Treatment of Nerve Injuries

By Babak Azizzadeh MD, Grigoriy Mashkevich, MD

treatment of nerve injuries 1treatment of nerve injuries 2

Motor Nerves Introduction

Surgical intervention remains a popular choice in patients seeking facial rejuvenation. Although uncommon, temporary or permanent peripheral nerve injury may complicate almost any type of invasive aesthetic procedure of the face, resulting in functional and psychological consequences for the patient. Prompt recognition and appropriate intervention are necessary to avoid the long-term sequelae and improve the chances of complete neurological recovery. Depending on the type of injury, various interventions may range from observation and close follow-up to interposition nerve grafting. This article reviews the pertinent anatomy of nerves at risk in facial cosmetic surgery and discusses various management strategies for inadvertent injury to peripheral nerves of the face.

Nerves at Risk in Facial Cosmetic Surgery: Anatomy and Sites of Injury

Motor Nerves

The dominant motor nerve to the face is the facial nerve (cranial nerve VII), and it is present throughout the region targeted by almost all cosmetic procedures of the face. As such, a thorough understanding of its anatomy is of paramount importance in preventing the injury to this critical structure.

The facial nerve, upon its exit from the stylomastoid foramen, penetrates the substance of the parotid gland, by which it is well protected in the pre-auricular region. Within the gland, it divides into five major branches, which exit the periphery of the gland deep to the superficial muscular aponeurotic system (SMAS). Anterior to the parotid gland, distal facial nerve branches (zygomatic and buccal) are situated evendeeper - under the masseteric fascia. This anatomic relationship creates a surgical plane between SMAS and the masseteric fascia, allowing for a sub-SMAS (or "deep plane") dissection anterior to the parotid gland.As zygomatic and buccal nerves course to innervate their target midfacial muscles from underneath (zygomaticus major and minor, levator labii, and superioris alaeque nasi), a sub-SMAS plane of dissection can be followed until the first midfacial muscle is encountered (zygomaticus major), at which point the dissection must proceed superficial to this muscle (and SMAS).

facial nerve Dissection in this area places zygomatic and buccal branches at risk for injury, due to their close proximity. Similarly, a subperiosteal midface dissection (when performed for a midface lift) makes these deep branches vulnerable while lifting the periosteum from the anterior surface of the maxilla. Great care must be taken if such surgical approachesare undertaken, and the use of cautery and forceful retraction should be avoided. Fortunately, anterior facial nerve branches substantiallyintercommunicate and innervate midfacial musculature with some redundancy. As such, single branch injuries are unlikely to cause significant dysfunction of the midface.

The temporal branch of the facial nerve exits the superior aspect of the parotid gland, deep to SMAS, and crosses the zygomatic arch at the junction of anterior one third and posterior two thirds. Additional surface landmarks may be utilized to approximate the course of the temporal branch. Pitanguy\'s line runs from 0.5 cm inferior to the tragus to 1.5 cm above the lateral eyebrow. This may be somewhat variable since the lateral aspect of the eyebrow is not always a precise landmark in some patients. A more consistent approximation is the line that begins at the inferior aspect of the ear lobule and bisects another line connecting the tragus and the lateral canthus (Fig 1). Above the zygoma, the temporal branch enters a more superficial layer of the temporoparietal fascia and courses to innervate the superior orbicularis and frontalis muscles. Secondary to this anatomical transition, surgical lifting of the forehead, temple, and the midface must be performed in a plane deep to the temporoparietal fascia. However, a face lift dissection carried over the zygoma must be in the subcutaneous plane, which is superficial to SMAS (where the temporal branch is transitioning to the temporoparietal fascia).

The marginal branch of the facial nerve exits from the inferior aspect of the parotid gland, at the angle of the mandible, and descends up to 2 cm inferior to the body of the mandible before returning to innervate the mentalis and depressor anguli oris muscles. As these muscles are superficial to the platysma, the marginal nerve penetrates through the platysma in this region, and becomes susceptible to injury in superficial procedures such as liposuction of the jowl region. During face and neck lifting, dissection deep to platysma in the neck, or sub-SMAS dissection inferior to the border of the mandible places the marginal nerve at risk for injury.

altThe spinal accessory nerve (cranial nerve XI) may be encountered during a neck lift if dissection is carried sufficiently inferior along the sternocleidomastoid (SCM) muscle. This nerve crosses the SCM approximately 1 cm superior to Erb\'s point (location along the posterior border of SCM at which the greater auricular nerve becomes superficial). Deep dissection over the SCM should be avoided as it can lead to spinal accessory nerve palsy. Clinically, this injury manifests as a potentially debilitating shoulder dysfunction, trapezius wasting, and dull pain in the shoulder region.

Sensory Nerves

Several sensory nerves are consistently encountered during commonly performed cosmetic procedures of the face and neck. These include the greater auricular, lesser occipital, infra-orbital, mental, zygomatico-temporal, and zygomatico-facial nerves.

Sensory Nerves Several external landmarks are available to localize the greater auricular nerve along the posterior border of the SCM. It runs 0.5-1cm parallel and posterior to the external jugular vein, and is approximately 6.5 cm inferior to the external auditory meatus. In this location over the SCM, platysma fibers become attenuated with little overlying subcutaneous tissue. This is further complicated by the fusion of the superficial and deep cervical fascias in this region. Thus,no surgical plane exists in this area, necessitating a sharp elevation of skin along SCM.

Therefore, great care must be taken to remainsuperficial in order to avoid the greater auricular nerve injury. Another pitfall lies in the placement of sutures for suspension of SMAS to the mastoid periosteum. If placed sufficiently inferior or under undue tension, this may result in a compressive injury of the greater auricular nerve and loss of sensation over the inferior aspect of the auricle.

The lesser occipital nerve runs parallel and approximately 1 cm posterior to the greater auricular nerve, providing sensation to the superior and posterior aspects of the ear. This nerve is vulnerable to injury for the same reasons as the greater auricular nerve.

Trigeminal nerve branches (infraorbital and mental) exit through respective foramina in the maxilla and mandible, and typically become susceptible to injury during subperiosteal dissection of the midface (midface lift, implant placement) or mandible (chin implant pocket creation). These nerves, while large in caliber, are susceptible to stretch injury or transection during a subperiosteal dissection.

Zygomatico-facial and zygomatico-temporal penetrate through the lateral surface of the zygomatic arch and innervate the lateral cheek and temple. Subperiosteal dissection over the zygomatic arch, as performed during the midface lift, may damage these sensory nerves and lead to a sensory deficit in the area of their distribution.

Listen To Dr. Azizzadeh Lecture On Facial Nerve Reconstruction & Facial Paralysis Surgery

Part 1: Facial Nerve Anatomy & Facial Nerve Reconstruction Overview

Part 2: Treating Facial Paralysis & Acoustic Neuromas

Part 3: Improving Facial Symmetry With Surgery

Part 4: Case Study: Actual Patient Overview

Part 5: Case Study: Actual Patient Overview

Cosmetic Facial Procedures and Associated Nerve Injuries

A wide variety of surgical approaches are currently utilized in facial cosmetic surgery. As such, nerve injuries tend to be specific to the approach favored by the surgeon. Depending on the anatomic region targeted by the specific procedure, select motor and sensory nerves can become susceptible to injury. Such relationships between the surgical approach and nerve injuries, as well as associated clinical manifestations, are listed in Table I.

Rates of Nerve Injury in Facial Cosmetic Surgery

A number of series in literature document complications of facial cosmetic surgery and report on rates of nerve injury. Most such reviews are retrospective in nature and may underestimate the true rate of nerve paresis and paralysis for the following reasons. First, complete neurological exams are likely not performed routinely in busy clinical practices. Also, while motor deficits may be obvious during the interaction with the patient (and documented), sensory assessment requires a thorough physical exam and is probably not routinely performed. In addition, sensory deficits of the head and neck, while bothersome in the beginning, are generally well tolerated long-term and usually are not the primary source of patient complaints. Second, motor dysfunction, especially in the midface region, may be difficult to assess due to post-operative swelling and redundancy of innervation. Third, large reports usually originate from high-volume practices and, therefore, likely represent the lowest end of the spectrum for nerve injuries simply from the experience standpoint. As such, published numbers reported in this manuscript should be interpreted with caution.

During rhytidectomy, the greater auricular nerve is the most commonly injured sensory structure (1-7%), while motor nerve injury reaches 2.6 % . Depending on the series, either the marginal or temporal branches of the facial nerve appear to sustain the highest rate of motor injury. This has been in part explained by the lack of anastomotic and intercommunicating branches, which are present in zygomatic and buccal nerves.

Several large rhytidectomy series focusing on complications and outcomes have been reported in the literature and are briefly reviewed here. For the endoscopic brow lift, Jones reported a single case of frontal branch paresis in 538 patients (0.19%), while Sabini found eight cases of paresis in 350 patients undergoing a combined endoscopic forehead and midface lifts (2.29%). For face lifts, Kamer presented a series of 100 deep plane rhytidectomies, with no reported events of paresis or paralysis (0%). In SMAS-platysma lifts, Daane documented cervical branch injuries in 34 of 2002 cases (1.7%). This injury was labeled as "pseudoparalysis of the marginal mandibular nerve" and full recovery in all cases occurred within 6 months. Tanna reported no cases of nerve injury in "short scar rhytidectomy with SMAS suspension" in one thousand cases (0%). In another SMAS series of 96 patients, Sullivan documented temporary facial nerve weakness in 3%, and permanent ear numbness in 1% of cases. While these large series document the overall low rate of nerve injuries during rhytidectomy, Baker noted that while the facial nerve injury occurs in "less than one percent of the cases," about 20% of such injuries fail to undergo spontaneous return of function.

The spinal accessory nerve injury has also been documented to occur during rhytidectomy . While this represents a highly unusual occurrence in cosmetic surgery of the neck, one should be cognizant of the nerve\'s location if such operation is undertaken.

Peripheral Nerve Anatomy and Classification of Injury

Peripheral nerves contain numerous nerve fibers, which are separated by layers of connective tissue sheaths. The endoneurium envelopes individual nerve fibers, perineurium wraps around multiple nerve fibers (creating nerve fascicles), and epineurium covers the entire nerve bundle (Fig 2). Mechanisms of nerve injury may be numerous and include direct trauma from anesthetic infiltration, surgical dissection, liposuction, suture placement, and use of electrocautery. Indirect trauma, such as traction injury, may also cause fiber disruption and edema within the nerve.

In 1968, Sunderland published a classification system for peripheral nerve injury based on the severity of nerve disruption (Table II). In this system, the most benign form of injury is neuropraxia (Grade I), in which a local conduction block is present (from nerve compression or ischemia) without disruption of axoplasmic continuity. Such nerves may continue to transmit the electrical signal beyond the site of the block and completely recover their function once the block is removed. This is the only type of nerve injury in which distal Wallerian degeneration does not occur.

In more significant nerve injuries, axoplasmic (axonotmesis, Grade II) or a neural tubule (neurotmesis, Grade III) disruption leads to a Wallerian degeneration of the nerve distal to the site of injury. Axonotmesis undergoes excellent functional recovery, secondary to axonal regeneration through intact neural tubules. In contrast, neural tubule disruption promotes aberrant regeneration of nerve fibers within fascicles, potentially resulting in synkinesis.

Grades IV (perineurium disruption, nerve sheath continuity preserved) and V (epineurium, or complete nerve transection) carry the worst prognosis for functional recovery, as neural regeneration is severely hampered by intra-neural scarring and aberrant pathway selection. Theoretically, Grade V injuries do not recover any function without anatomic re-approximation of the cut ends of the nerve.

Treatment of Nerve Injuries

Preserved Nerve Continuity

Most cases of post-operative nerve dysfunction occur in a setting where little doubt exists about nerve integrity. These typically recover well with conservative management alone. Patients must be counseled that recovery is anticipated, but that it may take some time. In the immediate post-operative period, it is not uncommon to observe motor branch paralysis secondary to local anesthesia, which wears off within several hours and warrants no additional intervention. For nerves that sustain direct injury (such as from traction, cautery, etc), a typical time frame for recovery may be anywhere from several weeks to 6 months. This is consistent with the time required to undergo complete Wallerian degeneration and re-growth of nerve fibers at a rate of approximately 1mm per day.

While intriguing from the anti-inflammatory standpoint, the role of steroids in hastening the functional recovery of nerves remains unclear. To our knowledge, there are no studies of steroid administration in a setting of cosmetic facial surgery. However, steroids have been evaluated in other clinical scenarios involving the facial nerve. Unfortunately, these reports offer conflicting recommendations. The strongest evidence to date against the use of post-operative steroids for facial nerve dysfunction stems from a prospective randomized trial of patients undergoing parotid surgery . The study group receiving perioperative dexamethasone derived no benefit and, in fact, displayed a median time of 150 days to recovery, compared to only 60 days in the control group. This finding is in contrast to studies documenting a beneficial impact of steroids in patients with Bell's palsy.

Nerve Transection Injuries

If nerve injury is confirmed intraoperatively, immediate repair should be attempted with direct anastomosis of the cut ends. Tensionless technique represents a critical aspect of any nerve repair; otherwise, regeneration of fibers may be compromised through the site of nerve coaptation. Both ends of the nerve should be freshly cut and three to four epineurial 9-0 nylon stitches should be placed circumferentially in order to achieve an effective anastomosis (Fig 3).

Nerve grafting may be required in cases where tensionless closure is not possible or in those where nerve transection spans a segment. For facial nerve grafting, it is not unreasonable to sacrifice a regional sensory nerve, such as the greater auricular. Sural and lateral antebrachial cutaneous nerves represent alternative sources for nerve grafting (Fig 4).

Post-operative Management of Poorly Recovered or Paralytic Facial Nerve Branches

Management of Poorly Recovered Poor recovery of the facial nerve may result in uncoordinated movement of affected muscle groups or complete paralysis. For the correction of facial synkinesis or asymmetry, botulinum toxin has been documented in several studies to be highly effective. In cases of paralysis, the approach should be site-specific (i.e. upper, middle, and lower face should be considered separately). For instance, marginal nerve paralysis may be treated with the contralateral botulinum toxin injection, depressor labii inferioris myectomy, or selective contralateral marginal mandibular neurectomy.


Several motor and sensory nerves are at risk during facial rejuvenation surgery. A thorough understanding of nerve anatomy is critical in avoiding neurologic injury, which may be severely debilitating for the patient. In the event of injury, its management depends on the degree of nerve disruption and may range from simple observation to exploration and grafting. Meticulous dissection technique, guided by knowledge of facial anatomy, should prevent most neurological sequelae during facial cosmetic surgery.


Cosmetic Facial Operation
Nerves at Risk
Clinical Manifestations

Forehead and Brow
Endoscopic, trichophytic, pre-trichial, or coronal brow lifts
Motor: Fronto-temporal division of the facial nerve Sensory: Supraorbital and supratrochlear nerves
Motor: Ipsilateral forehead paresis or paralysis, with resultant brow ptosis Sensory: deficit in the forehead distribution
Direct brow lift
Motor: None Sensory: Supraorbital, Supratrochlear
Motor: None Sensory: deficit in the forehead distribution
Subperiosteal midface lift, midfacial malar or sub-malar augmentation (implants)
Motor: Zygomatic and buccal branches of the facial nerve Sensory: zygomatico-temporal, zygomatico-facial, infraorbital nerves
Motor: Incomplete eye closure, external nasal valve collapse (nasal obstruction), drooping of the mouth corner, asymmetric smile, food spillage Sensory: Hyposthesia or numbness of the temporal, lateral facial, or midfacial regions
Face Lift
Motor: All branches of the facial nerve Sensory: Greater auricular, lesser occipital nerves
Motor: Paresis or paralysis of any portion of the face Sensory: Hyposthesia or numbness of the ear, inferiorly and/or superiorly.
Face and Neck
Chin Implant
Motor: Marginal branch of the facial nerve Sensory: Mental nerve
Motor: Depressor anguli muscle paresis or paralysis, with resultant asymmetric smile Sensory: Lower lip and chin hyposthesia or numbness
Neck Liposuction
Motor: Marginal branch of the facial nerve Sensory: None
Motor: Depressor labii inferioris muscle paresis or paralysis, with resultant asymmetric smile Sensory: None


Table I: Facial cosetic procedures, associated nerves at risk, and clinical manifestations of nerve injury.

Sunderland Classification
Anatomic Injury
Clinical Manifestation and Recovery

I (Neuropraxia)
Local conduction block, with preservation of axoplasmic continuity
Clinical recovery usually complete in several weeks
II (Axonotmesis)
Axoplasmic disruption, endoneurium intact, with preservation of nerve sheath continuity
Wallerian degeneration, with \'1mm/day\' regrowth, good to excellent recovery of function
III (Neurotmesis)
Endoneurium disruption, with preservation of nerve sheath continuity
Wallerian degeneration, worse degree of recovery, with synkinesis
IV (Perineurium Disruption)
Nerve sheath continuity preserved with intact epineurium
Wallerian degeneration, poor recovery with significant synkinesis
V (Epineurium Disruption)
V (Epineurium Disruption) Complete nerve transection


Table II: Sunderland classification of nerve injuries and anticipated clinical recovery.

Fig 1. External landmarks useful in approximating the course of the temporal division of the facial nerve. Blue line connects the tragus with the lateral canthus. Red point represents the midpoint of the blue line. Green line (temporal branch) bisects the blue line and runs from the inferior aspect of the lobule.

Fig 2. Peripheral nerve anatomy. The endoneurium envelopes individual nerve fibers, perineurium wraps around multiple nerve fibers (creating nerve fascicles), and epineurium covers the entire nerve bundle.

Fig 3. Nerve anastomosis performed with a 9-0 nylon suture (fine black strand in the photograph) spanning the epineurial layer of cut ends. Typically, 3-4 sutures are necessary to achieve stable closure. Nerve approximation must be performed under microscope magnification and without tension.

Fig 4. Sural nerve graft. A External marking on the left lower extremity prior to nerve harvest. The incision is placed approximately 2 cm posterior to the lateral malleolus of the fibula, and taken superiorly as necessary to obtain sufficient graft length. This nerve can also be harvested through a stab incision with a nerve stripper. B Internal anatomy (A - Achilles tendon, * - lesser saphenous vein, Arrow - sural nerve). Note the close relationship of the nerve to the vein, and a distal branching pattern, suitable in caliber to peripheral facial nerve branches.


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