Journal of Pediatric Rehabilitation Medicine: An Interdisciplinary Approach 7 (2014) 295305

DOI 10.3233/PRM-140300
IOS Press

295

Facial paralysis reconstruction in children and

adolescents with central nervous system
tumors
Andre Panossiana,b,
a

Division of Plastic and Maxillofacial Surgery, Childrens Hospital, Los Angeles, CA, USA
Keck School of Medicine, University of Southern California, Los Angeles, CA, USA

Accepted 13 July 2013

Abstract. Facial paralysis remains a vexing problem in the treatment of posterior cranial fossa tumors in children. Fortunately,
current techniques are available to reconstruct the paralyzed face in restoring balance, symmetry, and amelioration of functional
sequelae. The restoration of structure and function of the paralyzed face is tantamount to proper social integration and psychosocial rehabilitation. In addition, the facial nerve is important in preventing drying of the eyes, drooling, and speech abnormalities,
among other functions. The most visible evidence of facial paralysis is stark asymmetry, especially with animation. This is perhaps the most troubling aspect of facial paralysis and the one that leads to the greatest amount of psychosocial stress for the child
and family members. Management strategies include early and late intervention. Early reconstructive goals focus on preservation
and strengthening of intact motor end plates through native stimulatory pathways. Late reconstructive efforts are centered on
surgically reconstructing permanently lost function based on each third of the face. Use of adjunct modalities such as chemical
or surgical denervation and myectomies are also critical tools in restoring symmetry. Physical therapy plays a large role in both
early and late facial nerve paralysis in optimizing cosmetic and functional outcome.
Keywords: Facial paralysis, facial nerve palsy, facial asymmetry, facial reanimation, brain tumors, smile reconstruction, oral
continence, speech pathology, permanent denervation, facial rehabilitation

1. Introduction
Neurological deficits occur frequently in children afflicted with brain tumors [1]. Surgery remains the treatment of choice in the majority of these patients. As
such, the incidence of neurological complications increases when considering operative intervention. Cranial nerve impairment is frequently an associated manifestation, both pre- and post-operatively. Even in those
patients experiencing some recovery of nerve function,
more than two thirds continue to experience persistent
deficits from preoperative levels [2].
Corresponding author: Andre Panossian, MD, Facial Paralysis
Center, Childrens Hospital Los Angeles, 4650 Sunset Blvd, MS
#96, Los Angeles, CA 90027, USA. Tel.: +1 323 361 2154; Fax: +1
323 361 4106; E-mail: apanossian@chla.usc.edu.

Tumors of the posterior cranial fossa account for

50% to 70% of all pediatric brain tumors [1,3]. Surgical resection is associated with increased neurological
morbidity from 26 to 80 percent in patients undergoing total or subtotal resection [1,4]. These tumors typically arise in the fourth ventricle at the cerebellopontine angle, posing a significant surgical challenge [5].
Anatomically, the location of these tumors poses substantial risk of iatrogenic injury to the cranial nerves,
most notably the facial nerve. The severity and degree of cranial nerve damage will vary based on tumor
pathology, size, and extent of resection.
Facial nerve palsy secondary to central nervous system (CNS) tumors results in facial weakness or paralysis, presenting with dry eyes, facial asymmetry or
drooping, brow ptosis, drooling, and speech abnormalities. Facial paralysis is categorized grossly by congen-

c 2014 IOS Press and the authors. All rights reserved

1874-5393/14/$27.50 

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A. Panossian / Facial paralysis reconstruction in children and adolescents with central nervous system tumors

ital or acquired etiologies. Implications for reconstruction follow along these two classifications. Brain tumors in the pediatric population are considered acquired in origin and indicate the presence, at one point
in time, of a functioning facial nerve. Westin and Zuker
give a logical classification system to effectively enumerate the various presentations and etiologies of facial paralysis [6]. Understanding the origins of a particular patients facial paralysis provides a roadmap for
implementing available reconstructive strategies.
The goal of facial paralysis reconstruction is to restore mimetic function as close as possible to the native state. Thorough preoperative history and physical
exam are vital in formulating proper timing and implementation of medical and/or surgical interventions.
Considerations include a preference for dynamic reanimation procedures, use of nerve sources with analogous function, and application of therapeutic modalities and ancillary procedures to achieve symmetry at
rest and with animation.
2. Evaluation
The initial patient history requires an inventory of
pre-morbid disorders and symptoms, including the
presence of syndromic conditions, birthing history,
trauma, neuromuscular diseases, inflammatory conditions, infections, tumors, and surgical interventions of
the head and neck. Additional aspects address temporal onset of symptoms and gradual versus sudden exacerbation.
In the setting of pediatric brain tumors, further subcategorization will include benign or malignant tumors
and intracranial versus extracranial extension. Additionally, tumors may contribute to facial paralysis via
intrinsic or extrinsic mechanisms. Intrinsic sources are
less common and implicate tumorigenesis within the
structure of the facial nerve, such as schwannoma. Extrinsic sources exert pressure and destruction of the facial nerve within a confined space in the context of
CNS tumors. These tumors include acoustic neuromas,
meningiomas, gliomas, medulloblastomas, sarcomas,
ependymomas, astrocytomas, vascular malformations,
among other types.
Iatrogenic injury in the treatment of posterior cranial fossa tumors occurs in cases of planned or inadvertent sacrifice of the facial nerve, given the characteristics of a particular tumor. The nature of iatrogenic injuries suggests a well-defined point in time from which
symptoms ensue. This temporal onset has direct bearing on the type of reconstruction used and the timing
for implementing the interventions.

Often, the decision to intervene following the onset

of facial nerve palsy is difficult to make. In cases of
neurapraxia or axonotmesis, the structural framework
of peripheral nerves is preserved, with the expectation
of varying degrees of axonal regeneration and return of
neuromuscular function [7]. In cases of complete nerve
disruption (neurotmesis), the continuity of peripheral
nerves is violated with little to no return of function
observed [8]. Under these circumstances, surgical intervention is recommended. Distinguishing the type of
nerve injury can be quite elusive, often resulting in delay of treatment. In cases of facial paralysis following posterior cranial fossa tumor excision where sacrifice of the facial nerve was unplanned, a common practice is to allow an ambiguous period of time for return
of function. However, the waiting period is not unlimited and may, in fact, lead to permanent loss of motor
end plates at the neuromuscular junction and an inability to proceed with primary reconstruction [9,10]. This
length of time is debatable, but most investigators consider an appropriate waiting period of 9 to 18 months
for spontaneous recovery. Beyond this period of time,
gains may still be seen, but anecdotal evidence suggests that the return of clinically meaningful function
is poor. Therefore, management options in facial paralysis will vary based on subjective endpoints of facial
nerve recovery during the early or late period.
After establishing the etiology and temporal association of facial nerve palsy, the physical exam will focus
on division of the face into thirds (Fig. 1). The upper
third of the face demonstrates brow ptosis and absence
of rhytids in the forehead. Often, there is little cosmetic
or functional impairment requiring surgical intervention. Manifestations in the mid third of the face are centered on periocular function. Specifically, lagophthalmos is measured with volitional eye closure. Evidence
of chemosis, dry eyes, epiphora, and the presence of
a Bells phenomenon are recorded. Lower eyelid malposition is evaluated in comparison to the contralateral side, and a snap test is used for determining laxity. Perinasal paralysis may contribute to internal nasal
valve collapse and fixed obstruction. In the lower third
of the face, perioral function is affected. A softening
or complete lack of nasolabial fold production is seen.
Positioning of the oral commissure is quantified at rest
and with animation, most notably during smile [11].
Speech may be slurred and articulation errors are common. Paralysis of the buccinator may cause difficulty
with manipulation of food within the oral cavity. Loss
of lower lip depression is typical with gross asymmetry noted on smiling. Dynamic assessments are corre-

A. Panossian / Facial paralysis reconstruction in children and adolescents with central nervous system tumors

lated with videography. The function of the remaining cranial nerves must be documented for purposes of
identifying sources of donor nerves. Additionally, facial pulses are noted in determining suitability of specific reconstructive options, namely free muscle transplantation. Nerve conduction studies and electromyography may be useful in determining type, severity, and
prognosis of denervation in patients experiencing some
form of facial nerve recovery. However, they have little
value in guiding reconstruction for patients with established facial paralysis [12,13]. Similarly, imaging studies are not useful for patients requiring reconstruction,
but are a necessary tool in evaluating and monitoring
the growth or recurrence of brain tumors and in ruling
out other anatomical causes of facial paralysis.
Several grading systems for facial nerve palsy exist
to describe the severity of symptoms [1416]. However, there is currently no grading system that is universally accepted to give valuable prognostic data or to
algorithmically guide the implementation of interventional strategies. The subjective nature of facial paralysis and the spectrum of presentations render grading systems difficult to employ reliably. Much of the
decision-making regarding reconstructive options occurs jointly between the treating surgeon and the patient. Options for reconstruction will vary given similar
clinical presentations and based on patient preferences.

3. Early surgical management

Early management corresponds roughly to the first
1218 months following the onset of facial paralysis.
During this period, injured nerves will undergo a cycle of degeneration followed by recovery based on the
degree of injury, as described by Sunderland [8,17]. In
the first and second degrees of Sunderlands classification, nerve recovery occurs spontaneously and nearly
completely. In the third and fourth degrees, injury and
inflammation are more severe and may result in partial recovery or disorganized re-innervation (i.e., synkinesis). The fifth degree of injury indicates complete
disruption of the nerve structure with no potential for
recovery without surgery.
The distance of the injury from the motor end plates
also has a bearing on expected time course to recovery. Proximal peripheral nerve injuries (near the site of
injury) result in longer delays to functional recovery
than distal injuries (near the muscle target). Sunderland calculated the rate of nerve regeneration in radial
nerve injuries to progressively diminish from proxi-

297

Fig. 1. Evaluation of the paralyzed face in thirds. (A) Brow. (B) Midface. (C) Lower face. This patient demonstrates the typical appearance of complete unilateral facial nerve palsy, including poor eye
closure, distortion of nasal base, unopposed smile, lack of nasolabial
fold, and overpowering lower lip depression.

mal to distal. Cases of axonotmesis resulted in average rates of regeneration of 1.9 mm per day in proximal segments of the nerve and 0.8 mm per day in distal
sites [18]. This implies that high peripheral nerve injuries take longer to arrive at the neuromuscular junction than lower lesions, leading to irreversible loss of
motor endplates and permanent disuse atrophy [18
20].
Intervention for early facial nerve injury is aimed
at restoring neural continuity as close to the time of
injury as possible. The most direct method is to perform primary surgical repair with the use of an operating microscope. Alternatively, bridging a segmental defect may be accomplished with interpositional
nerve grafting from autogenous sources or with processed allografts, such as decellularized human peripheral nerve [21,22]. However, preliminary studies suggest that autogenous nerve grafting remains a superior
option histologically for bridging long gaps than its allograft counterparts [23]. Nonetheless, lengths of nerve
injury up to and beyond five centimeters have been
successfully reconstructed using processed allografts
with clinically measurable results [24]. Alternatives to
nerve grafts include the use of conduits, such as autogenous vein grafts or artificial nerve conduits [25,26].
However, these modalities are less viable options [23,
27]. In the setting of pediatric brain tumors, the location of nerve damage is often too proximal for repair
in a primary fashion. Hence, the aforementioned use

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A. Panossian / Facial paralysis reconstruction in children and adolescents with central nervous system tumors

of grafts and conduits are not applicable. Therefore,

reconstructive strategies are directed distal to the location of injury, thereby abandoning the native pathways for facial nerve stimulation. Nerve transfers are
the preferred choice in this setting. This typically involves borrowing or sacrificing one of the remaining
functional cranial nerves. Choices include CN V, XI,
XII, and the contralateral CN VII. Each option carries
benefits and drawbacks in reestablishing the mimetic
function provided by the facial nerve.
The mandibular division (V3) of the fifth cranial
nerve has become the donor of choice in most instances
of nerve transfer due to the increased cross-sectional
axon count, strength of stimulus, and analogous nature
of activation to the facial nerve. In fact, the muscles
of mastication (temporalis, masseter, medial and lateral pterygoid) activate at some level in natural smiling function, although not always. Therefore, retraining the patient to smile using V3 often requires longterm physical therapy with recent reports of excellent
cerebral adaptation and spontaneity in activation of
mimetic functions [28,29].
Use of CN XI (spinal accessory) and CN XII (hypoglossal) has been reported with variable results [30,
31]. The function of these donor nerves is not necessarily analogous to that of the facial nerve. Therefore, rehabilitation aimed at achieving spontaneity may
fail in a larger proportion of patients than with use of
CN V. The result is often disconcerting and uncontrollable jerking of the face, especially in adolescents and
adults. Interestingly, use of hypoglossal-to-facial nerve
transfers may have a theoretical role in maintaining
stimulation of facial musculature via the distal, uninjured portion of CN VII. Providing action potentials to
the neuromuscular junctions by this mechanism offers
protection from permanent atrophy during the early period of nerve injury [32].
The viable contralateral facial nerve may serve as a
donor for restoring function to the injured side. Typically, a small branch of the facial nerve (e.g., buccal or
zygomatic branch) may be sacrificed for this purpose
without losing native function. However, the length
of the donor nerve is a limiting factor. Therefore, a
cross-facial nerve graft using a free autograft (usually
the sural nerve) is necessary as a bridge to connect to
the distal stump of the injured facial nerve. Numerous
problems limit this technique as a viable option, including axonal fallout, central fibrosis of the graft, and
poor fidelity of the transmitted stimulation [33,34]. In
addition, cross-sectional mismatch between the small
donor branch and the target innervation site of the in-

jured distal stump of the contralateral facial nerve results in delivery of inadequate power.
All options above imply a donor and recipient nerve.
As such, an ideal donor nerve should mimic normal
facial nerve function in an analogous fashion. After
the facial nerve, the masseter nerve (CN V) provides
the most similarity in this regard, especially for mid
and lower facial function. In addition, sacrifice of a
suitable donor nerve should minimize loss of function in its native site. For example, in the setting of a
masseter-to-facial nerve transfer, sacrifice of the masseter nerve does not diminish masseter function significantly due to a dual innervation pattern [35,36]. Additionally, masticatory function is composed of four
muscles as described above. A weakening or loss of the
masseter muscle will typically not produce a functional
deficit.
Early management of facial paralysis in the setting
of pediatric brain tumors is ideally initiated when there
is high suspicion of proximal facial nerve injury. Dialogue between the ablative and reconstructive surgeons should be initiated early, preferably preoperatively when nerve injury is anticipated. Often, the decision to intervene is delayed due to uncertainty of complete disruption of the nerve (i.e., neurotmesis) and the
hope of spontaneous recovery from a neurapraxic state.
One must also keep in mind that although a waiting
period is reasonable in most cases, there must be evidence of gradual objective improvement of paralysis.
Serial electromyography and nerve conduction studies
may be helpful in this situation to quantify progress.
In some instances, improvement may plateau and obscure the expectation of clinically meaningful recovery. In other words, there may be some return of facial
nerve function; however, considerable facial asymmetry and other symptoms of profound paralysis may persist into adulthood. The waiting period must also incorporate the possibility of proceeding with early surgical reconstruction, if indicated. Specifically, one must
consider the time required for achieving nerve regeneration from the point of nerve transfer to the target muscles. This process alone may take up to 34 months. A
multidisciplinary approach for the treatment of facial
paralysis will streamline this process and avoid much
of the uncertainty related to decision-making during
the early versus late phases of facial nerve injury.

4. Late surgical management

Late management of facial paralysis occurs when
permanent changes take place at the neuromuscular

A. Panossian / Facial paralysis reconstruction in children and adolescents with central nervous system tumors

junction or when there is poor recovery or severely impaired residual nerve function. In both instances, the
patient remains permanently paralyzed or hemiparetic,
causing varying degrees of cosmetic and functional
disturbance. Some symptoms include facial asymmetry at rest, speech abnormalities, oral incontinence, dry
eyes with reliance on lubrication, and loss of rhytids
and expressive ability. There is no consensus on when
facial nerve paralysis is considered permanent, but
some suggest 18 months as an approximate cutoff
point for any further recovery [13].
The decision to pursue reconstruction for established facial paralysis follows a systematic approach.
As mentioned above, the face is divided into thirds,
each with its own considerations regarding restoration
of vital mimetic functions.
4.1. Upper face (Brow)
Paralysis of the brow may result in ptosis and decreased ability to raise the forehead. Often there is minimal cosmetic or functional deformity. Asymmetry is
visualized with animation and rarely causes deformity
at rest. Procedures to restore symmetry are namely
static in nature and focus on purposeful defunctionalization of the contralateral frontalis muscle [13].
Chemodenervation of the contralateral frontalis muscle
with botulinum toxin will improve symmetry aesthetically, but requires multiple injections at 34 months intervals to maintain results [37]. Alternatively, surgical
denervation of the frontalis branch of the contralateral
facial nerve will achieve a more permanent solution,
although results are variable [38].
4.2. Midface
Paralysis of the midface most visibly affects periocular function, namely proper eye closure. Symptoms
of periocular mimetic dysfunction include lagophthalmos, lower eyelid malposition, and lacrimal duct obstruction, all of which may produce corneal dessication, exposure keratopathy, epiphora, and cosmetic deformity [39]. Reconstructive principles focus on repositioning of the upper and lower eyelids simultaneously
or sequentially, depending on variations and severity.
Dynamic and static procedures that address the
problems of eye closure are available. Dynamic options to restore blinking include regional and distant
muscle transfers including temporalis myoplasty, pedicled frontalis transfer, and vascularized muscle grafts
such as pectoralis minor, gracilis, and platysma mus-

299

cles; however, results have been equivocal [40,41]. In

addition, palpebral spring implants dynamically augment residual blink by applying a downward force to
the upper eyelid that increases with upward eyelid excursion [42]. The final result is a stronger blink reflex
and a lowering of the lagophthalmic upper eyelid.
Static options are performed more commonly. These
include improving upper eyelid downward excursion
by lid loading and correcting lower eyelid ectropion.
Several techniques are available to accomplish these
tasks. Insertion of a gold or platinum weight into the
upper eyelid is relatively easy, with the advantage of
adjustability over time. Complications may include a
cosmetically unattractive prominence produced by the
weight, occasional extrusion, and astigmatism [43,44].
Resection of Mullers muscle has also been used to
counter the effects of lid retraction by allowing the upper eyelid to rest at a lower level.
Tessier et al. first described his approach to treating paralyzed eyelids by using a lengthening technique
of the levator mechanism of the upper eyelid [45]. In
this technique, an interpositional fascia graft is inserted
into a surgically created defect in the levator aponeurosis. The degree of lengthening may be adjusted as necessary. As much as seven millimeters of lengthening
is possible with good long-term relief of lagophthalmos [46]. Lateral tarsorrhaphy involves surgically joining the lateral aspect of the upper eyelid to the lower
eyelid. As an adjunct procedure, tarsorrhaphy provides
good relief of symptoms in combination with upper
eyelid weight insertion [47]. Rounding of the corner
between the two eyelids may occur, giving an unfavorable appearance.
In addressing lower eyelid ectropion, several options
exist to elevate ptotic structures and maintain lower
eyelid position. Lower tarsal strip resection is a commonly used procedure to elevate the eyelid [48]. A fullthickness segment of the lateral lower eyelid is excised,
including the associated tarsus, thus producing mild
elevation via a tightening effect along the lid margin.
Long-term correction is not as reliable as other techniques. Similarly, canthopexy involves tightening the
lower eyelid by repositioning the lateral canthus to a
higher level along the lateral orbit. Both of these procedures are used frequently in conjunction with upper
eyelid loading procedures such as platinum weight insertion [49]. Finally, lower eyelid repositioning using a
sling created from a tendon or fascia graft is effective in
producing sustained elevation of the lower eyelid [50].
Usually, the palmaris longus tendon or a strip of fascia lata is used due to advantages of autogenous grafts

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A. Panossian / Facial paralysis reconstruction in children and adolescents with central nervous system tumors

over alloplastic materials, such as expanded polytetrafluoroethylene (ePTFE or GORE-TEX , Newark,

DE) (Fig. 2) [51].
In some instances of facial paralysis resulting from a
posterior cranial fossa tumor or from its excision, collateral damage may occur to the trunk of the trigeminal nerve (CN V). Implications in the midface are related to anesthesia of the ipsilateral cornea via the ophthalmic nerve (V1). Patients demonstrating symptoms
may develop exposure keratitis and corneal trauma
due to disruption of the afferent limb of the blink
reflex. Terzis et al. describe a novel technique of
transferring the contralateral supraorbital and supratrochlear nerves to the anesthetic eye and implanting
the branches around the limbus [52]. Corneal sensory
testing demonstrated return of objective sensibility as
early as 9 months.
Facial paralysis may also affect nasal airflow by interfering with external nasal valve opening and contribute to descent of soft tissues in the cheek. Static
procedures such as tendon or fascia lata slings function
by elevating the cheek and recreating the nasolabial
fold. By targeting the alar base, they may augment
nasal airflow by drawing the ala laterally, thus opening the external nasal valve. Nasal valve suspension to
the infraorbital rim using Mitek bone anchors (Depuy
Mitek, Raynham, MA) is a simple technique used to
elevate the lateral portion of the nasal ala [53]. However, in most patients, relief of symptoms is successful in the short-term only (less than 22 months) [54].
Subperiosteal facelifts and sub-orbicularis oculi fat elevation have demonstrated promise in delivering more
durable results when used to suspend the midface and
lower eyelid [55,56]. Other techniques such as standard facelifts and thread lifting suffer from short-term
benefit and are, therefore, of limited use [57].
4.3. Lower face
Reconstruction of the lower face in established facial paralysis focuses on restoration of perioral function. Specific functions affected include smiling, articulation, and oral continence. As in midface reconstruction, static procedures using tendon and/or fascia lata
slings are effective in elevating the oral commissure.
However, static procedures carry the disadvantage of
producing a conspicuous appearance during animation,
although resting symmetry may be improved. To avoid
this problem, dynamic options in the form of regional
muscle transposition and free muscle transplantation
afford the paralyzed patient an opportunity to exert vol-

Fig. 2. The authors preferred technique for treatment of lower eyelid

paralytic ectropion. A palmaris longus tendon graft is harvested and
wrapped around the medial canthal tendon. It is then passed along
the margin of the lower eyelid subcutaneously and attached to the
lateral orbital rim. Tension is set to slightly overcorrect the deformity.

untary control over facial expression, namely smiling

and bilabial closure.
In 1934, Harold Gillies described a novel technique
of turning over the ipsilateral temporalis muscle and attaching it to the paralyzed oral commissure via a fascia
lata graft [58]. This was one of the earliest examples of
a regional muscle transfer that continues to be used today. Although patient satisfaction has been improved,
problems of excessive bulk over the zygomatic arch
and lack of spontaneous expressivity have been noted
to be drawbacks. In light of current improvements in
regional muscle transfers, the problems related to traditional temporalis turnover flaps is less than satisfactory.
More recently, Labbe and Hault introduced a new
technique that involves transferring the temporalis
muscle underneath the zygomatic arch, thereby eliminating the problem of excessive bulk with the traditional approach [59]. In addition, the muscle is disinserted from the coronoid process and carefully inserted
along the oral commissure and nasolabial fold to reanimate the smile. The procedure is reliable in accomplishing excursion at the oral commissure along the
proper vector and in improving resting symmetry of
the mouth.
The masseter muscle transfer has also been described, but with major limitations [60,61]. This includes hollowing over the border of the mandible and
an undesirable lateral vector of pull on the oral commissure. Refinements of this procedure by mobilization of both the insertion and origin of the masseter are
currently under investigation to improve direction of
pull on the oral commissure [62].
Free muscle transplantation has become the procedure of choice for many reconstructive surgeons in reanimating the paralyzed smile. Most reliable among
the options of donor muscles is the gracilis muscle [63]. Appropriate resting length, purely linear di-

A. Panossian / Facial paralysis reconstruction in children and adolescents with central nervous system tumors

Fig. 3. Eight-year-old boy with complete left facial paralysis following resection of a medulloblastoma. Preop and 3-month postop
following gracilis free muscle transfer to face with neurorrhaphy to
masseter branch of CN V. This patient had also undergone repositioning of the lower eyelid using a palmaris longus tendon sling.

rection and adjustability of pull, and the ability to

segmentalize the muscle in order to diminish bulk in
the cheek make the gracilis an ideal option. Other
candidates for free muscle transfer include the latissimus dorsi, serratus anterior, pectoralis minor, biceps
femoris, and extensor digitorum brevis, none of which
seem to approximate the ideal donor criteria exhibited
by the gracilis muscle [6468]. Smile reconstruction
in unilateral facial paralysis proceeds along one of two
basic strategies: recruitment of the contralateral buccal
or zygomatic branch of the facial nerve (CN VII) or
use of the ipsilateral masseteric branch of the trigeminal nerve (CN V). Each carries advantages and disadvantages, and the ultimate decision is made by the patient and family members in conjunction with the reconstructive surgeon. The availability of donor nerves
also has a bearing on this decision.
Use of the contralateral facial nerve carries the advantage of triggering the transplanted muscle via native
pathways of facial muscle stimulation; spontaneity is
inherent. However, several disadvantages limit its universal adoption. First, use of this nerve requires staged
procedures utilizing a cross-face nerve graft, followed
by definitive muscle transplantation and coaptation
with the nerve graft. Therefore, the time between initiation of reconstruction and activation of the transplanted muscle may be from 12 to 18 months. Second,
the power afforded by the contralateral facial nerve
branch may be variable (and often less forceful than the
masseter nerve) at its point of action in the transplanted
muscle. Lastly, the reproducibility of results may be
highly variable from patient to patient in comparison
to use of the ipsilateral CN V.
The advantages of using the ipsilateral masseter
nerve include a single stage procedure, shorter time
to smile actuation (approximately 3 to 4 months), and
more forceful contraction (Fig. 3). The major disad-

301

vantage is the development of, or lack thereof, spontaneous smiling, given the analogous pathway of action via CN V. This may be quite distressing to older
patients; however, recent evidence suggests excellent
cerebral adaptation and development of spontaneity in
both children and adults [29,69].
Restoration of mimetic functions of the lower face
is one of the most challenging goals in facial paralysis
reconstruction. This is likely due to the high level of
visibility and inherent expressivity that can stigmatize
an afflicted individual. However, much of patient and
surgeon gratification derives from the dramatic results
achieved in successfully reanimating the lower face.
4.4. Ancillary procedures
Achieving symmetry of form and function is the
goal of all strategies described in facial paralysis reconstruction. Often, it may be difficult to realize this
goal with a single procedure. In practice, multiple ancillary procedures help to restore symmetry in an incremental fashion.
Weakening contralateral facial movement is a common technique in adjusting final results from facial
paralysis reconstruction. Administration of botulinum
toxin is common practice for achieving this goal and
has numerous advantages, including ease of administration, controllability, and reproducibility. Botulinum
toxin acts at the neuromuscular junction by blocking
release of acetylcholine at the presynaptic nerve terminal [70]. Disadvantages include temporary effect (3
6 months), need for repeat injections, and high cost.
Common areas of injection include the contralateral
brow, the nasolabial fold, and the lower lip depressors.
However, many patients prefer a permanent solution
for facial asymmetry, especially in children who would
otherwise require a lifetime of botulinum toxin injections.
Surgical resection of muscles and nerves in the nonparalyzed half of the face provides a permanent solution. Denervation of the frontal branch of the facial
nerve will weaken frontalis muscle function most directly. This procedure may be performed alone or in
combination with contralateral browpexy as described
above. Overactive lower lip depression is perhaps the
most distressing aspect of post-reconstruction facial
asymmetry and may even diminish the affect of a transplanted muscle. Resection of the depressor labii inferioris (DLI) and depressor angularis oris (DAO) permanently disables the downward and lateral forces on
the lower lip and oral commissure [71]. Coupled with

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marginal mandibular nerve resection, a lasting result is

possible.
For those patients who experience partial facial
nerve palsy or full recovery of facial nerve function,
synkinesis may be a vexing problem. Disorganized reinnervation in this setting results in involuntary contraction of one group of facial muscles with purposeful activation of another muscle group. Botulinum
toxin has been effective in diminishing this distressing
symptom with good reliability [72]. Permanent solutions have targeted facial nerve branches in the paretic
side with selective denervation or micro-nerve transfers [73].
Other ancillary procedures are used to improve
structural symmetry. Debulking of transplanted muscle
flaps, selective fat injection, and oral commissuroplasties are some examples of other modalities [13,74,75].

5. Rehabilitation
Physical therapy is a critical aspect of both preoperative and postoperative management of patients with
facial paralysis. Numerous modalities exist for stimulation of muscle and nerve units in the paretic or paralytic face. These modalities also apply to the treatment
of patients following reconstructive surgery with only
slight differences depending on type of reconstruction
employed.
Preoperative assessment is critical in measuring the
efficacy of treatment. Various facial grading systems
are described to record symmetry of voluntary movement and synkinesis [6]. Measurements using calipers
and rulers are made from facial landmarks, and the
amount of excursion and direction are recorded [11].
Timing for starting therapy following reconstruction
usually corresponds to evidence of re-innervation or
voluntary muscle activation. Depending on the type of
reconstruction, this may be anywhere between 3 and 9
months following distant muscle transfer procedures.
In the case of regional muscle transfer such as a temporalis myoplasty, therapy is started 3 weeks postoperatively [59].
Therapy involves controlled active range of motion
exercises of available neuromuscular units, with the
aim of strengthening and coordinating movement. Specific functions are stressed, such as smiling, swallowing, and speech articulation [76]. Biofeedback is critical in order for patients to experience the result of volitional movement, due to the loss of intrinsic feedback in affected facial muscles following facial paral-

ysis. This is especially important in patients undergoing dynamic reconstruction using analogous muscle or
nerve transfers where the facial nerve is unavailable.
Biofeedback allows patients to combine visual cues of
facial movement to sensory changes in the face during
movement. It allows for error correction and coordination to occur rapidly in order to avoid development
of pathological habits. Biofeedback may be performed
with a mirror by the patient as facial exercises are performed. This is also known as mime therapy, and has
been shown to improve facial muscular contractions
and limit synkinesis [77,78]. Cooperation with therapy
is a key element to success; therefore, children must
be of an appropriate age (typically over five years of
age) to follow instructions and to remain focused on directed tasks. EMG biofeedback is an additional method
to mirror biofeedback and has demonstrated efficacy in
reducing synkinesis [79]. Electrodes are placed on the
face, whereby the amount of muscle stimulation is visualized by the patient in wave form. With visual cues,
the patient increases stimulation of re-innervated muscles by voluntarily elevating the threshold of the waveform.
Massage therapy or tactile stimulation of the face
is an important aspect of therapy to intended reduce
edema and promote symmetry of facial muscular contraction. Proprioceptive neuromuscular facilitation, as
proposed by Kabat, has demonstrated usefulness in
early recovery following Bells palsy and iatrogenic facial nerve injury [76,80,81]. Using this technique, a
combination of stretching of muscle groups, resistance
against contralateral contraction, and manual pressure
are employed to increase contractile power and resistance in the residual muscles or a transferred muscle.
Electrical stimulation of the paralyzed face or following dynamic muscle reconstruction may provide
some benefit in improving re-innervation or promoting
the health of the transplanted muscle [82,83]. Opinions regarding this modality are mixed. Some opponents argue that electrostimulation may provoke synkinesis and contractures [84,85]. Various types of electrostimulatory muscle therapy are available. Stimulation of pain fibers may be a drawback, especially in
children. However, the use of high-voltage pulsed current (HVPC) is a promising modality in promotion
of healthy muscles in the face of denervation. Wellknown for its efficacy in the treatment of wounds,
HVPC improves facial edema, promotes denervated
muscle circulation during the re-innervation period,
and may commence soon after reconstruction [86,87].
Currently, no single modality is superior as a standalone therapy. An effective physical therapy regimen

A. Panossian / Facial paralysis reconstruction in children and adolescents with central nervous system tumors

incorporates more than one of the methods above,

along with close supervision by a therapist and a cooperative patient. A significant portion of rehabilitation from facial paralysis or following reconstruction occurs at home. Compliance with home exercises
and other modalities is requisite to successful recovery from facial nerve palsy or following muscle and/or
nerve transfers.

6. Conclusion
Facial paralysis in children and adolescents with
brain tumors may be unavoidable in many instances.
Whether the cause is secondary to nerve involvement
or iatrogenic injury following resection of posterior
cranial fossa tumors, the social consequences are quite
severe to the patient and his or her family. Often,
prolonged psychological treatment is required. Fortunately, current advances in surgical reconstruction have
been shown to be effective in restoring movement in
the paralyzed face. Each reconstructive effort is tailored to the individual and may be categorized as an
early or late intervention. A discussion with the patient and family is critical in deciding whether or not to
proceed with reconstruction, as factors such as length
and intricacy of surgery, waiting period for results, and
compliance necessary for home therapy should all be
weighed. Finally, a multidisciplinary approach is crucial to maximizing success in the pediatric patient.
Interdepartmental communication within a designated
facial paralysis center is vital in treating children with
facial paralysis of any etiology. Identifying patients
early in the evolution of facial paralysis is key to preserving functioning muscle units that will activate facial expression naturally. Future directions will focus
on new rehabilitation strategies and other forms of dynamic reconstruction to improve spontaneity and symmetry simultaneously.

[2]

[3]

[4]

[5]

[6]

[7]
[8]
[9]

[10]

[11]

[12]

[13]

[14]

[15]

[16]

[17]

Conflict of interest
[18]

The author has no conflict of interest to declare.

[19]

References
[1]

Sonderkaer S, Schmiegelow M, Carstensen H, Nielsen LB,

Muller J, Schmiegelow K. Long-term neurological outcome
of childhood brain tumors treated by surgery only. J Clin Oncol. 2003; 21: 1347-1351.

[20]

[21]

303

Cochrane DD, Gustavsson B, Poskitt KP, Steinbok P, Kestle

JR. The surgical and natural morbidity of aggressive resection
for posterior fossa tumors in childhood. Pediatr Neurosurg.
1994; 20: 19-29.
Newman LA, Boop FA, Sanford RA, Thompson JW, Temple CK, Duntsch CD. Postoperative swallowing function after posterior fossa tumor resection in pediatric patients. Childs
Nerv Syst. 2006; 22: 1296-1300.
Albright AL, Wisoff JH, Zeltzer PM, Deutsch M, Finlay
J, Hammond D. Current neurosurgical treatment of medulloblastomas in children. A report from the Childrens Cancer
Study Group. Pediatr Neurosci. 1989; 15: 276-282.
Magliulo G, DAmico R, Forino M. Results and complications of facial reanimation following cerebellopontine angle
surgery. Eur Arch Otorhinolaryngol. 2001; 258: 45-48.
Westin LM, Zuker R. A new classification system for facial
paralysis in the clinical setting. J Craniofac Surg. 2003; 14:
672-679.
Seddon HJ. A Classification of Nerve Injuries. Br Med J.
1942; 2: 237-239.
Sunderland S. The anatomy and physiology of nerve injury.
Muscle Nerve. 1990; 13: 771-784.
Brown MC, Hopkins WG, Keynes RJ. Short- and long-term
effects of paralysis on the motor innervation of two different
neonatal mouse muscles. J Physiol. 1982; 329: 439-450.
Lentz TL. Development of the neuromuscular junction. 3. Degeneration of motor end plates after denervation and maintenance in vitro by nerve explants. J Cell Biol. 1972; 55: 93103.
Manktelow RT, Zuker RM, Tomat LR. Facial paralysis measurement with a handheld ruler. Plast Reconstr Surg. 2008;
121: 435-442.
Grosheva M, Wittekindt C, Guntinas-Lichius O. Prognostic
value of electroneurography and electromyography in facial
palsy. Laryngoscope. 2008; 118: 394-397.
Fattah A, Borschel GH, Manktelow RT, Bezuhly M, Zuker
RM. Facial palsy and reconstruction. Plast Reconstr Surg.
2012; 129: 340e-352e.
Kanerva M, Poussa T, Pitkaranta A. Sunnybrook and HouseBrackmann Facial Grading Systems: intrarater repeatability
and interrater agreement. Otolaryngol Head Neck Surg. 2006;
135: 865-871.
de Ru JA, Braunius WW, van Benthem PP, Busschers WB,
Hordijk GJ. Grading facial nerve function: Why a new grading system, the MoReSS, should be proposed. Otol Neurotol.
2006; 27: 1030-1036.
Yen TL, Driscoll CL, Lalwani AK. Significance of HouseBrackmann facial nerve grading global score in the setting
of differential facial nerve function. Otol Neurotol. 2003; 24:
118-122.
Allodi I, Udina E, Navarro X. Specificity of peripheral nerve
regeneration: interactions at the axon level. Prog Neurobiol.
2012; 98: 16-37.
Sunderland S. Course and rate of regeneration of motor fibers
following lesions of the radial nerve. Arch Neurol Psychiatry.
1946; 56: 133-157.
Sunderland S. Rate of regeneration of motor fibers in the ulnar
and sciatic nerves. Arch Neurol Psychiatry. 1947; 58: 7-13.
Sunderland S. Rate of regeneration in human peripheral
nerves; analysis of the interval between injury and onset of
recovery. Arch Neurol Psychiatry. 1947; 58: 251-295.
Stephanian E, Sekhar LN, Janecka IP, Hirsch B. Facial nerve
repair by interposition nerve graft: Results in 22 patients.
Neurosurgery. 1992; 31: 73-6; discussion 77.

304
[22]

[23]

[24]

[25]

[26]
[27]

[28]

[29]

[30]

[31]

[32]

[33]

[34]

[35]
[36]

[37]

[38]

[39]

[40]

[41]

A. Panossian / Facial paralysis reconstruction in children and adolescents with central nervous system tumors
Karabekmez FE, Duymaz A, Moran SL. Early clinical outcomes with the use of decellularized nerve allograft for repair of sensory defects within the hand. Hand (N Y). 2009; 4:
245-249.
Whitlock EL, Tuffaha SH, Luciano JP et al. Processed allografts and type I collagen conduits for repair of peripheral
nerve gaps. Muscle Nerve. 2009; 39: 787-799.
Brooks DN, Weber RV, Chao JD et al. Processed nerve allografts for peripheral nerve reconstruction: a multicenter study
of utilization and outcomes in sensory, mixed, and motor
nerve reconstructions. Microsurgery. 2012; 32: 1-14.
Wolford LM, Rodrigues DB. Autogenous grafts/allografts/
conduits for bridging peripheral trigeminal nerve gaps. Atlas
Oral Maxillofac Surg Clin North Am. 2011; 19: 91-107.
Taras JS, Nanavati V, Steelman P. Nerve conduits. J Hand
Ther. 2005; 18: 191-197.
Jones RH. The use of vein grafts in the repair of the inferior
alveolar nerve following surgery. Aust Dent J. 2010; 55: 207213.
Coombs CJ, Ek EW, Wu T, Cleland H, Leung MK.
Masseteric-facial nerve coaptationan alternative technique
for facial nerve reinnervation. J Plast Reconstr Aesthet Surg.
2009; 62: 1580-1588.
Manktelow RT, Tomat LR, Zuker RM, Chang M. Smile reconstruction in adults with free muscle transfer innervated by
the masseter motor nerve: effectiveness and cerebral adaptation. Plast Reconstr Surg. 2006; 118: 885-899.
Ozsoy U, Hizay A, Demirel BM et al. The hypoglossal-facial
nerve repair as a method to improve recovery of motor function after facial nerve injury. Ann Anat. 2011; 193: 304-313.
Griebie MS, Huff JS. Selective role of partial XI-VII anastomosis in facial reanimation. Laryngoscope. 1998; 108: 16641668.
Terzis JK, Tzafetta K. The babysitter procedure: minihypoglossal to facial nerve transfer and cross-facial nerve grafting. Plast Reconstr Surg. 2009; 123: 865-876.
Frey M, Happak W, Girsch W, Bittner RE, Gruber H. Histomorphometric studies in patients with facial palsy treated by
functional muscle transplantation: New aspects for the surgical concept. Ann Plast Surg. 1991; 26: 370-379.
Frey M, Koller R, Liegl C, Happak W, Gruber H. Role of a
muscle target organ on the regeneration of motor nerve fibres
in long nerve grafts: A synopsis of experimental and clinical
data. Microsurgery. 1996; 17: 80-88.
Klebuc MJ. Facial reanimation using the masseter-to-facial
nerve transfer. Plast Reconstr Surg. 2011; 127: 1909-1915.
Spira M. Anastomosis of masseteric nerve to lower division
of facial nerve for correction of lower facial paralysis. Preliminary report. Plast Reconstr Surg. 1978; 61: 330-334.
Clark RP, Berris CE. Botulinum toxin: a treatment for facial
asymmetry caused by facial nerve paralysis. Plast Reconstr
Surg. 1989; 84: 353-355.
Bulstrode NW, Harrison DH. The phenomenon of the late
recovered Bells palsy: Treatment options to improve facial
symmetry. Plast Reconstr Surg. 2005; 115: 1466-1471.
Patel V, Daya SM, Lake D, Malhotra R. Blink lagophthalmos and dry eye keratopathy in patients with non-facial palsy:
clinical features and management with upper eyelid loading.
Ophthalmology. 2011; 118: 197-202.
Frey M, Giovanoli P, Tzou CH, Kropf N, Friedl S. Dynamic
reconstruction of eye closure by muscle transposition or functional muscle transplantation in facial palsy. Plast Reconstr
Surg. 2004; 114: 865-875.
Terzis JK, Karypidis D. The outcomes of dynamic procedures

for blink restoration in pediatric facial paralysis. Plast Reconstr Surg. 2010; 125: 629-644.
[42] Levine RE, Shapiro JP. Reanimation of the paralyzed eyelid
with the enhanced palpebral spring or the gold weight: Modern replacements for tarsorrhaphy. Facial Plast Surg. 2000; 16:
325-336.
[43] Rofagha S, Seiff SR. Long-term results for the use of gold
eyelid load weights in the management of facial paralysis.
Plast Reconstr Surg. 2010; 125: 142-149.
[44] Mavrikakis I, Beckingsale P, Lee E, Riaz Y, Brittain P.
Changes in corneal topography with upper eyelid gold weight
implants. Ophthal Plast Reconstr Surg. 2006; 22: 331-334.
[45] Tessier P, Delbet JP, Pastoriza J, Lekiefre M. [Paralized eyelids]. Ann Chir Plast. 1969; 14: 215-223.
[46] Guillou-Jamard MR, Labbe D, Bardot J, Benateau H. Paul
Tessiers technique in the treatment of paralytic lagophthalmos by lengthening of the levator muscle: Evaluation of 29
cases. Ann Plast Surg. 2011; 67: S31-5.
[47] Tan ST, Staiano JJ, Itinteang T, McIntyre BC, Mackinnon CA,
Glasson DW. Gold weight implantation and lateral tarsorrhaphy for upper eyelid paralysis. J Craniomaxillofac Surg, 2012.
[48] Smith DS, Wax MK. The lower-eyelid tarsal-strip procedure.
Ear Nose Throat J. 2005; 84: 698.
[49] Nakazawa H, Kikuchi Y, Honda T, Isago T, Morioka K, Yoshinaga Y. Treatment of paralytic lagophthalmos by loading the
lid with a gold plate and lateral canthopexy. Scand J Plast Reconstr Surg Hand Surg. 2004; 38: 140-144.
[50] Carraway JH, Manktelow RT. Static sling reconstruction of
the lower eyelid. Oper Tech Plast Reconstr Surg. 1999; 6: 163166.
[51] Tollefson TT, Senders CW. Restoration of eyelid closure in
facial paralysis using artificial muscle: preliminary cadaveric
analysis. Laryngoscope. 2007; 117: 1907-1911.
[52] Terzis JK, Dryer MM, Bodner BI. Corneal neurotization: A
novel solution to neurotrophic keratopathy. Plast Reconstr
Surg. 2009; 123: 112-120.
[53] Yu K, Kim AJ, Tadros M, Costantino PD. Mitek anchoraugmented static facial suspension. Arch Facial Plast Surg.
2010; 12: 159-165.
[54] Nuara MJ, Mobley SR. Nasal valve suspension revisited.
Laryngoscope. 2007; 117: 2100-2106.
[55] Ramirez OM, Maillard GF, Musolas A. The extended subperiosteal face lift: a definitive soft-tissue remodeling for facial
rejuvenation. Plast Reconstr Surg. 1991; 88: 227-36; discussion 237-8.
[56] Horlock N, Sanders R, Harrison DH. The SOOF lift: its role
in correcting midfacial and lower facial asymmetry in patients
with partial facial palsy. Plast Reconstr Surg. 2002; 109: 83949; discussion 850-4.
[57] Stephens J, De Zoysa N, Hughes J, Mochloulis G. Silhouette lift for facial reanimation. [letter]. Clin Otolaryngol 2009;
34(4): 404-405.
[58] Gillies H. Experiences with Fascia Lata Grafts in the Operative Treatment of Facial Paralysis: (Section of Otology and
Section of Laryngology). Proc R Soc Med. 1934; 27: 13721382.
[59] Labbe D, Huault M. Lengthening temporalis myoplasty and
lip reanimation. Plast Reconstr Surg. 2000; 105: 1289-97; discussion 1298.
[60] Hastings S. Transplantation of Anterior Half of Masseter
Muscle for Facial Paralysis. Proc R Soc Med. 1920; 13: 6465.
[61] Hontanilla B, Qiu SS. Transposition of the hemimasseteric

A. Panossian / Facial paralysis reconstruction in children and adolescents with central nervous system tumors
muscle for dynamic rehabilitation of facial paralysis. J Craniofac Surg. 2012; 23: 203-205.
[62] Matic DB, Yoo J. The pedicled masseter muscle transfer for
smile reconstruction in facial paralysis: Repositioning the origin and insertion. J Plast Reconstr Aesthet Surg. 2012; 65:
1002-1008.
[63] Manktelow RT, Zuker RM. Muscle transplantation by fascicular territory. Plast Reconstr Surg. 1984; 73: 751-757.
[64] Harrison DH. The treatment of unilateral and bilateral facial
palsy using free muscle transfers. Clin Plast Surg. 2002; 29:
539-49, vi.
[65] Harrison DH, Grobbelaar AO. Pectoralis minor muscle transfer for unilateral facial palsy reanimation: An experience of
35 years and 637 cases. J Plast Reconstr Aesthet Surg. 2012;
65: 845-850.
[66] Hayashi A, Maruyama Y. Neurovascularized free short head
of the biceps femoris muscle transfer for one-stage reanimation of facial paralysis. Plast Reconstr Surg. 2005; 115: 394405.
[67] Alagoz MS, Alagoz AN, Comert A. Neuroanatomy of extensor digitorum brevis muscle for reanimation of facial paralysis. J Craniofac Surg. 2011; 22: 2308-2311.
[68] Lifchez SD, Sanger JR, Godat DM, Recinos RF, LoGiudice
JA, Yan JG. The serratus anterior subslip: anatomy and implications for facial and hand reanimation. Plast Reconstr Surg.
2004; 114: 1068-1076.
[69] Lifchez SD, Matloub HS, Gosain AK. Cortical adaptation to
restoration of smiling after free muscle transfer innervated by
the nerve to the masseter. Plast Reconstr Surg. 2005; 115:
1472-9; discussion 1480-2.
[70] Klein AW. The therapeutic potential of botulinum toxin. Dermatol Surg. 2004; 30: 452-455.
[71] Hussain G, Manktelow RT, Tomat LR. Depressor labii inferioris resection: An effective treatment for marginal mandibular
nerve paralysis. Br J Plast Surg. 2004; 57: 502-510.
[72] Toffola ED, Furini F, Redaelli C, Prestifilippo E, Bejor M.
Evaluation and treatment of synkinesis with botulinum toxin
following facial nerve palsy. Disabil Rehabil. 2010; 32: 14141418.
[73] Terzis JK, Karypidis D. Therapeutic strategies in post-facial
paralysis synkinesis in pediatric patients. J Plast Reconstr
Aesthet Surg. 2012; 65: 1009-1018.
[74] Takushima A, Harii K, Asato H, Momosawa A. Revisional
operations improve results of neurovascular free muscle trans-

305

fer for treatment of facial paralysis. Plast Reconstr Surg. 2005;

116: 371-380.
[75] Terzis JK, Olivares FS. Secondary surgery in paediatric facial
paralysis reanimation. J Plast Reconstr Aesthet Surg. 2010;
63: 1794-1806.
[76] Wilson CM, Ronan SL. Rehabilitation postfacial reanimation
surgery after removal of acoustic neuroma: a case study. J
Neurol Phys Ther. 2010; 34: 41-49.
[77] Pereira LM, Obara K, Dias JM, Menacho MO, Lavado EL,
Cardoso JR. Facial exercise therapy for facial palsy: systematic review and meta-analysis. Clin Rehabil. 2011; 25: 649658.
[78] Beurskens CH, Heymans PG. Mime therapy improves facial
symmetry in people with long-term facial nerve paresis: A
randomised controlled trial. Aust J Physiother. 2006; 52: 177183.
[79] Dalla Toffola E, Bossi D, Buonocore M, Montomoli C,
Petrucci L, Alfonsi E. Usefulness of BFB/EMG in facial palsy
rehabilitation. Disabil Rehabil. 2005; 27: 809-815.
[80] KABAT H, KNOTT M. Proprioceptive facilitation therapy for
paralysis. Physiotherapy. 1954; 40: 171-176.
[81] Barbara M, Monini S, Buffoni A et al. Early rehabilitation
of facial nerve deficit after acoustic neuroma surgery. Acta
Otolaryngol. 2003; 123: 932-935.
[82] Baricich A, Cabrio C, Paggio R, Cisari C, Aluffi P. Peripheral facial nerve palsy: how effective is rehabilitation? Otol
Neurotol. 2012; 33: 1118-1126.
[83] Targan RS, Alon G, Kay SL. Effect of long-term electrical
stimulation on motor recovery and improvement of clinical
residuals in patients with unresolved facial nerve palsy. Otolaryngol Head Neck Surg. 2000; 122: 246-252.
[84] Saito S, Moller AR. Chronic electrical stimulation of the facial nerve causes signs of facial nucleus hyperactivity. Neurol
Res. 1993; 15: 225-231.
[85] Sen CN, Moller AR. Signs of hemifacial spasm created by
chronic periodic stimulation of the facial nerve in the rat. Exp
Neurol. 1987; 98: 336-349.
[86] Bettany JA, Fish DR, Mendel FC. Influence of high voltage
pulsed direct current on edema formation following impact
injury. Phys Ther. 1990; 70: 219-224.
[87] Clemente FR, Matulionis DH, Barron KW, Currier DP. Effect
of motor neuromuscular electrical stimulation on microvascular perfusion of stimulated rat skeletal muscle. Phys Ther.
1991; 71: 397-404; discussion 404-6.

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