BackgroundSudden onset of unilateral weakness of the upper and lower muscles of one side of the face is defined as peripheral facial nerve palsy. Peripheral facial nerve palsy is often idiopathic and sometimes it could be due to infectious, traumatic, neoplastic, and immune causes. This study aimed to report the clinical manifestation, evaluation, and prognosis in children with peripheral facial nerve palsy.Methods57 children under 18 years of age diagnosed with peripheral facial nerve palsy at Çukurova University, Balcalı Hospital, between January 2018 and September 2021, were included in the study.ResultsThe mean age of the children at the time of diagnosis was 9.6 ± 7, 4 years. Thirty-two (56.1%) of the patients were female and 25 (43.9%) were male. A total of 57 patients were diagnosed with peripheral facial nerve palsy and categorized into many groups by etiology: idiopathic Bell’s palsy in 27 (47.5%), infectious in 11 (19.2%), traumatic in 6 (10.5%), and others (due to congenital, immune, neoplastic, Melkersson–Rosenthal syndrome, drug toxicity, and iatrogenic causes) in 13 (22.8%). Forty-six of the children achieved full recovery under oral steroids within 1–7 months. Four patients with acute leukemia, myelodysplastic syndrome, Mobius syndrome and trauma did not recover and two patients (schwannoma, trauma) showed partial improvement. Five patients could not come to follow-up control.ConclusionPeripheral facial nerve palsy is a rare condition in children with different causes. It could be idiopathic, congenital, or due to infectious, traumatic, neoplastic, and immune reasons. So, when a child presents with facial palsy, a complete clinical history and a detailed clinical examination are recommended. Giving attention to the red flag is very important. Peripheral facial nerve palsy in children is considered to have a good prognosis.

Peripheral facial paralysis, caused by damage to the lower motor neurons of the facial nerve, is a neurological disorder characterized by partial or complete loss of facial expression. It typically manifests suddenly with symptoms such as post-auricular pain, diminished taste, excessive tearing, difficulty speaking, and facial muscle twitching. Depending on the underlying cause, this condition can be categorized into spontaneous facial nerve palsy, peripheral facial paralysis induced by Guillain-Barré syndrome, and peripheral facial paralysis caused by brainstem lesions. Among these, the most common type is Bell’s palsy, which usually presents as sudden unilateral facial muscle paralysis. The incidence rate is approximately 20 to 40 cases per 100,000 people annually, with patients ranging in age from young to old, although it is most prevalent in those aged 20 to 40, and it tends to occur more frequently in men than in women. Conventional treatments for peripheral facial nerve paralysis include hormone therapy, antiviral medication, and surgical intervention. However, hormone therapy may not be effective for some patients due to its side effects, the efficacy of antiviral therapy remains controversial, and surgery is costly and may lead to postoperative complications. Traditional Chinese Medicine (TCM) acupuncture therapy, with a long-standing history, has been widely used to treat such facial nerve disorders as documented in the "Huangdi Neijing · Suwen."

Purpose: To evaluate the findings of normal facial nerve, as seen on oblique sagittal MRI using a TMJ (temporomandibular joint) surface coil, and then to evaluate abnormal findings of peripheral facial nerve palsy. Materials and Methods: We retrospectively reviewed the MR findings of 20 patients with peripheral facial palsy and 50 normal facial nerves of 36 patients without facial palsy. All underwent oblique sagittal MRI using a TMJ surface coil. We analyzed the course, signal intensity, thickness, location, and degree of enhancement of the facial nerve. According to the angle made by the proximal parotid segment on the axis of the mastoid segment, course was classified as anterior angulation (obtuse and acute, or buckling), straight and posterior angulation. Results: Among 50 normal facial nerves, 24 (48%) were straight, and 23 (46%) demonstrated anterior angulation; 34 (68%) showed iso signal intensity on T1WI. In the group of patients, course on the affected side was either straight (40%) or showed anterior angulation (55%), and signal intensity in 80% of cases was isointense. These findings were similar to those in the normal group, but in patients with post-traumatic or post-operative facial palsy, buckling, of course, appeared. In 12 of 18 facial palsy cases (66.6%) in which contrast materials were administered, a normal facial nerve of the opposite facial canal showed mild enhancement on more than one segment, but on the affected side the facial nerve showed diffuse enhancement in all 14 patients with acute facial palsy. Eleven of these (79%) showed fair or marked enhancement on more than one segment, and in 12 (86%), mild enhancement of the proximal parotid segment was noted. Four of six chronic facial palsy cases (66.6%) showed atrophy of the facial nerve. Conclusion: When oblique sagittal MR images are obtained using a TMJ surface coil, enhancement of the proximal parotid segment of the facial nerve and fair or marked enhancement of at least one segment within the facial canal always suggests pathology of the facial nerve. The use of this modality, together with the coil, is, therefore, an effective complementary technique for the evaluation of a facial nerve.

Cases of central nervous system (CNS) disorders manifesting peripheral type facial palsy are rare. We report a 70‐year‐old man with a small infarct of the pontine tegmentum who presented with acute‐onset peripheral facial palsy. In the case of infarction in this area, combined symptoms of peripheral facial palsy and abducens nerve palsy are often found, but peripheral facial palsy may occur as the only symptom as in our present case. In the differential diagnosis of peripheral facial nerve palsy, we should also consider the possibility of stroke such as pontine tegmentum infarction.

Facial nerve palsy is the most common cranial nerve disorder. There is no consensus on a single diagnostic tool deemed as the 'gold standard' for distinguishing between idiopathic (Bell's palsy) and symptomatic causes. The diagnosis is one of exclusion and most often made on physical examination. In the present study, we describe the etiological background of peripheral facial palsy in N = 509 patients and evaluate the relevance of cerebrospinal fluid (CSF) analysis and magnetic resonance imaging (MRI) in differential diagnosis. We carried out a retrospective data analysis of 509 patients with the clinical diagnosis of peripheral facial palsy admitted to our emergency unit between January 2006 and January 2017. All patients were seen clinically; their CSF was analyzed and MRI was performed. Of N = 526 patients with isolated facial palsy, 17 patients were excluded because they did not consent to CSF analysis. Of the remaining N = 509 patients, 383 patients (75.2%) were diagnosed with idiopathic facial palsy. In the remaining 126 patients (24.8%), the following etiologies for facial palsy could be found: Ramsay-Hunt-Syndrome (N = 34), Lyme Neuroborreliosis (N = 32), other viral/bacterial central nervous system (CNS) infections (N = 8), neoplasias (N = 18), autoimmune disease (N = 12), otogenous processes (N = 6), or other etiologies (N = 16). Analysis of the CSF showed 85% sensitivity for Ramsay-Hunt-Syndrome and 100% for Lyme Neuroborreliosis and other viral/bacterial CNS infections. CSF analysis proved a reliable diagnostic tool for identifying these subgroups. MRI with contrast compounds, as performed in 409 patients, was the most important tool in diagnosing neoplasias (88% sensitivity) and otogenous processes (83% sensitivity). MRI with contrast-enhancing compounds did not reveal additional information concerning inflammatory facial nerve lesions when performed the same day as hospital admission. Although peripheral facial palsy was predominantly idiopathic (75.3%) in our cohort, the disease was caused in approximately 25% of the patients by factors which require specific treatment. In the present study, CSF analysis proved to be the leading method for the diagnosis of Ramsay-Hunt-Syndrome, Lyme Neuroborreliosis, and other CNS infections. These subgroups made up approximately 15% of our cohort. To detect these subgroups reliably, routine use of CSF analysis in peripheral facial palsy may be advisable, whereas MRI proved to be useful for exclusion of otogenic and neoplastic processes with a sensitivity of 83% and 88%. We found that the use of MRI with contrast-enhancing compounds does not provide additional diagnostic information on the day of hospital admission. Hence, the potential benefits of routine use of MRI in patients with facial nerve palsy should be weighed against health care cost factors.

Objectives: This study reports on the efficacy of Korean medicine treatments for peripheral facial nerve palsy and sleep disorders that occur after microvascular decompression.Methods: A 57-year-old female patient with right facial palsy was treated with herbal medicines and acupuncture for 36 days. The treatment effect was evaluated using the House Brackmann Grading System (HBGS), Yanagihara’s Unweighed Grading System (Yanagihara’s score), and the Korean Modified Leeds Sleep Evaluation Questionnaire (KMLSEQ).Results: Following treatment, the patient showed a decrease in HBGS and an improvement in Yanagihara’s score and KMLSEQ score.Conclusions: Korean medicine treatments appeared to be effective in reducing facial nerve palsy. Further clinical research on patients with facial nerve palsy is needed.

Key words: Bell's palsy, brainstem glioma, magnetic reso- nance imaging Introduction Facial palsy of the peripheral type is generally seen in the pain clinic and is often treated with a stellate gang- lion block. The most common cause of peripheral facial nerve palsy is Bell's palsy, although its etiology remains controversial. The diagnosis of Bell's palsy is usually made by exclusion of other conditions such as herpes zoster oticus (Ramsay Hunt syndrome), trauma (including skull base fracture and surgery), otitis media, and neoplasm [1]. Isolated peripheral facial nerve palsy of neoplastic origin is uncommon. We herein describe a case of peripheral facial nerve palsy which was initially diag- nosed as Bell's palsy but was later found to be caused by an intrinsic brain stem tumor. Case report A 9-year-old boy presented to the Pediatric Depart- ment of our University Hospital in August 1990 with left facial weakness. His mother noticed the hyperemic conjunctiva and lacrimation of his left eye at the end of June. Consultation with the ophthalmologist revealed no abnormality in his left eye and the hyperemia im- proved with conservative therapy. In July, facial asym- metry became obvious. He was diagnosed as having Bell's palsy by a pediatrician in August and was referred to. our pain clinic. Address correspondence to: K. Kodama Received for publication on May 31, 1993; accepted on January 6, 1994 Upon examination, the patient had a left facial nerve palsy of the peripheral type (score of the facial paresis was 24/40), however, no other neurological deficits were seen. An audiogram failed to reveal a hearing abnormality. Although repeated stellate ganglion block was given, his facial palsy progressed slowly over a 2- month period, suggesting an etiology other than Bell's palsy. Magnetic resonance imaging (MRI) in September demonstrated a tumor in the left pons and brachium pontis extending into the left cerebellopontine angle (Fig. 1). The lesion was seen as a hypointense and hyperintense area on T1- and T2-weighted images, re- spectively. He was admitted to the Neurosurgical De- partment on September 29. The positive neurological findings on admission were Bruns' nystagmus, absence of left corneal reflex, decreased gag reflex, and mild trunkal ataxia, in addition to left facial nerve palsy. He underwent a wide suboccipital decompressive craniec- tomy, and biopsy of the tumor indicated low-grade glioma. In spite of postoperative radiation (60 Gy) and chemotherapy including Ranimustine and tumor necro- sis factor, he died due to tumor progression 17 months from the time of his initial symptom. Discussion Eighty percent of peripheral facial nerve palsy cases represent idiopathic or Bell's palsy, of which approxi- mately 20% can be demonstrated to have a specific etiology [2]. Peripheral facial nerve palsy with neoplas- tic origin is uncommon, and is estimated to be the cause in approximately 5% of all cases [3]. The diagnosis of Bell's palsy is unjustified unless an accurate history is taken along with a careful examina- tion of the ear and central nervous system (CNS). The differential diagnosis of neoplastic facial palsy is vast

Communication about diagnosis and medical treatment for children suffering from life-threatening illnesses is complex. It is a primary step in involving underage patients and families in care and lays the...

Background/Aims: The conventional systemic corticosteroid treatment for acute peripheral facial nerve palsy in patients with type 2 diabetes mellitus can induce hyperglycemia, and an alternative local therapy may be necessary. Our purpose in this study is to evaluate therapeutic effects of stellate ganglion block (SGB) on facial nerve palsy in patients with type 2 diabetes mellitus. Methods: A total of 361 cases of acute peripheral, chronic peripheral, acute central and chronic central facial nerve palsy treated with SGB or conventional therapy were included in this retrospective study. The facial nerve function score (Sunnybrook Facial Grading System) obtained at before and after treatment in non-SGB and SGB groups was used to assess the outcome. Furthermore, the blood glucose level in acute peripheral facial nerve palsy was measured. Results: The facial nerve function score in the SGB group was higher than that in the non-SGB group after treatment in peripheral facial nerve palsy, while the blood glucose level in the non-SGB group increased and was higher than that in the SGB group during the treatment in acute peripheral facial nerve palsy. Conclusions: Our findings suggest that SGB has better therapeutic effect than conventional treatment on acute and chronic peripheral facial nerve palsy in patients with type 2 diabetes mellitus.

Objectives: The purpose of this study is to investigate the effectiveness of using Korean medical treatment for peripheral facial nerve palsy.Methods: We primarily treated the patient’s peripheral facial nerve palsy during hospitalization (06/28/21~07/13/21) without any other steroids or antiviral drug treatments and additionally treated their spinal stenosis, using Korean medical treatments in both cases (herbal medicine, acupuncture, and herbal acupuncture therapy). The House-Brackmann grading system and Yanagihara’s unweighted grading system were used to assess facial symptom changes, and the Numerical Rating Scale was used to evaluate the back pain caused by the spinal stenosis.Results: Following treatment, the patient’s House-Brackmann and Numerical Rating Scale scores decreased, while their Yanagihara unweighted score improved.Conclusions: This study suggests that Korean medicine may be effective in the treatment of facial nerve palsy.

Background: This retrospective study aimed to determine whether there were correlations between the number and type of accompanying symptoms of peripheral facial nerve palsy, and surface electromyography (SEMG) and clinical assessment scales to help diagnosis.Methods: There were 30, cases of peripheral facial nerve palsy at Visit 1 to the Korean Medicine Hospital, Dong-eui University, 22 cases at Visit 2 and 10 cases at Visit 3. The study period was from July 19, 2021 to November 31, 2021. Symptoms were evaluated three times (with two-week intervals which began 7 days from onset) using SEMG, clinical assessment scales and accompanying symptoms. In this study, the House-Brackmann grading system (HBGS), and the Yanagihara’s unweighted grading system (Y-score) clinical assessment scales were used. The Pearson or Spearman correlation was used for statistical analysis.Results: On Visit 1, the number of accompanying symptoms of peripheral facial nerve palsy had no significant correlation with other measures. On Visits 1-3, the HBGS score had a significant negative correlation with the Y-score. On Visit 2, most of the mean values measured had significant correlations with each other although not between SEMG-Z and SEMG-O that Z means a zygomaticus muscle and O means a orbicularis oris muscle. On Visit 3, the number of accompanying symptoms significantly correlated with the clinical assessment scales. The HBGS score, Y-score, and SEMG measurements (except SEMG-Z) had significant correlations with each other. A significant positive correlation between SEMG-Z and SEMG-T was noted.Conclusion: We predict accompanying symptoms can be used to diagnose the peripheral facial nerve palsy including both clinical assessment scales and SEMG measurements at 2-5 weeks after onset.

Peripheral facial nerve palsy is one of the most common cranial nerve disease. There can be multiple etiologies including trauma, infection, idiopathic conditions. In rare case, during dental treatment including extraction, peripheral facial palsy also can occur. Based on the time of onset and duration of the symptom, facial palsy could be classified on immediate or delayed. Immediate facial palsy is relatively common and mainly associated with the injection of local anesthetic. However, in case that onset of facial palsy and symptom are delayed, it is difficult to determine the pathogenesis. We report a rare case of delayed facial palsy as a complication of tooth extraction, which occurred 5 days after the tooth extraction and subsided in about 1 month and discuss the possible etiology and management.

<p class="abstract"><strong>Background:</strong> A facial paralysis is one of the most emotionally traumatic deficits a person can experience. It is essential to understand the cause and nature of nerve injury and undertake proper measures for restoration and rehabilitation of facial symmetry. The present study was conducted to evaluate the various aetiologies of lower motor neuron facial paralysis that presented to our department. The aim of the present study is to investigate into the demographic data and etiology associated with peripheral facial nerve paralysis and to assess the site of lesion, severity grade and treatment outcome of peripheral facial nerve paralysis.</p><p class="abstract"><strong>Methods:</strong> A prospective longitudinal study conducted in a tertiary care hospital, over a time period of one and a half years from November 2014 to April 2016. All the patients were assessed regarding the time of onset of symptoms, rapidity of progression, duration and completeness of paralysis. Topo diagnostic tests were done to assess the site of lesion and response to treatment monitored. </p><p class="abstract"><strong>Results:</strong> The most common cause for LMN facial nerve paralysis was external trauma and Bell’s palsy. The mean age group was 37.5 years with a male preponderance. Majority of the lesions were suprageniculate and had a House Brackmann grade IV severity score.</p><p class="abstract"><strong>Conclusions:</strong> Peripheral facial paralysis showed a good response to treatment and timely intervention would result in a full or partial recovery at the end of a follow up.</p><p align="left"> </p>

A 40-year-old woman with Cat-scratch disease sought treatment for neuroretinitis OD and right peripheral facial nerve palsy. To our knowledge, this is the first case of an adult with a peripheral facial nerve palsy from Cat-scratch disease and the first case of a patient with both neuroretinitis and peripheral facial nerve palsy.

The prognosis of the peripheral facial nerve palsy is good on the whole. However, the prognosis is not favorable when nerve degeneration is severe in the early stage and when steroid therapy is delayed. The facial nerve decompression surgery could be applied to those patients with poor prognosis. The authors performed this study to analyze the results of the facial nerve decompression surgery using middle fossa approach and/or combined with transmastoid approach, and to evaluate its usefulness. This retrospective study was undertaken in 9 patients with peripheral facial nerve palsy who received facial nerve decompression surgery between Jan. 2003 and Dec. 2012. The number of patient with Bell's palsy and Herpes zoster oticus was 5 and 4, respectively. The patients comprise 3 men and 6 women, aged between 41 and 65 years (average age: 55.4 years). All patients had HB grade V of facial nerve palsy before surgery, and neural degeneration between 92 and 100% (average: 96.6%) in electroneurography (ENoG). The average time took until operation was 24.8 days (18–33). 7 out of 9 patients improved facial palsy to some extent within 1 week after operation. It took average of 7.3 weeks (1–15) to reach to HB grade III. It took average of 21.3 weeks (10–26) to reach the final degree of facial palsy which is HB grade I in 4 patients, and HB grade II in 5 patients on 1 year of follow-up. There was no relationship in causes of palsy or time to operation from onset of palsy with respect to the final degree of the palsy. 9 patients who have facial nerve palsy but not done surgical decompression are served as negative control. All of them showed facial palsy of H-B grade V. 6 of 9 patients were recovered to HB grade I or II. However, remaining 3 patients showed poor prognosis of facial palsy less than HB grade IV. Average 5 months (3–7 months) are required that improved to H-B grade III. The time taken to reach the final facial palsy status is average 9.12 months (3–24 months)