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Structural remodeling in related brain regions in patients with facial synkinesis.

ABSTRACT: Facial synkinesis is a troublesome sequelae of facial nerve malfunction. It is difficult to recover from synkinesis, despite improved surgical techniques for isolating the peripheral facial nerve branches. Furthermore, it remains unclear whether long-term dysfunction of motor control can lead to irreversible plasticity-induced structural brain changes. This case-control study thus investigated the structural brain alterations associated with facial synkinesis. The study was conducted at Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, China. Twenty patients with facial synkinesis (2 male and 18 female, aged 33.35 ± 6.97 years) and 19 healthy volunteers (2 male and 17 female, aged 33.21 ± 6.75 years) underwent magnetic resonance imaging, and voxel-based and surface-based morphometry techniques were used to analyze data. There was no significant difference in brain volume between patients with facial synkinesis and healthy volunteers. Patients with facial synkinesis exhibited a significantly reduced cortical thickness in the contralateral superior and inferior temporal gyri and a reduced sulcal depth of the ipsilateral precuneus compared with healthy volunteers. In addition, sulcal depth of the ipsilateral precuneus was negatively correlated with the severity of depression. These findings suggest that there is a structural remodeling of gray matter in patients with facial synkinesis after facial nerve malfunction. This study was approved by the Ethics Review Committee of the Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, China (approval No. 2017-365-T267) on September 13, 2017, and was registered with the Chinese Clinical Trial Registry (registration number: ChiCTR1800014630) on January 25, 2018.

SUBMITTER: Wu JJ

PROVIDER: S-EPMC8374555 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Background: There is no current standard for facial synkinesis rehabilitation programs. The benefit and stability of effect of an intensified 10-day facial training combining electromyography and visual biofeedback training was evaluated. Methods: Fifty-four patients (77.8% female; median age: 49.5 years) with post-paralytic facial synkinesis (median time to onset of paralysis: 31.1 months) were included in retrospective longitudinal study between January 2013 and June 2016. Facial function was assesses at baseline (T0), first days of training (T1), last day of training (T2), and follow-up visit (T3) at a median time of 6 months later using the House-Brackmann (HB) facial nerve grading system, Stennert index (SI), Facial Nerve Grading System 2.0 (FNGS 2.0), and Sunnybrook Facial Grading System (SFGS). Pairwise comparisons between the time points with post-hoc Bonferroni correction were performed. Results: No significant changes of the gradings and subscores were seen between T0 and T1 (all p > 0.01). The 10-day combined and intensified feedback training between T1 and T2 improved facial symmetry and decreased synkinetic activity. Facial grading with the FNGS 2.0 or the SFGS were most suited to depict the training effect. FNGS 2.0, regional score, FNGS 2.0, synkinesis score, and FNGS 2.0 total score improved significantly (all p ≤ 0.0001). Both, the FNGS 2.0 and the SFGS showed the strongest improvement in the nasolabial fold/zygomatic and the oral region. Neither the age of the patient (r = 0.168; p = 0.224), the gender (r = 0.126; p = 0.363) nor the length of the interval between onset of the palsy and training start (r = 0.011; p = 0.886) correlated with the changes of the SFGS between T1 and T2. The results remained stable between T2 and T3 without any further significant change. Conclusion: Intensified daily combined electromyography and visual biofeedback training over 10 days was effective in patients with facial synkinesis and benefits were stable 6 months after therapy.

Project description:ImportanceBotulinum toxin neuromodulators are an important treatment for facial synkinesis. Whether a difference in efficacy exists among the 3 different botulinum neuromodulators used in treating this condition remains unknown.ObjectiveTo evaluate the effectiveness of 3 commercially available botulinum toxin neuromodulators in the treatment of facial synkinesis.Design, setting, and participantsIn this single-blind, 3-arm comparison randomized clinical trial, 28 patients at the Facial Nerve Center, University of Utah, Salt Lake City, were randomized to onabotulinumtoxinA, abobotulinumtoxinA, or incobotulinumtoxinA treatment. Each patient was given the Synkinesis Assessment Questionnaire (SAQ) to assess severity of synkinesis before treatment and 1, 2, and 4 weeks after treatment, and improvements were compared among the groups. Data were collected from July 3, 2012, to March 31, 2015.InterventionsBotulinum toxin type A neuromodulator (onabotulinumtoxinA, abobotulinumtoxinA, or incobotulinumtoxinA) injected into synkinetic areas of the face.Main outcomes and measuresSynkinesis assessed using the SAQ (score range, 20-100; lower scores indicate less severe synkinesis) before treatment and 1, 2, and 4 weeks after treatment.ResultsA total of 28 patients (mean [SD] age, 49.1 [18.5] years; 8 [28.6%] male and 20 [71.4%] female), with 6 patients enrolled multiple times, received 38 treatments (15 onabotulinumtoxinA, 13 abobotulinumtoxinA, and 10 incobotulinumtoxinA). No significant difference existed in baseline pretreatment SAQ scores among the 3 groups. Mean (SD) SAQ score improvement at 4 weeks was 41% (31%) for the onabotulinumtoxinA, 42% (20%) for the abobotulinumtoxinA, and 17% (18%) for the incobotulinumtoxinA groups. No significant differences were noted in SAQ score improvements among the 3 groups at weeks 1 and 2 after treatment (week 1 mean improvements of 42% in the onabotulinumtoxinA, 45% in the abobotulinumtoxinA, and 26% in the incobotulinumtoxinA groups; P = .19; week 2 mean improvements of 43% in the onabotulinumtoxinA, 46% in the abobotulinumtoxinA, and 28% in the incobotulinumtoxinA groups; P = .20). The difference in mean SAQ score improvement for abobotulinumtoxinA vs incobotulinumtoxinA from pretreatment to 4 weeks after treatment was not significant (30 vs 12 points; P = .11) despite a significant difference in mean total SAQ score for abobotulinumtoxinA vs incobotulinumtoxinA (40.34 vs 58.00; P = .02).Conclusions and relevanceAbobotulinumtoxinA had similar efficacy to onabotulinumtoxinA and incobotulinumtoxinA for the management of facial synkinesis up to 4 weeks after treatment. IncobotulinumtoxinA had significantly less effect on SAQ score improvement than onabotulinumtoxinA at 4 weeks, perhaps because of the shorter duration of action. Shorter intervals between treatments or larger doses may be required when using incobotulinumtoxinA treatment for facial synkinesis.Trial registrationclinicaltrials.gov Identifier: NCT03048383.Level of evidence1.

Project description:BackgroundThe treatment of post-facial palsy synkinesis (PFPS) remains inadequate. Previous studies have confirmed that brain plasticity is involved in the process of functional restoration. Isolated activation has been well studied, however, the brain works as an integrity of several isolated regions. This study aimed to assess the alteration of the brain network topology with overall and local characteristics of information dissemination. Understanding the neural mechanisms of PFPS could help to improve therapy options and prognosis.MethodsPatients with facial synkinesis and healthy controls (HCs) were estimated using functional magnetic resonance imaging (fMRI) of resting-state. Subsequently, an independent component analysis (ICA) was used to extract four subnets from the whole brain. Then we used the measurements of graph theory and calculated in the whole-brain network and each sub-network.ResultsWe found no significant difference between the patient group and the HCs on the whole-brain scale. Then we identified four subnetworks from the resting-state data. In the sub-network property analysis, patients' locally distributed properties in the sensorimotor network (SMN) and ventral default mode network (vDMN) were reduced. It revealed that γ (10,000 permutations, P=0.048) and S (10,000 permutations, P=0.022) within the SMN progressively decreased in patients with PFPS. For the analysis of vDMN, significant differences were found in γ (10,000 permutations, P=0.019), Elocal (10,000 permutations, P=0.008), and β (10,000 permutations, P=0.011) between the groups.ConclusionsOur results demonstrated a reduction in local network processing efficiency in patients with PFPS. Therefore, we speculate that decreased characteristics in the intra-vDMN and intra-SMN, rather than the whole-brain network, may serve distinct symptoms such as facial nerve damage or more synkinetic movements. This finding of the alteration of network properties is a small step forward to help uncover the underlying mechanism.

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Structural remodeling in related brain regions in patients with facial synkinesis.

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