Eyelid Rehabilitation in Post-Facial Paralysis With Synkinesis

Background

Eyelid paralysis, related to facial nerve injury, is a debilitating condition that causes significant functional impairment and cosmetic disfigurement. The most common eyelid and ocular sequelae resulting from facial paralysis include upper and lower lid retraction, lagophthalmos, exposure keratopathy, ectropion, ocular discomfort, visual deficit, and epiphora. Some of these changes can also contribute to corneal decompensation and psychosocial detriment. An additional potential long-term sequela is synkinesis due to aberrant regeneration of the facial nerve which can lead to differing cosmetic and functional impairments.

In non- or partially recovered eyelid paralysis with reduced neural input, the orbicularis muscle tone is deficient, which is what underlies the physical findings. This paralytic component, with resultant lack of orbicularis contraction, can lead to secondary cicatricial changes, manifesting as anterior lamellar shortage.

The upper eyelid has two retractors (levator aponeurosis and Mueller’s muscle) and a single protractor (orbicularis oculi). These two opposing muscle groups are in a state of equilibrium, which controls the upper lid position. In paralysis patients, eyelid position favors the retractors and the upper lid elevates and eyelid closure is reduced. In the lower eyelid, the orbicularis muscle provides resting tone to maintain eyelid position. Eyelid position is further maintained by supportive soft tissue structures including the tarsus and canthal tendons. The dynamic upward forces of these structures are in equilibrium versus gravity. As the orbicularis weakens in eyelid paralysis patients, unopposed gravitational pull leads to lower lid retraction and development of ectropion. The severity of the symptoms and clinical presentations of eyelid palsy depends on the varying changes of the upper and lower eyelid function.

The orbicularis oculi muscle also serves as a tear pump and thus contributes to tear film stability, which has an important protective role for the cornea and refractive role for visual acuity optimization. With paralysis, the upper and lower eyelid blink function is weakened. This can trigger symptoms related to tear film instability including tearing, red eyes, foreign body sensation, visual acuity fluctuations, and corneal breakdown or scarring. These latter issues can lead to permanent vision loss in severe cases of exposure keratopathy.

Although most of the literature has focused on managing complications related to acute and complete eyelid paralysis, many patients present with post-facial paralysis synkinesis, which can develop following any form of facial nerve injury. Although the exact mechanism of synkinesis is unknown, the most widely accepted theory is that of aberrant regeneration of axons at the site of injury. Newly sprouted or misdirected axons reinnervate both original and inappropriate facial muscles. This results in the involuntary contraction of muscles during volitional movement of another muscle group. Eyelid manifestations of synkinesis are therefore very different from acute or irreversible orbicularis deficit, as these patients develop no muscle weakness, but rather increased muscle tone.

One of the most common manifestations of synkinesis is involuntary eye closure with smiling, known as oral-ocular synkinesis. As opposed to the ocular symptoms associated with the paralytic component of eyelid paralysis, patients with synkinesis experience a different set of symptoms related to increased dynamic muscle tone. This in itself leads to functional impairment and cosmetic deformity which can significantly impact one’s quality of life. ^, Ocular synkinesis can manifest as excessive narrowing of eyelid aperture, pain, twitching, fatigue, or gustatory lacrimation that can be very distressing to the patient.

The degree of synkinesis may vary from slight asymmetry to significant deformity and severity often depends on the etiology and the grade of paralysis at onset. ^, Thorough evaluation and understanding of the patient’s disease process is crucial to counseling and treatment. Multiple tools for evaluation are available; however, there is no one reliable, validated measure to assess patients over time. Therapeutic measures for the treatment of synkinesis include physiotherapy, neuromodulation, and surgery. Management of ocular synkinesis is often challenging and optimal treatment can be limited.

Given the risk of adverse ocular consequences with facial palsy, appropriate management of the associated eyelid and ocular sequelae of this disease requires a thorough understanding of the biomechanics of eyelid function as well as facial anatomy and topography.