[Synkinesis of the facial and oculomotor muscles]

Using literature data, to study the morphofunctional mechanisms of peripheral synkinesis, determine the contribution of trigger points to their development, and assess the potential of using peripheral synkinesis in medical rehabilitation.

A systematic analysis of 87 publications from the PubMed, Web of Science, Scopus, and Google Scholar databases was conducted for the period from 2020 to 2025. Selection criteria included reviews, clinical studies, and randomized controlled trials.

Peripheral synkinesis is predominantly related to III, IV, VI, and VII cranial nerves. The underlying mechanisms include aberrant axon regeneration with ephaptic transmission, hyperexcitability of cranial nerve nuclei, and cortical reorganization. The uniqueness of peripheral synkinesis is due to anatomical features: significant branching and short length of nerves, evolutionary resistance of extraocular and facial muscles to denervation, and the presence of alternative sources of proprioception. Trigger points play a significant role in the pathogenesis of peripheral synkinesis, increasing the hyperexcitability of the brainstem nuclei, and inactivation of the trigger points breaks this pathological system. There are no true contractures in facial muscle paralysis. Cicatricial and adipose degeneration are reported only in subjects with congenital defects of ocular muscle innervation.

Peripheral synkinesis is caused by the anatomical features of III-VII cranial nerves (pronounced branching and short length) and craniofacial muscles (presence of alternative sources of proprioception). Trigger points for facial palsy are an early marker of denervation that enhances synkinesis. Their inactivation is reasonable. There are no true contractures of facial muscles; they are mistaken for tonic synkinesis or myokymia. The use of peripheral synkinesis in medical rehabilitation has no pathogenetic ground.