Facial Neuromuscular Retraining for Synkinesis


We rarely think of facial movement. It is spontaneous and emotional as it morphs effortlessly from one mood and expression to the next. Facial palsy devastates normal function, often resulting in significant functional and psychosocial consequences that negatively impact quality of life for those afflicted. Facial muscles are unique in the human body. They move the facial skin in multiple directions to produce a wide range of movement patterns that enable nonverbal communication, eye closure, and oral motor functions. The subtleties of human expression require a delicate balance of activity among multiple facial muscles contracting and relaxing in a precise sequence.

Acutely, injury to the facial nerve causes a flaccid paralysis where the absence of muscle contraction is due to the lack of neural signal. Like flipping a switch to light the bulb of an unplugged lamp, no amount of effort can trigger the facial muscles to contract in the absence of a functional electrical circuit. In cases where the electrical circuit is still intact and recovery is delayed, flaccid paralysis can be followed by the development of uncoordinated, inappropriate movement termed synkinesis. Synkinesis is less common and often goes unrecognized by patients as well as medical professionals. What deceptively appears to be weakness in the synkinetic face may in fact be restriction of dynamic motion caused by simultaneous contraction of opposing muscles. Like stretching fabric in two or more directions at once, antagonistic co-contraction prevents normal mobility, excursion, range of motion, and therefore expression. For the patient with synkinesis, facial neuromuscular retraining (fNMR) offers a nonsurgical approach to rehabilitation for restoring and refining functional facial movement and expression.

The objectives of this chapter are to: (1) provide an overview of fNMR; (2) explain specific therapeutic approaches for treating contracture and synkinesis; and (3) discuss the use of neuromodulators such as botulinum toxin A (BTX-A) from an fNMR perspective to optimize dynamic outcomes in the synkinetic patient.

Facial Neuromuscular Retraining

fNMR is a clinical specialty program within the field of rehabilitation medicine created specifically for improving function in patients with facial paralysis, paresis, and/or synkinesis after facial nerve injury. fNMR uses selective neuromotor training to normalize resting tone, facilitate symmetrical movement, and control aberrant gross motor activity. It is a synthesis of therapeutic science, neurophysiology, neuropsychology, learning theory, and art. Unique training methods provide augmented sensory information to enhance neural adaptation and learning. The application of learning theory maximizes motivation through individualized instruction and active patient participation. Each patient presents a distinct functional profile and psychosocial response to the condition and so requires personalized, individual attention; each treatment program is unique. There is no generic “hand-out sheet of exercises.” The ability to create a myriad of expressions requires subtlety, accuracy, and precise control of the 23 plus pairs of facial muscles which no simple generic exercise can achieve.

The well-trained fNMR practitioner plays a vital role within the facial nerve multidisciplinary team, providing an innovative perspective for analyzing and explaining abnormal movement patterns in the synkinetic face. In addition, they provide patient support, continuity of care, education, and effective therapy based on the uniquely complex facial neuromuscular system.

To address the complexities of facial movement, the retraining process identifies neuromuscular sequencing abnormalities that impact expression and modifies them by improving coordination between muscles as opposed to simply increasing their strength. This is accomplished through practicing low amplitude, precisely coordinated movement patterns that mimic natural expressions. fNMR approaches motor control in a manner similar to that used to excel in a sport, play a musical instrument, or acquire any complex motor skill by providing “training” as opposed to “therapy”.

“Rehabilitation cannot be administered to the patient, in contrast to the treatment for many other disorders. The psychosocial and educational aspects of the rehabilitation process are thus of very great importance. In spite of the existence of biological bases for recovery, it does not occur without the appropriate environment, the attitude, and the involvement of the patient.”

This comprehensive clinical program was first described by Balliet and colleagues in 1982, who reported improved function in patients more than two years after facial nerve injury. Acquisition of new motor behaviors was attributed to brain plasticity, the capacity of the central nervous system to modify its organization, resulting in lasting functional change. Current programs are based largely on the works of Balliet, , Beurskens, Diels, and Ross, the most important features being detailed evaluation, patient education, individualized program development using a wide variety of motor learning techniques, and active patient participation.

In stark contrast to the precise, low amplitude, functional patterns that exemplify fNMR, general therapy techniques may include nonspecific, maximum effort exercises intended to strengthen muscles without regard for inhibiting or coordinating abnormal patterns. Simply strengthening facial muscles does not develop the accuracy and precision required to normalize facial action nor does it acknowledge the emotional stimuli that drive communicative expression.

Electrical stimulation is another general therapy modality that continues to be widely used despite evidence suggesting it may interfere with neural regeneration , and no evidence indicating its effectiveness. Acute administration of electrical stimulation coincides with the spontaneous recovery period where improvements can erroneously be attributed to the stimulation rather than the natural course of recovery. Multiple adjacent muscles may contract simultaneously which may further reinforce poor coordination. Clinical experience amongst fNMR practitioners suggests patients who receive it acutely may develop more synkinesis and mass action than those who do not. There is no indication that electrical stimulation can either inhibit or recoordinate synkinetic patterns, and surely there is no need to stimulate already active muscles. The unfounded use of electrical stimulation in the synkinetic face speaks to the common misinterpretation that limited movement indicates weakness rather than abnormal hyperactivity. Both gross exercises and electrical stimulation can reinforce already abnormal patterns and may be contraindicated in treating this population.

Physiological Basis of fNMR

The distinct techniques that comprise fNMR are based on characteristics unique to the facial neuromuscular system. These include:

  • 1.

    Facial muscles lack muscle spindles. The muscle spindle is a physiologic mechanism in skeletal muscle that produces a contraction in response to therapeutic facilitatory stimuli such as quick stretch, vibration, and tapping. These common techniques, effectively used for treating other disabilities, are ineffective for stimulating facial muscles in the absence of muscle spindles.

  • 2.

    Facial muscles have small motor units. Small motor units enable precise refinement, complexity, and subtlety of movement. Practicing gross facial movements confounds normal precision by producing unnaturally large motions which can cause overflow from neighboring muscles, further reinforcing abnormal patterns.

  • 3.

    Facial muscles degenerate slowly. They may remain viable for an extended period, so procedures used to maintain muscle viability (e.g., electrical stimulation) are unfounded.

  • 4.

    Facial muscles receive emotional as well as volitional neural inputs. There is a well-established distinction between the upper motor neuron pathways used for volitional facial movements and those used for emotional expression. In other words, facial muscles not only have a biomechanical action, but a specific emotional “signature” as well. The depressor anguli oris (DAO), for example, depresses the angle of the mouth to display sadness. It never conveys happiness. This is a critical concept in the synkinetic patient where “cross-wiring” results in wrong or confusing emotional expression.

  • 5.

    Facial muscles move skin. Unlike other skeletal muscles which attach to bone at origin and insertion and are biomechanically restricted by a joint, facial muscles have only one bony attachment (if that) and insert into other muscles or to skin. The facial skin is responsive to even a very slight, low amplitude contraction which displaces it in the many directions that comprise communicative facial expression.

Goals of fNMR

The goals of fNMR are consistent with the goals of surgical rehabilitation and include improving eye closure to decrease corneal exposure, increasing oral motor function for speech and mastication, improving facial tone, symmetry, and volitional and spontaneous movement.

Patient goals identified during the initial evaluation most often include increased eye closure, improved smile, and lip function. They may also include decreasing facial tightness, twitching, or abnormal movements such as eye closure while speaking or eating. Realistic, attainable goals are discussed and established by the patient and therapist prior to proceeding with treatment and are revised as progress is achieved.

Patients with bilateral facial palsy or those who have undergone surgical reanimation procedures such as hypoglossal anastomosis, temporalis transfer, cross face, or masseteric nerve graft, require specialized retraining programs which are beyond the scope of this chapter. ,

Timing of fNMR

Not every synkinetic patient is a good retraining candidate. Patients must be cognitively intact and motivated to participate in the program. The therapy is challenging and requires mindful, self-directed practice between sessions. Children with synkinesis can actively participate when they are of an age and maturity level sufficient to engage in the cognitive aspects of retraining; this is typically age 8 for girls, age 10 for boys. Younger children may benefit from aspects of the program via parental coaching.

Patients may be referred for retraining when tone increases or synkinesis is appreciated, typically 3 to 5 months after injury. This timeline is highly variable. Referral should still be considered if the patient appears flaccid at 6 to 8 months as subtle return of function may be masked by contracture or synkinesis and mistaken for flaccidity. ,

Treatment frequency and scheduling varies widely depending on multiple factors including proximity to clinic, compliance to daily home program, and financial considerations.

Local patients may be scheduled once a month, whereas those traveling a distance might return several months later. Typical duration of fNMR is 18 months to 3 years with an estimated 90% of the therapy completed by the patient on their own at home. Consistent and accurate home program practice between clinic visits is essential to achieve progress. Time spent on home practice between clinic visits far exceeds the number of hours spent with therapist resulting in a cost-effective program that greatly amplifies the effect of treatment. This process empowers patients to assume control of their own recovery.


Facial palsy is rare in the practice of rehabilitation medicine, one of the few peripheral nerve (lower motor neuron) injuries requiring rehabilitative intervention. Most commonly, therapy is provided for musculoskeletal, orthopedic, or brain (central, upper motor neuron) injuries. As synkinesis following peripheral nerve injury occurs so rarely, there is no precedent for identifying, understanding, or treating it. Training in its accurate evaluation and effective management is limited and inadequate. The treatment of facial paralysis and synkinesis is a highly specialized field that requires advanced clinical training. With proper instruction, occupational and physical therapists, as well as speech pathologists, can be trained to administer fNMR.

Synkinesis is the most common condition treated by the fNMR therapist. It is one of the most perplexing and challenging to treat as it “links” muscles that do not normally contract together. It distorts the face into unusual, unfamiliar expressions that are difficult to decipher. Interpretation of synkinetic patterns is particularly challenging because, to the untrained eye, the lack of motion is simply assumed to be weakness, when, in fact, it is caused by simultaneous contraction of agonist and antagonist muscles exerting tension on the facial skin in opposing directions. This abnormal muscle action can visually mimic flaccidity ( Fig. 9.1 ). On closer examination, visible bulking of the midfacial musculature clearly indicates active flexion of the zygomaticus (ZYG) contradicting the presence of flaccidity ( Fig. 9.2 ). Other common examples of this paradox include (1) lack of lip excursion during pucker, where synkinesis of midfacial and depressor musculature retracts the angle of the mouth such that it cannot move toward midline ( Fig. 9.3 ), and (2) impaired lower lip depression restricted by synkinesis, often interpreted as depressor labii inferioris (DLI) weakness ( Fig. 9.4 ). Like cars in traffic navigating a busy interchange with a broken signal, it is particularly challenging to “untangle” the “busy intersection” of opposing muscular actions of the lower third of the face.

Fig. 9.1

Lack of elevation at the affected left angle of the mouth during smile is visually perceived as weakness of zygomaticus major and minor rather than inability to elevate due to synkinetic co-contraction.

Fig. 9.2

Synkinetic depression/retraction caused by antagonistic co-contraction of ipsilateral depressor anguli oris, buccinator, and platysma (red arrows) while zygomaticus is activated during smile (green arrows).

Fig. 9.3

(A, B) During pucker, movement of the lips to midline (orbicularis oris superioris and inferioris [green arrows] ) is restricted by synkinetic co-contraction of opposing muscles, zygomaticus, levators, buccinator, and platysma (red arrows) . Visually it appears as though the lips are weak.

Fig. 9.4

Limited lower lip depression due to synkinetic co-contraction of buccinator and zygomaticus retracting/elevating the lower lip and angle, and mentalis elevating it (red arrows).

Synkinesis varies in location, occurrence, and severity from mild to severe (mass action), where it can result in gross deformity during facial movements. This gross, mass action results in a “frozen” face where many opposing muscles co-contract to the extent that no dynamic movement occurs. Like two teams pulling on opposite ends of a rope in a “tug-of-war,” the rope does not move though both teams are pulling with all their might. Easy to miss with the untrained eye, the contrast between flaccidity and synkinesis is striking. A drooped angle of the mouth in flaccid paralysis is due to decreased tone and weakness in the midfacial muscles ( Fig. 9.5A ); in the synkinetic face the angle may be actively depressed and/or retracted by synkinetic flexion of DAO, platysma (PLA), or buccinator (BUC) ( Fig. 9.5B ). In both cases, the angle of the mouth is “down” as compared to the unaffected side.

Fig. 9.5

Comparison of Mouth Angle Position in a Flaccid Versus Synkinetic Patient.

While appearing the same to the untrained eye, the angle in flaccid paralysis is “drooped” due to weakness of the ipsilateral midfacial musculature (A). In the synkinetic face, it is “pulled down” due to opposing synkinesis in the depressors and platysma (B).

Accurate assessment is paramount to developing appropriate retraining strategies. Flaccidity may call for strengthening; synkinesis, however, requires improving mobility and coordination, even in the presence of weakness. It is clear to see why applying strengthening strategies to synkinesis will result in poor outcomes and patient dissatisfaction. Increasing strength in the synkinetic patient does not improve expression.

Synkinesis causes more muscles to contract than are required for a particular expression. The aim of treatment is to diminish the unwanted, aberrant movements to reveal more appropriate expression. The concept is counterintuitive: in this case, more is not better. Too much movement actually impairs function.

We can think of each muscle of facial expression as having two base functions: (1) it performs a biomechanical action that displaces the skin in a specific direction; and (2) it expresses distinct emotional content. For example, when the ZYG muscles contract, the angle of the mouth is elevated. The corresponding emotional expression is smile or “happy.” When the DAO contracts, the angle of the mouth is depressed or pulled down. The corresponding emotional expression is frown or “sad.” When the two contract together during smile (a common pattern in synkinesis) the sum of ZYG + DAO equals a “sad” or “confused” smile as opposed to a “happy” one ( Fig. 9.6 ). The two opposing emotional states communicated simultaneously confound nonverbal communication: the message is unclear to the viewer. Additionally, the patient’s own proprioceptive sense detects the dichotomy between the two sides of the face resulting in self-consciousness and a lack of confidence which, in and of itself, can negatively impact social interactions.

Fig. 9.6

In the synkinetic patient opposing emotional states are communicated simultaneously, confounding nonverbal communication. In this case, the unaffected (right) side communicates happy (zygomaticus), whereas the synkinetic side communicates happy + sad (zygomaticus + depressor anguli oris).

The fNMR Process

fNMR addresses two separate but related issues in the synkinetic face:

  • 1.

    Increased muscle tone, spasm, and contracture at rest, resulting in rigidity and immobility.

  • 2.

    Abnormal motor patterns which impair/distort dynamic movement.

Appropriate intervention begins by first reducing elevated muscle tone. Rigidity caused by contracture must be reduced first to access the dynamic movement required for inhibiting synkinesis.

Reduce Resting Tone

Contracture is defined as a shortening of muscular or connective tissue that results in distortion or deformity. A tenet of rehabilitation medicine states that normal movement cannot be superimposed on abnormal tone. , Therefore, the first phase of fNMR for synkinesis is to decrease hypertonus. Increased facial tone, tightness, or rigidity may be noted in any area of the ipsilateral face. Although similar to a muscle spasm that reduces mobility and range of motion in any skeletal muscle, its presentation may not be as self-evident because the facial muscles move skin only and are not restricted by a biomechanical joint. The lack of dynamic movement caused by contracture can easily be mistaken for weakness.

The ipsilateral face may appear “full,” immobile, and contracted at rest. On palpation the tissues feel dense and rigid as compared with the contralateral side. Specific manifestations of hypertonus may include any or all of the following: deepened nasolabial fold (levators, ZYG), narrowed palpebral fissure (orbicularis oculi), retraction at the angle of the mouth (ZYG, risorius [RIS], BUC), dimpling of the chin (mentalis [MEN]), depression of the angle of the mouth (DAO, DLI, PLA), and banding of the neck (PLA). Increased tone of the orbicularis oris may present as a thickening or “puffiness” of the lips ( Fig. 9.7 ).

Fig. 9.7

Vectors of hypertonic muscles at rest indicated by blue arrows . These include corrugator, orbicularis oculi superioris and inferioris, levators, zygomaticus, buccinator, depressor anguli oris, mentalis, and platysma.

Patients frequently complain of “heaviness,” tightness, spasms, persistent discomfort, and pain with pressure. They may use the word “swollen” or “numb” to describe it. To develop an effective program, it is important to clarify whether “numb” is descriptive of trigeminal nerve impairment or a sensory perception associated with tightness/rigidity. Facial sensation is tested by having the patient close their eyes and respond affirmatively to a light touch over the three divisions of the trigeminal nerve. “Is it the same ‘numbness’ as going to the dentist?”; “Does it feel ‘heavy’ or ‘light’ compared to the unaffected side?” Such self-examination may lead a patient to become aware that what is perceived as “numbness” is actually a sensation associated with tightness, not weakness. In the absence of trigeminal involvement, guiding the patient to use alternative words to clarify the sensation provides another opportunity for explaining these counterintuitive concepts to improve understanding and reinforce new learning.

Soft Tissue Mobilization

Soft tissue mobilization elongates the contracted, tense muscles of the affected side, decreasing contracture and improving suppleness, mobility, and comfort. , , The basic technique consists of firm but gentle stretching of each affected muscle group in the opposite direction from which it contracts.

In the midfacial muscles, for example, the opposite thumb is placed inside the affected cheek while the second and third digits are placed on the facial skin over the target muscle as close to the origin as possible. Grasping the tissue between fingers and thumb, the cheek is slowly stretched toward and through the mouth. The patient or therapist may encounter trigger points, areas of discrete pain caused by focal contraction of that and nearby motor units. Pain will resolve with maintained gentle to moderate, not forceful, pressure ( Fig. 9.8 ).

Nov 21, 2021 | Posted by in OTOLARYNGOLOGY | Comments Off on Facial Neuromuscular Retraining for Synkinesis
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