortex. However, at times, pial or brain invasion may complicate identification of the tumor margin.4 In addition, meningiomas parasitize pial and cortical vessels and can be densely adherent to the adventitia of cerebral blood vessels or even completely encase a vessel, posing particular challenges to the surgeon attempting to separate native vasculature from tumor.5 Generally, sharp microdissection techniques are employed, but vessel manipulation is frequently unavoidable.

Cerebral arterial vasospasm (CAV) is commonly encountered after aneurysmal subarachnoid hemorrhage (SAH), especially in cases involving significant blood in the subarachnoid cisterns. The Fisher scale, which categorizes extent of SAH on the initial presenting computed tomography (CT) scan, is predictive of the occurrence of arterial vasospasm associated with delayed cerebral ischemia, one of the leading causes of morbidity and death in these patients.6,7 Posttraumatic SAH may also lead to CAV.8 The occurrence of CAV after brain tumor resection is less commonly recognized but has been previously reported.9 Nonetheless, ischemic defects noted on postoperative magnetic resonance imaging (MRI) studies are usually attributed to the sacrifice of vessels that may supply tumor and cortical tissues simultaneously, rather than to CAV. Hence, a high index of suspicion is essential to recognize this phenomenon in a timely manner to facilitate early therapeutic interventions. We report two cases of cerebral ischemia induced by CAV after resection of supratentorial skull base meningiomas. The semiology, presentation, and angiographic studies mimicked the pattern of CAV that would be observed after aneurysmal SAH. Early recognition and timely intervention to treat the CAV resulted in salutary outcomes.

Illustrative Cases

Case 1

A 38-year-old right-handed male presented with a new-onset generalized tonic-clonic seizure and was found to have a right medial sphenoid wing and clinoidal meningioma on cranial MRI (Fig. 1 left). His neurological examination was normal. A diagnostic cerebral angiography (DCA) showed a significant tumor blush with the tumor largely supplied by the right M1 segment of the middle cerebral artery (MCA) and the right anterior choroidal artery (AChA). The tumor was noted to encase and cause mild stenosis of the supraclinoid segment of the right internal carotid artery (ICA) and M1 segment but without any significant flow limitation. Safe embolization was not considered feasible and thus was not performed. The patient underwent a right-sided cranio-orbito-zygomatic craniotomy and subtotal resection of the tumor (Simpson grade IV). Residual tumor was left within the cavernous sinus and at points of adhesion to the distal M1 and AChA. There were no intraoperative complications. The pathology was reported as a World Health Organization (WHO) grade 1 meningioma without atypical features.

FIG. 1
FIG. 1

Case 1. Brain MRI before (left) and after (right) resection, demonstrating a small amount of residual tumor around the cavernous sinus and distal M1 and AChA. Tumor dimensions prior to resection measured 3.3 × 3.1 × 3.2 cm.

The patient remained neurologically intact postoperatively, and routine cranial CT demonstrated a thin SAH (4-mm thickness) under the craniotomy site; this was expectantly managed. Postoperative cranial MRI demonstrated the expected residual tumor (Fig. 1 right) along with restricted diffusion surrounding the operative bed. The patient’s postoperative course was notable for waxing and waning consciousness suspected to be due to a simple partial seizure without electrographic evidence. Nine days after surgery, the patient was noted to have progressively worsening weakness in his left face and left upper extremity. A cranial CT scan demonstrated worsened edema around the tumor resection bed, and the patient was started on dexamethasone and mannitol without improvement in his symptoms. Cranial MRI and magnetic resonance angiography on postoperative day 10 showed marked narrowing of the clinoid and supraclinoid segments of the distal right ICA extending to the right A1 segment of the anterior cerebral artery (ACA) and right M1 segment. The patient was taken for an emergent DCA, which revealed severe vasospasm of the right supraclinoid ICA and right M1 (Fig. 2 left). Nitroglycerin 200 µg and verapamil 10 mg were administered into the cervical ICA with minor improvement in antegrade flow. Balloon angioplasty was therefore performed across the supraclinoid ICA and M1 segment, which greatly improved vessel caliber (Fig. 2 right). No intraoperative complications were noted during the procedure. The patient was brought to the intensive care unit and started on a phenylephrine drip to maintain a systolic blood pressure goal of 140 to 160 mm Hg for induced hypertension to improve cerebral perfusion. His condition improved, but he had residual weakness of the left upper extremity. No further angiograms were obtained given the patient’s continued clinical improvement. He gradually improved over the next few months, and at 2 years he had complete resolution of the weakness. However, follow-up imaging demonstrated slow growth of the residual tumor; this was treated with fractionated radiation therapy to a total dose of 50.4 Gy with no further growth noted on follow-up studies 2 years later.

FIG. 2
FIG. 2

Case 1. DCA of the right ICA before (left) and after (right) vasospasm treatment with vasodilators and angioplasty, demonstrating an improvement in vessel caliber and the flow of contrast into the capillary phase.

Case 2

A 60-year-old right-handed female presented with progression of a residual anterior cranial base WHO grade 1 meningioma after a prior endoscopic endonasal subtotal resection 6 years prior. She was noted to have significantly decreased visual acuity in the right eye and blindness in the left eye. Cranial MRI revealed an enhancing large sellar mass extending into the suprasellar and subfrontal space with significant mass effect on the optic nerves and optic chiasm (Fig. 3). The ICA and ACA branches on both sides were encased by the tumor. Preoperative DCA was performed, revealing arterial feeders from the left posterior ethmoidal artery. Safe tumor embolization was not considered feasible and therefore not performed. The patient underwent a left-sided cranio-orbital craniotomy and resection of the meningioma (Simpson grade II). Intraoperatively, the tumor was noted to be densely adherent to both optic nerves, the optic chiasm, the left ICA, the left ACA, and the anterior communicating artery. Postoperatively, the patient developed diabetes insipidus, which improved with intravenous desmopressin administration, and panhypopituitarism requiring hormonal replacement therapy. She was also noted to be hypertensive, and she developed urinary tract candidiasis requiring antifungal therapy.

FIG. 3
FIG. 3

Case 2. Brain MRI before (left) and after (right) resection, demonstrating an enhancing sellar/suprasellar mass measuring 3.0 × 3.2 × 2.6 cm and encasing the bilateral ICA and ACA branches.

Thirteen days after surgery, the patient was noted to have acute-onset gaze deviation to the left, aphasia, and right hemiparesis. CT angiography demonstrated stenosis of the left ICA and M1. DCA revealed severe vasospasm of the supraclinoid left ICA and proximal left MCA, as well as complete occlusion of the left A1 segment (Fig. 4 left). Nitroglycerin 300 µg and verapamil 20 mg were slowly infused into the left ICA, with slight improvement noted in vessel caliber. Balloon angioplasty was then performed with marked rebound in the left MCA vessel caliber (Fig. 4 right). Postoperatively, she was started on scheduled nimodipine, which was eventually discontinued 6 days after endovascular intervention. Midodrine was then started to facilitate cerebral perfusion. The remainder of her hospital course was complicated by dysphagia secondary to her neurological deficits for which she required percutaneous endoscopic gastrostomy tube placement. A CT perfusion study was obtained during an episode of somnolence, which did not demonstrate any new perfusion deficit. Given this, repeat angiograms were not obtained.

FIG. 4
FIG. 4

Case 2. DCA of the left carotid arteries before (left) and after (right) vasospasm treatment with vasodilators and angioplasty, demonstrating a significant improvement in vessel caliber.

One month postoperatively, the patient was discharged to subacute rehabilitation with persistent but stable right-sided weakness. During a continued follow-up over the course of 5 months, she had several hospitalizations related to hypernatremia, for which her desmopressin dosage was appropriately titrated. Cranial MRI showed no gross recurrent tumor but was notable for a chronic left ACA distribution ischemic infarct (Fig. 3B). The patient now lives at home with significant improvement in her hemiparesis and can ambulate with an assistive device. However, she continues to have persistent and unchanged visual deficits since before her surgery.

Patient Informed Consent

The necessary patient informed consent was obtained in this study.

Literature Review

A PubMed search was performed for articles indexed through the MEDLINE database using the phrase “meningioma AND vasospasm” on September 20, 2023. A total of 39 articles were identified. Twenty-seven articles were excluded, because their subject matter did not include CAV after meningioma resection. Two articles were excluded because the cases described vasospasm related to postsurgical bacterial meningitis and Candida meningitis. Ten articles were of interest and described 15 cases (Table 1).7,10–18 One case was excluded because it described an infratentorial meningioma resection. A qualitative analysis was performed on the included cases, and the findings are presented.

TABLE 1

Literature review of previously reported cases of supratentorial meningioma resection complicated by cerebral vasospasm

Authors & YearAge (yrs), SexTumor PresentationTumor LocationVessels InvolvedSurgeryVasospasm PresentationVasospasm Vessel(s)Time to VasospasmVasospasm TreatmentSequelae
Amuluru et al., 20161054, FSeveral wks lt-sided visual lossLt spheno-clinoido-cavernousLt CS ICALt modified orbitozygomatic transcavernous approachProgressive visual worsening in lt eyeLt ophthalmic, clinoid & ophthalmic segments of ICA6 hrsIA verapamil, HHH, high-dose corticosteroids, aspirinDecreased lt eye visual acuity
Bejjani et al., 19991148, FUNKRt spheno-cavernousRt ICAUNKHemiparesisRt ICA, rt MCA30 daysHHH, IBP, angioplastySignificant improvement
50, FUNKLt orbital apex, CSLt ICAUNKPoorly responsiveLt ACA, lt MCA4 daysHHHSignificant improvement
57, MUNKRt petroclival, CSBilat ICA, VAUNKHemiparesisRt M11 dayHHH, IA papaverineSignificant improvement
59, FUNKRt CSRt ICAUNKLethargy, hemiparesisRt M1, rt A14 daysHHHSignificant improvement
50, FUNKPlanum sphenoidNoneUNKRt UE monoparesisLt ICA, lt M11 dayHHH, angioplastySignificant improvement
38, FUNKLt CSLt ICAUNKAsymptomaticLt A1/A2, lt M1/2/36 daysNoneSignificant improvement
Budnick et al., 20201236, FMild rt homonymous hemianopsiaTuberculum sellaeLt P1, partial bilat supraclinoid ICA &t A1 segmentsEndoscopic TSSAMS, rt hemiparesisSevere lt paraclinoid ICA, mod lt A1 & M116 daysBalloon arthroplasty for paraclinoid lt ICA, IA papaverine for lt A1 & proximal lt M2, vasopressorsMild rt hemiparesis & preop visual deficits
LeRoux et al., 19911342, F2-yr Hx of progressive lt frontal & retro-orbital headacheLt sphenoid wingNoneLt frontotemporal craniotomyConfusion, rt side neglect, expressive dysphasia, motor weaknessLt M1, lt A110 daysHHH, nimodipineResolving expressive dysphasia
Lessa et al., 20221423, F3 mos headache, diplopia, lt amaurosisLt sphenoid wingLt supraclinoid ICA, lt CSLt FOZ craniotomyObtunded, complete, & proportionate rt hemiparesis & rt Babinski’s signLt supraclinoid carotid artery, lt M17 daysIA milrinoneIntact
Mallereau et al., 2022752, F6 mos diplopia, headaches, olfaction disorderOlfactory grooveNoneRt pterional craniotomyDysphasia & rt facio-brachial hemiparesis.status epilepticusProximal lt M1, diffuse rt M1, bilat PCA12 daysInduced HTN, antiplatelet, & nimodipineMild dysphagia
Pan et al., 20211553, FSeizures, episodic diplopia, facial numbness, & lt eye vision changesLt clinoidalLt cavernous ICA2-staged bifrontotemporal craniotomy, nasal osteotomy, & lt zygomatic osteotomyRt hemiparesisLt A1, lt M16 daysIA nicardipine & balloon angioplastyPartial lt CN III palsy at 6-wk FU
Rosen et al., 20001648, FHeadaches for 1 yr, rt eye vision loss, LE weakness, memory issues, decreased CN V in all distributionsRt spheno-cavernousRt ICA, rt MCAFrontotemporal craniotomy w/ orbital zygomatic osteotomyHemiparesisRt ICA, rt MCA30 daysHHH, IPB due to MI, angiography of rt ICA & MCANo hemiparesis, baseline postop
Simonato et al., 20191770, M1 yr of mixed aphasia, severe rt-sided hemiparesisLt sphenoid wingLt M1Lt fronto-pterional craniotomyRt hemiparesis, aphasiaLt M1, proximal lt A112 daysIA nimodipine, IV nimodipine, Solitaire stentPersistence of rt-sided hemiparesis & mild aphasia, w/o new neurological deficits
Taussky et al., 20121841, F4-mo Hx of progressive proptosis of rt eye & headachesRt sphenoid wingLat wall of rt CSRt pterional craniotomyLt arm weakness, lt leg paralysisRt MCA, lt A1-A2, rt A1-A2, rt ICA14 daysIA verapamil, HHHLt central facial nerve paralysis. 3/5 strength LLE, 4/5 strength LUE

AMS = altered mental status; CN = cranial nerve; CS = cavernous sinus; FOZ = fronto-orbitozygomatic; FU = follow-up; HTN = hypertension; Hx = history; IA = intraarterial; IBP = intraaortic balloon pump; IV = intravenous; LE = lower extremity; LLE = left lower extremity; LUE = left upper extremity; MI = myocardial infarction; TSS = transsphenoidal surgery; UE = upper extremity; UNK = unknown; VA = vertebral artery.

Fifteen patients with possible CAV associated with supratentorial meningioma resection were identified in 10 articles published between 1991 and 2022.7,10–18 The mean age was 48.1 ± 11.1 years, with a majority of the population being female (13 patients, 86.6%). Seven patients (46.7%) had tumors on the left, whereas five patients (33.3%) had tumors on the right. Three patients (20.0%) had midline tumors. Six patients (40.0%) had tumors in the anterior skull base, 13 (86.7%) in the middle skull base, and one (6.7%) in the posterior skull base. There were no tumors that were located along the cerebral convexities. The most commonly named location of the tumor was the sphenoid wing. Arteries were described as “encased” or “displaced” by the tumor in 11 patients (73.3%). Preoperative angiograms were obtained for seven patients (46.7%), with preoperative embolization occurring in six patients (40.0%).

In seven patients (46.6%), vasospasm occurred in at least one of the tumor-encased arteries. Ten patients (66.6%) had vasospasm occur ipsilateral to the tumor, one patient (6.7%) had a right-sided tumor with bilateral vasospasm, three patients (20.0%) had a midline tumor with unilateral vasospasm, and one patient (6.7%) had a midline tumor with bilateral vasospasm. The mean time to vasospasm was 10.2 ± 9.4 days after the index surgery. The most common presenting symptom was hemiparesis of the contralateral side (12 patients, 80.0%). Three patients (20.0%) also exhibited an altered mental status, and one (6.7%) was completely asymptomatic.

The most common treatment was endovascular intervention for selective injection of intraarterial vasodilators (7 patients, 46.6%) and/or angioplasty procedures (4 patients, 26.7%). Commonly used vasodilators included nimodipine, milrinone, nicardipine, and verapamil. In total, 10 patients (66.7%) underwent endovascular intervention. Six patients (40.0%) received hypertensive hypervolemic hemodilutional (HHH) therapy in conjunction with endovascular laboratory intervention, whereas four patients (26.7%) received HHH therapy alone. One patient required a stent to be placed for a “kink” in the M1 segment of the MCA within the operative bed. In the asymptomatic patient, vasospasm was found incidentally and managed expectantly. None of the patients required repeat endovascular treatment. All 15 patients were discharged with significant improvement in neurological deficits presumed to be secondary to vasospasm, with eight patients (53.3%) experiencing only minor deficits and no patients experiencing major deficits or death.

Discussion

Observations

Cerebral vasospasm is a rare sequela after supratentorial meningioma resection. To minimize associated morbidity and mortality, treatment providers should recognize the signs and symptoms to allow for prompt workup and intervention. The most common presenting symptom noted in our literature review was hemiparesis (80%). The mean time to vasospasm after index surgery was 10.2 days, although this widely ranged from 6 hours to 30 days. The median time to posthemorrhagic vasospasm was 7 days, suggesting a right-skewed distribution. Our patients experienced vasospasm 9 and 13 days after the index surgery, respectively.

Despite several decades of research, the definitive mechanism behind posthemorrhagic CAV has not been elucidated. Much of the current research is aimed toward studying vasospasm as it pertains to SAH. Furthermore, it is postulated that subarachnoid blood and its breakdown products cause free radical production and inflammation, which triggers Ca2+-dependent and Ca2+-independent (nitric oxide depletion) smooth muscle contraction, ultimately causing vasoconstriction.19 Likewise, some cases in our review suggested the presence of subarachnoid blood during resection as a possible cause of postresection vasospasm.13,14,18 Others suggested vessel manipulation and dissection as a potential trigger for vasospasm.7,10–12,14–17 Indeed, a majority of patients in our literature review had meningiomas encasing major arteries, which ultimately required manipulation and dissection. Although the laterality of vasospasm varied among cases, there were no cases in which isolated vasospasm occurred contralateral to the meningioma resection. Additionally, there were no case reports within our literature search of cerebral convexity meningioma resections causing vasospasm.

CAV after skull base tumor resection is a known phenomenon. It has been described in the anterior skull base (e.g., after pituitary adenoma resections12,20) and in the posterolateral skull base (e.g., after vestibular schwannoma resections21) but can also occur with the resection of tumors such as astrocytomas and gliomas.22 CAV after supratentorial meningioma resection is less well described. Various techniques have been proposed to decrease the risk of CAV after tumor resections, including the use of intracisternal vasodilator irrigation and papaverine-soaked Gelfoam.23 To our knowledge, there are currently no comparative studies demonstrating the efficacy of these techniques in preventing CAV.

Traditionally, cases of cerebral vasospasm after SAH have been treated with HHH therapy.24 However, studies examining the safety and efficacy of HHH have been limited, with several complications of therapy noted, including pulmonary edema, increased intracranial pressure, and hemorrhagic infarction.25,26 With advances in endovascular therapy, many providers now treat cerebral vasospasm with balloon angioplasty, local intraarterial delivery of vasodilators, or both with the goal of restoring vessel caliber and minimizing cerebral ischemia.27,28 Our review reflected this paradigm shift in the treatment of vasospasm: cases published earlier were treated predominantly with HHH, whereas more recently published cases were treated with endovascular intervention and “induced hypertension.”9,10,19,25–27 Vasodilators used during endovascular intervention in our literature review were mostly calcium channel blockers. Our institution typically utilizes verapamil (10–20 mg) and nitroglycerin (200–300 µg) to target both Ca2+-dependent and Ca2+-independent vasospasm mechanisms, with additional verapamil injected if there is minimal improvement on successive angiogram runs. We resort to angioplasty if the vasodilator injection does not result in a significant improvement of vasospasm or if hemodynamic instability is encountered and precludes the use of vasodilators. Based on our review, the role of intracranial stenting remains unclear, with only one patient having received a stent because of a postoperative “kink” noted in M1.

In our literature review, all patients were discharged with only mild neurological deficits. Although these outcomes may be attributable to the rapid diagnosis of vasospasm and emergent intervention, this finding could also be attributable to a positive result bias or publication bias. More research is necessary to fully ascertain the pathophysiology and natural history of this rare but important phenomenon.

Lessons

CAV is a rare sequela of supratentorial meningioma resection, particularly if the tumor is adherent to major cerebral arteries. Early clinical recognition of lateralizing signs associated with focal cerebral ischemia facilitates appropriate diagnostic studies, including cranial MRI and DCA, allowing for the institution of appropriate medical and endovascular therapies. Expeditious treatment can potentially prevent significant morbidity and mortality.

Acknowledgments

We thank Dr. William W. Ashley and Dr. Asterios Tsimpas for their contribution and dedication to the care of the patient described within this report.

Author Contributions

Conception and design: Pickles, Tsiang, Serrone, Prabhu. Acquisition of data: Pickles, Tsiang. Analysis and interpretation of data: Pickles, Tsiang, Bond, Germanwala, Serrone, Prabhu. Drafting the article: Pickles, Tsiang, NC Pecoraro, Jani, Serrone, Prabhu. Critically revising the article: all authors. Reviewed submitted version of manuscript: Pickles, Tsiang, NC Pecoraro, Jani, Bond, Germanwala, Serrone, Prabhu. Statistical analysis: Pickles, Tsiang. Administrative/technical/material support: Germanwala. Study supervision: Serrone.

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  • 26

    Treggiari MM, Walder B, Suter PM, Romand JA Systematic review of the prevention of delayed ischemic neurological deficits with hypertension, hypervolemia, and hemodilution therapy following subarachnoid hemorrhage. J Neurosurg. 2003;98(5):978984.

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  • 27

    Boulouis G, Labeyrie MA, Raymond J, et al. Treatment of cerebral vasospasm following aneurysmal subarachnoid haemorrhage: a systematic review and meta-analysis. Eur Radiol. 2017;27(8):33333342.

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  • 28

    Mindea SA, Yang BP, Bendok BR, Miller JW, Batjer HH Endovascular treatment strategies for cerebral vasospasm. Neurosurg Focus. 2006;21(3):E13.

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  • FIG. 1

    Case 1. Brain MRI before (left) and after (right) resection, demonstrating a small amount of residual tumor around the cavernous sinus and distal M1 and AChA. Tumor dimensions prior to resection measured 3.3 × 3.1 × 3.2 cm.

  • FIG. 2

    Case 1. DCA of the right ICA before (left) and after (right) vasospasm treatment with vasodilators and angioplasty, demonstrating an improvement in vessel caliber and the flow of contrast into the capillary phase.

  • FIG. 3

    Case 2. Brain MRI before (left) and after (right) resection, demonstrating an enhancing sellar/suprasellar mass measuring 3.0 × 3.2 × 2.6 cm and encasing the bilateral ICA and ACA branches.

  • FIG. 4

    Case 2. DCA of the left carotid arteries before (left) and after (right) vasospasm treatment with vasodilators and angioplasty, demonstrating a significant improvement in vessel caliber.

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    Treggiari MM, Walder B, Suter PM, Romand JA Systematic review of the prevention of delayed ischemic neurological deficits with hypertension, hypervolemia, and hemodilution therapy following subarachnoid hemorrhage. J Neurosurg. 2003;98(5):978984.

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    Boulouis G, Labeyrie MA, Raymond J, et al. Treatment of cerebral vasospasm following aneurysmal subarachnoid haemorrhage: a systematic review and meta-analysis. Eur Radiol. 2017;27(8):33333342.

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    • Export Citation
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    Mindea SA, Yang BP, Bendok BR, Miller JW, Batjer HH Endovascular treatment strategies for cerebral vasospasm. Neurosurg Focus. 2006;21(3):E13.

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