Facial Neuromuscular Retraining for Synkinesis

Introduction

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.

Synkinesis

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.

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.

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.

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.