Facial nerve palsy after middle meningeal artery embolization for chronic subdural hematoma: illustrative case

Abstract

BACKGROUND

Middle meningeal artery embolization (MMAE) has emerged as a safe and effective minimally invasive alternative to surgical evacuation of chronic subdural hematoma (cSDH), both as adjuvant therapy and as a stand-alone treatment. Despite its advantages, rare complications such as facial nerve palsy (FNP) may occur. Such complications have rarely been reported in the literature in the context of cSDH, with only 7 other cases.

OBSERVATIONS

The authors present the case of FNP after MMAE for cSDH and highlight the mechanism of injury, management, and preventive strategies that should be considered prior to endovascular interventions, while summarizing the previously reported cases.

LESSONS

Special attention must be given to the endovascular technique implicated and to the complex anatomy of the middle meningeal artery (MMA) to reduce the incidence of such complications. Management of such complications is extrapolated from the available literature on facial nerve injuries and is mainly supportive through eye moisturization, facial muscle rehabilitation, and steroids. Although no consensus has been reached for prevention, some recommendations have been given throughout the literature, such as distal microcatheter positioning, proximal mechanical blockage with balloon-assisted flow reversal, and the use of coil-only embolization or high-viscosity embolic agents with a particle size ≥ 150 μm.

https://thejns.org/doi/10.3171/CASE25866

The incidence of chronic subdural hematoma (cSDH) has been increasing due to the shift toward an aging population.¹ The classic management option is surgical evacuation.² Middle meningeal artery embolization (MMAE) is a safe and effective minimally invasive alternative that is adopted for cSDH, either as stand-alone therapy or an adjunct following surgical evacuation to reduce recurrence.³ It is safe in frail or older patients who do not qualify for surgery.⁴ It is also recommended in hematoma recurrence, occurring in approximately 5%–76% of patients after surgical evacuation, compared to around 6%–7% after MMAE.³ However, MMAE complications are mainly due to complex middle meningeal artery (MMA) anatomy. Of concern is facial nerve palsy (FNP), partially explained by the vascular anatomy of the facial nerve (FN) and geniculate ganglion. The geniculate ganglion receives supply from the petrosal branch of the MMA and the stylomastoid artery, which arises from the occipital or posterior auricular artery. Inadvertent embolization of these branches can compromise FN perfusion, causing ischemic neuropathy.⁵ In some cases, FNP occurs despite patency of the branches. Such injuries may involve liquid embolic material toxicity or microembolization of the vasa nervorum causing nerve ischemia.⁶ In this report, we present a case of FNP after MMAE and review the literature.

Illustrative Case

A 90-year-old right-handed female with hypertension, dyslipidemia, and dementia presented with decreased consciousness. Two months earlier, she had sustained a fall requiring right hip replacement. CT at the time revealed a large, 2.3-cm left frontoparietal subdural hematoma (SDH) with 1.3 cm of midline shift (Fig. 1), for which she underwent left parietal burr hole evacuation. One month later, she presented again with somnolence and right-sided weakness. Repeat CT (Fig. 2) showed acute-on-chronic subdural collection. Redo left parietal burr hole evacuation was performed, draining mixed acute blood and xanthochromic fluid consistent with hygroma. Her postoperative course was complicated with pneumonia and a urinary tract infection, for which she was promptly treated. Her neurological status improved postoperatively.

FIG. 1.

Axial (A) and coronal (B) CT images of the brain showing a large left SDH with a significant acute component.

FIG. 2.

Axial CT image of the brain showing an increase in the left subdural collection with new densities, denoting an acute on top of chronic bleed.

To reduce recurrence risk, left MMAE was performed after the patient was stable. Angiography confirmed no ophthalmic anastomoses (Fig. 3), and both frontal and parietal MMA branches were embolized with Onyx. The procedure was uneventful. On postoperative day 1, she was alert and cooperative but developed new left peripheral FNP (House-Brackmann [HB] grade III). She was discharged with lubricating eye drops without steroids and was lost to follow-up.

FIG. 3.

Lateral angiograms revealing Onyx deposition in the MMA with occlusion of the frontal and parietal branches (A) and occlusion of the petrosal branch after embolization (B).

Informed Consent

The necessary informed consent was obtained in this study.

Discussion

Observations

Despite the high safety of MMAE, rare neurological complications such as cranial nerve palsies may still occur. In our case, FNP occurred after MMAE. The mechanism of injury is based on the blood supply of the FN. The proximal one-third of the FN is supplied by branches of the internal auditory artery, originating from the cerebellolabyrinthine branch of the anterior inferior cerebellar artery. The distal two-thirds of the FN is typically supplied by the facial arch, which spans from the petrosal branch of the MMA to the stylomastoid branch of the occipital or posterior auricular artery.⁷ The petrosal branch usually originates from the MMA after it enters the cranial cavity through the foramen spinosum. It then continues its path to the geniculate ganglion accompanied by the superficial petrosal nerve. The distal two-thirds of the FN, through the geniculate ganglion, is supplied by the petrosal branch in approximately 90% of cases, although some variation exists where the stylomastoid artery can contribute as well.⁸ Based on this distribution, MMAE may pose a risk to the petrosal branch, through either direct embolization or backflow of liquid material, leading to FN ischemic neuropathy.⁹

Although the anatomical distribution may offer an explanation, multiple cases have been described in which FNP occurred despite sparing the petrosal branch and collaterals. In some cases in which MMAE was performed at least 1 cm above the MMA angle at the internal foramen spinosum orifice or above the level of the petrosal branch, where flow of the embolic agent and the microcatheter positioning were carefully observed to avoid any backflow, and where anatomical variations were assessed, FNP still occurred, albeit at a lower rate. In addition, the time of symptom onset varied widely among those cases.¹⁰ Therefore, the mechanism of FNP in such cases remains unclear. One hypothesis is that embolic agents may injure the FN via occlusion of anastomotic channels between the distal parts of the MMA branches and the surrounding collateral perineural vessels, which are not seen on conventional angiograms.¹⁰ Another mechanism of injury when using Onyx embolization is the toxicity of dimethyl sulfoxide, the ethylene vinyl alcohol solvent used in the embolic agent formula.¹¹ FNP can also be precipitated by flow of embolization material into the vasa nervorum, a process that is difficult to visualize on imaging due to tantalum sedimentation, especially with prolonged Onyx injection.¹² This hypothesis is supported by Geibprasert et al.⁷ who described that liquid embolic materials can enter and occlude small anastomotic channels that are visualized on initial angiograms.

FNP after MMAE may also depend on the use of microparticles instead of liquid embolizing material. Microparticles can penetrate tiny capillaries such as the vasa nervorum, leading to ischemic neuropathy. This is true when using microparticles < 80 μm in size, as the size of the nonvisualized anastomoses and the vasa nervorum ranges from 50 to 80 μm.⁶

Coil-only MMAE has recently emerged as a new technique that may be used for embolization without the use of liquid agents.¹³ This technique may reduce the risk of cranial neuropathies, as it causes proximal occlusion of the artery without the risk of distal penetration of liquid embolics into anastomotic branches or the vasa nervorum.¹³ A retrospective study of 137 patients who underwent MMAE for cSDH revealed that no neuropathies were reported in patients who underwent coil-only embolization.¹⁴ The authors of this study discussed the advantage of coiling in reducing embolization of skull base collaterals, and they succeeded in embolizing the MMA without any proximal trunk reflux. Although this is promising, current data are limited to small retrospective series and mechanistic observations from adjunctive coiling studies, and further prospective studies and trials are needed to directly compare coil-only versus liquid agent techniques.

FNP after MMAE for cSDH is a rare complication that is not widely reported in the literature. More than 50 cases of FNP have been reported after endovascular procedures. However, the injury was related to surgical complications, where the MMA ruptured and was immediately embolized, and an endovascular procedure was not performed for cSDH.¹⁵ Of the available literature, only 7 cases of FNP after MMAE for cSDH have been described.^3,10,16–18 In those cases, the time of symptom onset, treatment, and outcomes were variable. A summary of those findings is provided in Table 1.

TABLE 1.

Summary of reported cases of FNP after MMAE in cSDH

Authors & Year	Study Type	Age (yrs), Sex	Onset	Laterality	Treatment	Outcome	Embolic Agent	Notes
Kan et al., 20213	Multicenter series of 154 MMAEs	NA	NA	Rt	NA	No FU reported	NA	Included for context to demonstrate rarity
Ferber et al., 202316	Case report	81, F	Immediately	Lt	Symptomatic (artificial tears, lubricating ointment)	HB grade V initially, HB grade III after 63 days	NA	1st report of persistent palsy
Lambert-Cheatham et al., 202417	Case report	76, M	Immediately	Lt	NA	Significant partial recovery after 9 mos	Onyx	Combined oculomotor & facial palsy
Cristaldi et al., 202418	Case report	61, F	24 hrs	Lt	High-dose steroids, eye rehabilitation	HB grade V initially, minimal improvement after 6 mos	Polyvinyl alcohol microparticles w/ diluted acrylic	Palsy despite particle size >150 μm
Pilawska et al., 202510	Case series	82, M	24 hrs	Lt	Eye moisturization, facial muscle rehabilitation	HB grade IV initially, lost to FU	Onyx	Largest case series to date (3 patients)
		36, M	2 days	Lt	Steroids, facial muscle rehabilitation	HB grade III initially, HB grade II & partial recovery after 3 yrs	Onyx
		82, M	7 days	Lt	Eye moisturization, facial muscle rehabilitation, tarsorrhaphy	HB grade V initially, FNP still present at 4-mo FU	Onyx

FU = follow-up; NA = not available.

Because of the rarity of this condition in the setting of cSDH, management is extrapolated from that of iatrogenic or idiopathic facial palsy and Bell’s palsy. The initial management step involves assessing the severity of injury, typically done via the HB grade, to allow for appropriate monitoring of treatment effectiveness.¹⁹ After FNP is diagnosed, treatment is initially supportive. This involves symptomatic eye care via ophthalmic lubricant solutions, artificial tears, closed eye taping, and upper eyelid stretching.²⁰ In addition, facial muscle rehabilitation and physical therapy accompanied by diet modifications are used to improve facial function and reduce risk of aspiration.²¹ In the acute setting, a 10-day taper of high-dose steroids may be used to reduce inflammatory changes and edema.²² This can also be coupled with FN decompression.²³ In prolonged or refractory cases, surgical correction and chemodenervation may offer long-term aesthetic and functional improvement for patients.²⁴ In the reported cases, symptomatic management with steroids was used, with most patients exhibiting partial recovery after follow-up.

Because of to the limited number of reported cases, a temporal relationship between onset and recovery may not be easily delineated, and the recovery timeline is summarized in Table 1. Recovery ranged from no recovery to significant partial improvement within 3 years. Prognostic factors of FNP described in the literature may be extrapolated and applied to our case. Older age, higher baseline HB grade, presence of comorbidities, and extent of ischemia and FN degradation (evaluated via electroneurography degradation index) were crucial negative predictors of outcome at follow-up. In addition, early initiation of treatment with steroids and supportive therapy (within 5 days of diagnosis) was associated with a more favorable outcome.²⁵ Therefore, prompt identification and treatment may offer patients better long-term outcomes.

A standardized consensus on the optimal preventive strategies during MMAE to avoid FNP has not yet been established due to the limited number of reported cases. Nevertheless, several authors have emphasized technical precautions that may mitigate this risk, as summarized in Table 2.

TABLE 2.

Summary of preventive strategies to reduce FN after MMAE

Strategy	Rationale	Supporting Literature
Distal microcatheter positioning beyond the petrosal branch w/ slow injection	Reduces reflux into collaterals that may supply the FN	Shapiro et al., 20215; Pilawska et al., 202510
Proximal mechanical blockage (coil protection or large particles)	Prevents embolic material from entering collateral branches	Lazzaro et al., 201126; Campos et al., 202414
Balloon-assisted flow reversal	Minimizes retrograde collateral flow into FN-supplying branches	Campos et al., 202414
Particle size ≥150 μm	Nonvisualized vasa nervorum anastomoses measure 50–80 μm; larger particles reduce risk of nerve ischemia	Jindal et al., 20126; Lazzaro et al., 201126
Choice of embolic agent (favor higher viscosity)	Higher-viscosity liquid embolics & calibrated particles limit deep penetration into small vasa nervorum; low-viscosity formulations may increase risk	Iida et al., 20249; Mason et al., 201812
Slow, controlled proximal injection	Reduces risk of distal migration & reflux	Shapiro et al., 20215; Lazzaro et al., 201126
Meticulous angiographic mapping	Identifies subtle or dangerous extracranial-intracranial anastomoses involving the FN	Geibprasert et al., 20097; Ozanne et al., 20088; Pilawska et al., 202510
Postprocedure monitoring & early management	Early recognition & treatment of cranial neuropathies is a positive prognostic factor for recovery	Feng et al., 202115; Ferber et al., 202316; Lambert-Cheatham et al., 202417; Cristaldi et al., 202418

Lessons

FNP is a rare but significant complication of MMAE for cSDH. The vulnerability of the geniculate ganglion’s vascular supply from the MMA petrosal branch coupled with microvascular occlusion of the vasa nervorum and embolization material toxicity may explain the development of this complication, although the mechanism of injury remains unclear in some patients. The management of FN injury is mainly supportive through eye moisturization, facial muscle rehabilitation, and steroids, with most patients demonstrating at least partial recovery.

On reviewing the literature, some prevention techniques have been suggested. One important technique involves reducing reflux into collateral vessels. This may be achieved via distal microcatheter positioning beyond the petrosal branch with slow and controlled delivery of liquid embolics,^5,10 proximal mechanical blockage of the collateral branch with coiling or large particles prior to embolization,^14,26 or flow reversal of the collaterals using proximal balloon occlusion of the targeted vessel of the external carotid artery.²⁵ Another strategy relates to the caliber of nonvisualized anastomoses connecting to the vasa nervorum, estimated at 50–80 μm; thus, the use of embolic particles ≥ 150 μm may theoretically reduce the risk of occlusion of these critical microvessels.^6,26 Coil-only embolization may also provide benefit in reducing the risk of such complications, although current evidence remains sparse.¹⁴ Importantly, FNP can be avoidable if the anatomy is carefully evaluated. Detailed angiographic assessment of the MMA and the anatomical distribution prior to embolization remains a cornerstone of proper technique and preoperative evaluation to reduce the risk of reflux and cranial neuropathies.^7,8 The petrosal branch, which often arises within 10 mm of the foramen spinosum, is a major supplier of the FN and geniculate ganglion and represents a critical danger point.²⁷ Therefore, preoperative angiography should aim at precisely identifying the anatomical branches of the MMA and the presence of collaterals, allowing for patient stratification into safe candidates and those in whom embolization should be avoided when dangerous anastomoses exist.²⁸ In equivocal cases, a lidocaine provocation test may help identify the cranial nerve supply and the extent of reflux and collaterals before permanent embolization.²⁹ These steps emphasize the importance of meticulous anatomical assessment of the MMA in minimizing the risk of avoidable cranial neuropathies such as FNP.

Additional suggested precautions include careful selection of embolic agents of higher-viscosity formulations to limit deep penetration and unintended spread,^9,12 and maintaining slow, proximal injection to prevent distal migration.^5,26 Finally, patient counseling regarding this rare but potentially permanent complication and vigilant postprocedural monitoring for early signs of cranial neuropathy are also advocated.¹⁰

Despite these recommendations, a few limitations still exist. Most evidence on the management of FNP after MMAE is extrapolated from existing evidence on iatrogenic injuries or Bell’s palsy. Also, although the latest American Heart Association consensus on MMAE for cSDH reviewed the complications and efficacy of this procedure across available trials, FNP was reported in only 1 patient, highlighting the rarity of this complication.³⁰ In addition, the consensus primarily did not discuss prevention strategies aimed at reducing neuropathies such as FNP. Therefore, this complication remains rare, and evidence on prevention strategies is from expert opinions, case reports, and small case series.

Prevention depends on sound endovascular technique with proper angiographic mapping of collaterals and appropriate selection of particle size. Combining distal embolization with proximal coil protection appears to offer the best balance of safety and efficacy. Future studies should quantify the true incidence of cranial neuropathies after MMAE for cSDH and establish standardized preventive protocols to allow for optimal management.

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: Kawtharani, Shouman, Mosleh. Acquisition of data: Mosleh, Mahmoud. Analysis and interpretation of data: Mosleh, Mahmoud. Drafting the article: Kawtharani, Shouman, Mosleh, Ftouni. Critically revising the article: Darwish, Kawtharani, Shouman, Mosleh, Ftouni. Reviewed submitted version of manuscript: Darwish, Kawtharani, Shouman, Ftouni. Approved the final version of the manuscript on behalf of all authors: Darwish. Administrative/technical/material support: Darwish, Kawtharani, Ftouni. Study supervision: Darwish, Kawtharani.

Correspondence

Houssein Darwish: American University of Beirut Medical Center, Beirut, Lebanon. hd17@aub.edu.lb.