Selected References These references are in PubMed. This may not be the complete list of references from this article. Bennett MV. Physiology of electrotonic junctions.
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Types[ edit ] 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 the size of the muscles. Synkinesis can also involve the upper limbs, especially hands which is quite rare, at 1 case in 1 million.
As the nerve attempts to recover, nerve miswiring results see Mechanism of Action below. In patients with severe facial nerve paralysis, facial synkinesis will inevitably develop. Unfortunately, this has been shown to be disruptive to normal re-innervation and can promote the development of synkinesis.
This has been attributed to neural interaction between the salivary glands and the lacrimal glands. 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: On attempted abduction of an affected eye, the eye adducts and the eyelid retracts. This is an interaction between the abducens nerve and a branch of the oculomotor nerve.
Voluntary activation of the abducens nerve eye abduction causes involuntary activation of the oculomotor nerve eye adduction and eyelid elevation. This accommodation-convergence synkinesis can result in esotropia, or eyes that turn in when the ratio between accommodation and convergence is unusually high. Thus, involuntary abduction of an involved eye will occur upon eating or chewing. This causes weakness in voluntary chewing; also, facial movements such as blinking cause the muscles to contract.
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. Genetic mutations associated with congenital mirror hand movements are in the DCC gene or RAD51 gene, which account for about 35 percent of cases.
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 ,  and physical injury. Aberrant nerve regeneration[ edit ] The aberrant nerve regeneration hypothesis is the most widely accepted mechanism for synkinesis. These aberrant branches can simultaneously innervate different subdivisions of the facial nerve. Once the compression has relieved, regeneration of axons from the lesion site begins.
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  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[ edit ] 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. The post-synaptic cell consequently becomes deprived of input and becomes more sensitive to neurotransmitters e. 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.
Since synkinesis is observed much earlier, aberrant regeneration and ephaptic communication fail to explain for this observation thus providing evidence that nuclear hyper-excitability is an important factor in the mechanism of synkinesis development.
Measurement[ edit ] Until May , there was no clinical scale to measure synkinesis. A study led by Mehta et al. 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[ edit ] 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. Treatments for synkinesis in general include facial retraining, biofeedback, mime therapy, and Botox and surgery, as a last resort.
Facial retraining[ edit ] 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 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.
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.
A study by Nakamura et al. Due to the extreme efforts needed to achieve improvements during synkinesis, Nakamura et al. 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. It was then later observed that people who had post-facial palsy synkinesis also benefited from this therapy. Furthermore, later studies by Beurskens et al. The components include: massage, stretching exercises, exercises to coordinate both halves of the face, etc.
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[ edit ] Botox botulinum toxin is a new and versatile tool for the treatment of synkinesis.
Initially used for reducing hyperkinesis after facial palsy,  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.
More notable is that in a majority of patients, various synkinetic movements completely disappeared after sessions of trimonthly Botox injections. 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.
Neurolysis has been shown to be effective in relieving synkinesis but only temporarily and unfortunately symptoms return much worse than originally.
Curr Opin Neurobiol. Ephaptic interactions within a chemical synapse: hemichannel-mediated ephaptic inhibition in the retina. Kamermans M 1 , Fahrenfort I. A third, less well known, form of communication is ephaptic transmission, in which electric fields generated by a specific neuron alter the excitability of neighboring neurons as a result of their anatomical and electrical proximity. Ephaptic communication can be present in a variety of forms, each with their specific features and functional implications. One of these is ephaptic modulation within a chemical synapse. This type of communication has recently been proposed for the cone-horizontal cell synapse in the vertebrate retina.
Ephaptic transmission between single nerve fibres in the spinal nerve roots of dystrophic mice.
Early experiments, like those by du Bois-Reymond,  demonstrated that the firing of a primary nerve may induce the firing of an adjacent secondary nerve termed "secondary excitation". This effect was not quantitatively explored, however, until experiments by Katz and Schmitt  in , when the two explored the electric interaction of two adjacent limb nerves of the crab Carcinus maenas. Their work demonstrated that the progression of the action potential in the active axon caused excitability changes in the inactive axon. These changes were attributed to the local currents that form the action potential. For example, the currents that caused the depolarization excitation of the active nerve caused a corresponding hyperpolarization depression of the adjacent resting fiber.