Resection of sphenoid wing meningioma with blood pressure augmentation reverses acute symptomatic left middle cerebral artery syndrome: illustrative case

Abstract

BACKGROUND

Meningiomas are typically benign, slow-growing tumors, but in rare cases, they can also cause symptomatic compression of cerebral arteries, potentially leading to stroke. Historically, management of such cases often required supplementary revascularization procedures. This report reviews cerebral artery compression secondary to meningiomas and presents a case of a left sphenoid wing meningioma causing compression of the left middle cerebral artery (MCA) with resulting acute neurological deficits, which resolved after emergency tumor resection and blood pressure optimization.

OBSERVATIONS

A 28-year-old female with a history of migraines presented with acute right hemiplegia, numbness, and dysarthria (National Institutes of Health Stroke Scale score 11). Imaging revealed a 4.5-cm dura-based mass in the left middle cranial fossa, displacing and compressing the left MCA, with early signs of infarction. An angiogram revealed limited treatment options, and she underwent an urgent left frontal craniotomy for tumor resection and neurovascular decompression. Pathological examination confirmed meningioma. Following surgery, she experienced near-complete recovery of motor and language function.

LESSONS

Meningiomas are a rare cause of symptomatic MCA stenosis. While revascularization strategies have been described, surgical decompression can potentially provide rapid neurological improvement. Urgent tumor resection with medical optimization should be considered as an effective treatment strategy for symptomatic meningioma-induced cerebral artery stenosis.

https://thejns.org/doi/10.3171/CASE2515

Meningiomas are typically benign, slow-growing tumors that, when sufficiently large, can lead to progressive symptoms due to mass effect. Although rare, these tumors can also cause acute focal neurological deficits by compromising vascular structures. We present a case of a left sphenoid wing meningioma that led to stenosis of the left middle cerebral artery (MCA). The patient underwent emergency tumor resection and decompression. Postoperatively, there was consideration for neurovascular intervention due to persistent symptomatic occlusion of the proximal left M1 segment, resulting in hypoperfusion. However, the decision was made to pursue medical management with targeted hypertension, aiming to promote circulation through collateral vessels, as the diagnostic angiogram revealed limited treatment options.

Illustrative Case

History and Examination

A 28-year-old Caucasian female with a medical history notable for migraines and recent tonsillectomy 10 days prior presented to the emergency department with acute-onset dysarthria, word-finding difficulties, and right-sided paralysis of the face, arm, and leg. The patient had awakened at 6:00 am with complete right-sided paralysis and slurred speech, which were not present the previous night. Head and neck CT angiography (CTA) performed at an outside hospital revealed a left frontotemporal mass, likely a meningioma. On arrival, the patient demonstrated intermittent right-sided motor function (grade 4/5 strength) for approximately 15 minutes, followed by complete paralysis, suggesting “stuttering” MCA occlusion.¹,²

MRI of the brain with and without contrast (with no prior comparisons) revealed a 4.1 × 4.2 × 4.4–cm homogeneously contrast-enhancing mass arising from the left anterior clinoid process and anterior floor of the left middle cranial fossa (Fig. 1A). The mass exerted significant mass effect on adjacent structures, including medial and superior displacement/compression of the left MCA, compression of the left lateral ventricle and third ventricle, and a 5-mm rightward midline shift (Fig. 1B). Edema secondary to mass effect was also noted. MRI also demonstrated acute to subacute infarctions in the territories of the anterior choroidal and limbic striate arteries, along with scattered infarctions within the MCA territories of the left frontal and parietal lobes (Fig. 1C and D). No acute intracranial hemorrhage was noted.

FIG. 1.

Preoperative images. A:Axial T1-weighted postcontrast MR image showing a homogeneously enhancing 4.1 × 4.2 × 4.4–cm mass arising along the left anterior clinoid process and medial floor of the left middle cranial fossa. B: Coronal MR image demonstrating that this medial sphenoid wing mass causes superior and medial compression of the lateral and third ventricles. C and D: Axial apparent diffusion coefficient (ADC) (C) and diffusion-weighted (D) MR images showing acute to subacute infarcts in the anterior choroidal and limbic striate territories.

The patient was started on 1 g of Keppra twice daily, intravenous (IV) fluids, and norepinephrine to maintain a systolic blood pressure (sBP) > 160 mm Hg. At this time, we considered preoperative angiography and the potential for a bypass procedure, which could be beneficial, particularly in light of the vascular stenosis observed. However, after consultation with our on-call neurovascular surgeon, it was determined that the current imaging sequences were sufficient for decision-making and that a delay in surgery would pose a greater risk to the patient. Therefore, the immediate priority was to alleviate the mass effect and address the evolving ischemic events through tumor resection. The neurovascular team would be available for revascularization procedures, either intraoperatively or if needed in the future.

A left pterional craniotomy was performed using intraoperative navigation. The pterional incision was made preserving the periosteum and temporalis fascia via the cranial stair-step approach.³ The mass was fairly tough and heterogeneous during the resection, with significant vascularized and calcified portions, at times resembling calcifying pseudoneoplasm of the neuraxis.⁴ The abnormal tumor borders were delineated through surface dissection. The tumor was resected using ultrasonic aspiration and blunt dissection. Ultimately, a subtotal resection was achieved, leaving adherent portions of the tumor along the sylvian fissure and MCA branches, as seen on imaging (Fig. 2). The frozen pathology confirmed the diagnosis of meningioma, WHO grade 1. Immunohistochemical analysis revealed focal positivity for epithelial membrain antigen and progesterone receptors, while glial fibrillary acidic protein was negative.

FIG. 2.

Postoperative images. A: Axial T1-weighted postcontrast MR image showing postsurgical changes and residual tumor. B: Coronal postcontrast sequence demonstrating some preserved blood flow along the M1 segment, along with decreased compression of the third ventricle and stable midline shift. C and D:Axial ADC (C) and diffusion-weighted (D) MR images demonstrating similar/persistent multifocal acute to subacute infarcts in the left hemisphere, unchanged from preoperative imaging findings.

Postoperative MRI (Fig. 2A and B) revealed typical postsurgical changes and a small expected residual margin with encroachment on the left cavernous sinus and suprasellar cistern. Compression of the left MCA was still notable but improved. There was also a decrease in the compression of the left lateral and third ventricles. No new infarcts were seen (Fig. 2C and D), and the midline shift remained similar.

On postoperative day 1 (POD 1), the patient showed early signs of recovery, with a newly regained right hand grip and the ability to wiggle her right thumb. She was able to speak in full sentences, although with some mixed aphasia (phrases), but had no volitional movement in her right lower extremity (RLE). However, she experienced intermittent hypotensive episodes, with sBP dropping to the 90- to 100-mm Hg range, which were associated with temporary loss of all right-sided motor function. IV fluids and phenylephrine were used to maintain an sBP goal of 120–180 mm Hg, which resulted in regaining right grip strength and right thumb movement.

CTA performed on POD 1 during these hypotensive episodes showed high-grade stenosis in the left M1 segment with distal reconstitution (Fig. 3). Consultation with the stroke neurology and neurovascular surgery teams resulted in a recommendation for a diagnostic cerebral angiogram to evaluate potential revascularization options for the left M1 artery. The diagnostic angiogram revealed significant occlusion of the proximal left M1 segment, with no filling of the distal M1 or M2 segments (Fig. 4A). The distal MCA territory was being supplied by leptomeningeal collaterals arising from both the left anterior cerebral artery and left posterior cerebral artery (Fig. 4B and C). The patient began daily physical therapy (PT) and occupational therapy (OT) on POD 2. Ultimately, the neurovascular surgical team did not recommend endovascular interventions such as stenting or bypass, as the patient showed continued improvement in her right-sided motor function and angiographic evidence of robust collateral vessels. Medical management with aspirin (81 mg daily) and a target sBP of 120–180 mm Hg was continued to allow further collateralization. On POD 5, she was cross-titrated to midodrine (5 mg three times per day, increasing to 20 mg three times per day) and fludrocortisone (0.1 mg daily) to maintain the blood pressure goal in an outpatient regimen.

FIG. 3.

POD 1 CT angiogram obtained during the symptomatic hypotensive episodes. A:Coronal sequence showing high-grade stenosis of the left M1 segment of the MCA. B: 3D reconstruction of the cerebral vasculature, providing an enhanced view of the stenosis.

FIG. 4.

Anteroposterior (AP) digital subtraction angiogram of the left internal carotid artery (A), showing only the proximal portion of the left M1 segment (purple arrow), with no filling of the distal M1 segment or distal MCAs. AP digital subtraction angiogram of the left vertebral artery (B), demonstrating the occluded left MCA territory (orange arrow), which is supplied a few seconds later by leptomeningeal collaterals (blue arrows) arising from the left posterior cerebral artery (green arrow) in the subsequent frame (C).

The patient was discharged to acute rehabilitation on POD 11 with grade 4/5 strength throughout the right upper extremity (RUE) and grade 4+/5 in the RLE aside from the right iliopsoas, which was grade 4/5, with some decreased gait speed and right foot clearance. She used a rolling walker for assistance at discharge. After just 2 days of acute rehabilitation, she was discharged home due to significant functional improvement. At a 2.5-week follow-up in our multidisciplinary brain tumor clinic, the patient was walking independently and reported being 90%–95% back to her baseline function. She had regained the ability to handwrite and type on her phone, although she still had minor difficulty brushing her teeth. She was showering independently and had no further speech impairment.

The patient’s physical examination at follow-up showed grade 4/5 strength in the right deltoid and triceps and grade 5/5 in the remaining RUE and RLE. Mild sustained clonus in the RLE was noted, likely a sequela of the recent stroke, with reflexes at grade 2+ in the RUE. The patient was advised to discontinue and avoid high-dose progesterone medications due to the progesterone receptor positivity of the meningioma. Close follow-up continued, with further improvements leading to full-strength recovery. More than 1 year postsurgery, the patient now leads a fully normal and functional lifestyle.

Informed Consent

The necessary informed consent was obtained in this study.

Discussion

Observations

Meningiomas are the most commonly diagnosed benign intracranial tumors in adults.⁵ However, they rarely cause acute neurological deficits due to cerebral artery stenosis.⁶ This rarity can be attributed to the arachnoid cap–based cellular origin of meningiomas, which leads them to grow with more distinct borders along the dura. As a result, meningiomas tend to invade less frequently into adjacent parenchyma and vascular structures.⁷ In contrast, atypical and anaplastic meningiomas that invade beyond the dura often show high expression of matrix metalloproteinase, aquaporin, and plasminogen activators, with these proteins being more intensely expressed at sites of cell invasion.⁸,⁹ Other studies have demonstrated that the upregulation of angiogenic factors like vascular endothelial growth factor and abnormal expression of cyclins and cyclin-dependent kinases and inhibitors are linked to increased invasion and cellular proliferation. However, such invasive meningiomas typically correspond to higher WHO grades.⁵,¹⁰,¹¹

A parallel paucity of literature exists on meningiomas causing cerebral artery stenosis.⁶,^12–22 Few reports address the decision-making involved in managing these cases—whether resection, neurovascular intervention, or medical management is the most appropriate strategy—and the time line for functional recovery following the chosen intervention. Table 1 summarizes existing reports on meningiomas causing cerebral artery stenosis and provides insight into the decision-making process and patient outcomes.

TABLE 1.

Literature review of existing case reports detailing meningiomas causing cerebral artery stenosis and acute-onset focal neurological deficits

Authors & Year	Location	Age (yrs), Sex	Tumor Presentation	Sx	Tumor Location	Artery Affected	Tx	Op Details Provided?	Reperfusion Achieved?	Stent vs Anastomosis Considered?	Tx Outcome
Komotar et al., 200315	US	Case 1: 49, M	Acute	LUE weakness; lt facial droop	Rt cavernous sinus	Rt cavernous ICA	Focused RT	No	Yes	No	Sx improved, then presented 6 mos later w/ lt leg weakness due to fresh thrombus in rt cavernous ICA
	US	Case 2: 31, M	Acute	Rt eye vision loss, painless, did not seek care; 2 yrs later: lt-sided numbness	Rt parietal; olfactory groove	Rt ICA; rt optic nerve	Complete tumor resection	No	Yes	No	No vision in rt eye; lt arm numbness; otherwise recovered
Heye et al., 20066	Belgium	48, F	Acute	Lt hemiparesis	Rt sphenoid sinus; rt cavernous sinus	Rt ICA	Endovascular stent placement	Yes	Yes	Yes, also considered decompression of optic nerves & rt postop RT ≥12 mos postop	Incomplete recovery of lt hemiparesis at 2 wks postop; partial recovery of lt hemiparesis; residual motor deficits of 4th & rt 5th fingers
Masuoka et al., 201017	Japan	31, M	Acute	Recurrent & transient lt LE weakness	Rt frontal lobe in planum sphenoidale	Rt ACA	Bilat frontal craniotomy; GTR	Yes	Yes	No	No new neuro deficits; no comment on improvement of condition or if there are residual deficits
Chivoret et al., 201120	France	44, F	Acute	Rt hemiparesis; aphasia	Lt medial sphenoid	Lt MCA at M1 segment; lt ACA at A1 segment; terminal lt ICA	Antiplatelets; BP monitoring; rehab; 3 wks later: preop endovascular angioplasty w/o stent placement (to aid tumor resection); complete resection	Yes	Yes	Yes	Partial recovery in several days w/ medical management alone; lt visual deficit & rt oculomotor nerve paresis in early postop; recovered w/in 1 mo
Fernandez-Valverde et al., 201312	Spain	48, F	—	Rt hand hemiparesis; HA; aphasia	Lt planum sphenoidale	Lt MCA	Endovascular recanalization; total tumor resection	—	Yes	Yes	Not detailed
Mathis et al., 201321	France	30, F	Acute	HA; lt hemiparesis	Rt sphenoid	Rt MCA	Complete tumor resection	No	Yes	No	Recovered most functions over several wks; Residual mod spasticity of rt upper & rt lower limbs
Ko et al., 201413	South Korea	52, M	Acute	Lt hemiparesis; dysarthria	Rt sphenoid ridge	Rt MCA	EC-IC bypass	No	Yes	Yes, also considered GKRS to resect tumor	Preop weakness resolved dramatically in 48 hrs postop
Tantikittichaikul et al., 201522	US	68, F	Acute	Episodic; rt hand dyspraxia; rt facial numbness; dysarthria	Lt planum, sphenoid clinoid, & rt supraclinoid	Lt ICA; lt MCA	Medical management only	No	Not detailed	No	Complete resolution of Sx
Kim et al., 201614	South Korea	75, F	Acute	Lt homonymous hemianopia	Lt petroclival area	Rt PCA	4 courses of RT 6 yrs prior; no intervention at repeat presentation 6 yrs later	No	Not detailed	No	Not detailed
Huang et al., 201819	China	63, F	Subacute	HA; rt eyesight weakness	Lt medial sphenoid ridge	Lt ICA	Lt frontotemporal craniotomy; subtotal resection; end-to-side anastomosis of frontal branch of lt superficial temporal artery to M2 segment of MCA bypass (EC-IC bypass); ipsilat decompressive craniectomy	Yes	Yes	Yes, also considered superselective embolization	Rt limbs grade 4, 10 days postop (worse than on admission when grade 5); similar visual acuity as on preop; muscle strength returned to grade 5 at 6 mos postop
Gopal et al., 202316	Nepal	36, F	Acute	HA; nausea; vomiting; loss of consciousness; rt hemiplegia	Lt medial sphenoid; lt planum sphenoidal area	Lt ICA; lt MCA at M1 segment	Lt pterional craniotomy; GTR	Yes	Yes	Yes	Extubated, walking, speaking few words at 3 wks postop; remained severely disabled
Current case, 2024	US	28, F	Acute	Rt-sided paralysis; rt facial droop; dysarthria	Lt sphenoid ridge	Lt MCA	STR to free lt MCA; medical management; in-pt PT/OT & rt acute rehab	Yes	Yes	Yes	RUE motor strength improved to grade 4 to 4+; RLE motor strength improved to grade 5; dysarthria resolved; full recovery achieved 6 wks postop (complete resolution of Sx, grade 5 strength throughout)

ACA = anterior cerebral artery; EC-IC = extracranial-intracranial; GKRS = Gamma Knife radiosurgery; GTR = gross-total resection; HA = headache; ICA = internal carotid artery; LE = lower extremity; mod = moderate; neuro = neurological; PCA = posterior cerebral artery; pt = patient; RT = radiation therapy; STR = subtotal resection; Sx = symptoms; Tx = treatment.

Our case is unique in that it describes tumor resection and blood pressure augmentation as sufficient to achieve near-total functional recovery in the acute postoperative period. Notably, the case described by Huang and colleagues is the only other report in the literature that discusses subtotal resection as a treatment for symptomatic cerebral artery stenosis due to meningioma.¹⁹ However, in addition to the subtotal resection, the authors performed an extracranial-intracranial bypass using an end-to-side anastomosis of the frontal branch of the left superficial temporal artery to the M2 segment of the MCA.¹⁹ This contrast highlights the potential for diverse management strategies, with some opting for additional revascularization procedures based on the severity of arterial compromise and collateral flow.

Several considerations must guide the management approach in patients with meningioma-induced cerebral artery stenosis. Our case was particularly urgent, as the patient presented within 24 hours of symptoms with no prior history of neurological symptoms. In contrast, Huang and colleagues’ patient had a more subacute presentation over a span of 6 months.¹⁹ While the tumor size was not detailed in their report, it was described as compressing the left ICA and left MCA at the M1 segment, which likely contributed to their decision to pursue an extracranial-intracranial bypass in addition to tumor resection.

The decision between tumor resection with medical management alone or in conjunction with endovascular procedures, radiotherapy, or immunotherapy depends on multiple factors, including the location of the mass, the area of infarction, the patient’s hemodynamic stability at presentation and during the intervention, and their response to initial interventions. These factors can help determine whether gross-total resection is feasible, if subtotal resection is sufficient, or if adjunctive procedures such as stenting or bypass are warranted. The chronicity and severity of symptoms also play an important role in the decision-making process.

Ultimately, our case emphasizes that in some instances, particularly when the patient presents acutely and demonstrates favorable collateral circulation, tumor resection and blood pressure augmentation might be sufficient to restore function without the need for complex revascularization techniques.

Lessons

Although rare, meningiomas can cause symptomatic cerebral artery stenosis through extrinsic compression, leading to acute focal neurological deficits. Early recognition and prompt imaging are crucial to avoid delayed diagnosis and subsequent treatment to achieve cerebral reperfusion. MRI should be performed at the earliest sign of neurological deterioration, especially when cerebral artery stenosis is suspected. If a meningioma is identified as the underlying cause of cerebral artery stenosis, the treatment approach should be carefully considered. The decision to pursue tumor resection, either complete or partial, might depend on tumor size and location and might be combined with additional interventions, such as open or endovascular procedures, if deemed necessary. In some cases, following tumor resection, medical management, particularly blood pressure augmentation, might suffice to support collateral circulation and promote cerebral reperfusion, leading to functional recovery.

Our case represents the first known report in the literature in which subtotal resection with medical optimization was successful in managing a large symptomatic medial sphenoid wing meningioma inducing an acute left MCA syndrome, resulting in favorable functional recovery. The value of our case lies in its comparison with existing reports, helping to define treatment trends and outcomes for meningiomas causing cerebral artery stenosis. By consolidating knowledge from prior cases, we gain insights into treatment strategies for this rare yet treatable condition. Furthermore, our case highlights the importance of a multidisciplinary approach, integrating both surgical and medical interventions, to optimize patient outcomes.

Acknowledgments

We thank the patient and her family for their cooperation and for the patient’s willingness to share her experience through this case report. Our appreciation extends to the neurovascular and stroke neurology teams for their clinical expertise and assistance with the diagnosis and treatment of this patient.

Disclosures

The authors report no conflict of interest concerning the materials or methods used in this study or the findings specified in this paper.

Author Contributions

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

Correspondence

Rafael A. Vega: Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA. rvega@bidmc.harvard.edu.