Long-standing and chronic facial palsies represent multifaceted medical conditions with multiple etiologies ranging from Bell’s palsy and trauma to iatrogenic and neoplastic causes. The epidemiological impact is significant, affecting individuals across all demographics. This has profound implications for emotional well-being and social interaction. The impairment of facial movements can severely compromise quality of life, given the face’s role in expression and communication.

The spectrum of facial paralysis manifests in various forms. Flaccid facial paralysis denotes a complete loss of muscle tone and movement. Contrarily, postparalysis synkinesis reflects involuntary muscle contractions from aberrant reinnervation, leading to unwanted facial movements as is the case with crocodile tear syndrome. Mixed paralysis features regions of flaccidity alongside areas of synkinetic activity, whereas isolated muscle paralysis, such as congenital unilateral lower lip palsy (CULLP), is characterized by singular, unilateral muscular dysfunction ( Fig. 35.1 ). The resultant asymmetry and functional loss pose unique reconstructive challenges to restore facial symmetry and expression.

Spectrum of facial paralysis before and after treatment by any indicated method. (A) Flaccid facial paralysis, showing unilateral complete loss of muscle tone and movement. (B) Post-paralysis synkinesis, showing residual right lower facial weakness and involuntary contraction of the right eyelid muscles. (C) Mixed paralysis, depicting loss of the left nasolabial crease and hypercontraction of the muscles at the left oral commissure. (D) Isolated muscle paralysis, as seen in congenital unilateral lower lip palsy (CULLP). With permission from the Center for Advanced Facial Plastic Surgery.

The management of flaccid versus synkinesis necessitates distinct therapeutic strategies, as they present very different functional and aesthetic issues. In the periorbital region, flaccid paralysis results in lagophthalmos and a widened palpebral aperture which, if untreated can lead to corneal ulceration and blindness. Conversely, synkinesis can result in peripheral visual defects due to narrowed palpebral aperture. Synkinetic brow dysfunction (SBD), distinct from flaccid brow paralysis, arises from the synkinesis-induced co-contraction of the frontalis muscle with other brow depressor muscles like the corrugator. This can result in a “frozen eyebrow” effect and a limited range of movement, creating appearances ranging from depressed to hypercontracted eyebrows. This form of brow palsy is characterized by hypertonicity and involuntary muscle contractions rather than a complete paralysis of the frontalis muscle.

In the midface and lower face, flaccid paralysis is characterized by a complete or near-complete absence of muscular movements and tone, resulting in ptosis of the face and modiolus, effacement of the nasolabial folds, and a complete inactivity of the smile mechanism. Midface and lower face synkinesis, on the other hand, most often presents with a normal appearance at rest. Smile dysfunction is a result of overactivity of the buccinator, depressor anguli oris (DAO), and platysma. Similarly, synkinetic unilateral lower lip palsy (SULLP) mimics the cosmetic appearance of flaccid CULLP but is actually due to co-contractions involving the depressor labii inferioris (DLI) and mentalis muscle following aberrant neural regeneration. This co-activation pattern leads to complex facial dynamics and asymmetries, particularly in the lower face, which can complicate the restorative efforts. ^, These details highlight the nuanced differences in pathophysiology between these types of paralysis, underscoring the complexity of diagnosis and the importance of targeted therapeutic interventions.

Optimal outcomes in facial palsy treatment are achieved when a multimodality approach is used, typically with surgery as the first-line treatment. Surgical procedures such as modified selective neurectomy, gracilis muscle transfer, cross facial nerve graft, cranial nerve substitution techniques, temporalis myoplasty, static sling, and aesthetic procedures are the cornerstone of treatments for patients with facial palsy. Noninvasive treatments and neuromuscular retraining (NMR) also play a critical role in addressing this complex neurological disorder. The dichotomy between flaccid paralysis and synkinesis, each with its distinct pathophysiology and clinical manifestations, underscores the necessity for a tailored, patient-specific approach in treatment. This background forms the cornerstone upon which the efficacy of office-based treatments such as botulinum toxin A (BTX), dermal fillers, and NMR therapy can be further explored throughout this chapter.

Upon first encounter with patients with facial paralysis, it is imperative that the clinician takes a detailed history and physical prior to starting treatment. This detailed assessment enables the physician to create a tailored treatment plan, utilizing combinations of chemodenervation, filler, NMR, and/or surgery. It also gives patients time to determine the course of action with which they feel most comfortable. While surgical options remain critical in the treatment of facial paralysis, the growing importance of nonsurgical NMR and soft-tissue mobilization (STM) in conjunction with a multimodal treatment is paramount in achieving the most optimal outcomes. As a patient undergoes treatment, it is critical to have photo documentation as well as records of injection sites to have objective data to trend throughout the length of treatment.

Facial NMR and STM, initially described in 1983, are invaluable nonsurgical tools for treating peripheral facial nerve disorders. They are specifically indicated for patients with synkinesis. For patients with mixed facial palsy, paresis, or synkinesis, we recommend starting with NMR with STM as soon as possible with a facial therapy specialist. Patients with flaccid paralysis will not benefit from this therapy since there would not be any movement without a functioning nerve. Hence, the NMR model truly holds most value once the facial nerve begins to recover, in the case of complete facial nerve paralysis. It should be noted that the goal of NMR is focused more on coordination instead of strength, while STM (stretching, massage, etc.) helps decrease muscle contracture and spasm that may otherwise limit excursion and range of motion. Still, patients must be well informed with regard to interventions for flaccid paralysis such as eye care, gentle stroking of the affected side for sensory awareness, and letting the muscles rest in the flaccid period. Attempts at muscle activation may paradoxically strengthen the contralateral side and worsen asymmetry.

There are a variety of toxins used for chemodenervation in facial paralysis. Onabotulinumtoxin A, commonly referred to as BOTOX (BTX), is used the most frequently for patients with synkinesis or hyperkinesis. Injection of BTX into the spastic muscle irreversibly blocks the release of acetylcholine at the neuromuscular junction, resulting in muscle paralysis that begins within a few days and peaks by 2 weeks. This effect continues until the new axon terminals regain synaptic contact with the muscle, which usually takes between 3 and 6 months. ^,

Patients with flaccid paralysis may desire a more natural and symmetric appearance at rest prior to their reanimation surgery. In these instances, BTX is injected into the contralateral functioning muscle to balance movement with the paralyzed side, creating a more symmetric facial appearance at rest. In patients with partial facial neuromuscular recovery who develop synkinesis, BTX is used on the ipsilateral affected side to help minimize the synkinetic movement and potential pain that may be present. Some patient populations have isolated muscle paralysis, such as in CULLP, and BTX on the unaffected side helps restore symmetry both at rest and with movement.

Similar to its use in facial paralysis, BTX has shown promise in other conditions. Vázquez-Costa et al. conducted a pilot study on the use of BTX-A for treating spasticity in amyotrophic lateral sclerosis (ALS) patients. The study found that all treated patients experienced improvement in walking speed and functional ambulation status. The study suggests that BTX-A could be considered as part of a comprehensive neurorehabilitation program in carefully selected ALS patients.

Overall, BTX is a safe procedure for the majority of the population, but there are a few absolute and relative contraindications. Absolute contraindications include a known BTX allergy or previous adverse reaction, pregnancy or lactation, ongoing local infections at the treatment sites, peripheral motor neuropathies, and neuromuscular diseases such as myasthenia gravis. Patients on anticoagulation medications and some herbal supplements that result in anticoagulation as well such as ginseng and Ginkgo biloba may have increased risk of bruising and hematoma formation postinjection.

Similarly, within the realm of nonsurgical injectable treatments for facial palsy, there exist a number of dermal fillers that can be used to create facial symmetry. They are primarily classified by their source or their longevity in tissues. Sources for fillers include human-derived, animal-derived, and synthetically derived, and they typically last along one of three timeframes: temporary, semipermanent, and permanent. ^, Furthermore, they are separated into moderate and long-duration biodegradable fillers versus nonbiodegradable fillers. Further classifications exist, such as varying degrees of fluidity and flexibility (G′) and particulate versus nonparticulate, though longevity of activity remains among the most clinically pertinent forms of classification.

Common dermal fillers include collagen, autologous fat, hyaluronic acid (HA), poly-L-lactic acid (PLLA), calcium hydroxylapatite (CaHA), and polymethylmethacrylate (PMMA). HA and its derivatives are some of the most commonly used facial dermal fillers. Given their ability to be degraded by the body naturally via hyaluronidase, total degradation generally occurs within 6 to 12 months. Other biodegradable fillers such as CaHA and PLLA stimulate surrounding cells to produce collagen and mild inflammation, thus leading to an average duration of effect from 15 months to 2 years. ^, Nonbiodegradable fillers such as PMMA stimulate a foreign body response with the consequent fibroelastic deposition of collagen; this allows for the PMMA to become integrated into the soft tissue, hence being the longest-lasting in duration, ranging from 1 year to 5 years. ^,

Indications and preference for dermal filler may be influenced by a patient’s desired outcomes as well as the location of the affected anatomy. Muscle atrophy is an indication for filler in patients with facial paralysis as filler may help reduce the cosmetic effects of this atrophy. To this end, fillers are used in facial contouring and volume restoration, specifically around the cheek, tear trough, and chin. Facial dermal fillers also play a role in depressed scar restoration as well as systemic diseases such as lipodystrophy or dermal atrophy.