Synkinesis is a neurological phenomenon characterized by the involuntary movement of one muscle group when a person intentionally attempts to move a different, unrelated group. This condition is a consequence of damage and subsequent misrepair of a cranial nerve, most often the facial nerve, which controls expression. It represents an abnormal recovery state following temporary nerve weakness or paralysis. The result is a lack of independent control over facial movements, which can affect daily functions and communication.
Defining Synkinesis
The word synkinesis literally translates from Greek as “simultaneous movement.” This condition is defined by an unwanted muscle contraction that accompanies a person’s deliberate facial expression. For instance, when an individual tries to smile, their eye on the affected side might involuntarily narrow or partially close. Synkinesis is not a new disease but rather a sequela, or after-effect, of an earlier nerve injury, such as from trauma, surgery, or Bell’s palsy.
The primary characteristic is the inability to isolate muscle movements on the affected side of the face. The message sent from the brain to initiate one action is incorrectly rerouted, causing other muscles, such as those around the eye or neck, to contract simultaneously. Synkinesis can range from subtle twitching to pronounced mass movement that significantly impacts facial symmetry and function. This simultaneous activation often causes the affected side of the face to feel tight and fatigued, even at rest.
The Neurological Basis of Synkinesis
Synkinesis develops due to aberrant regeneration of the facial nerve (the seventh cranial nerve). After the nerve is damaged, the axons—the projections that conduct electrical impulses—begin to regrow and seek out their target muscles. During this regeneration phase, the sheaths that normally guide the axons to their original destinations are often compromised or destroyed.
This disruption leads to “miswiring,” where regenerating axons grow toward the wrong target muscles, creating an abnormal circuit. For example, an axon originally destined for the mouth muscles might mistakenly grow toward the eye muscles instead. Consequently, a signal intended to produce a smile is sent through the misrouted axon, causing the eye to close simultaneously.
The entire facial nerve system on the affected side may also become over-excitable, leading to increased muscle tone and contracture even when the face is at rest. This hypertonicity contributes to a feeling of stiffness and can deepen the facial folds.
Typical Presentation of Facial Synkinesis
The most common manifestation of this miswiring is known as ocular-oral synkinesis, where movement of the mouth triggers an unwanted response around the eye. When a person attempts to smile, talk, or chew, the orbicularis oculi muscle involuntarily contracts, causing the eye to squint or narrow. The reverse can also occur, causing the corner of the mouth to pull upward when the person blinks or closes their eye tightly.
Another frequent presentation is cervical synkinesis, involving the neck and chin muscles. For example, a voluntary action like smiling can cause the platysma muscle in the neck to contract, creating visible neck banding or tightness. Many patients also experience mentalis involvement, where the chin develops an involuntary dimpling or puckering during facial movement.
A highly specific form of synkinesis is gustatory lacrimation, sometimes called Crocodile Tears Syndrome. This occurs when the nerve fibers intended for the salivary glands are misrouted to the lacrimal gland, which produces tears. As a result, the eye on the affected side begins to water or tear excessively while the person is eating or chewing.
Treatment and Management Strategies
The goal of managing synkinesis is to reduce involuntary movements and improve facial symmetry and function. The most common non-surgical strategies involve a combination of physical therapy and chemodenervation. Specialized physical therapy, often called neuromuscular retraining, is designed to help the patient consciously re-learn how to move individual muscle groups. This involves targeted exercises and biofeedback techniques to inhibit unwanted contractions while encouraging desired movements.
Botulinum Toxin Type A (BTX-A) injections are a primary treatment modality for controlling synkinesis symptoms. The toxin is injected directly into the overactive, miswired muscles, such as the orbicularis oculi or the platysma. BTX-A works by blocking the release of acetylcholine at the neuromuscular junction, temporarily weakening the muscle. This reduces the strength of the involuntary contraction, lessening the synkinetic movement and associated facial tightness. The effects of the injection are temporary, typically lasting three to four months, and the treatment is often used in conjunction with physical therapy.