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Management of Facial
Paralysis after Intracranial Surgery
by Mack Chen, MD and Michael McKenna,
M.D
Stephen B. Tatter, M.D., Ph.D., HTML
editor
Index
Despite improvements
in microsurgical techniques and intraoperative facial nerve monitoring,
it is often impossible to preserve normal facial nerve function
when removing tumors with intrinsic facial nerve involvement. This
is especially true for large acoustic tumors and posterior fossa
meningiomas. Although the facial nerve is anatomically preserved
in many cases, the function may be completely lost, resulting in
a complete facial paralysis. In this circumstance, full facial paralysis
is often physiologically and psychologically devastating to the
patient. Associated problems include painful corneal irritation,
visual loss, difficulties in eating and speaking and in the worse
circumstance, self-imposed social isolation. The successful management
of this problem is best accomplished by a multi-disciplinary approach
utilizing ihe expertise of neurosurgeons, oculoplastic surgeons,
otolaryngologists, psychologists, psychiatrists, and facial reconstructive
surgeons. Successful facial reanimation requires careful analysis
of the patient's deficits, appropriate reconstructive procedures,
and a concentrated period of rehabilitation following surgical reconstruction.
Although a variety of reconstructive
methods for the management of facial paralysis have been described,
the great majority of patients can be successfully managed with
a few relatively simple and reliable techniques. Patient age, general
health, skin laxity, neurological deficits, and expected nerve recovery
must all be taken into consideration. Even under the best of circumstances,
it is impossible to restore perfect dynamic facial symmetry. For
this reason, it is essential to accurately assess the patient's
expectations and counsel them as to reasonable expected results.
The use of patient pre- and post-operative video tapes and discussion
with other patients who have undergone similar procedures can be
extremely useful.
Numerous scales for the assessment
of facial nerve paralysis and recovery have been proposed. Although
they are useful for purposes of discussion, pre- and post-operative
photographic documentation is essential in patient evaluation and
in the evaluation of surgical results.
In the past it has been common practice
to allow for up to two years of complete recovery after complete
paralysis before contemplating surgical reanimation. With this approach,
it is often three to four years before rehabilitation occurs. This
unnecessary delay may be significantly reduced by offering patients
early reanimation procedures that do not adversely affect normal
facial nerve regeneration and potential facial movement. We have
found the temporalis muscle transposition in conjunction with a
gold-weight implant and lower lid tightening to be the most useful
combination of techniques in achieving this goal. Although it is
difficult to predict the overall long-term recovery in many cases,
the length of time for recovery to occur can usually be predicted
by certain clinical criteria. Early surgical rehabilitation should
be considered in cases where prolonged recovery is expected or when
the overall recovery is uncertain. This approach can reduce the
period of facial disability from years to weeks.
Patients with complete facial paralysis
require immediate attention to the eye to prevent problems associated
with corneal exposure. These patients should undergo oculoplastic
surgery for corneal protection. This may be in the form of tarsorrhaphy,
gold-weight implantion, placement of an ocular spring, or a combination
of these procedures. All of these procedures are reversible if facial
nerve recovery occurs. Aggressive corneal protection is especially
important if a fifth cranial nerve deficit is present in conjunction
with a full facial paralysis For this reason, if patients are reluctant
to consider full facial reanimation, surgical protection of the
eye must be encouraged. Preoperative patient counseling of the possible
need for surgery to correct the eye should be included in the discussion
concerning the potential for postoperative facial paralysis.
Predicting Facial Nerve Recovery
Accurate prediction of the long-term facial
nerve recovery with complete paralysis after intracranial surgery
is difficult, and although general guidelines are useful, the long-term
results are not always uniform. Facial movement in the immediate postoperative
period is the best prognostic sign for long term recovery, even if
complete paralysis ensues. The ability to stimulate the facial nerve
at the brain stem with a low voltage is another good prognostic sign.
However, inability to stimulate the nerve at low voltage does not
always correspond to poor recovery.
Table 1.
Ancillary procedures.
Facial nerve
is transected at surgery and grafted.
These are among the least predictable
group of patients. Results in this group vary from no recovery to
recovery of all movement in all divisions with synkinesis. The endpoint
for recovery may require 12 to 18 months. Electrical testing is
of no use in predicitng recovery. Based on experience, the surgeon
who has performed the repair can give the best prediction for recovery.
Facial nerve
is anatommically intact but does not stimulate at the brainstem
and there is no facial movement in the immediate postoperative period.
Recovery in this group of patients is generally poor. If recovery
does occur, the endpoint may requir 18 months. The best recovery
to be reasonably hoped for is reinstutuion of resting tone and weak
movement with synkinesis. Electroneurography (ENoG) in the early
postoperative period generally demonstrates an absent compound action
potential suggestive of sever neural degeneration.
Facial nerve
is anatomically intact, stimulates at low voltage, but no movement
immediately after surgery. In this group of patients, ENoG
may be particularly useful in the postoperative period. If the compound
action potential of the paralyzed side remains greater that 10%
of that of the normal side after one week, then a good recovery
usually occurs, although it may require several months.
Facial nerve
is anatomically intact, there is some movement in the immediate
postoperative period, but complete paralysis ensues within hours.
This group generally has a satisfactory recovery. It is important
that real significant movement is appreciated
ENoG is only of limited value in predicting
the degree of overall recovery. It is most helpful during the first
two postoperative weeks. It may be useful in distinguishing severe
injuries with neural degeneration from neuropraxic irjury. Intramuscular
electromyography may be useful in detecting reinnervation after
injury and prolonged paralysis, before detectable motion is present.
It is of no value in the late postoperative period.
Ocular Management in Facial Paralysis
Paresis of the orbicularis oculi muscle
results in diminished blink, incomplete eyelid closure (lagophthalmos),
impairment of the nasolacrimal pumping system, and occasional eyelid
malposition (paralytic ectropion). The blink reflex and lid position
are important in maintaining the ocular surface epithelial integrity.
Each blink physically spreads the tear film over the ocular surface
and allows for a continuous layer of moisture. The precorneal tear
film continuity is also dependent on the volume of tears produced
by the lacrimal gland, the surfectant properties of the tear film
resulting from its biochemical composition, and the microanatomic
state of the surface epithelium. Lack of blinking and incomplete eyelid
closure result in increased evaporation from the ocular surface, discontinuity
of the precorneal tear film, and degenerative changes in the surface
erosions (exposure keratitis) and ulceration which ultimately can
result in permanent visual loss. When intrinsic corneal disease coexists
with paralytic lagophthalmos (e.g. neurotrophic keratitis with
corneal anesthesia) or decreased tear production (e.g. autonomic
facial nerve involvement), ocular surface deterioration is often accelerated.
The ophthalmic management of paralytic
lagophthalmos is directed at maintaining a normal corneal epithelium
which provides comfort and preserves visual acuity. Initial management
would include an ocular lubricant such as a tear substitute or ointment
(Lacrilube, Hypotears ointment, etc.) used at varying intervals.
Ointments are more effective in corneal protection; however, they
often substantially blur vision. If this is not effective or if
the paralysis is expected to persist, more permanent therapy would
include procedures which narrow the palpebral fissure such as tarrsorhaphy,
lower-lid elevation with spacers, medial canthoplasty or procedures
which increase the amplitude of the blink reflex such as gold weight
or spring implant. If paralytic ectropion is present, correction
of this lid malposition can be very helpful in relieving symptoms
and signs of corneal exposure.
Tarsorrhaphy has been the standard
method of managing exposure keratitis and is often effective if
large enough. However, larger tarsorrhaphies are disfiguring and
do limit peripheral vision. Generally, a lateral tarsorrhaphy of
<5 mm is not noticeable and can be integrated with other procedures
to obtain optimal results. Medial tarsorrhaphies are always disfiguring
and should only be used as a last resort in managing surface exposure.
The tarsorrhaphy should include a tongue-in-groove technique that
does not disturb the lash follicles at the anterior lid margins.
"Bedside" lid margin scraping procedures with suture approximation
may disrupt the lash line and lead to trichiasis or heal with lateral
palpebral angle webbing.
If a 5 mm tarsorrhaphy is not sufficient
to manage the exposure keratitis, then a reanimation procedure should
be considered. Gold-weight implantation is the most direct and effective
method of enhancing the blink reflex. Gold was chosen for this implant
because this metal best matches Caucasian skin color. The weights
are supplied by the Meddev Corporation and vary from 0.6 to 1.6
grams. The weights are taped to the pretarsal portion of the upper
lid to determine which size will be needed to reduce the lagophthalmos.
The heavier weights can induce ptosis and patients should be warned
of this complication. .1.0 to 1.2 grams are most commonly used.
An incision is made at the upper lid crease exposing the anterior
surface of the tarsal plate, and the weight is fixed to the anterior
surface of the tarsus with at least 8-0 nylon through three separate
holes (Fig 1 ). The skin-muscle flap is closed in separate layers.
Edema of the upper lid often persists for several weeks. Complications
include extrusion and distortion of the lid fold and crease, infection,
ptosis, and persistent corneal exposure symptoms.
Figure
1. The gold weight is placed over the anterior surface of the
tarsal plate and fixed with 8-0 nylon through three separate holes.
This procedure is potentiated by concomitant
lateral tarsorrhaphy or lower-lid elevation with spacers. Spring
implants made from orthodontic wire can increase the amplitude of
the blink reflex. The orthodontic wire spring is fixed to the lateral
orbital rim periosteum with the other end of the spring passed under
the orbicularis muscle to the mid-tarsal position. The tension produced
by the spring is also judged and adjusted by preoperatively fixing
one limb of the spring to the lateral orbital rim and assessing
the reduction in lagophthalmos. In order to limit extrusions, the
pretarsal end of the spring is covered with a Dacron sleeve.
Paralytic ectropion often responds
to horizontal lid shortening. This lid malposition is often more
common in older patients with pre-existing lid laxity and canthal
tendon dehiscences.
Lower lid elevations can be accomplished
with cartilage or scleral spacers. The spacer is placed between
the lower-lid retractor (capsulopalpebral fascia) and the inferior
border of the tarsal plate. A subciliary or a transconjunctival
approach can provide the surgical exposure to insert the spacer.
Ophthalmic follow-up with slit lamp
examination and flourescein staining are advised to assess corneal
and visual status after any lid procedure.
Reconstruction of the Paralyzed Face
Each patient with facial paralysis requires
a detailed analysis of the individual's particular concerns and physical
deformities. Multiple surgical techniques have been described and
advocated for facial reanimation after facial nerve paralysis. In
our experience the most versatile technique for early facial reanimation
utilizes temporalis muscle transposition. This technique can be used
to achieve early facial reanimation and improve facial symmetry without
affecting potential facial nerve recovery. Because of this, it can
be performed in the early postoperative period when long-term results
remain uncertain. Patients can expect an immediate improvement in
facial symmetry at rest, and in the majority of cases, movement in
the corner of the mouth which allows the patient to produce an organized
and controlled smile within six weeks of the operation. This procedure
can be performed in conjunction with a hypoglossal-facial nerve anatomosis
in which the hypoglossal nerve is split and anastomosed to a lower
branch of the facial nerve. This results in limited problems with
movement of the tongue and prevents mass facial movement which has
been a recurrent problem in full hypoglossal nerve procedures. In
our experience the resultant reanimation using the parital hypoglossal-facial
nerve is more natural than that achieved by anastomosis of the entire
hypoglossal nerve to the main trunk of the facial nerve
Preoperative Planning
Temporalis muscle transfer for reconstruction
of the paralyzed face is not a difficult surgical maneuver. However,
the use of this technique to create a meaningful, organized, and
symmetrical smile pattern is challenging. The preoperative evaluation
of the patient's smile pattern, the selection of the proper amount
and orientation of the temporalis muscle, and the optimal insertion
and tension of the temporalis muscle at the time of surgery all
affect the final surgical result.
Figure
2: The vascular and neural supply to the temporalis muscle lies
on the medial aspect of the muscle with dtstribution in an arcadian
pattern from the trigeminal nerve and the internal maxillary artery.
Operative Technique
The temporalis muscle itself is broadly
based, arises from the temporal line, and inserts into the coronoid
process of the mandible. The vascular supply from the internal maxillary
artery is of surgical importance as the preservation of this consisient
blood supply is important to the viability of the muscle to be transferred
for facial reanimation. The neural supply is from the trigeminal
nerve and courses into the undersurface of the muscle in the area
of the zygomatic arch to provide innervation to the muscle in an
arcadian pattern.
(Fig. 2) The temporalis muscle has
many characteristics which make it highly suitable for use in facial
reanimation. The muscle is relatively short (3-5 cm), thin (2-3
mm), and has a contractual capability of 1 to 1.5 cm. The mid-portion
of the muscle has sufficient strength to adequately mobilize the
face and to resist the forces of soft tissue fibrosis.
Figure
3: The incisions utilized in temporalis muscle transfer reconstruction
extend from the midportion of the superior auricular helix to a
point above the temporal line. An extension of this incision may
be executed if partial cranial nerve 7 to 12 anastomosis is performed.
The vermilion incision is designed 1.5 to 2.0 cm along the upper
and lower borders of the lips.
After adequately evaluating the orientation
of the patient's smile on the unaffected side, temporalis muscle
transposition is planned. The incision is designed to extend from
the midportion of the superior auricular helix and courses above
the temporal line with tangential extensions of the vertical incision
above the temporal line to gain full exposure of the temporalis
muscle (Fig 3). The initial incision allows for the development
of a separate temporoparietal fascial flap. This flap is mobilized
laterally and is used to reconstruct the secondary temporal fossa
defect which is created when the temporalis muscle is used. The
muscular fascia is exposed anteriorly to the temporal hairline and
posteriorly for a distance of 5 to 6 cm. The incision is then extended
in the pretragal area to allow access for facial disseclion. An
important point is the transfer of the plane of dissection to the
temporoparietal fascia. By transferring to this plane of dissection,
the risks of peripheral facial nerve injury are minimized. This
technical detail is especially important in those patients in whom
eventual recovery of facial function is anticipated. Using sharp
dissection, an area of approximately 4 to 5 cm is undermined from
the zygomatic arch to the oral commissure. A vermilion incision
is made at the oral commissure extending 1.5 to 2 cm along the upper
and lower lip. The lateral aspect of the orbicularis oris muscle
varies in its fullness and anatomical characteristics depending
upon the duration of facial paralysis.
With the facial flap fully elevated
and with the surgeon able to pass both index fingers comfortably
from the zygomatic arch to the vermilion border at the oral conimissure
(Fig. 4), determination of temporalis muscle width, orientation
and elevation of the muscle flap are pursued. As a general rule
approximately 2 to 2.5 cm of temporalis muscle is utilized for facial
rehabilitation. It has been our experience that the muscle best
suited for facial rehabilitation lies in the central one third of
the temporalis muscle. The anterior one third of the muscle has
a heavy tendency to be short, bulky, and poorly oriented for useful
reanimation of the face. On the other hand, the posterior one third
of the muscle lacks appropriate contractile properties and is poorly
oriented for rehabilitation purposes. The central one third of the
temporalis muscle provides adequate length and exhibtis active contractile
properties, which make it the ideal donor muscle source for transfer
(Fig 5). The muscle is harvested from the temporal fossa and is
elevated with pericranium on its medial surface. Using blunt elevation
and careful attention to the inferior aspect of the muscle in the
area of ihe zygomatic arch, the vascular and neural supply to the
muscle is preserved. A central incision is made in the muscle flap
which represents the point of placement of the temporalis muscle
to the oral commissure. Three 3-0 Prolene sutures are placed into
the fascia and muscle at the disial tip using a figure-of-eight
suture technique (Fig. 6). The muscle is then transferred into the
lower face and suture stabilized using 3-0 Prolene at appropriate
points along the lateral border of the orbicularis oris muscle.
As a rule, we rely upon muscle-to-muscle contact between the temporalis
muscle and the orbicularis oris muscle, as this results in increased
dynamic postoperative movement (Fig 7). Overcorrection at the time
of surgery is essential with an attempt made to expose the second
to third molar of the upper dental arch at the time of muscle transposition.
The vermilion border is closed using a horizontal mattress suture
to accentuate this landmark. The donor site is reconstructed using
the previously developed temporoparietal fascial flap and a silicone
drain is placed in the temporal and fascial regions for 24 to 36
hours. A bulky compressive dressing is used in the first 24 hours
postoperatively in an attempt to reduce the risk of hematoma formation
and to reduce facial swelling.
Figure
4: A facial flap is created that extends from the temporal region
to the oral commissure. This flap is elevated to allow for both
index fingers of the surgeon to pass comfortably from the zygomatic
arch to the oral commissure.
Figure
5: The central one third of the temporalis muscle is best suited
for rehabilitation of the paralyzed face. The orientation of the
muscle can be varied to individualize the muscular repair.
Figure
6: Temporalis muscle is harvested from the temporal fossa mobilzed
to the zygomatic arch, and transferred into the midface with 3-0
Prolene suture.
Figure 7: The temporalis rnuscle
is sutured to the lateral border of the orbicularis orbis muscle
with 3-0 Prolene.
Partial hypoglossal-facial nerve anastomosis
The partial hypoglossal-facial nerve
anatomosis is utilized in specific clinical circumstances in which
ihe facial nerve has been sacrificed at the time of surgery and
the surgeon is unable to immediately graft the neural defect. This
technique is utilized in conjunction with the temporalis transposition
flap and is important in providing resting tone and improving facial
symmetry of the lower lip, commissure, and the nasolabial fold regions.
In keeping with our philosophy of dividing ihe face into three zones
of reconstruction, the partial hypoglossal-facial nerve anastomosis
directs its neural input to the middle and lower zones of the facial
nerve. The incision is an extension of the incision used for the
temporalis muscle transposition technique. The pretragal incision
is carried around the auricular lobule and into the cervical region
2 to 2.5 cm below the angle of the mandible (Fig 3). The facial
nerve is identified as it courses from the stylomastoid foramen
and is dissected peripherally distal to the point where the two
major divisions of the faciai nerve are clearly identified. At this
point the surgical dissection is carried into the neck where the
posterior belly of the digastric muscle and the anterior border
of the sternocleidomastoid muscle are utilized for hypoglossal nerve
identification. Rather than a complete transection of the hypoglossa1
nerve, this technique utilizes a 30% selected neural graft which
is mobilized distal to the takeoff of the ansa hypoglossal nerve
and is superiorly rotated for microsurgical anastomosis with the
lower division of the facial nerve. The superior division of the
facial nerve is ligated. An epineural anastomosis is then performed
to approximate the partial hypoglossal nerve to the lower division
of the facial nerve. In our sreies of patients this technique has
provided improve resing tone to the loer division of the face and
has eliminated the donor defect of hemiparesis of the tongue, which
has been associated with the full resection of the hypoglossal nerve.
Aberrant Regeneration of the Facial
Nerve
Following prolonged facial paralysis,
facial nerve regeneration can often be associated with misdirected
axonal regrowth, which can cause abnormal synkinetic movements of
the facial muscles, epiphora, and barying degrees of hemifacial
contracture. The most troubling of the synkiectic movements in involuntary
eyelid closure with movements of the jaw and lower face. The clinician
will observe internittent ptosis at the patient speaks with return
to a resting state (reverse Marcus-Gunn sign). The eyelid closure
is often associated with distortion in the nasolabial fold and lip
position, or asymmetric dimpling near the lateral angle of the mouth.
Therapy with botulinum A toxin injection
is directed at relieving the involuntary blepharospasm. Injections
are given in the mideial and lateral extremes of the pretarsal orbicularis
muscle with tow additional injections along the lateral orbicularis.
the total dose in each injeciton site probably should not exceed
four international unite (IU) as excessive weakening of the orbicularis
oculi muscle may result in lagophthalmos and exposure keratitis.
The injection results in a substantial reduction in the degree of
involuntary eyelid closure for a periof of four to five months.
It is especially important not to exceed 15 IU on initial injection
because the orbicularis already is partially denervated and is exceptionally
sensitive to botulinum toxin injection. Patient acceptance of this
therapy is excellent and injections can be repeated without reduction
of efficacy.
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