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This study aimed to determine the preferred timing and measurement sites for electroneuronography (ENoG) to predict early recovery from acute peripheral facial paralysis. We retrospectively evaluated 42 patients with acute peripheral facial paralysis who received standard treatment with oral corticosteroids. The severity of facial paralysis was assessed at the initial visit and after 1 month using the House-Brackmann grading system. Patients were classified into recovery and non-recovery groups according to changes in the grade. ENoG was performed at the initial visit and after 2 weeks. ENoG amplitudes of four facial muscles (frontalis, nasalis, orbicularis oculi, and orbicularis oris) at the initial visit and after 2 weeks, as well as age, sex, affected side, and diagnosis, were compared between the two groups. No differences were observed in degeneration ratios across all subsites in the initial ENoG, which can be explained by the fact that Wallerian degeneration is not yet complete at this early stage. However, the second ENoG, performed after degeneration had progressed, showed significant differences across all subsites. Binary logistic regression analysis revealed that the degeneration ratio of the orbicularis oris muscle was the best predictor of early recovery (odds ratio, 0.961; p = 0.014). Receiver operating characteristic curve analysis also revealed that the degeneration ratios of all subsites measured in the second ENoG were useful in predicting early recovery, with the highest possibility at the orbicularis oris muscle (area under the curve = 0.789). When the degeneration ratio exceeded 60% in all subsites in the second ENoG, a favorable prognosis was not expected. This study provides the preferred testing time and measurement sites for ENoG to predict early recovery from facial paralysis. Given the personal and social impact of facial paralysis, predicting early recovery is crucial for reassuring patients, providing better treatment, and encouraging early reintegration into society.

The subjective assessment of facial paralysis relies on the expertise of clinicians; the main limitation is intra-observer and inter-observer reproducibility. In this paper, we proposed a deep learning approach combining point clouds of facial movements with expert consensus to objectively quantify the severity of facial paralysis. A dynamic 3D photogrammetry imaging system was used to capture the facial movements of five facial expressions. Point clouds of the face at rest and at maximum expressions were extracted. These were integrated with the experts grading of the severity of facial paralysis to train a PointNet network to quantify the severity of facial paralysis. The results showed an accuracy exceeding 95% for assessing facial paralysis.

Severe axonal damage in the peripheral nerves results in retrograde degeneration towards the central side, leading to neuronal cell death, eventually resulting in incomplete axonal regeneration and functional recovery. Therefore, it is necessary to evaluate the facial nerve nucleus in models of facial paralysis, and investigate the efficacy of treatments, to identify treatment options for severe paralysis. Consequently, we aimed to examine the percentage of facial nerve cell reduction and the extent to which intratympanic administration of a basic fibroblast growth factor (bFGF) inhibits neuronal cell death in a model of severe facial paralysis. A severe facial paralysis model was induced in Hartley guinea pigs by freezing the facial canal. Animals were divided into two groups: one group was treated with gelatin hydrogel impregnated with bFGF (bFGF group) and the other was treated with gelatin hydrogel impregnated with saline (control group). Facial movement scoring, electrophysiological testing, and histological assessment of facial neurons were performed. The freezing-induced facial paralysis model showed a facial neuronal cell death rate of 29.0%; however, bFGF administration reduced neuronal cell death to 15.8%. Facial movement scores improved in the bFGF group compared with those in the control group. Intratympanic bFGF administration has a protective effect on facial neurons in a model of severe facial paralysis. These findings suggest a potential therapeutic approach for treating patients with refractory facial paralysis. Further studies are required to explore the clinical applicability of this treatment.

Objective To systematically review the published cases of bilateral facial palsy (BFP) to gather evidence on the clinical assessment and management of this pathology. Methods Following PRISMA statement recommendations, 338 abstracts were screened independently by two authors. Inclusion criteria were research articles of human patients affected by BFP, either central or peripheral; English, Italian, French or Spanish language; availability of the abstract, while exclusion criteria were topics unrelated to FP, and mention of unilateral or congenital FP. Only full-text articles reporting the diagnostic work-up, the management, and the prognosis of the BFP considered for further specific data analysis. Results A total of 143 articles were included, resulting a total of 326 patients with a mean age of 36 years. The most common type of the paralysis was peripheral (91.7%), and the autoimmune disease was the most frequent aetiology (31.3%). The mean time of onset after first symptoms was 12 days and most patients presented with a grade higher than III. Associated symptoms in idiopathic BFP were mostly non-specific. The most frequently positive laboratory exams were cerebrospinal fluid analysis, autoimmune screening and peripheral blood smear, and the most performed imaging was MRI. Most patients (74%) underwent exclusive medical treatment, while a minority were selected for a surgical or combined approach. Finally, in more than half of cases a complete bilateral recovery (60.3%) was achieved. Conclusions BFP is a disabling condition. If a correct diagnosis is formulated, possibilities to recover are elevated and directly correlated to the administration of an adequate treatment.

Background and Objectives: Peripheral facial paralysis (PFP) is a condition with diverse etiologies, requiring multidisciplinary management. This study aimed to describe the sociodemographic, clinical, and functional characteristics of patients with PFP treated at the Rehabilitation Service of the University Hospital of Burgos and to evaluate factors associated with the initial degree of impairment. Materials and Methods: A descriptive, cross-sectional study was conducted on 45 patients referred to the Rehabilitation Service from July 2018 to July 2023. Inclusion criteria included first-time rehabilitation visits for PFP during the study period with signed informed consent. Patients with prior PFP on the affected side or severe comorbidities, such as stroke, were excluded. Data were collected from medical records and initial evaluations. The Sunnybrook Facial Grading System (SFGS) was used to assess impairment. Results: Idiopathic paralysis was the most common etiology, with a predominance in men (60.9%) and middle-aged or older adults. Otorhinolaryngology was the leading referral service, though primary care referrals were underrepresented. Delays in initiating rehabilitation were identified, especially in complex cases like acoustic neurinoma. The ANOVA test revealed no significant differences in functional assessments based on age, sex, or etiology, likely due to the limited sample size. Conclusions: The study highlights the predominance of idiopathic etiology in PFP and the importance of otorhinolaryngology in referrals. Greater awareness in primary care and early identification are crucial. Future studies with larger samples are needed to evaluate predictors of impairment and optimize rehabilitation strategies.

With the continuous progress of technology, the subject of life science plays an increasingly important role, among which the application of artificial intelligence in the medical field has attracted more and more attention. Bell facial palsy, a neurological ailment characterized by facial muscle weakness or paralysis, exerts a profound impact on patients’ facial expressions and masticatory abilities, thereby inflicting considerable distress upon their overall quality of life and mental well-being. In this study, we designed a facial attribute recognition model specifically for individuals with Bell’s facial palsy. The model utilizes an enhanced SSD network and scientific computing to perform a graded assessment of the patients’ condition. By replacing the VGG network with a more efficient backbone, we improved the model’s accuracy and significantly reduced its computational burden. The results show that the improved SSD network has an average precision of 87.9% in the classification of light, middle and severe facial palsy, and effectively performs the classification of patients with facial palsy, where scientific calculations also increase the precision of the classification. This is also one of the most significant contributions of this article, which provides intelligent means and objective data for future research on intelligent diagnosis and treatment as well as progressive rehabilitation.

Peripheral facial paralysis (PFP) is a common neurological disorder characterized by facial-nerve dysfunction. Identifying therapeutic targets and understanding the molecular and cellular mechanisms underlying PFP are crucial for developing effective treatment strategies. This study combined Mendelian randomization (MR) analysis and single-cell RNA sequencing (scRNA-seq) to explore potential therapeutic candidates and their roles in PFP pathophysiology. The MR analysis included 1925 publicly available plasma protein cis-heritability instruments. Instrumental variables were selected for MR analysis to identify plasma proteins associated with PFP, followed by colocalization analysis to evaluate shared genetic variants between the identified proteins and PFP. After the initial identification of plasma proteins associated with Bell’s palsy using MR analysis, a rat model of facial-nerve injury was established to further dissect underlying mechanisms at cellular and molecular levels. Using scRNA-seq technology, we delved deeply into cellular Heterogeneity and dynamic changes in gene expression in the facial-nerve nucleus tissues under both injured and control conditions, thereby achieving a systematic study ranging from macroscopic genetic associations to microscopic cellular functions. Finally, expression patterns were preliminarily validated by performing in vitro immunofluorescence analysis on the facial-nerve nucleus samples of SD rats. The MR analysis results identified 30 plasma proteins significantly associated with PFP, with nine target genes showing differential expression in the scRNA-seq data. Colocalization analysis demonstrated that slit guidance Ligand 2 (SLIT2), semaphorin 4D (SEMA4D), EGF containing fibulin extracellular matrix protein 1 (EFEMP1), and sprouty related EVH1 domain containing 2 (SPRED2) shared causal variants with PFP. SLIT2 was highly expressed in the microglia and inhibitory neurons in the experimental group, whereas SEMA4D showed elevated expression across multiple glial cell types in the same group. In contrast, EFEMP1 and SPRED2 showed distinct expression patterns in fibroblasts and oligodendrocytes. The role of SLIT2 has been previously well-documented in many central nervous system diseases. However, for the first time, this study detected SLIT2 alteration after facial-nerve injury. Altered intercellular signaling, particularly enhanced SLIT2-ROBO signaling between neurons and glial cells, was observed in the PFP group. Pseudotime analysis revealed dynamic SLIT2 expression during microglia and inhibitory neuron differentiation, mirroring changes in ROBO1 expression. Immunofluorescence analysis of rat facial-nerve nucleus samples verified that SLIT2 protein levels were significantly increased in the facial-nerve nuclei of injured samples. In conclusion, despite the fact that this study is primarily founded on animal models and despite notable differences existing between animals and humans in terms of the facial motor nucleus, this study successfully identified SLIT2 as potential therapeutic targets for PFP. The SLIT2-ROBO axis stands out as a particularly promising candidate. SLIT2 may play a role in modulating neuroimmune interactions and promoting nerve repair. These findings provide a foundation for future clinical studies and targeted interventions to enhance recovery from PFP. Future research should focus on human sample validation to enhance clinical translation.

A 56-year-old man presented with right-sided drooping of the mouth corner and eyelid, along with weakness in the left lower limb. His MRI revealed a corona radiata lacunar infarction on the left and an acute infarction on the right. However, the needle electromyography (EMG) results were unremarkable. It was determined that his unilateral peripheral facial paralysis (PFP)-like symptoms were secondary to bilateral corona radiata infarctions. This case highlights that some patients with cerebral strokes may present with PFP-like symptoms. To minimize misdiagnosis, clinicians should consider the possibility of central lesions manifesting as PFP.

Previous research has shown that observers tend to form inaccurate and negatively biased first impressions of people with facial paralysis (FP). It has been hypothesised that this may be ameliorated by encouraging people to focus on channels of expression other than the face. This was tested in a web-based study of 466 participants. Participants in the Trained Condition received tips for perceiving expressiveness in individuals with FP, while those in the Untrained Condition received general medical information about FP. We observed no significant differences between groups for accuracy of emotion recognition, but a significant effect of the training upon perception of emotional intensity. These results show that attending to non-facial cues may improve social perception and reduce bias.

COVID-19 pandemic revealed several neurological syndromes related to this infection. We describe the clinical, laboratory, and radiological features of eight patients with COVID-19 who developed peripheral facial palsy during infection. In three patients, facial palsy was the first symptom. Nerve damage resulted in mild dysfunction in five patients and moderate in three. SARS-Cov-2 was not detected in CSF by PCR in any of the samples. Seven out of eight patients were treated with steroids and all patients have complete or partial recovery of the symptoms. Peripheral facial palsy should be added to the spectrum of neurological manifestations associated with COVID-19.