Topographic Consideration on the Occurrence of Ipsilesional Facial Paresis in Lateral Medullary Infarction.

INTRODUCTION: The purpose of this study was to identify course of the corticobulbar tract and factors associated with the occurrence of facial paresis (FP) in lateral medullary infarction (LMI). METHODS: Patients diagnosed with LMI who were admitted to tertiary hospital were retrospectively investigated and divided into two groups based on the presence of FP. FP was defined as grade 2 or more by the House-Brackmann scale. Differences between the two groups were analyzed with respect to anatomical location of the lesions, demographic data (age, sex), risk factors (diabetes, hypertension, smoking, prior stroke, atrial fibrillation, and other cardiac risk factors for stroke), large vessel involvement on magnetic resonance angiography, other symptoms and signs (sensory symptoms, gait ataxia, limb ataxia, dizziness, Horner syndrome, hoarseness, dysphagia, dysarthria, nystagmus, nausea/vomiting, headache, neck pain, diplopia, and hiccup). RESULTS: Among 44 LMI patients, 15 patients (34%) had FP, and all of them had ipsilesional central-type FP. The FP group tended to involve upper (p < 0.0001) and relative ventral (p = 0.019) part of the lateral medulla. Horizontally large lesion was also related to the presence of FP (p = 0.044). Dysphagia (p = 0.001), dysarthria (p = 0.003), and hiccups (p = 0.034) were more likely to be accompanied by FP. Otherwise, there were no significant differences. CONCLUSION: The results of present study indicate that the corticobulbar fibers innervating the lower face decussate at the upper level of the medulla and ascend through the dorsolateral medulla, where the concentration of the fibers is densest near the nucleus ambiguus.

Rare cases of Guillain-Barré syndrome after COVID-19 vaccination, Germany, December 2020 to August 2021.

BackgroundGuillain-Barré syndrome (GBS) has been associated with vaccination against COVID-19.AimWe aimed to compare clinical characteristics and analyse excess GBS cases following administration of different COVID-19 and influenza vaccines in Germany versus the expected numbers estimated from pre-pandemic background incidence rates.MethodsWe analysed safety surveillance data reported to the German national competent authority between 27 December 2020 and 31 August 2021. GBS cases were validated according to Brighton Collaboration (BC) criteria. We conducted observed vs expected (OvE) analyses on cases fulfilling BC criteria levels 1 to 4 for all four European Medicines Agency-approved COVID-19 vaccines and for influenza vaccines.ResultsA total of 214 GBS cases after COVID-19 vaccination had been reported, of whom 156 were eligible for further analysis. Standardised morbidity ratio estimates 3-42 days after vaccination were 0.34 (95% confidence interval (CI): 0.25-0.44) for Comirnaty, 0.38 (95% CI: 0.15-0.79) for Spikevax, 3.10 (95% CI: 2.44-3.88) for Vaxzevria, 4.16 (95% CI: 2.64-6.24) for COVID-19 Vaccine Janssen and 0.60 (95% CI: 0.35-0.94) for influenza vaccines. Bilateral facial paresis was reported in 19.7% and 26.1% of the 156 GBS cases following vaccination with Vaxzevria and COVID-19 Vaccine Janssen, respectively, and only in 6% of cases exposed to Comirnaty.ConclusionThree and four times more GBS cases than expected were reported after vaccination with Vaxzevria and COVID-19 Vaccine Janssen, respectively, therefore GBS might be an adverse event of vector-based vaccines. Bifacial paresis was more common in cases with GBS following vaccination with vector-based than mRNA COVID-19 vaccines.

Expanding the Phenotype of Hereditary Congenital Facial Paresis Type 3.

The HOXB1 gene encodes a homeobox transcription factor pivotal in the development of rhombomere 4. Biallelic pathogenic variants in this gene are associated with congenital facial paresis type 3 (HCFP3). Only seven single nucleotide variants have been reported in the literature to date. Here, we report a 27-year-old female with a unique presentation of HCFP3 with two novel compound-heterozygous missense variants: c.763C>G, p.(Arg255Gly), which arose de novo and an inherited c.781C>T, p.(Arg261Cys) variant. The patient exhibited HCFP3 symptoms with mild upward esodeviation and lacked the documented ear malformations common in HCFP. For many years, she was misdiagnosed with facio-scapulo-humeral muscular dystrophy, due to complaints of shoulder girdle and neck muscle weakness. No alternative genetic or acquired causes of neck and shoulder girdle weakness were found, suggesting its potential inclusion in the phenotypic spectrum.

Magnetic resonance imaging-negative myeloneuropathy and bilateral facial paresis unfurling systemic lupus erythematosus.

Systemic lupus erythematosus is a chronic autoimmune connective tissue disorder that can affect all the neuroaxes in the central and peripheral nervous systems. Myelopathy in systemic lupus erythematosus is one of the least common neuropsychiatric syndromes accounting for 1%-2% of cases. Myelopathy has long been diagnosed based on clinical findings, laboratory tests, and gold-standard gadolinium-enhanced magnetic resonance imaging (MRI). MRI-negative myelopathy is a recently described subset of myelopathies. Here, we report the case of a young woman from rural West Bengal, India, who presented with overlapping features of white-matter and gray-matter myelopathy associated with peripheral neuropathy and bilateral asymmetric lower motor neuron-type facial paresis. The historical analysis yielded clues toward an etiological diagnosis of systemic lupus erythematosus, further substantiated by seropositivity of lupus-specific autoantibodies. Her neurological disabilities responded poorly to oral administration of hydroxychloroquine, bolus intravenous administration of methylprednisolone, and high-dose cyclophosphamide therapy but eventually responded remarkably well to cyclical rituximab therapy. This case adds to the tally of cases of MRI-negative lupus myelopathy. MRI-negative myelopathy in systemic lupus erythematosus can be easily missed if not meticulous attention is paid during clinical history taking and examinations.

Differentiating Moebius syndrome and other congenital facial weakness disorders with electrodiagnostic studies.

INTRODUCTION: Congenital facial weakness (CFW) can result from facial nerve paresis with or without other cranial nerve and systemic involvement, or generalized neuropathic and myopathic disorders. Moebius syndrome is one type of CFW. In this study we explored the utility of electrodiagnostic studies (EDx) in the evaluation of individuals with CFW. METHODS: Forty-three subjects enrolled prospectively into a dedicated clinical protocol and had EDx evaluations, including blink reflex and facial and peripheral nerve conduction studies, with optional needle electromyography. RESULTS: MBS and hereditary congenital facial paresis (HCFP) subjects had low-amplitude cranial nerve 7 responses without other neuropathic or myopathic findings. Carriers of specific pathogenic variants in TUBB3 had, in addition, a generalized sensorimotor axonal polyneuropathy with demyelinating features. Myopathic findings were detected in individuals with Carey-Fineman-Ziter syndrome, myotonic dystrophy, other undefined myopathies, or CFW with arthrogryposis, ophthalmoplegia, and other system involvement. DISCUSSION: EDx in CFW subjects can assist in characterizing the underlying pathogenesis, as well as guide diagnosis and genetic counseling.

The course of facial corticobulbar tract fibers in the dorsolateral medulla oblongata.

BACKGROUND: The course of the corticobulbar tract (CBT) to the facial nucleus has been investigated by some previous studies. However, there are some unclear points of the course of the CBT to the facial nucleus. This study aimed to elucidate the detailed course of the CBT to the facial nucleus through the analysis of lateral medullary infarction (LMI) cases. METHODS: The neurological characteristics and magnetic resonance imaging findings of 33 consecutive patients with LMI were evaluated. The location of the lesions was classified rostro-caudally (upper, middle, or lower) and horizontally. Further, we compared the neurological characteristics between the groups with and without central facial paresis (FP). RESULTS: Eight (24%) patients with central FP ipsilateral to the lesion were identified. Dysphagia and hiccups were more frequently observed in the group with central FP than in the group without central FP. In patients with central FP, middle medullary lesions and those including the ventral part of the dorsolateral medulla were more frequently observed. Contrastingly, patients with lesions restricted to the lateral and dorsal regions of the dorsolateral medulla did not present with central FP. CONCLUSION: The results of this study indicate that the CBT to the facial nucleus descends with the corticospinal tract at least to the middle portion of the medulla, and then ascends to the facial nucleus through the medial and ventral areas of the dorsolateral medulla after decussation.

Variants affecting diverse domains of MEPE are associated with two distinct bone disorders, a craniofacial bone defect and otosclerosis.

PURPOSE: To characterize new molecular factors implicated in a hereditary congenital facial paresis (HCFP) family and otosclerosis. METHODS: We performed exome sequencing in a four-generation family presenting nonprogressive HCFP and mixed hearing loss (HL). MEPE was analyzed using either Sanger sequencing or molecular inversion probes combined with massive parallel sequencing in 89 otosclerosis families, 1604 unrelated affected subjects, and 1538 unscreened controls. RESULTS: Exome sequencing in the HCFP family led to the identification of a rare segregating heterozygous frameshift variant p.(Gln425Lysfs*38) in MEPE. As the HL phenotype in this family resembled otosclerosis, we performed variant burden and variance components analyses in a large otosclerosis cohort and demonstrated that nonsense and frameshift MEPE variants were significantly enriched in affected subjects (p = 0.0006-0.0060). CONCLUSION: MEPE exerts its function in bone homeostasis by two domains, an RGD and an acidic serine aspartate-rich MEPE-associated (ASARM) motif inhibiting respectively bone resorption and mineralization. All variants associated with otosclerosis are predicted to result in nonsense mediated decay or an ASARM-and-RGD-truncated MEPE. The HCFP variant is predicted to produce an ASARM-truncated MEPE with an intact RGD motif. This difference in effect on the protein corresponds with the presumed pathophysiology of both diseases, and provides a plausible molecular explanation for the distinct phenotypic outcome.

Magnetic resonance imaging of developmental facial paresis: a spectrum of complex anomalies.

PURPOSE: Despite its clinical implications, the MRI features of developmental facial paresis (DFP) were described in a few case reports. This study aims to describe MRI features of DFP in relation to the embryological development with a proposed radiological new grading system. METHODS: The clinical records and MRI of the brain and internal auditory canal of 11 children with DFP were retrospectively reviewed. The following sequences were analyzed: axial, oblique sagittal SPACE of the internal auditory canal and brainstem; axial T2, T1WI and coronal T2WI of the brain. The severity of the maldevelopment of the seventh nerve was graded from 0 to 4: 0 = no abnormalities, 1 = unilateral facial nerve hypoplasia, 2 = unilateral facial nerve aplasia, 3 = aplasia or hypoplasia involving facial nerves on both sides, and 4 = facial nerve aplasia or hypoplasia associated with other cranial nerve palsy. RESULTS: Isolated facial nerve palsy was diagnosed in seven patients. It was of grade 1 in five and grade 3 in two. Hypoplasia of the nerve with interrupted course was encountered in two cases. Other associated cranial nerve abnormalities (grade 4) were seen in four patients; two of them were diagnosed previously as Moebius syndrome. In addition to inner ear anomalies, middle and external ear and parotid gland anomalies were described. CONCLUSION: To our knowledge, this is the largest series of patients with DFP that represents a continuum of isolated and combined malformations. Understanding of embryological basis can give insights into the anomalous development of the facial nerve.

Progressive cranial nerve involvement and grading of facial paralysis in gelsolin amyloidosis.

INTRODUCTION: Hereditary gelsolin amyloidosis (GA) is a rare condition caused by the gelsolin gene mutation. The diagnostic triad includes corneal lattice dystrophy (type 2), progressive bilateral facial paralysis, and cutis laxa. Detailed information on facial paralysis in GA and the extent of cranial nerve injury is lacking. METHODS: 29 GA patients undergoing facial corrective surgery were interviewed, examined, and studied electroneurophysiologically. RESULTS: All showed dysfunction of facial (VII) and trigeminal (V) nerves, two-thirds of oculomotor (III) and hypoglossal (XII) nerves, and half of vestibulocochlear (acoustic) (VIII) nerve. Clinical involvement of frontal, zygomatic, and buccal facial nerve branches was seen in 97%, 83%, and 52% of patients, respectively. Electromyography showed marked motor unit potential loss in facial musculature. CONCLUSIONS: Cranial nerve involvement in GA is more widespread than previously described, and correlates with age, severity of facial paralysis, and electromyographic findings. We describe a grading method for bilateral facial paralysis in GA, which is essential for evaluation of disease progression and the need for treatment.

Botulinum Toxin Injections to Manage Sequelae of Peripheral Facial Palsy.

Long-standing facial palsy sequelae cause functional, aesthetic, and psychological problems in patients. Botulinum toxin is an effective way to manage them, but no standardized recommendations exist. Through this non-systematic review, we aimed to guide any practitioner willing to master the ins and outs of this activity. We reviewed the existing literature and completed, with our experience as a reference center, different strategies of botulinum toxin injections used in facial palsy patients, including history, physiopathology, facial analysis, dosages, injection sites, and techniques, as well as time intervals between injections. The reader will find all the theorical information needed to best guide injections according to the patient's complaint, which is the most important information to consider.

Management of paracondylar process fracture in three horses.

BACKGROUND: Fractures of the paracondylar process of the occipital bone may cause headshaking, neck pain and neurologic deficits. The condition is being recognised more frequently with increasing availability of computed tomography. However, to date only limited information is available as to presentation, treatment, surgical approach and outcome. OBJECTIVES: To describe the clinical signs, imaging findings, treatment, surgical approach and outcome in three horses diagnosed with paracondylar process fracture. STUDY DESIGN: Retrospective case series. METHODS: Clinical records and diagnostic images of affected cases were reviewed. RESULTS: Two cases had ventral nonunion fractures-one of these presented with neck pain, headshaking and behavioural changes, while in the other the fracture was a suspected incidental finding in a case of poor performance. A third case with a more dorsal fracture presented with acute facial nerve paralysis. Diagnosis was by computed tomography in all cases, although imaging of ventral fractures by radiography was found to be feasible. Where clinical signs could be associated confidently with the fracture, conservative management resulted in improvement but not complete resolution. Repeated recurrence of clinical signs after prolonged periods of remission necessitated surgical removal in one case, which was readily accomplished with the aid of ultrasound guidance, and led to rapid resolution of clinical signs without significant post-operative complications. The surgical approach is described. MAIN LIMITATIONS: Limited follow-up was available. CONCLUSIONS: Paracondylar process fracture should be considered as a differential diagnosis for headshaking, neck pain, poor performance and facial paresis, and is a justification for performing computed tomography in such cases. A multi-disciplinary approach is beneficial due to the potential for orthopaedic, neurologic, ophthalmologic and behavioural clinical signs, with additional need for expertise in diagnostic imaging and pain management. Surgical fragment removal should be considered for ventral fractures.

Facial palsy at the onset of SARS-CoV-2 infection. A case report.

Introduction: SARS-CoV-2 infection has been associated with an increased number of deaths, due to severe respiratory damage, cardiovascular impairment, acute renal failure, and also neurological injury, including stroke, which is most commonly responsible for death. These are elements that determine patients to seek medical advice. Case report: This is a case report of a female Caucasian patient, aged 65 years, with type 2 diabetes mellitus on metformin 1000 mg twice/day, and hypertension, who presented to the emergency department with one day history of left orbital hyperlacrimation and chewing and swallowing difficulty. On physical examination there was a decreased blink reflex, flattened nasolabial fold, and drooping left corner of the mouth, with left conjunctival hyperemia, and a present corneal reflex. Motion limited head CT and MRI revealed no pathological changes suggestive for the appearance of paresis. The patient was transferred to the Department of Infectious Diseases after laboratory confirmation of SARS-CoV-2 infection. Under treatment, improvement of paresis after three days was observed, with minimal asymmetry left five days after admission. A reassessment one month after discharge revealed complete recovery of the paresis, physical asthenia, and headache, in the context of long-COVID syndrome. Conclusions: The appearance of paresis may be a consequence of the direct action of the virus on the nervous system, of hypercoagulability, or, later, of an immune mechanism. The case presented is judged as an early, direct action of the virus on the central nervous system, the respiratory symptoms were minimized by the patient at the time of presentation.

V to VII Nerve Transfer for Smile Reanimation.

Using the wording "facial reanimation," surgeons mean restoring movements to the paralyzed face. According to the condition of mimic muscle, facial palsy can be classified as recent (mimic muscle still alive) and chronic (atrophy of mimic muscle) palsy. The treatment is quite different because in the former group the mimic muscles can be still used so long as a new motor source would be connected to the damaged facial nerve. In the latter group, muscular transplantation is needed to substitute the atrophied mimic muscles of the middle part of the face. In both cases, the neural impulse that makes the muscles (mimic muscle in the former, transplanted muscle in the latter) move come from a new motor nerve. Nowadays, the masseteric nerve is widely used as a new motor source in recent facial reanimation; the same nerve has also a main role in the treatment of both chronic facial palsy where it is used as the new nervous stimulus for the new transplanted muscle and facial paresis where the nervous stimulus coming from the masseteric nerve is used to empower the stimulus coming from the injured facial nerve. The masseteric nerve can be usually connected directly to the facial nerve without the interposition of a nerve graft, with a faster reinnervation. Moreover, the use of the masseteric nerve gives no morbidity to the masticatory functions.

Moebius Syndrome: What We Know So Far.

Moebius syndrome (MBS) is a rare congenital cranial nerve disorder characterized by unilateral, bilateral symmetrical, or asymmetrical facial (VII) and abducens (VI) nerve palsies. Genetics and rhombencephalon vascular disturbances from intrauterine environmental exposures have been attributed to its development. It can present with various orofacial abnormalities. Although the diagnosis is purely clinical, certain characteristic features are present in the brain's images. With no cure, it is essential to devise management on a personalized basis. We discuss etiology, presentation, diagnostic approaches, and effective management in the existing literature. This comprehensive review examines the clinic-pathological aspects of Moebius syndrome. The authors employed the PUBMED base index to identify pertinent literature and reference it according to research keywords. Findings suggest the most popular etiology is the theory of intrauterine vascular disruption to the brainstem during embryogenesis, followed by the genetic hypothesis. Intrauterine environmental exposures have been implicated as potential risk factors. Facial and abducens nerve palsies are the most common presenting features. However, clinical manifestations of lower cranial nerves (IX, X, XI, XII) may be present with orthopedic anomalies and intellectual deficiencies. The diagnosis is clinical with minimal defined diagnostic criteria. Characteristic radiological manifestations involving the brainstem and cerebellum can be observed in imaging studies. With no definitive treatment options, a multidisciplinary approach is employed to provide supportive care. Despite radiological manifestations, Moebius syndrome is diagnosed clinically. Although incurable, a multidisciplinary approach, with personalized rehabilitative measures, can manage physical and psychological deficits; however, standard guidelines need to be established.

Assessment of Nerve Conduction in Patients With Lower Motor Neuron Facial Paralysis.

Introduction Bell's palsy (BP), a lower motor neuron facial paralysis, commonly causes dysfunction of muscles of facial expression. Nerve conduction electrodiagnostic studies differentiate early-stage minor conduction blocks from later-stage Wallerian degeneration. Nerve conduction studies (NCSs) assess facial nerve function by delivering supramaximal electrical stimulus at the stylomastoid foramen. The amplitude loss percentage of the affected side is calculated with reference to the normal side. Aim The study's aim was to characterize the ncs in BP cases and to evaluate the correlation between the Compound Muscle Action Potential (CMAP) of the muscles affected. Materials and methods One hundred and four NCS data of BP cases were retrospectively collected over the period of two years. Statistical analyses of variables were done using the Chi-square test, one-way ANOVA, and Pearson correlation coefficient. Result The greater amplitude loss was seen in the orbicularis oris muscle innervated by buccal and mandibular branches of the facial nerve. The bivariate correlation between the Right Nasalis versus Right Orbicularis Oculi and Left Orbicularis Oculi versus Left Nasalis showed a highly significant moderately Strong Positive Correlation with an R-value of 0.687 and 0.558, respectively. The amplitude drop percentage was statistically significant in the affected left and right sides with P values of 0.008 and 0.007 respectively (P value < 0.05). The amplitude drop between the nasalis, orbicularis oculi and orbicularis oris muscles of both sides was statistically significant with a P value of 0.001. Conclusion NCS should be mandatorily included as an assessment protocol in BP cases for quantification of nerve degeneration and as a prognostic tool during the course of treatment.

Systemic Steroids for Otolaryngology-Head and Neck Surgery Disorders: An Evidence-Based Primer for Clinicians.

OBJECTIVE: To offer pragmatic, evidence-informed guidance on the use of systemic corticosteroids (SCS) for common otolaryngologic disorders. DATA SOURCES: PubMed, Cochrane Library, and American Academy of Otolaryngology-Head and Neck Surgery Foundation clinical practice guidelines. REVIEW METHODS: A comprehensive search of published literature through November 2021 was conducted on the efficacy of SCS, alone or in combination with other treatments, for managing disorders in otolaryngology and the subdisciplines. Clinical practice guidelines, systematic reviews, and randomized controlled trials, when available, were preferentially retrieved. Interventions and outcomes of SCS use were compiled to generate summary tables and narrative synthesis of findings. CONCLUSIONS: Evidence on the effectiveness of SCS varies widely across otolaryngology disorders. High-level evidence supports SCS use for Bell's palsy, sinonasal polyposis, and lower airway disease. Conversely, evidence is weak or absent for upper respiratory tract infection, eustachian tube dysfunction, benign paroxysmal positional vertigo, adenotonsillar hypertrophy, or nonallergic rhinitis. Evidence is indeterminate for acute laryngitis, acute pharyngitis, acute sinusitis, angioedema, chronic rhinosinusitis without polyps, Ménière's disease, postviral olfactory loss, postoperative nerve paresis/paralysis, facial pain, and sudden sensorineural hearing loss. IMPLICATIONS FOR PRACTICE: Clinicians should bring an evidence-informed lens to SCS prescribing to best counsel patients regarding the risks, anticipated benefits, and limited data on long-term effects. Alternate routes of corticosteroid administration-such as sprays, drops, inhalers, and intralesional injections-may be preferable for many disorders, particularly those that are self-limited or require a prolonged duration of therapy. Prudent use of SCS reduces the risk of medication-related adverse effects. Clinicians who are conversant with high-level evidence can achieve optimal outcomes and stewardship when prescribing SCS.

Is There a Difference in Facial Emotion Recognition after Stroke with vs. without Central Facial Paresis?

The Facial Feedback Hypothesis (FFH) states that facial emotion recognition is based on the imitation of facial emotional expressions and the processing of physiological feedback. In the light of limited and contradictory evidence, this hypothesis is still being debated. Therefore, in the present study, emotion recognition was tested in patients with central facial paresis after stroke. Performance in facial vs. auditory emotion recognition was assessed in patients with vs. without facial paresis. The accuracy of objective facial emotion recognition was significantly lower in patients with vs. without facial paresis and also in comparison to healthy controls. Moreover, for patients with facial paresis, the accuracy measure for facial emotion recognition was significantly worse than that for auditory emotion recognition. Finally, in patients with facial paresis, the subjective judgements of their own facial emotion recognition abilities differed strongly from their objective performances. This pattern of results demonstrates a specific deficit in facial emotion recognition in central facial paresis and thus provides support for the FFH and points out certain effects of stroke.

Dysarthria-Facial Paresis and Rostral Pontine Ischemic Stroke.

We describe an acute, postoperative dysarthria-facial paresis. While the rare stroke syndrome has been described previously, we present an under-described clinical nuance to its presentation with a particularly clear imaging correlation. A 78-year-old, right-handed man with a past medical history of aortic stenosis presented after a transcatheter aortic valve replacement. Immediately postoperatively, no neurological deficits were noted. That evening, he described his speech as "drunken." He was later noted to have a right lower facial droop in addition to the speech change. His speech exhibited labial, lingual, and (to a lesser degree) guttural dysarthria. At the patient's request due to claustrophobia, he received 2 mg of oral lorazepam prior to cranial imaging. Afterwards, he was sleepy but arousable, yet was unable to put pen to paper when asked to write. Right lower facial paresis persisted, but he now demonstrated a right pronator drift, which resolved after 14 h without other evolution to his clinical examination. Brainstem lesions above the level of the pontine facial nucleus may present with central facial paresis contralateral to the lesion. An associated dysarthria may have both labial and lingual features in the absence of tongue or pharyngeal weakness. Our review of reported cases of dysarthria in isolation, dysarthria in combination with facial paresis, and facial paresis finds that all presentations may result from cortical, subcortical, or brainstem involvement. Stroke mechanisms are most commonly thromboembolic or small-vessel-ischemic in either the anterior or posterior circulations.

Facial Paresis After Mandibular Reconstruction.

Condylar neck fractures are common injuries that occur in the facial and mandibular regions. The proximity of this area to the vital neurovasculature creates the increased importance of proper surgical intervention to limit damage to the underlying structures. Here, we report a case of a condylar neck fracture that resulted in temporary paresis of the facial nerve. In addition, a review of the literature regarding condylar fracture treatment and its complications was conducted.

Mild Facial Paresis in a Recipient of Gam-COVID-Vac Vaccine: A Case Report.

Facial paralysis has been reported as a rare side effect of mRNA COVID-19 vaccines. The Gam-COVID-Vac was introduced in August 2020 in Russia. There was no report of facial paralysis in phase I to III clinical trials of the vaccine. To our knowledge, there is no post-marketing report of facial paresis with Gam-COVID-Vac vaccination to this date. The Gam-COVID-Vac vaccine has a reported efficacy of 90%, but its safety and efficacy have not been approved by international organizations to this date. Iran is among the countries using the Gam-COVID-Vac vaccine. Here, we present a case of mild facial paresis that occurred shortly after the Gam-COVID-Vac vaccine administration in a female healthcare worker.