Synkinesis

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Synkinesis
Specialty Neurology

Synkinesis is a neurological symptom in which a voluntary muscle movement causes the simultaneous involuntary contraction of other muscles. An example might be smiling inducing an involuntary contraction of the eye muscles, causing a person to squint when smiling. Facial and extraocular muscles are affected most often; in rare cases, a person's hands might perform mirror movements.

Contents

Synkinesis is usually caused by dysfunction of a particular nerve. Potential causes include improper healing after nerve trauma or neurodegeneration, as occurs in Parkinson's disease. In congenital cases, mutations of genes involved in nerve growth, specifically axonal growth have been found. Rarely, it occurs as part of syndromes with neuroendocrine problems, such as Kallman syndrome. The prognosis is usually good with normal intelligence and lifespan. Treatment depends on the cause, but is largely conservative with facial retraining or mime therapy, if needed, while Botox and surgery are used as last resort.

Types

Most cases involve the cranial nerves, which innervate many small cranial muscles, such as the facial muscles and the extraocular muscles. This is in contrast to areas of body where miswiring of the larger muscles is less evident due to the size of the muscles. Synkinesis can also involve the upper limbs, especially hands which is quite rare, at 1 case in 1 million. [1] In some cases, nerves improperly regenerate into glands, such as lacrimal glands, leading to a condition known as crocodile tears or Bogorad's syndrome.

Facial synkinesis

Facial synkinesis is a common sequela to Idiopathic Facial Nerve Paralysis, also called Bell's Palsy or Facial Palsy. [2] Bell's Palsy, which is thought to occur due to a viral reactivation which can lead (through unknown mechanisms) to diffuse axon demyelination and degeneration of the seventh cranial nerve, results in a hemifacial paralysis due to non-functionality of the nerve. As the nerve attempts to recover, nerve miswiring results (see Mechanism of Action below). In patients with severe facial nerve paralysis, facial synkinesis frequently develops. [3] Additionally, a common treatment option for facial palsy is to use electrical stimulation. Unfortunately, this has been shown to be disruptive to normal re-innervation and can promote the development of synkinesis. [4] The most common symptoms of facial synkinesis include: [5]

Extra-ocular muscle synkinesis

The six muscles around the eye (extraocular muscles) are innervated by three different cranial nerves: Abducens (6th nerve), Trochlear (4th nerve), and Oculomotor (3rd nerve). After nerve trauma around the eye, a combination of any two of these three cranial nerves have been shown to be involved with extra-ocular synkinesis. Moreover, while the abducens and the trochlear nerve each innervate one specific muscle, the oculomotor nerve has many functions including eyelid retraction and pupil constriction. Thus, during synkinesis, one of these functions may be involved. Examples include:

Other less common variations of synkinesis involving the cranial nerves include:

Bimanual Synkinesis

Bimanual Synkinesis occurs when left and right upper limbs, especially the hands and fingers execute exactly the same movement even though only one hand is intentionally moved. It is also called "mirror hand movements" and persists throughout life. When it occurs by itself without other associated signs and symptoms it is associated with normal intelligence and lifespan. It can also develop in the course of Parkinson's disease. [1] In association with other abnormalities, mirror hand movements are a hallmark of Kallmann syndrome.

Genetic mutations associated with (congenital) mirror hand movements are in the DCC (gene) or RAD51 gene, which account for about 35 percent of cases. [1] In DCC mutation, impaired or missing netrin 1 receptor protein impairs control of axon growth during nervous system development. [1]

Causes

Almost all cases of synkinesis develop as a sequel to nerve trauma. (The exception is when it is congenitally acquired as in Duane-Retraction Syndrome and Marcus Gunn phenomenon.) Trauma to the nerve can be induced in cases such as surgical procedures, nerve inflammation, neuroma, [12] and physical injury. [7]

Mechanism

There are three proposed mechanisms for synkinesis: aberrant nerve regeneration, interneuronal ephaptic transmission, and nuclear hyperexcitability.

Aberrant nerve regeneration

The aberrant nerve regeneration hypothesis is the most widely accepted mechanism for synkinesis. [13] The hypothesis states that, after trauma, axons project from the facial nucleus to incorrect peripheral muscle groups. These aberrant branches can simultaneously innervate different subdivisions of the facial nerve. [3]

For example: compression to the facial nerve causes a lesion and the set of axons that innervates the orbicularis oris (mouth muscle) degenerate. Once the compression has relieved, regeneration of axons from the lesion site begins. This time though, only 50% of the set of axons that innervate the orbicularis oris successfully reinnervate the original site. The other half aberrantly branched off and innervated the orbicularis oculi(eye muscle). Thus, when the patient purses their lips, the ipsilateral eye will squint.

The hypothesis assumes that disorganized regeneration occurs at the site of the lesion. On the contrary, recent research by Choi and Raisman [14] has provided a more thorough understanding of synkinesis through aberrant axonal regeneration. Their study has shown that regenerating axons become disorganized throughout the length of the nerve and not only at the site of the lesion. Previously, many developed treatment strategies (that inevitably failed) were invented based on the original hypothesis by only focusing on the lesion site for improving the organization of regeneration. The new modification to the hypothesis could allow for better success in developing treatments.

Ephaptic transmission

Ephaptic transmission is when two nerves communicate with each other via an artificial synapse between nerves. Healthy peripheral nerves are insulated with a myelin sheath that helps to both enhance electric transmission and to prevent cross-talk between parallel nerves. After a lesion, it has been observed that regenerating nerves might not be myelinated effectively. Consequently, the two nerve fibers can come into contact and provide a means for an impulse to be directly conducted through the nerve membrane. An analogy for this is having two uninsulated electrical wires placed adjacent to each other. Thus, the two nerves are able to “cross-talk” and send action potentials in both directions. [15]

Nuclear hyperexcitability

The basis of this hypothesis is as follows: after a lesion, axonal degeneration (via Wallerian degeneration) occurs. The post-synaptic cell consequently becomes deprived of input and becomes more sensitive to neurotransmitters (e.g. creating additional receptors). Subsequently, nearby residual undamaged axons can provide a source of neurotransmitter to the deprived post-synaptic cell. Since the post-synaptic cell is hypersensitive, the neurotransmitters that reach it from an axon of another nerve will successfully provide stimulation. This consequently creates undesired peripheral movement (i.e. synkinesis). [16]

Although these three mechanisms have been argued for and against in various ways, it has become more accepted that synkinesis develops through a combination of these mechanisms.

Diagnosis

Measurement

Until May 2007, there was no clinical scale to measure synkinesis. A study led by Mehta et al. [5] has validated the use of a newly designed instrument to evaluate facial synkinesis called the Synkinesis Assessment Questionnaire (SAQ). The instrument, consisting of nine questions, was found to be both reliable and valid. In addition, it is simple, easy to administer, and inexpensive. Its analyses can allow for treatment options to be evaluated.

Treatment

Experimental research for treatment has been mostly focused on facial synkinesis due to its abundant prevalence compared to extra-ocular synkinesis. Additionally, since the extra-ocular muscles are hidden within the orbits, there is a limit on the type of practical treatments that can be established (e.g. massage). Treatments for synkinesis in general include facial retraining, biofeedback, mime therapy, and Botox and surgery, as a last resort.

Facial retraining

Facial retraining therapy builds upon the idea that neurons are constantly in a dynamic state. In other words, there is constant growth and regression of neuronal projections dependent on the stimuli produced. To reduce synkinesis, facial retraining teaches the patient techniques for increasing wanted movements while focusing on restricting unwanted movement. If, for example, the mouth moves whenever the eyes blink voluntarily, facial retraining techniques will teach the patient to slowly close the eyes while actively focusing on keeping the mouth muscles still. Facial retraining has shown to be very successful with almost a 60-70% average decrease in synkinesis reported after 7 months. [18]

Biofeedback

Biofeedback therapy for facial synkinesis aims to increase the patient's awareness of the facial muscle posture and movement. Facial muscles contain few to none intrinsic muscle sensory receptors (used for proprioceptive feedback) and additionally they do not span movable joints and so lack joint receptors (another source for proprioceptive feedback). [18] Thus, biofeedback allows the patient to actively sense the motion of their muscles. The two common forms of biofeedback used are electromyographic feedback and mirror feedback. Electromyographic feedback includes visual EMG signals (coming from facial muscle sites displayed to the patient from a computer in the form of waveform traces) or auditory signals that indicate strength of muscle contraction. [19] The subsequent role of the patient is to control the movement of undesired muscle during volitional movement by incorporating the information perceived through the EMG. While mirror feedback is a much more basic way of providing the patient feedback on muscle movement, studies have shown that both are very effective options for synkinesis/paresis reduction. [20] Biofeedback is commonly coupled to facial retraining techniques to achieve maximal effectiveness.
A study by Nakamura et al. has shown that biofeedback works better for prevention of synkinesis as opposed to treatment of synkinesis. Due to the extreme efforts needed to achieve improvements during synkinesis, Nakamura et al. observed that patients will often fail to reach their desired goal because of the difficulty of maintaining motivation during training. The desired course of action is to catch the patient shortly after facial nerve trauma and teach the patient biofeedback techniques. This course of action has been experimentally proven to significantly reduce the development of synkinesis. [3]

Mime therapy

Mime therapy was introduced in the Netherlands in 1980. [21] It was initially designed to treat facial palsy by improving symmetry of the face both at rest and during movement. It was then later observed that people who had post-facial palsy synkinesis also benefited from this therapy. It wasn't until 2003 that Beurskens and Heymans were able to experimentally conclude that mime therapy was indeed a good treatment choice for synkinesis. Furthermore, later studies by Beurskens et al. have shown that benefits obtained from mime therapy are stable one year after therapy. [22] Current mime therapy consists of a combination of procedures designed to promote symmetry of the face at rest and during movement to control synkinesis. The components include: massage, stretching exercises, exercises to coordinate both halves of the face, etc. [2] The overall aim of mime therapy is to develop a conscious connection between the use of facial muscles and emotional expression. While facial retraining therapy is more focused on treating slight synkinetic movements, mime therapy aims to increase the overall vigor of the muscles through active exercises, while in the process of doing so, teaching the face to decrease unwanted synkinetic movements.

Botox

Botox (botulinum toxin) is a new and versatile tool for the treatment of synkinesis. Initially used for reducing hyperkinesis after facial palsy, [23] Botox was later attempted on patients with post-facial palsy synkinesis to reduce unwanted movements. The effects of Botox have shown to be remarkable, with synkinetic symptoms disappearing within 2 or 3 days. The most common treatment targets are the orbicularis oculi, depressor anguli oris (DAO), mentalis, platysma and the contralateral depressor labii inferioris muscles. [24] Due to the short span of Botox effects though, patients must come back to the doctor for re-injection approximately every 3 months. More notable is that in a majority of patients, various synkinetic movements completely disappeared after 2-3 sessions of trimonthly Botox injections. [25] A more specific synkinesis, crocodile tears syndrome (hyperlacrimation upon eating), has been shown to respond exceedingly well to Botox injection. Botox is injected directly into the lacrimal gland and has shown to reduce hyperlacrimation within 24–48 hours. The procedure was shown to be simple and safe with very little chance of side-effects (although on rare occasions ptosis can occur due to botulinum toxin diffusion). [6] Furthermore, reduction in hyper-lacrimation was shown to last longer than the expected 3 months (about 12 months). [25] Since Botox can mimic facial paralysis, an optimized dose has been determined that reduces involuntary synkinesis of the muscle while not affecting muscle tone. [25]

Surgery

Practical surgical procedures used for treating synkinesis are neurolysis and selective myectomy. Neurolysis has been shown to be effective in relieving synkinesis but only temporarily and unfortunately symptoms return much worse than originally. [26] Selective myectomy, in which a synkinetic muscle is selectively resected, is a much more effective technique that can provide permanent relief and results in a low recurrence rate; post-operative complications may include edema, hematoma, and ecchymosis. [3]

See also

Related Research Articles

<span class="mw-page-title-main">Ramsay Hunt syndrome type 2</span> Presentation of shingles in the geniculate ganglion

Inflammation of the geniculate ganglion of the facial nerve is a late consequence of varicella zoster virus (VZV) known as Ramsay Hunt syndrome (RHS), commonly known as herpes zoster oticus. In regard to the frequency, less than 1% of varicella zoster infections involve the facial nerve and result in RHS. It is traditionally defined as a triad of ipsilateral facial paralysis, otalgia, and vesicles close to the ear and auditory canal. Due to its proximity to the vestibulocochlear nerve, the virus can spread and cause hearing loss, tinnitus (hearing noises that are not caused by outside sounds), and vertigo. It is common for diagnoses to be overlooked or delayed, which can raise the likelihood of long-term consequences. It is more complicated than Bell's palsy. Therapy aims to shorten its overall length, while also providing pain relief and averting any consequences.

<span class="mw-page-title-main">Cranial nerves</span> Nerves that emerge directly from the brain and the brainstem

Cranial nerves are the nerves that emerge directly from the brain, of which there are conventionally considered twelve pairs. Cranial nerves relay information between the brain and parts of the body, primarily to and from regions of the head and neck, including the special senses of vision, taste, smell, and hearing.

<span class="mw-page-title-main">Bell's palsy</span> Facial paralysis resulting from dysfunction in the cranial nerve VII (facial nerve)

Bell's palsy is a type of facial paralysis that results in a temporary inability to control the facial muscles on the affected side of the face. In most cases, the weakness is temporary and significantly improves over weeks. Symptoms can vary from mild to severe. They may include muscle twitching, weakness, or total loss of the ability to move one or, in rare cases, both sides of the face. Other symptoms include drooping of the eyebrow, a change in taste, and pain around the ear. Typically symptoms come on over 48 hours. Bell's palsy can trigger an increased sensitivity to sound known as hyperacusis.

<span class="mw-page-title-main">Abducens nerve</span> Cranial nerve VI, for eye movements

The abducens nerve or abducent nerve, also known as the sixth cranial nerve, cranial nerve VI, or simply CN VI, is a cranial nerve in humans and various other animals that controls the movement of the lateral rectus muscle, one of the extraocular muscles responsible for outward gaze. It is a somatic efferent nerve.

<span class="mw-page-title-main">Facial nerve</span> Cranial nerve VII, for the face and tasting

The facial nerve, also known as the seventh cranial nerve, cranial nerve VII, or simply CN VII, is a cranial nerve that emerges from the pons of the brainstem, controls the muscles of facial expression, and functions in the conveyance of taste sensations from the anterior two-thirds of the tongue. The nerve typically travels from the pons through the facial canal in the temporal bone and exits the skull at the stylomastoid foramen. It arises from the brainstem from an area posterior to the cranial nerve VI and anterior to cranial nerve VIII.

<span class="mw-page-title-main">Oculomotor nerve</span> Cranial nerve III, for eye movements

The oculomotor nerve, also known as the third cranial nerve, cranial nerve III, or simply CN III, is a cranial nerve that enters the orbit through the superior orbital fissure and innervates extraocular muscles that enable most movements of the eye and that raise the eyelid. The nerve also contains fibers that innervate the intrinsic eye muscles that enable pupillary constriction and accommodation. The oculomotor nerve is derived from the basal plate of the embryonic midbrain. Cranial nerves IV and VI also participate in control of eye movement.

<span class="mw-page-title-main">Pyramidal tracts</span> Include both the corticobulbar tract and the corticospinal tract

The pyramidal tracts include both the corticobulbar tract and the corticospinal tract. These are aggregations of efferent nerve fibers from the upper motor neurons that travel from the cerebral cortex and terminate either in the brainstem (corticobulbar) or spinal cord (corticospinal) and are involved in the control of motor functions of the body.

<span class="mw-page-title-main">Medial longitudinal fasciculus</span> Nerve tracts in the brainstem

The medial longitudinal fasciculus (MLF) is an area of crossed over tracts, on each side of the brainstem. These bundles of axons are situated near the midline of the brainstem. They are made up of both ascending and descending fibers that arise from a number of sources and terminate in different areas, including the superior colliculus, the vestibular nuclei, and the cerebellum. It contains the interstitial nucleus of Cajal, responsible for oculomotor control, head posture, and vertical eye movement.

<span class="mw-page-title-main">Lateral rectus muscle</span> Muscle on lateral side of the eye

The lateral rectus muscle is a muscle on the lateral side of the eye in the orbit. It is one of six extraocular muscles that control the movements of the eye. The lateral rectus muscle is responsible for lateral movement of the eyeball, specifically abduction. Abduction describes the movement of the eye away from the midline, allowing the eyeball to move horizontally in the lateral direction, bringing the pupil away from the midline of the body.

<span class="mw-page-title-main">Abducens nucleus</span>

The abducens nucleus is the originating nucleus from which the abducens nerve (VI) emerges—a cranial nerve nucleus. This nucleus is located beneath the fourth ventricle in the caudal portion of the pons near the midline, medial to the sulcus limitans.

<span class="mw-page-title-main">Ciliary ganglion</span> Bundle of nerves, parasympathetic ganglion

The ciliary ganglion is a bundle of nerves, parasympathetic ganglion located just behind the eye in the posterior orbit. It is 1–2 mm in diameter and in humans contains approximately 2,500 neurons. The ganglion contains postganglionic parasympathetic neurons. These neurons supply the pupillary sphincter muscle, which constricts the pupil, and the ciliary muscle which contracts to make the lens more convex. Both of these muscles are involuntary since they are controlled by the parasympathetic division of the autonomic nervous system.

<span class="mw-page-title-main">Sixth nerve palsy</span> Medical condition

Sixth nerve palsy, or abducens nerve palsy, is a disorder associated with dysfunction of cranial nerve VI, which is responsible for causing contraction of the lateral rectus muscle to abduct the eye. The inability of an eye to turn outward, results in a convergent strabismus or esotropia of which the primary symptom is diplopia in which the two images appear side-by-side. Thus, the diplopia is horizontal and worse in the distance. Diplopia is also increased on looking to the affected side and is partly caused by overaction of the medial rectus on the unaffected side as it tries to provide the extra innervation to the affected lateral rectus. These two muscles are synergists or "yoke muscles" as both attempt to move the eye over to the left or right. The condition is commonly unilateral but can also occur bilaterally.

<span class="mw-page-title-main">Facial motor nucleus</span>

The facial motor nucleus is a collection of neurons in the brainstem that belong to the facial nerve. These lower motor neurons innervate the muscles of facial expression and the stapedius.

<span class="mw-page-title-main">Fazio–Londe disease</span> Medical condition

Fazio–Londe disease (FLD), also called progressive bulbar palsy of childhood, is a very rare inherited motor neuron disease of children and young adults and is characterized by progressive paralysis of muscles innervated by cranial nerves.

<span class="mw-page-title-main">Marcus Gunn phenomenon</span> Medical condition

Marcus Gunn phenomenon is an autosomal dominant condition with incomplete penetrance, in which nursing infants will have rhythmic upward jerking of their upper eyelid. This condition is characterized as a synkinesis: when two or more muscles that are independently innervated have either simultaneous or coordinated movements.

<span class="mw-page-title-main">Oculomotor nerve palsy</span> Medical condition

Oculomotor nerve palsy or oculomotor neuropathy is an eye condition resulting from damage to the third cranial nerve or a branch thereof. As the name suggests, the oculomotor nerve supplies the majority of the muscles controlling eye movements. Damage to this nerve will result in an inability to move the eye normally. The nerve also supplies the upper eyelid muscle and is accompanied by parasympathetic fibers innervating the muscles responsible for pupil constriction. The limitations of eye movement resulting from the condition are generally so severe that patients are often unable to maintain normal eye alignment when gazing straight ahead, leading to strabismus and, as a consequence, double vision (diplopia).

The term gaze is frequently used in physiology to describe coordinated motion of the eyes and neck. The lateral gaze is controlled by the paramedian pontine reticular formation (PPRF). The vertical gaze is controlled by the rostral interstitial nucleus of medial longitudinal fasciculus and the interstitial nucleus of Cajal.

<span class="mw-page-title-main">Cranial nerve disease</span> Impaired functioning of one of the twelve cranial nerves

Cranial nerve disease is an impaired functioning of one of the twelve cranial nerves. Although it could theoretically be considered a mononeuropathy, it is not considered as such under MeSH.

<span class="mw-page-title-main">Smile surgery</span> Surgical procedure to restore smile

Smile surgery or smile reconstruction is a surgical procedure that restores the smile for people with facial nerve paralysis. Facial nerve paralysis is a relatively common condition with a yearly incidence of 0.25% leading to function loss of the mimic muscles. The facial nerve gives off several branches in the face. If one or more facial nerve branches are paralysed, the corresponding mimetic muscles lose their ability to contract. This may lead to several symptoms such as incomplete eye closure with or without exposure keratitis, oral incompetence, poor articulation, dental caries, drooling, and a low self-esteem. This is because the different branches innervate the frontalis muscle, orbicularis oculi and oris muscles, lip elevators and depressors, and the platysma. The elevators of the upper lip and corner of the mouth are innervated by the zygomatic and buccal branches. When these branches are paralysed, there is an inability to create a symmetric smile.

Alternating hemiplegia is a form of hemiplegia that has an ipsilateral cranial nerve palsies and contralateral hemiplegia or hemiparesis of extremities of the body. The disorder is characterized by recurrent episodes of paralysis on one side of the body. There are multiple forms of alternating hemiplegia, Weber's syndrome, middle alternating hemiplegia, and inferior alternating hemiplegia. This type of syndrome can result from a unilateral lesion in the brainstem affecting both upper motor neurons and lower motor neurons. The muscles that would receive signals from these damaged upper motor neurons result in spastic paralysis. With a lesion in the brainstem, this affects the majority of limb and trunk muscles on the contralateral side due to the upper motor neurons decussation after the brainstem. The cranial nerves and cranial nerve nuclei are also located in the brainstem making them susceptible to damage from a brainstem lesion. Cranial nerves III (Oculomotor), VI (Abducens), and XII (Hypoglossal) are most often associated with this syndrome given their close proximity with the pyramidal tract, the location which upper motor neurons are in on their way to the spinal cord. Damages to these structures produce the ipsilateral presentation of paralysis or palsy due to the lack of cranial nerve decussation before innervating their target muscles. The paralysis may be brief or it may last for several days, many times the episodes will resolve after sleep. Some common symptoms of alternating hemiplegia are mental impairment, gait and balance difficulties, excessive sweating and changes in body temperature.

References

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  15. ↑ Sadjadpour K. (1975). "After Postfacial palsy phenomena: faulty nerve regeneration or ephaptic transmission?". Brain Res. 95 (2–3): 403–6. doi:10.1016/0006-8993(75)90117-1. PMID   168941. S2CID   41333187.
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  20. ↑ Ross B, Nedzelski JM, McLean JA (1991). "Efficacy of feedback training in long-standing facial nerve paresis". Laryngoscope. 101 (7): 744–50. doi:10.1288/00005537-199107000-00009. PMID   2062155. S2CID   44951069.
  21. ↑ Beurskens CH, Heymans PG (2003). "Positive effects of mime therapy on sequelae of facial paralysis: stiffness, lip mobility, and social and physical aspects of facial disability". Otol. Neurotol. 24 (4): 677–81. doi:10.1097/00129492-200307000-00024. PMID   12851564. S2CID   15792060.
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  26. ↑ May, Mark; Barry M. Schaitkin (1999). The Facial Nerve. Thieme. p. 467. ISBN   0-86577-821-3.
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