Treatment of Nerve Injuries
By Babak Azizzadeh MD, Grigoriy Mashkevich, MD
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.
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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 even |
deeper - 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).
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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).
treatment of nerve injuries 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.
The 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.
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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.
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
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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. |
Summary
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. Tables
|
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 |
Midface |
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 cosmetic 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 |
Paralysis |
Table II: Sunderland classification
of nerve injuries and anticipated clinical recovery.
Figures
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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