Anatomy of the Middle Meningeal Artery: Implications for Middle Meningeal Artery Embolization in Chronic Subdural Hematoma

Abstract

Chronic subdural hematoma (cSDH) is among the most common neurosurgical conditions, particularly affecting older adults and patients receiving anticoagulation. While burr-hole evacuation has long been the standard therapy, recurrence rates and associated morbidity remain significant. Middle meningeal artery (MMA) embolization has recently emerged as a promising alternative or adjunctive treatment, offering durable hematoma control with reduced recurrence. To understand the rationale and safety of this endovascular approach, detailed knowledge of MMA anatomy, embryology, and variations is essential. This review synthesizes current understanding of the MMA from gross and microvascular perspectives, integrating embryological origins, common and rare anatomical variants, and dural angioarchitecture, with emphasis on how these factors inform embolization strategies for cSDH. By bridging historical anatomical insights with contemporary angiographic and clinical evidence, we aim to provide a comprehensive resource for clinicians and researchers involved in neuroendovascular therapy.

Introduction

Chronic subdural hematoma (cSDH) is a progressive accumulation of blood and inflammatory fluid in the subdural space, affecting predominantly older adults and patients with coagulopathies or receiving antithrombotic therapy. Traditional management with burr-hole evacuation achieves hematoma decompression but is associated with recurrence rates of up to 20% in some series.¹⁾ In recent years, middle meningeal artery (MMA) embolization has gained attention as an alternative or adjunctive treatment, with multiple studies demonstrating reduced recurrence rates and favorable safety profiles.^2–4) The underlying rationale is to target the vascular supply to the fragile neocapillary networks within the cSDH membranes, thereby interrupting the cycle of rebleeding and exudation.⁵⁾

The success and safety of MMA embolization depend on detailed anatomical knowledge. While the MMA is the principal dural artery supplying the cranial convexity, it demonstrates considerable embryological complexity, anatomical variability, and extensive anastomotic connections.⁶⁾ Understanding these features is not merely academic—it is critical for avoiding complications such as cranial nerve palsies or inadvertent embolization of ophthalmic or cerebral arteries.

This review provides a comprehensive overview of the MMA in the context of cSDH embolization. We first trace the embryologic origins of the vessel, then describe its normal and variant anatomy, followed by the microvascular dural angioarchitecture. Finally, we discuss how these insights directly inform the practice of MMA embolization for cSDH.

Embryology of the MMA

Development from the stapedial artery system

The MMA originates from one of the most fascinating processes in cranial vascular embryology: the development and regression of the stapedial artery system. During early embryogenesis, the stapedial artery emerges from the hyoid artery—a remnant of the 2nd aortic arch—and traverses the stapes ring within the middle ear cavity. This transient but critical vessel contributes to the formation of the definitive cranial arterial network. It divides into 2 main branches: supraorbital (intracranial superior division) and maxillomandibular (extracranial inferior division). The ventral pharyngeal artery originates from the remnant vascular network of the ventral part of the 2nd aortic arch and merges with the maxillomandibular branch, finally forming the external carotid artery (ECA) with regression of the stapedial artery. The proximal part of the maxillomandibular branch forms the main trunk of the MMA, which passes through the foramen spinosum and anastomoses with the dorsal branch of the supraorbital branch. After this anastomosis, the MMA is supplied by the ECA via the internal maxillary artery. The supraorbital branch connects to the future ophthalmic artery. Through this process, the stapedial artery serves as a bridge between the internal and external carotid circulations.^6–8)

As the embryo develops, the proximal portion of the stapedial artery typically regresses, leaving behind its distal cranial segments. These distal remnants are incorporated into the developing maxillary artery, which arises as a branch of the ECA. The remnant incorporated into the maxillary system ultimately becomes the trunk of the MMA. This transition from an internal carotid-based supply (via the stapedial artery) to an external carotid origin exemplifies how embryological vessel regression and persistence shape adult anatomy.⁸⁾

Persistence and regression

Aberrations in this developmental sequence explain many clinically significant variations of the MMA. If the proximal stapedial artery fails to regress, a persistent stapedial artery may remain in continuity with the internal carotid artery (ICA), producing unusual origins of the MMA from the petrous or cavernous segment of the ICA. Similarly, incomplete incorporation by the maxillary artery can result in the MMA arising from the ophthalmic artery. Other rare variations, such as origin from the basilar artery, reflect persistence of primitive anastomotic channels between the primitive trigeminal artery and stapedial branches.⁹⁾

Normal Anatomy of the MMA

Origin and course

In most individuals, the MMA arises from the 1st segment of the maxillary artery, a terminal branch of the ECA. It ascends through the infratemporal fossa, passing posterior to the lateral pterygoid muscle, and enters the cranial cavity via the foramen spinosum, which is typically present and patent bilaterally. Once within the middle cranial fossa, the artery courses laterally across the greater wing of the sphenoid bone before dividing into its principal anterior and posterior branches.^10,11)

Segmentation

Detailed angiographic studies have classified the MMA into several distinct segments, each with characteristic branching patterns and relationships to surrounding bone and dura matter¹¹⁾ (Fig. 1A and 1B):

• •  Extracranial segment: Extends from its maxillary artery origin to the foramen spinosum.
• •  Horizontal segment: Courses anterolaterally within the middle cranial fossa, giving rise to cavernous and petrosal branches.
• •  Temporal segment: Ascends over the temporal convexity and gives rise to posterior convexity branches.
• •  Pterional segment: Travels toward the pterion, typically dividing into anterior and posterior branches.
• •  Coronal segment: Extends toward the coronal suture, forming rich anastomoses across the midline.

Fig. 1 Normal segments of the middle meningeal artery. (A) Anterior–posterior view and (B) lateral view.

br, branches; FS, foramen spinosum

This segmentation framework is particularly useful in endovascular planning, as each segment carries distinct anastomotic risks and opportunities for embolization.

Major branches and anastomoses

The MMA has several clinically important branches:

• •  Anterior branch: Supplies the dura of the frontal and anterior parietal convexities. Anastomoses with the lacrimal branch of the ophthalmic artery via the meningolacrimal artery are of high clinical significance, as reflux in this region risks retinal ischemia.
• •  Posterior branch: Supplies the parietotemporal dura and posterior convexity. It is frequently targeted during embolization for cSDH because it supplies membranes overlying the parietal convexity.
• •  Petrosal branch: Usually arises from the 10-mm segment of the MMA after it passes through the foramen spinosum, though it may also originate within or just below the foramen.¹²⁾ (Figs. 2 and 3) This branch runs toward the petrous apex and may anastomose with the internal auditory artery branching off from the anterior inferior cerebellar artery.
• •  Petrosquamosal branch: Courses along the petrosquamous suture, contributing to transosseous supply to the posterolateral floor of the middle fossa, the lateral tentorium, and the dura of the superior posterior fossa. It anastomoses with the jugular branch of the ascending pharyngeal artery, the lateral/medial tentorial artery, and the mastoid branch of the occipital artery.
• •  Falcine arteries: Arise from the anterior and posterior branches. They anastomose with the anterior falcine artery, ethmoidal branches of the ophthalmic artery, anterior cerebral artery, and posterior meningeal artery.
• •  Cavernous branch: Arises from the petrosal branch and supplies the lateral wall of the cavernous sinus (Fig. 4).

Fig. 2 Petrosal branch. A case with transverse sinus dural arteriovenous fistula. Left external carotid angiography (A, anteroposterior view; B, lateral view) revealed petrosal branch (white arrow). It arises just after passing through the foramen spinosum.

Fig. 3 The same case as in Fig. 2. Cone-beam CT (A) coronal, (B) sagittal, and (C) axial views clearly showed the petrosal branch (white arrow) of the middle meningeal artery.

Fig. 4 Cavernous branch of the MMA. A case of a cavernous sinus dural arteriovenous fistula. The left internal maxillary artery angiogram (A, anteroposterior view; B, lateral view) shows a small cavernous branch (black arrow, anterior; double black arrow, posterior). The artery of the foramen rotundum (white arrow) is also observed as a feeder.

MMA, middle meningeal artery

These anastomoses highlight the importance of selective angiography and precise microcatheter positioning during embolization.

Territory supplied

The MMA supplies the majority of the supratentorial dura, including the lateral convexities, falx cerebri, tentorial insertions, and calvarial bone via transosseous branches. This extensive distribution explains why MMA embolization can effectively devascularize the membranes of cSDH, which rely heavily on MMA supply for their pathological neovasculature.^5,6,13)

Anatomical Variations of the MMA

Variability in origin

Although the classic origin of the MMA is from the maxillary artery, several important anatomical variations have been reported. The most clinically relevant of these originates from the ophthalmic artery (Fig. 5). An ophthalmic-origin MMA is relatively uncommon, reported in 0.5%–2% of angiographic series.¹⁴⁾ Embolization from such ophthalmic-rigin MMA presents a high risk of vision loss if embolic material enters the central retinal artery. Three main types of this variation have been described.¹⁵⁾ The 1st type involves the entire MMA territory being supplied by the ophthalmic artery through the recurrent meningeal artery. In the 2nd type, only the anterior branch of the MMA originates from the ophthalmic artery, while the posterior branch retains its origin from the internal maxillary artery. The 3rd type is not a true ophthalmic origin of the MMA but rather an anastomosis between the ophthalmic artery and the accessory meningeal artery (via the deep recurrent ophthalmic artery). As a result, the anterior meningeal territory is supplied by both the MMA and the ophthalmic artery without direct communication between them.

Fig. 5 MMA arising from the ophthalmic artery. A case of right recurrent chronic subdural hematoma. (A) CT scan at recurrence. Right external carotid angiography (B, anteroposterior view; E, lateral view) showed no MMA originating from the internal maxillary artery. Right internal carotid angiography (C, anteroposterior view; F, lateral view) showed the MMA (arrow) originating from the ophthalmic artery. 3D rotational angiography of the right internal carotid artery (D, anteroposterior view; G, lateral view) clearly showed the MMA (white arrow, colored line) originating from the ophthalmic artery. Due to the high treatment risk, MMA embolization via the ophthalmic artery was not performed.

MMA, middle meningeal artery

Origins from the cavernous or petrous ICA are rarer and are often associated with persistence of embryonic stapedial artery remnants¹⁴⁾ (Fig. 6). The MMA may also arise from the cervical segment of the ICA, ascend along the cervical ICA, enter the tympanic cavity through the inferior tympanic canaliculus, and then follow the typical course of the stapedial artery. In this variant, annexation of the stapedial artery by the inferior tympanic artery (a branch of the ascending pharyngeal artery), along with regression of the proximal stapedial artery, explains this vascular configuration.

Fig. 6 Middle meningeal artery originating from the petrous portion of the internal carotid artery. Right internal carotid angiography (A, anteroposterior view; B, lateral view) showed the middle meningeal artery (white arrow) originating from the petrous portion of the internal carotid artery. (C) Cone-beam CT showed the origin of this middle meningeal artery (white arrow).

Rare cases describe the MMA arising from the basilar artery, usually between the anterior inferior cerebellar artery and the superior cerebellar artery.^16,17) This reflects persistence of trigeminal–basilar connections (the trigeminostapedial variant).⁹⁾ Recognition of these variants requires meticulous angiography of both the external and internal carotid circulations.

Variations in course and foramina

In some cases, the MMA does not traverse the foramen spinosum.^18,19) The absence of the foramen spinosum on imaging often indicates a variant origin. These variants can complicate catheter navigation and may alter the embolization target territory. In an analysis of 140 MMAs,²⁰⁾ dominance of the anterior branch was observed in 41%. The posterior convexity branch originated proximally (at or near the foramen spinosum) in 36% of cases, at an intermediate point in 44%, and distally in 21%. In cases where the posterior convexity branch originates proximally, particular care is required to avoid inadvertent migration into the petrosal branch during microcatheter navigation toward the posterior convexity branch.

Embryological basis and clinical significance

All these variations are best understood in the context of embryology. Persistence of stapedial connections explains ophthalmic and ICA origins. Orbital branches of the MMA also represent potentially hazardous anastomoses. Reflux of embolic agents into the ophthalmic artery has long been considered a potential risk during MMA embolization. These dangerous anastomoses between the MMA and the ophthalmic artery arise from their embryological relationship.⁸⁾ Clinically, knowledge of these variants is crucial for patient safety: failure to identify an ophthalmic origin can result in catastrophic vision loss, while unrecognized ICA connections may lead to cerebral infarction.

Microvascular Angioarchitecture of the Dura

Layered structure of the dura

The cranial dura mater is not a uniform sheet but a complex structure composed of distinct histological layers. Classically, 3 components are recognized^5,21):

• •  Periosteal layer: The outermost layer, firmly adherent to the inner table of the skull. It is richly vascularized by arterial branches from the MMA and other extracranial vessels that penetrate the skull. This layer serves as the main structural anchor of the dura and contains vessels that participate in transosseous anastomoses.
• •  Meningeal layer: Located beneath the periosteal layer, this intermediate zone is relatively less vascular and functions as a fibrous supportive sheet separating the outer and inner vascular networks.
• •  Border cell (inner) layer: Adjacent to the arachnoid, this thin cellular layer is crucial to the pathophysiology of cSDH. cSDH arises within this dural border cell layer—a loose cellular layer devoid of intercellular collagen and tight junctions—situated between 2 firm meningeal layers.²¹⁾ It contains fragile microvascular networks that are prone to leakage and neovascular proliferation.

This layered organization is central to understanding why certain vascular compartments are targeted during embolization.

Outer arterial network

The outer periosteal network is characterized by relatively large-caliber vessels, typically 100–300 μm in diameter.²²⁾ These arteries, derived from MMA branches, demonstrate extensive anastomoses across sutures and through the diploë of the calvarium. Key features include:^5,6)

• •  Cross-midline connections: Small branches traverse the sagittal suture, enabling collateral supply from the contralateral MMA.
• •  Transosseous pathways: Nutrient arteries pass through diploic channels, linking extracranial vessels (such as the superficial temporal or occipital arteries) with the intracranial dura.
• •  Sutural channels: Arteries course along cranial sutures, forming connections with contralateral dural networks.

These pathways explain why angiography often shows bilateral or transosseous supply to cSDH membranes. Therapeutically, they may justify bilateral MMA embolization even in unilateral cSDH, as contralateral feeders can sustain vascularization.²³⁾ However, the potential benefits of bilateral embolization require further investigation in future studies.

Transitional penetrating vessels

From the outer network, penetrating arterioles pass through the relatively avascular meningeal layer into the border cell layer.²⁴⁾ These vessels, ranging from 30–80 μm, represent a crucial link between larger convexity arteries and the fragile inner plexus. They are prone to pathological remodeling, becoming tortuous and leaky in disease states. The fact that these transitional vessels are supplied by proximal MMA branches underscores why selective embolization of distal convexity branches can effectively deprive hematoma membranes of their vascular supply.

Inner capillary plexus

The innermost border cell layer contains a delicate capillary plexus approximately 5–15 μm in diameter. This plexus is normally sparse, but in conditions such as cSDH, it undergoes significant angiogenesis. The vessels are immature, with thin walls lacking tight junctions, making them prone to leakage of both plasma and erythrocytes. Inflammatory mediators—including vascular endothelial growth factor (VEGF), interleukins, and matrix metalloproteinases—further destabilize these vessels, perpetuating a cycle of exudation and microhemorrhage.^24,25)

Histopathological studies consistently demonstrate hemosiderin-laden macrophages, fibrin breakdown products, and ongoing microvascular leakage within this layer. This pathological vascular bed, supplied by MMA arterioles, represents the therapeutic target of embolization.

Angiographic correlates

The microvascular architecture of the dura appears on angiography⁵⁾ as:

• •  Dural blush: Hypertrophied MMA convexity branches show a fine, persistent capillary stain corresponding to the vascularized outer membrane of a cSDH.
• •  Transosseous channels: Contrast opacification across sutures and diploic veins reflects collateral supply from the outer network.
• •  Delayed membrane enhancement: On flat-panel CT or contrast-enhanced MRI, thickened vascular membranes demonstrate contrast uptake, mirroring the neovascular plexus.

Successful embolization typically results in the disappearance or attenuation of this blush, correlating with subsequent hematoma involution.²⁶⁾

Clinical significance

The layered and interconnected nature of dural vasculature has several important implications:

• •  Target of therapy: Embolization is effective because it occludes proximal convexity branches of the MMA that ultimately feed the fragile inner plexus.
• •  Risk of recurrence: If embolization fails to reach distal feeders or if contralateral collaterals persist, the pathological cycle may continue.
• •  Anatomical safety: Awareness of hazardous collaterals to the ophthalmic and ICA branches is crucial to prevent complications.
• •  Predictive imaging: The extent of dural blush and membrane enhancement may predict responsiveness to embolization, reflecting the activity of the vascularized inner plexus.

Pathophysiological Basis of MMA Embolization in cSDH

Traditional vs. modern theories

The earliest descriptions of cSDH in the 19th century emphasized a traumatic origin, often attributing the condition to rupture of cortical bridging veins following minor head trauma. This explanation persisted for decades, supported by observations of older adults with brain atrophy, in whom veins appeared stretched and more susceptible to tearing. Rowbotham and Little advanced this venous rupture hypothesis, suggesting that small tears permitted the slow accumulation of blood in the subdural space.²⁷⁾

However, surgical and histopathological evidence over the past 5 decades has challenged this view. Many patients with cSDH have no clear history of trauma, and intraoperative exploration rarely reveals torn veins. Instead, surgeons consistently observe thickened, vascularized outer membranes lining the hematoma cavity. These membranes contain proliferating capillaries, hemosiderin deposits, inflammatory cells, and evidence of repeated microhemorrhages.^28,29) Such findings indicate that the hematoma is not a static collection but a biologically active lesion sustained by ongoing vascular processes rather than a single traumatic event.

The cycle of membrane vascularization

Modern understanding posits that cSDH represents a self-perpetuating cycle of inflammation, neovascularization, and rebleeding.^28,29) Initial trauma or subdural effusion may trigger proliferation of dural border cells, with subsequent angiogenesis driven by VEGF and other cytokines. The newly formed vessels are immature, thin-walled, and permeable.³⁰⁾ They leak plasma and red blood cells, generating further mass effect and inflammation. Fibrin degradation products within the hematoma cavity further stimulate angiogenesis, sustaining this pathological cycle.²⁴⁾

The MMA plays a pivotal role in this process. As the principal arterial supply to the outer dural membrane, it delivers blood to these fragile neocapillaries. Histological studies demonstrate direct continuity between MMA arterioles and the capillary plexus of the outer hematoma membrane.²⁷⁾ Embolization of the MMA interrupts this vascular input, thereby disrupting the cycle of hemorrhage and exudation.

Hemodynamic considerations

The dural vascular network exhibits low-resistance flow. In the presence of cSDH, angiography demonstrates hypertrophied MMA branches with persistent blush corresponding to the vascularized outer membrane. Embolization reduces or eliminates this blush, which correlates with gradual hematoma volume reduction over time.^5,26) Importantly, the inner hematoma membrane—which interfaces with the brain surface—is less vascularized and is not primarily supplied by the MMA.⁵⁾ This distinction explains why embolization targets the outer membrane, leading to gradual resorption of the hematoma rather than immediate decompression.

Imaging evidence of pathophysiology

Modern angiographic and cross-sectional imaging corroborate these pathophysiological insights. On DSA, cSDH membranes appear as diffuse dural staining fed by convexity branches of the MMA.⁵⁾ Dynamic contrast-enhanced MRI and flat-panel CT can show enhancement of the outer membrane, reflecting active vascular proliferation.²⁶⁾ These imaging findings strengthen the rationale for embolization by demonstrating that the hematoma is sustained by ongoing MMA-dependent perfusion.

Clinical–pathological correlation

Clinically, patients undergoing MMA embolization exhibit significantly lower recurrence rates compared to those treated with conventional burr-hole drainage alone. This outcome aligns with the proposed mechanism: surgical evacuation removes the hematoma mass but does not address the vascular source, whereas embolization deprives the membrane of its arterial supply, leading to involution. In refractory cases, embolization performed after surgery reduces the likelihood of reaccumulation.³¹⁾ Thus, the pathophysiological basis for MMA embolization is supported not only by theory but also by clinical outcomes.

Dangerous Anastomoses Relevant to MMA Embolization

The MMA develops embryologically from the stapedial artery, which originates from the hyoid artery, it maintains numerous potential connections with both the ophthalmic artery and the ICA in adulthood. In addition, the MMA supplies a wide territory extending from the cranial vault to the skull base; therefore, a detailed understanding of its collateral pathways is crucial for MMA embolization (Fig. 7).

Fig. 7 Dangerous anastomoses between the MMA and the ophthalmic artery/the inferolateral trunk and in the middle ear. The 2 dotted lines indicate potential anastomoses.

AphA, ascending pharyngeal artery; br, branches; CTA, caroticotympanic artery; FS, foramen spinosum; ICA, internal carotid artery; ILT, inferolateral trunk; IMA, internal maxillary artery; MLF, meningolacrimal foramen; MMA, middle meningeal artery; OcciA, occipital artery; SOF, superior orbital fissure

Orbital region

In the orbital region, the anterior branch of the MMA forms clinically significant anastomoses with the lacrimal branch of the ophthalmic artery. Anatomical studies have demonstrated the presence of orbital branches of the MMA in approximately 64.9% of individuals.³²⁾ The routes by which the MMA enters the orbit include: menigolacrimal foramen (meningolacrimal artery): 43.2%, superior orbital fissure (via the recurrent meningeal artery or sphenoidal artery): 16.2%.

The anterior branch of the MMA courses along the anterior margin of the greater wing of the sphenoid bone and may anastomose with branches of the inferolateral trunk (ILT) or the meningohypophyseal trunk (MHT). Through the recurrent meningeal artery, it also connects to the tentorial artery.

Because these anastomoses lead directly to the ophthalmic circulation, any reflux of embolic material during MMA embolization carries a risk of retinal ischemia and vision loss.

Cavernous region

The ILT of the ICA plays a central role in the anastomotic network around the cavernous sinus. According to Lasjaunias et al., the ILT typically divides into anterior, posterior, and superior branches.³³⁾ The marginal tentorial artery usually arises from the meningohypophyseal trunk, but may arise from the ILT.

The cavernous branch of the MMA arises from the petrosal branch and supplies the dura of the middle fossa and the lateral wall of the cavernous sinus. This branch frequently anastomoses with the posterolateral branch of the ILT. It may also communicate with the carotid branch of the ascending pharyngeal artery and the recurrent artery of the foramen lacerum.

Small tentorial branches arising from the posterior or petrosal divisions of the MMA may anastomose with: the superior branch of the ILT, or the tentorial artery from the MHT.

These connections constitute potential pathways for inadvertent ICA embolization.

Middle ear region

The petrosal branch of the MMA has additional connections within the middle ear.⁸⁾ It may anastomose with the internal auditory artery (from the anterior inferior cerebellar artery) and gives rise to the superior tympanic artery, contributing to the tympanic arterial network. The tympanic plexus includes: superior tympanic artery (MMA–petrosal branch), anterior tympanic artery (internal maxillary artery), inferior tympanic artery (ascending pharyngeal artery), and posterior tympanic (stylomastoid) artery. The stylomastoid artery and the superior tympanic artery form the facial arcade, which plays a major role in supplying the facial nerve. Thus, embolization in this region carries a risk of facial nerve palsy.

Conclusion

The MMA is central to both the vascular physiology of the dura and the pathophysiology of cSDH. Its embryological development, anatomical variations, and complex angioarchitecture explain the feasibility, efficacy, and potential risks of MMA embolization. A thorough understanding of these factors is essential for neurointerventionalists to perform safe and effective procedures, minimizing recurrence of cSDH while avoiding complications. As MMA embolization continues to gain prominence, mastery of the relevant anatomy and pathophysiology remains a cornerstone of optimal patient outcomes.

Disclosure Statement

The author declares no conflicts of interest.

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