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    Electromyographic analysis of joint-dependent global synkinesis in the upper limb of healthy adults: Laterality of intensity and symmetry of spatial representation
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    Oculostapedial synkinesis following Bell’s palsy, Ramsay Hunt syndrome and traumatic facial nerve paralysis is a rarely reported phenomenon. Oculostapedial synkinesis accompanying with hemifacial spasm also has been reported. We experienced a 51-year-old woman with persistent loud rumbling noise from her left ear related with voluntary left eye closure compatible with oculostapedial synkinesis after Bell’s palsy. We objectively proved this oculostapedial synkinesis with impedance audiometry. The patient was successfully treated by transmeatal tenotomy of the left stapedius muscle tendon under local anesthesia. (Korean J Otolaryngol 2002;45:817-20)
    Synkinesis
    Hemifacial spasm
    Tenotomy
    Facial paralysis
    Citations (1)
    Objectives: The researchers analyzed facial patterns in subjects with facial synkinesis after facial paralysis and evaluated the involved muscles to aid in the development of effective treatments for facial synkinesis.Methods: A total of 142 subjects were included in the study, the primary measure for synkinesis was determined by video analysis involving the strongest combination of two muscle groups that contributed to facial expression. The secondary measure of synkinesis was the analysis of its severity using the SB grading system, while observing the number of facial synkinetic movements.Results: The most common type of facial synkinesis was oral–ocular synkinesis (n = 137). Other synkinesis such as ocular–oral, ocular–nasal, ocular–chin, ocular–stapedial, chin–ocular and chin–oral synkinesis continued to coexist together with oral–ocular synkinesis. The results of BTX-A treatment are assessed based on the number of facial synkinetic movements observed and the evaluation of initial facial function.Conclusion: The effectiveness of botulinum toxin A (BTX-A) treatment should be considered on an individual basis, according to the initial state of facial function. A patient with mild facial synkinesis restricted to the oral–ocular area and with a high score on the Sunnybrook (SB) facial nerve grading system would be the best candidate for BTX-A treatment.
    Synkinesis
    Facial paralysis
    Facial muscles
    We examined the relationship between the time course of development of facial synkinesis in patients with Bell's palsy and the severity of facial nerve damage.Retrospective study.Tertiary referral center.Thirty-nine consecutive patients with Bell's palsy who developed synkinesis.Diagnostic.Subjects were divided into groups A (electroneurographic [ENoG] value, <10%; n = 31) and B (ENoG value, > or =10%; n = 8). Development of facial synkinesis was assessed based on the appearance of synkinetic potentials from the orbicularis oris muscle on the blink reflex test. Times to appearance of facial synkinesis in groups A and B were compared. The proportion of patients who developed facial synkinesis after complete recovery of facial movement was also assessed in 14 patients whose facial movement recovered completely.The mean time to maximal recovery of facial movement was significantly longer in group A than in group B (p < 0.001), whereas the duration between the appearance of facial synkinesis and the onset of facial paralysis did not differ significantly between the 2 groups (p = 0.72). The proportion of patients who developed facial synkinesis after complete recovery of facial movement was significantly greater in group B than in group A (p = 0.015).During the course of recovery from Bell's palsy, the patients with an ENoG value of 10% or greater have a higher risk of developing facial synkinesis after complete recovery of facial movement.
    Synkinesis
    Facial paralysis
    Facial muscles
    Facial synkinesis is a well-known disabling occurrence following severe facial palsy. Platysma muscle, innervated by the facial nerve, can be involved in synkinesis as well, but thus far has been little investigated. The aim of our study is to evaluate the presence of platysma synkinesis and its clinical evolution after onabotulinumtoxinA (BoNT-A) (Botox(®) ; Allergan Pharmaceuticals, Irvine, CA) injections.Retrospective study.Sixty-nine patients were treated for synkinesis following facial palsy. Of those, 45 were affected by platysma synkinesis and thus were injected in the platysma muscle. The total number of sessions was 124. The Sunnybrook Facial Grading System (SFGS) and a specific platysmal evaluation for the presence and severity of synkinesis and local symptoms were performed before and after BoNT-A treatments.Platysma synkinesis was present in 65.2% of the sample and was associated with subjective complaints in 85.5% of the cases. The facial expressions more related to platysma synkinesis were snarl, followed by open-mouth smile and lip pucker. After each BoNT-A treatment, there was an improvement in facial symmetry at rest and during voluntary movements, a global reduction of synkinesis, and a specific reduction of synkinesis and symptoms related to the platysma. No adverse reaction to BoNT-A occurred.Platysma involvement represents a recurring and symptomatic problem in patients affected by synkinetic recovery following facial palsy. After BoNT-A injections, there is a reduction in platysma synkinesis and related symptoms.4.
    Synkinesis
    Facial muscles
    Facial paralysis
    Citations (42)
    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.
    Synkinesis
    Facial paralysis
    Facial muscles
    Citations (9)
    Synkinesis of the facial muscles are common sequelae of peripheral facial nerve palsy. However, treatment for synkinesis is limited. The case of an 18-year-old woman with right-sided Bell's palsy is reported. An electroneurography (ENoG) test showed complete degeneration of the facial nerve on the right side. There was a good possibility that the patient would eventually be troubled by synkinesis. As prophylactic treatment for the prevention of synkinesis, biofeedback rehabilitation was undertaken using a mirror and electromyography. Subsequently, the patient showed no simultaneous activation of the orbicularis oculi during mouth movements, which is the most common clinical symptom of Synkinesis. It is proposed that biofeedback rehabilitation is an effective prophylactic treatment for synkinesis.
    Synkinesis
    Biofeedback
    Electroneuronography
    Facial paralysis
    Citations (0)
    Purpose. To assess the effect and efficacy of botulinum toxin type A (BTX-A) in reducing synkinesis in aberrant facial nerve regeneration (following facial paralysis).Method. A total of 55 sessions of BTX-A (Botox®) infiltration were performed on 30 patients (23 female) with synkinesis after facial palsy. Each subject was injected with 2.5 units of BTX-A in each injection site (the sites were chosen on a case-by-case basis). The synkinetic muscles targeted include: orbicularis oculi, zygomaticus major, depressor labii inferioris, platysma, healthy frontalis and healthy corrugator supercilii. The patients were examined using the Sunnybrook Facial Grading System, both before the BTX-A treatment and after an average of 35 days.Results. All 30 patients experienced improvement to the synkinesis after treatment. Total scores: median pre-BTX-A: 40; post 53 p = 0.004. Resting symmetry scores: mean pre-BTX-A −7.1; post: −3.5; median pre −5 [interquartile range (IQR) −10 to −5]; post: −5 (IQR −5 to 0); p = 0.0001. Symmetry of voluntary movement median pre-BTX-A: 56 post 60 p = 0.10. Synkinesis scores: median pre-BTX-A: −9 post −3 p < 0.0001. Mean duration of improvement was 4 months.Conclusions. BTX-A injection treatment was effective in reducing facial synkinesis, thus improving facial expression symmetry both at rest and in voluntary movements.
    Synkinesis
    Facial paralysis
    Citations (88)
    Background. Patients with an upper limb motor impairment are likely to develop wrist hyper-resistance during the first months post stroke. The time course of wrist hyper-resistance in terms of neural and biomechanical components, and their interaction with motor recovery, is poorly understood. Objective. To investigate the time course of neural and biomechanical components of wrist hyper-resistance in relation to upper limb motor recovery in the first 6 months post stroke. Methods. Neural (NC), biomechanical elastic (EC), and viscous (VC) components of wrist hyper-resistance (NeuroFlexor device), and upper limb motor recovery (Fugl-Meyer upper extremity scale [FM-UE]), were assessed in 17 patients within 3 weeks and at 5, 12, and 26 weeks post stroke. Patients were stratified according to the presence of voluntary finger extension (VFE) at baseline. Time course of wrist hyper-resistance components and assumed interaction effects were analyzed using linear mixed models. Results. On average, patients without VFE at baseline (n = 8) showed a significant increase in NC, EC, and VC, and an increase in FM-UE from 13 to 26 points within the first 6 months post stroke. A significant increase in NC within 5 weeks preceded a significant increase in EC between weeks 12 and 26. Patients with VFE at baseline (n = 9) showed, on average, no significant increase in components from baseline to 6 months whereas FM-UE scores improved from 38 to 60 points. Conclusion. Our findings suggest that the development of neural and biomechanical wrist hyper-resistance components in patients with severe baseline motor deficits is determined by lack of spontaneous neurobiological recovery early post stroke.
    Stroke
    Citations (8)