Laryngeal Synkinesis: A Viable Condition for Laryngeal Pacing.

Laryngeal synkinesis as a form of defective healing is the rule rather than the exception in persistent vocal fold paralysis. It typically occurs 4-6 months after the onset of the recurrent laryngeal nerve paralysis. The incidence is up to 85%. Not all laryngeal muscles need to be equally affected. Reliable evidence can only be provided by a laryngeal electromyography. Physiological co-activation of the laryngeal muscles during antagonistic maneuvers must be considered. Although synkinesis undeniably worsens the prognosis for a motion recovery, it protects the muscle fibers from degeneration. A differentiation is required between favorable synkinesis (type I according to Crumley), which does not always require further therapy in the case of unilateral paralysis, and unfavorable forms of synkinesis (type II-IV) according to Crumley, which are associated with a functionally relevant malposition of the vocal fold(s) or with vocal fold jerks. Particularly when bilateral vocal fold motion does not return, type I synkinesis can be a good prerequisite for new dynamic therapy approaches, such as laryngeal pacing. The rarely occurring type II-IV synkinesis should, whenever possible, be transformed into a more favorable type I synkinesis by selective or non-selective reinnervation at an early stage of the disease. The latter applies to expected muscle atrophy with insufficient regrowth of nerve fibers.

Electroneurography cannot predict when facial synkinesis develops in patients with facial palsy.

The objective of this study is to clarify when facial palsy patients with lower value of Electroneurography (ENoG) should begin the rehabilitation to prevent the development of facial synkinesis. For this purpose, we examined the relationship between the value of ENoG measured 10-14 days after facial palsy onset and the onset day of the development of oral-ocular synkinesis. Sixteen patients with facial palsy including 11 with Bell's palsy and 5 with Ramsay Hunt syndrome (7 men and 9 women ; 15-73 years old ; mean age, 41.6 years) were enrolled in this study. There was no correlation between ENoG value and the onset day of the development of oral-ocular synkinesis (ρ = .09, p = .73). Oral-ocular synkinesis began to develop in 4.0 ±â€…0.7 months (mean ±â€…SD ; range : 3.1-5.0 months) after facial palsy onset regardless of ENoG value. In conclusion, ENoG value cannot predict when facial synkinesis develops in patients with facial palsy. We recommend that facial palsy patients with a high risk for the development of synkinesis begin the biofeedback rehabilitation with mirror to prevent the development of facial synkinesis 3 months after facial palsy onset. J. Med. Invest. 67 : 87-89, February, 2020.

The Contribution of Surface Electromyographic Assessment for Defining the Stage of Peripheral Facial Paralysis: Flaccid or Sequelae Stage

Abstract Introduction Surface electromyographic activity may not be symmetric, even in subjects with no facial paralysis history. Objective To evaluate the contribution of the index of electromyographic (IEMG) activity in the identification of the two extremes of the facial paralysis course. Methods Thirty-four subjects with unilateral peripheral facial paralysis were selected. A control group was composed of volunteers without a history of facial paralysis. The electromyographic assessment of the facial muscle was performed by placing surface electrodes during movements of the forehead, eyes and lips using MIOTEC equipment, such as the MIOTOOL (Miotec, Porto Alegre, Brazil) software. The electromyographic activity was also recorded in other channels during the primary activity to identify the presence of synkinesis. The statistical analysis was performed using the Statistical Package for Social Sciences for Macintosh (SPSS Inc, Chicago, IL, USA). The IEMG activity was obtained from the division of the electromyographic activity root mean square (RMS) values on both sides. Results There was a statistically significant difference among the groups in all the analyzed indexes. The ocular-oral synkinesis in all patients must be correctly identified (with 100% sensitivity and specificity) using an IEMG activity of 1.62 as a cutoff point. The oral-ocular synkinesis must be correctly identified (93.3% sensitivity and 95.9% specificity) using the IEMG activity of 1.79 as a cutoff point. Conclusion The IEMG activity is below the normal scores in patients in the flaccid stage, whereas patients in the sequelae stage can either show normal values or values above or below the normal scores. The IEMG activity was shown to have high sensitivity and specificity in the identification of synkinesis.

Management of synkinesis.

Facial synkinesis is one of the most distressing consequences of facial paralysis. Synkinesis refers to the abnormal involuntary facial movement that occurs with voluntary movement of a different facial muscle group. The pathophysiologic basis of facial synkinesis is likely multifactorial although the predominant mechanism appears to be aberrant regeneration of facial nerve fibers to the facial muscle groups after facial nerve injury. Patients experience hypertonic contractures and synkinetic movements such as eye closure with volitional movement of the mouth or midfacial movement during volitional or reflexive eye closure. Synkinesis can cause functional limitation with activities such as eating, drinking, smiling, and may even lead to social isolation. Evaluation of synkinesis is primarily subjective with facial grading scales such as the Sunnybrook scale. Objective measures of synkinesis using computerized video analysis show promise although no objective techniques are currently widely used. The most common therapeutic modalities for the treatment of facial synkinesis include (1) botulinum toxin type A (BTX-A) injections for selective chemodenervation of affected muscle groups and (2) facial neuromuscular retraining. Biofeedback using mirrors or electromyography has been used both for the treatment and prevention of facial synkinesis. Other treatment options include surgical therapies, such as selective neurolysis or myectomy, although these have been rendered nearly obsolete with the advent of BTX-A.