Facial Retraining – Therapy



Physical and occupational therapists have been treating facial paralysis for decades. As early as 1927, physical therapy treatment of Bell’s palsy was advocated17 using treatment methods that have become “standard” in the decades since. Treatment modalities, originally developed for and successfully used on the extremities, were applied to the face. Gross facial exercises18,19, massage, electrical stimulation, and prosthetic devices or taping to lift a drooping, flaccid face were the treatments of choice.20-22 These non-specific procedures continue to be recommended and practiced today.

Traditional Therapy Techniques

Electrical Stimulation
Electrical stimulation continues to be widely used in the treatment of facial paralysis20,23 although there is mounting evidence that it may be contraindicated. It has been suggested that electrical stimulation may interfere with neural regeneration post peripheral nerve injury24,25 and studies proving its efficacy with facial muscles are lacking in the literature. A 1984 report by the National Center for Health Services Research concluded that “Electrotherapy treatment for Bell’s palsy…has no demonstrable beneficial effect in enhancing the functional or cosmetic outcomes in patients with Bell’s palsy.”26

Additionally, patients who undergo electrical stimulation acutely may demonstrate more synkinesis and mass action than those who do not.27 It is difficult to produce an isolated contraction of the facial muscles using electrical stimulation due to their small size and close proximity to each other. The contraction produced causes mass action which reinforces abnormal motor patterns and can be painful.20

Gross Exercises
Gross facial exercises are another staple in the therapy repertoire. However, because of their non-specificity, gross exercises typically given to patients reinforce abnormal movement patterns.28 Instructions such as “close your eyes as hard as you can”, “smile broadly” or “pucker your lips” do not produce the desired facial symmetry and control required for normalized facial function. The use of maximum effort exercises recruits excessive motor units producing patterns that differ from typical facial expressions which are gentle and fluid.


The ineffectiveness of traditional therapy methods for facial paralysis stems from their non-specificity and lack of adaptation to the unique characteristics of facial muscle.

Facial Muscles Differ from Skeletal Muscles

Facial muscle differs from most other skeletal muscle in several significant ways. Facial muscles:

– Lack muscle spindles29-32
– Have small motor units30,33
– Are relatively slow to degenerate10,34
– Receive emotional as well as volitional neural inputs.35

Muscle Spindles
The muscle spindle is the physiologic mechanism by which a muscle contraction is produced in response to a shortening of its fiber during a percutaneous stretch.36 Therapeutic facilitory techniques such as quick stretch, vibration and tapping rely upon the muscle spindle to stimulate muscle contraction.37 Because they lack spindles, the use of these techniques to elicit a contraction is ineffective in facial muscles.

Small Motor Units
A motor unit is defined as one motoneuron and all of the muscle fibers it innervates.38 The ratio of muscle fibers to motoneurons determines the refinement of a movement. In the facial muscles the ratio is approximately 25 muscle fibers to one motoneuron allowing great complexity of movement compared to limb muscles which have a much higher ratio (e.g. 2000 muscle fibers to one motoneuron in the gastrocnemius)33. The intricacy of movement that can be achieved by the facial muscles should preclude the use of maximum effort, gross exercises, where motor units other than those targeted are recruited due to overflow39.

Resistance to Degeneration
Facial muscle appears to resist degeneration post denervation for longer periods of time than other skeletal muscle, and may remain viable for three or more years.10,34 Because of this unique characteristic, the use of electrical stimulation to maintain viability of facial muscle during regeneration is unfounded.

Cortical Connections for Emotional Expression
There is a well-established distinction between volitional and emotional facial movements.35 Volitional movements of the face use different upper motor neuron pathways (pyramidal tract) than those used for emotional movements (extrapyramidal motor system). The use of emotional inputs during neuromuscular retraining may be helpful to reestablish more natural motor control post paralysis.

Lack of Specific Clinical Training
Most therapists receive no specialized training in facial muscle anatomy, physiology, or specific facial therapy techniques. The peripheral nerve injured facial paralysis patient has been treated ineffectively; therapy has been initiated too early and terminated too soon, before neural recovery had taken place. The naturally occurring spontaneous recovery of patients with Bell’s palsy reinforced the seeming “appropriateness” of whatever treatment modality was utilized. After 6 to 12 months, patients who did not regain function were classified as “chronic” with no further therapy attempted. No techniques were described for treating the aberrant, unsynchronous facial movements that characterize synkinesis. Given the non-specific nature of the therapy provided, it is not surprising that many clinicians found the treatment of facial paralysis to be frustrating and ineffective.40


Specific neuromuscular retraining techniques for facial paralysis appeared in the literature 30 years ago.41-45 Patients demonstrated improved facial function using EMG feedback to modify the manner in which they contracted their muscles. A comprehensive review of case studies using similar techniques is presented by Balliet.46 More recent studies have included both acute (less than 1 year post) and post acute patients and the effect of spontaneous recovery of function could not be ruled out.47,48

In 1982, Balliet, et. al. described a comprehensive clinical program that combined EMG feedback, mirror exercises and detailed, individualized home exercise programs and demonstrated improved function with patients more than two years post facial nerve injury.46 The authors hypothesized that brain plasticity, the capacity of the central nervous system to modify its organization to bring about lasting functional change, explained the acquisition of new motor behaviors in the post acute patient.

In 1991, Ross, et al 49 compared two treatment groups with a third control group that received no treatment. All patients were more than 18 months post injury to control for spontaneous recovery effect. After comprehensive evaluation, one group was trained with EMG and mirror feedback, while the second group used mirror feedback alone. Patients were reevaluated after one year of treatment. A significant difference was found between the treatment groups and the control group. Patients in both treatment groups demonstrated improvements in facial motor control, excursion of movement and decreased synkinesis. The control group showed no change, or decreased function. A follow-up study one year later concluded that gains acquired during treatment had been maintained without continued therapy.50

It is clear from research thus far, that the application of neuromuscular retraining techniques specifically designed for the treatment of facial paralysis can effectively reduce sequelae after facial nerve injury.