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Frontal nerve

The frontal nerve is the largest terminal branch of the ophthalmic division (CN V1) of the trigeminal nerve (cranial nerve V), a purely sensory nerve that originates from the trigeminal ganglion in the middle cranial fossa and provides general somatic afferent innervation to the skin and mucous membranes of the upper face, including the forehead, upper eyelid, and frontal sinus.^[1]^[2] The frontal nerve emerges as the middle and thickest branch of the ophthalmic nerve within the orbit, traveling forward along the superior aspect of the levator palpebrae superioris muscle and beneath the periosteum of the orbital roof.^[1]^[3] It enters the orbit through the superior orbital fissure, lateral to the tendinous ring, and typically divides into two main branches near the midpoint of the roof: the supraorbital nerve laterally and the supratrochlear nerve medially.^[2]^[4] The supraorbital nerve exits the orbit via the supraorbital foramen or notch, supplying sensory fibers to the conjunctiva and skin of the upper eyelid, the frontal sinus mucosa, and the skin of the forehead and scalp as far back as the vertex; it further divides into superficial and deep branches for broader distribution.^[1]^[2] The supratrochlear nerve, the smaller medial branch, passes superior to the trochlea of the superior oblique muscle, emerging near the superomedial angle of the orbit to innervate the medial conjunctiva and skin of the upper eyelid, as well as the skin of the lower forehead and the medial aspect of the eyebrow.^[4]^[2] Together, these branches ensure comprehensive sensory coverage of the anterior scalp and periorbital region, contributing to tactile sensation, pain, and temperature perception in these areas.^[1]

Anatomy

Origin and relations

The frontal nerve is the largest branch of the ophthalmic division (V1) of the trigeminal nerve (cranial nerve V), emerging from it just prior to entry into the orbit.^[5] It arises within the superolateral aspect of the superior orbital fissure, where the ophthalmic nerve divides into its three main branches: the frontal, lacrimal, and nasociliary nerves.^[1] Upon entering the orbit, the frontal nerve passes through the superolateral compartment of the superior orbital fissure, positioned superolateral to the annulus of Zinn (common tendinous ring) and without traversing the ring itself.^[6] In this compartment, it lies between the lacrimal nerve laterally and the trochlear nerve (cranial nerve IV) medially, while running parallel to the superior ophthalmic vein, which is positioned most laterally.^[7] Within the orbit, the nerve courses anteriorly between the periosteum of the orbital roof (periorbita) superiorly and the levator palpebrae superioris muscle inferiorly; it maintains proximity to the superior ophthalmic vein as this vein courses through the orbital contents.^[6] Embryologically, the sensory neurons of the frontal nerve derive from contributions of the trigeminal placode, associated with the first branchial arch placodes that form the sensory components of the trigeminal ganglion.^[8]

Course and branches

The frontal nerve, arising from the ophthalmic division of the trigeminal nerve, enters the orbit via the superior orbital fissure and courses anteriorly along its superior wall, positioned between the levator palpebrae superioris muscle and the periorbita.^[9] Approximately midway through the orbit, it divides into two terminal branches: the larger lateral supraorbital nerve and the smaller medial supratrochlear nerve.^[9]^[2] The supraorbital nerve proceeds superiorly and laterally, exiting the orbit through the supraorbital notch or foramen, which is typically located 2–2.5 cm lateral to the midline.^[9]^[5] After emerging, it travels with the supraorbital artery over the forehead and divides into superficial (anterior) and deep (posterior) branches; the superficial branch courses over the frontalis muscle toward the scalp, while the deep branch pierces the frontalis to reach the pericranium, distributing to the forehead up to the vertex.^[2]^[9] The supratrochlear nerve courses medially and anteriorly, passing superior to the trochlea of the superior oblique muscle before exiting the orbit near the medial orbital margin, often between the trochlea and the supraorbital notch.^[9]^[2] It then ascends along the medial forehead between the frontalis and orbicularis oculi muscles, distributing to the medial forehead, bridge of the nose, and upper eyelid skin.^[9]^[2] Anatomical variations of the frontal nerve include an undivided single trunk in approximately 0.5–10% of cases (varying by study), with the division occurring variably in the proximal or distal half of the orbit in others.^[9]^[5] The supraorbital notch or foramen position can vary, with single openings (notch or foramen) predominant in 78–80% of specimens and double openings in 20–22%.^[5] Duplication of the supratrochlear nerve is rare, observed in roughly 4% of cases.^[9]^[5]

Function

Sensory innervation

The frontal nerve serves as a purely sensory branch of the ophthalmic division (V1) of the trigeminal nerve (CN V), carrying general somatic afferent fibers that transmit sensations of touch, pain, temperature, and proprioception from the upper face.^[1] These fibers originate from pseudounipolar neurons in the trigeminal ganglion and convey impulses centrally to the brainstem nuclei.^[1] The supraorbital branch of the frontal nerve provides sensory innervation to the conjunctiva, skin of the upper eyelid, mucosa of the frontal sinus, skin of the forehead extending to the lambdoid suture, and the pericranium of the frontal bone.^[1] In contrast, the supratrochlear branch supplies the medial aspect of the upper eyelid, the skin over the root of the nose, and the medial forehead.^[10] These distributions ensure comprehensive coverage of the superior orbital and frontal regions without significant motor components.^[1] Sensory impulses from the frontal nerve travel proximally through the ophthalmic division to the trigeminal ganglion, where cell bodies of the afferent neurons reside, before projecting to the principal sensory nucleus in the pons for discriminative touch and proprioception, or to the spinal trigeminal nucleus for pain and temperature sensations.^[1] From these nuclei, second-order neurons ascend via the trigeminal lemniscus to the ventral posteromedial nucleus of the thalamus and ultimately to the somatosensory cortex.^[1] Collectively, the frontal nerve contributes to sensory innervation of approximately the upper third of the face, with minimal overlap from the maxillary division (V2) primarily at the midline.^[1] This targeted distribution supports fine spatial discrimination and protective sensory feedback in the periorbital and frontal areas.^[10]

Reflex mechanisms

The frontal nerve, as a branch of the ophthalmic division of the trigeminal nerve (CN V1), serves as the afferent limb in the corneal reflex, particularly for stimuli applied to the upper eyelid and conjunctiva via its supratrochlear and supraorbital branches. These branches detect tactile or noxious stimuli, transmitting sensory signals through the trigeminal ganglion to the spinal trigeminal nucleus in the brainstem, where interneurons connect to the facial nerve (CN VII) for the efferent response. This results in bilateral contraction of the orbicularis oculi muscle, producing a protective blink to shield the eye from potential harm.^[11]^[12] In addition to the corneal reflex, the frontal nerve contributes to the frontalis muscle reflex through the trigeminofacial pathway. Sensory input from the forehead and scalp, carried by the supraorbital and supratrochlear nerves, can elicit a delayed electromyographic response in the frontalis muscle approximately 33 milliseconds after stimulation, mediated by polysynaptic connections in the brainstem. The efferent limb involves motor fibers of the facial nerve (CN VII) that innervate the frontalis muscle, causing eyebrow elevation to protect the eyes from overhead threats, such as falling debris. This reflex enhances facial expressivity and environmental vigilance beyond simple eyelid closure.^[13]^[12] Physiologically, these mechanisms augment the efficiency of the blink reflex by incorporating scalp and forehead sensation, promoting rapid environmental awareness and preventing ocular injury during dynamic activities. The frontal nerve's role underscores its importance in multisynaptic circuits that prioritize eye protection through integrated sensory-motor feedback.^[11]^[13]

Clinical significance

Injuries and trauma

The frontal nerve, a branch of the ophthalmic division of the trigeminal nerve (V1), is vulnerable to direct trauma due to its course through the superior orbital fissure and along the orbital roof, where it divides into the supraorbital and supratrochlear nerves.^[14] Common trauma types include orbital roof fractures, often resulting from high-energy impacts such as motor vehicle accidents, falls, or assaults; forehead lacerations; and blunt head injuries that compress the nerve against the orbital roof.^[14] These injuries frequently occur in the context of maxillofacial trauma, with orbital roof fractures representing 1-9% of all facial bone fractures.^[14] Mechanisms of injury typically involve shear forces at the supraorbital notch during frontal impacts, where the nerve transitions from an intraorbital to a subcutaneous position, or compression and stretching within the orbit from displaced bone fragments in blowout or roof fractures.^[15] Iatrogenic trauma can arise during endoscopic sinus surgery or orbital decompression procedures, particularly when dissecting near the superomedial orbit or superior wall, potentially damaging the nerve during fat removal or bony manipulation. In orbital roof fractures, the nerve's superficial location along the supraorbital rim heightens its susceptibility to direct laceration or contusion.^[14] Symptoms of frontal nerve injury manifest as ipsilateral hypoesthesia or numbness in the forehead and upper eyelid, with loss of pain and temperature sensation in the nerve's distribution, often accompanied by paresthesia or tenderness at the supraorbital notch.^[16] These sensory deficits arise from neuropraxia, axonotmesis, or neurotmesis depending on the injury severity, and may contribute to post-traumatic headaches if the supraorbital branch is involved.^[17] Frontal nerve injuries are common in maxillofacial trauma, particularly with orbital involvement; for instance, trigeminal nerve branches, including V1, are impaired in up to 71% of facial fractures per prospective analyses (as of 2004), though V1-specific rates are lower (around 20-25% of nerve injuries).^[18]^[19] In orbital decompression surgeries for conditions like thyroid eye disease, supraorbital nerve hypesthesia occurs in approximately 8-18% of cases, with about 8% permanent (as of 2016).^[20] Risks are elevated in high-impact activities like sports or motor vehicle accidents, where orbital fractures account for 20-25% of facial trauma presentations.^[21] Initial management focuses on neuroimaging with computed tomography (CT) to assess bony involvement and fracture extent, guiding decisions on conservative versus surgical intervention.^[22] For neuropraxic injuries without significant entrapment or displacement, conservative observation with sensory monitoring and analgesics is often sufficient, as many resolve spontaneously within weeks to months.^[14]

Pathologies and disorders

The frontal nerve, as a branch of the ophthalmic division (V1) of the trigeminal nerve, can be affected by trigeminal neuralgia in its V1-predominant variant, manifesting as sudden, paroxysmal episodes of lancinating, electric-shock-like pain confined to the supraorbital and supratrochlear distributions. These attacks are typically brief, lasting seconds to minutes, and frequently triggered by innocuous stimuli such as light touch to the forehead or eye closure, reflecting hypersensitivity in the affected nerve territory.^[23] The underlying etiology often involves neurovascular compression at the trigeminal root entry zone, where a looping superior cerebellar artery or vein impinges on the nerve, or demyelination of the nerve sheath, which lowers the threshold for ectopic firing.^[24] This condition is more common in individuals over 50 and disproportionately affects women, with V1 involvement less common, occurring in less than 5% of cases for isolated V1 (up to 25% when multiple branches affected), though pure V1 neuralgia remains rare compared to V2 or V3 distributions (as of 2024).^[23]^[25] Herpes zoster ophthalmicus represents a significant infectious pathology impacting the frontal nerve, arising from reactivation of latent varicella-zoster virus within the trigeminal ganglion, specifically along the V1 division. Clinically, it presents with a painful vesicular rash in the dermatomes supplied by the frontal, lacrimal, and nasociliary branches, often beginning with prodromal sensory disturbances like paresthesia or itching in the forehead and upper eyelid before the eruption appears.^[26] Ocular complications occur in up to 50% of cases, but the frontal nerve's involvement can lead to persistent postherpetic neuralgia, characterized by chronic burning or stabbing pain in the supraorbital region lasting beyond three months after rash resolution, affecting sensory fibers and potentially causing corneal hypoesthesia.^[27] Risk factors include advanced age, immunosuppression, and prior varicella infection, with the virus traveling retrogradely along the nerve axon to cause inflammation and neuronal damage.^[26] Schwannomas of the frontal nerve are uncommon benign neoplasms originating from Schwann cells of the nerve sheath, typically presenting with insidious onset of symptoms such as progressive numbness, tingling, or a palpable mass in the superomedial orbit. These tumors grow slowly, often measuring 1-3 cm at diagnosis, and exert mass effect on adjacent structures, potentially leading to proptosis, diplopia, or visual field defects without significant motor involvement.^[28] They are characteristically located along the intraorbital course of the frontal nerve, between the superior orbital fissure and the supraorbital foramen, where the nerve is relatively superficial and amenable to surgical access.^[29] Imaging typically reveals a well-circumscribed, enhancing lesion with cystic components in some cases, confirming the diagnosis histologically as spindle-cell proliferation with Antoni A and B patterns.^[30] Such schwannomas account for less than 1% of orbital tumors and are usually sporadic, though rare associations with neurofibromatosis type 2 have been reported.^[28] Additional pathologies involving the frontal nerve include demyelination in multiple sclerosis, where plaques in the trigeminal sensory nuclei or brainstem tracts disrupt sensory conduction, resulting in neuropathic pain or dysesthesia mimicking V1 neuralgia in the frontal distribution.^[31] Ischemic neuropathy from giant cell arteritis may also affect the nerve through vasculitis of the vasa nervorum or orbital branches, leading to acute or subacute sensory deficits and headache, often as part of systemic symptoms like temporal tenderness.^[32] Diagnosis of these frontal nerve disorders relies on magnetic resonance imaging (MRI) to detect soft tissue abnormalities, such as nerve enhancement in inflammation, mass lesions in tumors, or demyelinating plaques in multiple sclerosis, with high-resolution sequences providing detailed visualization of the nerve from the superior orbital fissure onward.^[33] Clinical correlation is essential, including sensory testing to map deficits in the trigeminal V1 distribution, alongside serological tests for infectious or autoimmune etiologies to guide management.^[34]

Surgical considerations

The frontal nerve, consisting of the supraorbital and supratrochlear branches, holds significant relevance in surgical procedures of the forehead and periorbital region, including brow lifts, frontal sinus surgery, orbital tumor resection, and facelifts, where inadvertent injury can lead to sensory deficits in the forehead and scalp. In brow lifts, such as endoscopic or direct approaches, the supraorbital nerve is at risk during dissection near the supraorbital rim, necessitating careful mobilization to maintain sensation. Frontal sinus surgery, often via osteoplastic flaps or endoscopic methods, requires preservation of the nerve to avoid postoperative forehead numbness, particularly in tumor resections involving the anterior table. During orbital tumor resections, the nerve's proximity to the superior orbit demands precise exposure to prevent iatrogenic damage. In facelifts, the supratrochlear branch is vulnerable during midline forehead undermining, potentially causing medial brow anesthesia if not identified early. Surgical identification of the frontal nerve relies on reliable anatomical landmarks to minimize risks. The supraorbital nerve typically emerges from the supraorbital foramen or notch at the supraorbital rim, approximately 2 cm lateral to the midline or aligned with the medial iris, providing a consistent topographical guide during incisions. Intraoperative nerve monitoring or Doppler ultrasonography can further assist in locating finer branches, enhancing precision in endoscopic brow lifts or sinus procedures. Awareness of anatomical variations, such as a supraorbital foramen rather than notch in up to 10-20% of cases, informs incision planning to avoid blind dissection. Preservation techniques emphasize atraumatic handling to safeguard nerve integrity. Gentle retraction with non-compressive instruments prevents neuropraxia during brow lift periosteal elevation, while avoidance of electrocautery near the supraorbital notch reduces thermal injury risk in frontal sinus approaches. In orbital tumor resections, subperiosteal dissection planes help isolate the nerve from tumor margins. For iatrogenic sectioning encountered intraoperatively, immediate microneural repair or nerve grafting using sural nerve autografts—harvested from the lateral calf for their suitable diameter and length—restores continuity and promotes axonal regeneration. Postoperative outcomes vary by injury severity. Neuropraxia, the mildest form involving conduction block without axonal disruption, typically resolves spontaneously within 3-6 months through remyelination, restoring forehead sensation in most cases. Axonotmesis, with axonal disruption but intact endoneurium, often requires surgical intervention like microneural repair or grafting to achieve sensation recovery, with functional improvement observed over 6-12 months via reinnervation. Complications from frontal nerve injury include postoperative dysesthesia or anesthesia, reported in up to 15% of frontal sinus surgeries due to direct trauma or edema. Sensation recovery is evaluated using standardized tests such as two-point discrimination, which measures the minimal distance for distinguishing two stimuli (normal <40 mm on forehead), or Semmes-Weinstein monofilaments, assessing touch-pressure thresholds from normal (blue filament) to diminished protective sensation (red). Early detection allows for targeted rehabilitation, improving patient-reported outcomes.

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