There are three proposed mechanisms for<unk> : aberrant nerve regeneration, interneuronal ephaptic transmission, and nuclear hyperexcitability. Aberrant nerve regeneration The aberrant nerve regeneration hypothesis is the most widely accepted mechanism for<unk> . 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. 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 has provided a more thorough understanding of<unk>  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. 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.<unk> . *Since<unk>  has been reported in patients within 1–2 months, the nuclear hyper-excitability hypothesis is being supported by more researchers. Furthermore, axonal regeneration is a slow process (~1 mm/day growth) and regeneration at this rate of the facial nerve would roughly take 4–8 months. Since<unk>  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<unk>  development. Although these three mechanisms have been argued for and against in various ways, it has become more accepted that<unk>  develops through a combination of these mechanisms.
Synkinesis
Myoclonus
Pseudoathetosis
Chorea 
Chorea
Aniseikonia
Myotonia
Parkinsonian gait