[Evolution of synkinesis in children; the place of synkinesis in motor debility].
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As patients with facial paralysis regain facial nerve function, they must endure and adapt to complications associated with recovery, such as synkinesis. Synkinesis is the presence of unintentional movement in one area of the face when intentionally performing movement in another area of the face. We used the Maximal Static Response Assay of facial motion to better define the differences between eye closure-associated perioral motion in normal individuals, motion of the affected side in patients with synkinesis, and motion of the unaffected side in patients with synkinesis, thereby characterizing the syndrome of ocular to oral synkinesis. The study population consisted of 78 patients with clinically defined ocular to oral synkinesis of the left or right hemiface and 27 individuals without facial impairment (control subjects). We used the Maximal Static Response Assay to quantify facial motion on the affected and unaffected sides during the motions of eye closure and smile in both groups. Patients with ocular to oral synkinesis had decreased supraorbital and infraorbital motion of the orbicularis oculi during eye closure on both the affected and unaffected sides relative to control subjects. They also had increased modiolar motion during eye closure on both sides relative to control subjects. On the affected side, the modiolus tended to move laterally; on the unaffected side, the modiolus tended to move medially (i.e., toward the side affected by the synkinesis). Modiolar motion present during eye closure in patients with ocular to oral synkinesis was not statistically different from modiolar motion present during smile on the affected side (eye closure, 0.39 cm +/- 0.25; smile, 0.47 cm +/- 0.30, p > 0.05). Using the Maximal Static Response Assay, we have quantitatively defined synkinesis of the affected hemiface and have shown that movement of the unaffected hemiface is influenced by the synkinetic movements of the affected hemiface. These data may provide the basis for a rational system of facial neuromuscular rehabilitation in this patient group.
OBJECTIVES/HYPOTHESIS: To compare the sensitivity of an objective, computerized approach to measurement of facial synkinesis with that for a subjective approach and to examine the test-retest reliability of these approaches. STUDY DESIGN: Prospective, nonrandomized, and blinded. METHODS: Remote facial motion at the upper eyelids and oral commissures during a closed-lip smile and eyelid closure were measured using a commercially available computerized motion analysis system. Thirty healthy adults with normal facial nerve function were enrolled to establish normative data and a threshold value for synkinesis. Thirty consecutive patients were analyzed based on the synkinesis threshold value. Blinded subjective evaluations by two observers were also performed independently on the same patients. RESULTS: Facial synkinesis was detected significantly more frequently with objective than subjective analysis for eyelid closure; no significant differences between approaches were shown for the closed-lip smile. Interestingly, five (17%) patients developed early synkinesis within 3 months from the onset of the facial nerve injury. The test-retest reliability of all objective measures was excellent for both expressions. Close agreement in percent of patients with synkinesis between test and retest subjective evaluations was obtained for both observers for both expressions. CONCLUSIONS: The objective, computerized approach to detection of facial synkinesis has excellent reliability and is more sensitive than the subjective approach to assessment to the presence of facial synkinesis associated with eyelid closure. The finding of early synkinesis suggests that central nervous reorganization plays a role in regeneration of the facial nerve.
PURPOSE Various patterns of synkinesis have been observed following both congenital and acquired III nerve palsies. Aberrant regeneration is the most widely accepted mechanism which explains this synkinesis. Two models of aberrant regeneration have been proposed, namely central collateral axon sprouting, and misdirection of regenerating neurones at the site of nerve injury. We have studied the clinical patterns of III nerve recovery and synkinesis following III nerve palsies and relate the findings to the proposed models of synkinesis. MATERIALS AND METHODS Twelve patients with acquired and two with early onset III nerve synkinesis were reviewed. The type, rate and pattern of recovery of III nerve palsy was established from case notes. Observations and measurements of ocular motility, pupil movements, eyelid position and intraocular pressure changes were performed on each patient. Signs of contralateral synkinetic movements were also sought. RESULTS Upper lid retraction on attempted down gaze and in adduction was the most frequent synkinetic movement recorded. Observation of pupil size revealed evidence of pupillary-extraocular muscle synkinesis in all gaze positions except abduction. Similarly, intraocular pressure changes and signs of globe retraction showed widespread extraocular muscle co-contraction. Synkinetic levator innervation of extraocular muscles [i.e., LPS to MR, IR, SR] was also observed, a finding not previously reported in III nerve palsy but predicted by our model of misdirection of regenerating neurones at the site of nerve injury. There was no evidence of contralateral aberrant innervation. CONCLUSION Evidence of III nerve synkinesis in patients with III nerve palsy is widespread and the patterns of synkinesis observed were broadly similar for all patients irrespective of the aetiology. Random aberrant III nerve regeneration at the site of nerve injury best explains the patterns of synkinesis observed. Central collateral axon sprouting does not seem to play a major part in the synkinetic movements observed in acquired III nerve lesions.
The purpose of this paper is to describe the outcome of facial neuromuscular retraining for brow to oral and ocular to oral synkinesis in individuals with facial nerve disorders. Fourteen patients with unilateral facial nerve disorders and oral synkinesis who were enrolled in physical therapy for retraining were studied. Synkinesis was measured with quantitative video facial position analysis prior to the initiation of physical therapy and at regular intervals during retraining. Retraining included surface electromyographic biofeedback-assisted specific strategies for facial muscle reeducation and a home exercise program of specific facial movements. Twelve of 13 patients with brow to oral synkinesis and 12 of 14 patients with ocular to oral synkinesis reduced their synkinesis with retraining. Patients with a 1-year on greater duration of a facial neuromuscular disorder (excluding patients with unusually marked changes) demonstrated a significant decrease in brow to oral synkinesis and in ocular to oral synkinesis; there was a mean percentage decline in abnormal movement of 60.5 percent (SD = 26.48) and 30.1 percent (SD = 62.57), respectively. We conclude that brow to oral and ocular to oral synkineses associated with partial recovery from facial paralysis were reduced with facial neuromuscular retraining for individuals with facial nerve disorders.
Laryngeal synkinesis involves the misdirected reinnervation of an injured recurrent laryngeal nerve to vocal fold abductor and adductor musculature. The resultant laryngeal dyscoordination can cause vocal fold immobility and airway compromise. Although this entity is sometimes considered in the differential diagnosis, it is only demonstrable with laryngeal electromyography (EMG). We propose a new EMG definition of synkinesis to assist in its identification during workup of vocal fold immobility. A retrospective chart review from 1992 to 1997 in the Voice Disorders Clinic identified 10 patients with laryngeal synkinesis. Five patients had bilateral immobility, and 5 had unilateral immobility. Monopolar EMG was performed on all patients. Fine-wire EMG was performed when monopolar EMG did not elucidate the cause of the immobility. The EMG studies revealed synkinetic reinnervation in all subjects. On the basis of the EMG results, 7 of the 10 patients were treated with botulinum toxin to weaken the undesired reinnervation. Three of the 7 patients had benefit from this therapy. Laryngeal synkinesis should be considered as part of the differential diagnosis of vocal fold immobility. Awake laryngeal EMG is the only method to demonstrate synkinesis of the larynx. The diagnosis of synkinesis is clinically significant in cases of immobility to identify patients who might benefit from botulinum toxin therapy. Additionally, the presence of synkinesis in cases of unilateral immobility may be a contraindication to laryngeal reinnervation procedures. The benefit of botulinum toxin therapy is likely greater in the treatment of bilateral as opposed to unilateral immobility.
First described in 1982, laryngeal synkinesis continues to play an important diagnostic and therapeutic role following recurrent laryngeal nerve (RLN) injury. Vocal fold motion impairment (formerly called "vocal cord paralysis"), hyperadducted and hyperabducted vocal folds, and certain laryngeal spasmodic and tremor disorders are often best explained by synkinesis. A closer look at these mechanisms confirms that following RLN injury, immobile vocal folds may be nearly normally functional (favorable), or spastic, hyperadducted, or hyperabducted (unfavorable). This has resulted in a functional classification of laryngeal synkinesis as follows: type I laryngeal synkinesis, with satisfactory voice and airway (vocal fold poorly mobile, or immobile); type II synkinesis, with spasmodic vocal folds and an unsatisfactory voice and/or airway; type III synkinesis, with hyperadducted vocal folds and airway compromise; and type IV synkinesis, with hyperabducted vocal folds, poor voice, and possible aspiration. This classification facilitates the understanding of laryngeal pathophysiology following RLN injuries and promotes a more scientific basis for management.
Facial nerve synkinesis is an extremely distressing sequela of facial paralysis, and its prevention and treatment are less than adequate. Improved therapeutic interventions await better understanding of its pathogenesis. In this study, 11 patients with synkinesis and 11 normal control subjects were quantitatively assessed using a new computer-assisted, motion-sensitive system. Two additional, informative cases presenting at the completion of the study are also briefly reported. The observed synkinetic patterns appear predictable and nonrandom. In addition, these observations tend to raise doubts that the aberrant fiber regeneration hypothesis is the sole explanation of synkinesis. They further implicate facial nuclear hyperexcitability as an explanation in at least some cases of synkinesis. Understanding these patterns enhances clinical detection and evaluation and may lead to a better knowledge of the fundamental pathophysiology of synkinesis and its prevention.
PURPOSE: To report the outcomes of a management protocol for Marcus Gunn jaw winking synkinesis. METHODS: The records of 31 patients (16 female, 15 male) presenting to a tertiary referral center with Marcus Gunn jaw winking synkinesis between 1993 and 2003 were retrospectively analyzed. Generally, patients with mild wink and a small degree of ptosis underwent unilateral upper eyelid retractor surgery. Patients with a moderate or marked wink and ptosis underwent bilateral levator weakening procedures and brow suspension. Patients were assessed and treated for amblyopia and vertical strabismus before ptosis surgery. RESULTS: Mean patient age was 11.23 years (median, 8 years; range, 10 weeks to 31 years). Ipsilateral hypotropia was noted in 8 patients (26%), with a median visual acuity in the ptotic eye of 20/30 (range, 20/20 to 20/40), compared with 20/20 in those without hypotropia. Patients who underwent unilateral surgery had good correction of ptosis, with equal palpebral apertures and symmetrical contour but had a detectable wink on formal testing. Patients who underwent bilateral surgery had equal palpebral apertures and symmetrical contour, with wink elimination. Mean follow-up was 31 months (all patients) and mean postoperative follow-up was 22 months. CONCLUSIONS: Patients with Marcus Gunn jaw winking synkinesis can present at a wide age range. There may be an associated vertical muscle imbalance, which should be managed before ptosis surgery to avoid ptosis undercorrection and allow amblyopia management. Nearly all patients use the synkinesis to reduce the underlying true ptosis to a less noticeable "habitual" ptosis or to maintain binocularity. Surgical approach will differ, depending on whether the synkinesis, ptosis, or both are the main concern. Satisfactory results with a low complication rate can be achieved with the use of this management protocol.
In this study, the development of clinical synkinesis after facial nerve paralysis (FP) and its relationship to electrophysiological findings were investigated. Thirty-four patients who were examined within the first 5 days after onset of FP and who could also be followed up for at least 4 months were included in the study. Electrophysiological investigations consisted of: (1) recording of the direct responses by facial nerve stimulation at the stylomastoid fossa; (2) recording of the 'synkinetic spread' of the supraorbital nerve reflex to the lower facial muscles; (3) recording of the 'lateral spread responses' by stimulating the mandible and zygomatic branches of the facial nerve. Clinical synkinesis developed in 14 of 18 patients (78%) with a direct response ratio (DRr) of less than 40%. Among the 16 patients with a DRr of 40% or more, synkinesis was observed in 3 cases (18.7%) only. The DRr provided reliable information concerning the development of synkinesis. Forty percent seemed to be a reasonable limit to distinguish the high-risk group for the development of clinical synkinesis.
By conducting electrophysiological tests on patients with facial nerve paralysis, the characteristics of synkinesis and the mechanisms of its manifestations were examined. The subjects were 114 patients of facial nerve paralysis on whom electroneurography (ENoG) and the blink reflex were conducted. As a result, it was indicated that synkinesis could be determined by the blink reflex, and that the frequency of synkinesis manifestation increased with severity of paralysis. From examination during the latent period, early component (SI) recognized in the cases of synkinesis was found to be the waveform which passed the fibers with a slow conducting speed. It was not related to the degree of degeneration of nerves for either the severe or light degeneration of nerves. From the above result it was concluded that synkinesis is generated as a misdirection of reproduced nerves.
Three patients with Marcus Gunn's synkinesis were examined. The clinical variants and time-course of synkinesis are offered. Factors provoking synkinesis manifestations are considered. Various hypotheses of the etiology of Marcus Gunn's synkinesis are compared. Palpebro-mandibular synkinesis may be considered as a return to the primitive kinetics and actualization of the normal links of the phylogenetic past.
Neuromuscular rehabilitation can reduce the severity of chronic facial paralysis, but complete recovery is frequently impeded by synkinesis. We evaluated whether or not such synkinesis could be minimized by preventing its possible reinforcement during rehabilitation. We compared "standard" therapy, which uses the appearance of synkinesis to guide rehabilitation, with a new "small-movement" therapy, which uses smaller movements that should minimize possible subthreshold reinforcement of synkinesis. Ten subjects who had had facial paralysis for 0.5 to 27 years were randomly assigned to either therapy group. Blinded assessments were performed before and after ten 1-hour treatments given over a 1-month interval. Facial movements in both groups were significantly more symmetric after treatment. Although synkinesis tended to be reduced in the small-movement group, this reduction was not significant. The new therapy was at least as good as the standard one, and it may be better. Further studies are required to demonstrate this.
In a patient with temporal arteritis, ophthalmoplegia developed associated with a transient oculomotor synkinesis or aberrant regeneration. The synkinesis suggests that the ophthalmoplegia was neurogenic rather than myogenic. Based on published experiments, it appears that transient synkinesis is compatible with the hypothesis that aberrant regeneration of axons in the third nerve is the cause of oculomotor synkinesis.
PURPOSE: To describe a previously unreported type of ptosis associated with abnormal synkinesis between the superior rectus muscle and the levator palpebrae superioris. DESIGN: Retrospective noncomparative case series. PARTICIPANTS: Seven cases with congenital or longstanding unilateral ptosis presenting to a regional, tertiary referral, oculoplastic service. Six of these cases were seen within a period of 2 years. METHODS: Detailed observations of eyelid, ocular, and pupil movements of both eyes were performed before the planning of ptosis surgery anterior levator resection. MAIN OUTCOME MEASURES: Magnitude of ptosis and its variation with the position of gaze. RESULTS: Ptosis present in the primary position disappeared or markedly reduced with upgaze so that measurements of levator function were apparently normal. Close examination of the relative movement of the eyelids revealed evidence of superior rectus to levator synkinesis occurring during upgaze. In three cases the synkinesis was recognized only after failed ptosis surgery. Once recognized, two of these cases underwent further surgery with an excellent result. Three other patients all had successful surgery. CONCLUSIONS: Superior rectus to levator synkinesis may be easily overlooked if eyelid elevation in upgaze is ascribed to normal levator function rather than a synkinetic movement. We draw attention to the importance of identifying this relatively common condition to plan appropriate ptosis surgery. The lack of levator muscle tone in the primary position of gaze means that an augmented resection of the levator muscle should be performed.
OBJECTIVE: We developed a new training method of biofeedback rehabilitation for the prevention of synkinesis after facial palsy and evaluated the efficacy of the training. METHODS: Twenty-seven patients with complete facial palsy were divided randomly into 2 groups. Twelve of the patients were treated with the training method, and the other 15 patients served as controls. Patients were instructed to keep their eyes open symmetrically during mouth movements using a mirror. Thirty minutes of daily training was continued for a period of 10 months. The degree of synkinesis was evaluated by computing the percent asymmetry of eye opening width. RESULTS: The percent asymmetry of eye opening width was significantly greater in the training group than in the control group (P < 0.05). The results indicate that the degree of synkinesis is much less in the training group than in the control group. CONCLUSION: Our new training method is very effective for preventing the development of synkinesis after facial palsy.
In 95 patients with hemifacial spasm, synkinetic actions were measured objectively using electromyographic examination of the blink reflex and impedance audiometry. Abnormal synkinesis between the orbicularis oculi and the orbicularis oris muscles was recorded in 93% of cases, while synkinesis between the stapedius muscle and the facial muscles was recorded in 87%. Neither of these effects could be demonstrated on the unaffected side. The examinations were performed before and after microvascular decompression in 66 cases. Rapid disappearance of synkinesis, often within 10 days, was observed after the relief of vascular compression in 81% of patients who had not undergone previous peripheral facial nerve block procedures. These findings indicate that the synkinesis seen in hemifacial spasm is essentially a reversible condition, and suggest that axonal ephaptic conduction at the vascular compression site plays an important role in the pathophysiological mechanism of hemifacial spasm.
Facial synkinesis is an involuntary activation of muscles innervated by the zygomatic or mandibular branch of the facial nerve in conjunction with voluntary activation of the other branch. It appears frequently after recovery from peripheral facial nerve paralysis. We report 10 patients with facial synkinesis following Bell's palsy with a mean duration of synkinesis of 7 +/- 4 years before treatment with periorbital injections of Botulinum toxin type A. 9 had marked subjective and objective improvement starting a few days after injection and lasting 4-9 months. The results suggest a useful treatment option for post-Bell's palsy facial synkinesis with Botulinum toxin type A.