Cause Of Peripheral Facial Palsy Research Articles

Paralisi periferica monolaterale del VII nervo cranico da riattivazione di virus varicella zoster: la sindrome di Ramsay Hunt

Ramsay Hunt syndrome is the second leading cause of peripheral facial palsy in children, and it is due to reactivation of Varicella Zoster Virus. A characteristic feature of this syndrome is the triad of ipsilateral facial palsy, otalgia and vesicular rash in the auricle or auditory canal. The diagnosis is clinical, and currently there is no international protocol on its paediatric management and treatment. The paper reports the case of a 10-year-old girl, who presented with symptoms suggestive of peripheral facial palsy and, consequently, was treated with steroid therapy at first. After the appearance of vesicles in the auricular site and having ruled out the other causes of peripheral paralysis of the VII cranial nerve, antiviral therapy was undertaken and, given the poor clinical improvement, was later enhanced corticosteroid therapy. One month after onset, the child recovered com-pletely.

An Interesting Case of Bell’s Palsy in Pregnancy Associated with COVID-19 Infection

Recent studies have reported that Coronavirus Disease 2019 (COVID-19) can be the cause of peripheral facial paralysis and neurological symptoms may be the only manifestation of the disease. Hereby, the authors report an interesting case of a pregnant COVID-19 positive female with Bell's palsy, in third trimester of pregnancy. A 33-year-old female, G3P0L0A2, presented with left-side deviation of angle of mouth, excessive lacrimation and redness of right eye for the past three days. She had involuntary drooling on right and left side labial commissural deviation, absence of forehead frowning, inability to close her right eye (positive Bell’s phenomena), and ipsilateral lagophthalmos. No lesions were seen on the external ear and otoscopy was normal. She was confirmed to have right-sided facial nerve palsy. She had an uneventful course of pregnancy till term and underwent caesarean section at 40 weeks, in view of foetal distress. Pregnancy and Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection, both are immunocompromised state, and hence could be a risk factor for Bell’s palsy. But larger studies with more cases are required to prove the causal association.

Ramsay Hunt's Syndrome in Pediatric Age

AbstractThe Ramsay Hunt's syndrome (RHS), caused by the reactivation of the varicella-zoster virus (VZV), is an infrequent cause of peripheral facial palsy in the pediatric patients. A 16-year-old adolescent boy presented with headache, right earache, and signs of lower motor neuron type facial palsy. He was medicated with deflazacort. Four days later, he developed blurry vision in the right eye, gait imbalance, and vesicular lesions in the right ear with decreased ipsilateral hearing acuity. A diagnosis of RHS was considered. Cerebrospinal fluid (CSF) analysis showed pleocytosis, as well as VZV DNA. Magnetic resonance imaging of the brain identified abnormal uptake of gadolinium contrast in the right seventh cranial nerve, reinforcing the diagnosis. The patient was treated with acyclovir (14 days) and prednisone, with progressive clinical improvement. We emphasize the importance of recognizing this syndrome in patients with facial palsy, since the early antiviral treatment significantly improves the prognosis.

Is There Any Relation between Serum Levels of Interleukin-10 and Neurophysiological Abnormalities in Bell's Palsy?

Background:Bell’s palsy is the most common cause of peripheral facial palsy. The etiology and treatment of Bell’s palsy are still controversial. Previous studies emphasize the role of herpes simplex and herpes zoster viruses in this ailment. The role of Interleukin-10 (IL-10) in Bell’s palsy is yet unknown, and few studies have shed light on the matter. This study intended to assess the prognostic value of IL-10 and its relation to the intensity of electrodiagnostic abnormalities and evaluate its potential use as a factor for judging the need for medical or surgical interventions.Materials and Methods:30 patients in the acute phase of Bell’s palsy participated in this study. Peripheral blood samples were obtained for IL-10 assessment within the first 72 hours (before commencing treatment), and a nerve conduction study (NCS) was performed six days after symptom onset.Results:There was no significant correlation between IL-10 serum levels and the severity of nerve conduction pathology in Orbicularis oculi and Orbicularis oris muscles. Also, IL-10 serum levels did not show any meaningful relationships with participants’ age, gender, or symptoms.Conclusion:The IL-10 serum levels are not relevant to the pathology of Bell’s palsy, and the assessment of IL-10 serum levels cannot be used as an alternative to NCS for evaluating the severity of acute Bell’s palsy.

A Rare Cause of Facial Paralysis in Children: A Case of Ramsay Hunt Syndrome

AbstractPeripheral facial paralysis in children can have many causes including trauma, otitis media, head and neck tumors, congenital anomalies, viral infections, as well as metabolic and genetic factors. One cause of peripheral facial paralysis is Ramsay Hunt syndrome (RHS), which is also known as herpes zoster oticus, affecting the seventh and eighth cranial nerves. It is characterized by inner ear dysfunction, periauricular pain, and peripheral facial paralysis accompanied by the presence of an erythematous vesicular rash around the ear pinna and outer ear canal or in the oral mucosa. RHS is very rare in children when compared with its prevalence in adults. A 13-year-old male with no prior medical history applied to the pediatric emergency department after having first developed a vesicular rash on the left ear pinna and pain around the left ear, which was followed 1 day later by the development of ipsilateral facial asymmetry. The patient was hospitalized and simultaneously started on 2 mg/kg/d methylprednisolone for 10 days (followed by a 15-day taper), 100 mg/kg/d intravenous ceftriaxone twice per day (stopped on day 10), 30 mg/kg/d intravenous acyclovir three times per day (stopped on day 21), ciprofloxacin ear drops, tobramycin eye drops, ointment, and artificial tear drops with eye patching. However, only a minimal improvement was observed in the patient's peripheral facial paralysis by day 21. When compared with the prevalence in adults, RHS is very rare in children, which is why reports of pediatric RHS are limited in the literature. Therefore, additional studies are needed to provide information about the pathophysiology, diagnosis, and treatment of pediatric RHS.

Facial palsy caused by an intrameatal metastatic disease - Reconstruction with an autologous sural nerve graft

Dysfunction of the facial nerve is frequently attributed to inflammation, followed by traumatic injury. Knowledge of the complex anatomical course of the facial nerve is critical to localize the site of pathology and for successful management. The multiplicity of etiologies and its complex anatomy often make facial paralysis a diagnostic challenge. Neoplasms are a fairly rare cause of peripheral facial palsy, and are frequently overlooked in search of the more frequent traumatic or inflammatory etiologies of facial paralysis. Isolated metastatic lesions to the cerebellopontine angle (CPA) and internal auditory canal (IAC) are extremely rare. Their accurate diagnosis is difficult, since they share common clinical and radiological characteristics with vestibular schwannomas. We report a case of a 63-year-old female with a rapidly progressive left-sided hearing loss and complete facial palsy. Magnetic resonance imaging revealed a left intrameatal lesion. A provisional diagnosis of intracanalicular schwannoma or meningioma was made, although the possibility of metastasis due to her rapid neurological deterioration was considered. The patient underwent a translabyrinthine complete removal of the tumor followed by facial nerve reconstruction. The final histopathological findings revealed a metastatic breast adenocarcinoma. To our knowledge only seven prior cases of an isolated metastatic CPA lesion have been reported. In patients without a known malignancy, a rapid progression of hearing loss, disequilibrium, and facial palsy might be the first sign of a metastatic CPA lesion.

Borrelia burgdorferi sensu lato infection in patients with peripheral facial palsy

The aims of the study were to determine the frequency of borrelial infection in patients with peripheral facial palsy (PFP) and to compare clinical and laboratory characteristics of patients with borrelial PFP and patients with PFP of unknown etiology.Adult patients with PFP who presented at our department between January 2006 and December 2013 qualified for the study if they had undergone lumbar puncture and also been tested for the presence of borrelial IgM and IgG antibodies in serum and cerebrospinal fluid (CSF) in indirect chemiluminescence immunoassay. Patients with PFP who had obvious signs/symptoms indicating a disease other than Lyme borreliosis (LB) were excluded. Patients who qualified for the study were classified into three groups according to the clinical and microbiological criteria: those having confirmed LB, those with possible LB, and those with PFP of unknown etiology.Of 589 patients diagnosed with PFP during the eight-year period, 436 patients (240 males, 196 females) with median age 42.5 years (15–87 years) qualified for the study. Among these patients, 64 (14.7%) fulfilled criteria for confirmed LB, 120 (27.5%) had a diagnosis of possible LB, and in 252 (57.8%) the cause of their PFP remained unknown. When compared with patients with unknown cause of PFP, the patients with confirmed LB were older, more often presented in summer, more often reported tick bites, more frequently had LB in the past, more often complained of constitutional symptoms and radicular pain, and more often had bilateral palsy and CSF pleocytosis. Among the patients with possible LB and patients with unknown cause of PFP there were no differences in frequency of constitutional symptoms, radicular pain, bilateral palsy or CSF pleocytosis.Presentation in summer, tick bites, constitutional symptoms and radicular pain, bilateral palsy, and CSF pleocytosis strongly suggest borrelial etiology of PFP.

La paralysie faciale périphérique a frigore

Idiopathic peripheral facial palsy, also named Bell's palsy, is the most common cause of peripheral facial palsy in adults. Although it is considered as a benign condition, its social and psychological impact can be dramatic, especially in the case of incomplete recovery. The main pathophysiological hypothesis is the reactivation of HSV 1 virus in the geniculate ganglia, leading to nerve edema and its compression through the petrosal bone. Patients experience an acute (less than 24 hours) motor deficit involving ipsilateral muscles of the upper and lower face and reaching its peak within the first three days. Frequently, symptoms are preceded or accompanied by retro-auricular pain and/or ipsilateral face numbness. Diagnosis is usually clinical but one should look for negative signs to eliminate central facial palsy or peripheral facial palsy secondary to infectious, neoplastic or autoimmune diseases. About 75% of the patients will experience spontaneous full recovery, this rate can be improved with oral corticotherapy when introduced within the first 72 hours. To date, no benefit has been demonstrated by adding an antiviral treatment. Hemifacial spasms (involuntary muscles contractions of the hemiface) or syncinesia (involuntary muscles contractions elicited by voluntary ones, due to aberrant reinnervation) may complicate the disease's course. Electroneuromyography can be useful at different stages: it can first reveal the early conduction bloc, then estimate the axonal loss, then bring evidence of the reinnervation process and, lastly, help for the diagnosis of complications.

Bilateral peripheral facial palsy and mastoid infiltration as symptoms of relapsed acute myeloid leukemia

BackgroundAlthough Bell's palsy (BP) is the most common cause of peripheral facial palsy (PFP), other etiologies merit investigation. Case reportA 60-year-old female patient presented with recurrent bilateral PFP. Although the patient had a history of acute myeloid leukemia (AML), she had initially been diagnosed with BP-related PFP and had been treated accordingly. When the PFP recurred, additional diagnostic tests were performed. The resulting immunohistochemical profile included CD3 positivity in a few reactive T lymphocytes; positivity for myeloperoxidase in atypical cells; and focal positivity for CD34 and proto-oncogene c-kit proteins in neoplastic cells, thus confirming the suspicion of mastoid infiltration caused by relapsed AML. ConclusionIn patients with neoplastic disease, a finding of PFP calls for extensive investigation in order to rule out the involvement of the temporal bone.

Clinical characteristics and cerebrospinal fluid parameters in patients with peripheral facial palsy caused by Lyme neuroborreliosis compared with facial palsy of unknown origin (Bell's palsy)

BackgroundBell's palsy and Lyme neuroborreliosis are the two most common diagnoses in patients with peripheral facial palsy in areas endemic for Borrelia burgdorferi. Bell's palsy is treated with corticosteroids, while Lyme neuroborreliosis is treated with antibiotics. The diagnosis of Lyme neuroborreliosis relies on the detection of Borrelia antibodies in blood and/or cerebrospinal fluid, which is time consuming. In this study, we retrospectively analysed clinical and cerebrospinal fluid parameters in well-characterised patient material with peripheral facial palsy caused by Lyme neuroborreliosis or Bell's palsy, in order to obtain a working diagnosis and basis for treatment decisions in the acute stage.MethodsHospital records from the Department of Infectious Diseases, Sahlgrenska University Hospital, for patients with peripheral facial palsy that had undergone lumbar puncture, were reviewed. Patients were classified as Bell's palsy, definite Lyme neuroborreliosis, or possible Lyme neuroborreliosis, on the basis of the presence of Borrelia antibodies in serum and cerebrospinal fluid and preceding erythema migrans.ResultsOne hundred and two patients were analysed; 51 were classified as Bell's palsy, 34 as definite Lyme neuroborreliosis and 17 as possible Lyme neuroborreliosis. Patients with definite Lyme neuroborreliosis fell ill during the second half of the year, with a peak in August, whereas patients with Bell's palsy fell ill in a more evenly distributed manner over the year. Patients with definite Lyme neuroborreliosis had significantly more neurological symptoms outside the paretic area of the face and significantly higher levels of mononuclear cells and albumin in their cerebrospinal fluid. A reported history of tick bite was uncommon in both groups.ConclusionsWe found that the time of the year, associated neurological symptoms and mononuclear pleocytosis were strong predictive factors for Lyme neuroborreliosis as a cause of peripheral facial palsy in an area endemic for Borrelia. For these patients, we suggest that ex juvantibus treatment with oral doxycycline should be preferred to early corticosteroid treatment.

Is antiviral medication for severe Bell's palsy still useful?

Bell's palsy is the most common cause of peripheral facial paralysis, and treatment needs to be started as soon as possible after the onset of paralysis. Treatments include corticosteroids to reduce swelling and antiviral drugs to combat infection with the herpes simplex virus, which is a possible cause of the disorder.1,2 In their article, Engström and colleagues3 aimed to compare the efficacy of the corticosteroid prednisolone and the antiviral drug valaciclovir for treating facial paralysis. Consistent with the conclusion of an earlier trial,4 Engström and colleagues concluded that early treatment with prednisolone alone shortened the time to facial recovery and that valaciclovir did not affect recovery.

Infizierte Parotiszyste als Ursache einer Fazialisparese

Inflammatory processes are a rare cause of peripheral facial palsy. In most cases even massive infection does not lead to a loss of facial nerve function. In the literature, only 8 cases of facial paralysis associated with parotid cyst have been described. We present a case of facial palsy caused by an inflamed cyst of the parotid gland. The patient was operated on with the diagnosis malignant parotid tumor. The pathological report showed a squamous epithelial cyst, massive lymphocytic infiltration. As a rule the combination parotid gland lesion and facial palsy is a sign of malignancy, clinicians should be aware that, on rare occasions, facial nerve dysfunction may result from benign parotid gland disease.

Bell’s Palsy: Incidence, Etiology, and Results of Medical Treatment

The aims of the study were to determine the frequency of borrelial infection in patients with peripheral facial palsy (PFP) and to compare clinical and laboratory characteristics of patients with borrelial PFP and patients with PFP of unknown etiology.Adult patients with PFP who presented at our department between January 2006 and December 2013 qualified for the study if they had undergone lumbar puncture and also been tested for the presence of borrelial IgM and IgG antibodies in serum and cerebrospinal fluid (CSF) in indirect chemiluminescence immunoassay. Patients with PFP who had obvious signs/symptoms indicating a disease other than Lyme borreliosis (LB) were excluded. Patients who qualified for the study were classified into three groups according to the clinical and microbiological criteria: those having confirmed LB, those with possible LB, and those with PFP of unknown etiology.Of 589 patients diagnosed with PFP during the eight-year period, 436 patients (240 males, 196 females) with median age 42.5 years (15–87 years) qualified for the study. Among these patients, 64 (14.7%) fulfilled criteria for confirmed LB, 120 (27.5%) had a diagnosis of possible LB, and in 252 (57.8%) the cause of their PFP remained unknown. When compared with patients with unknown cause of PFP, the patients with confirmed LB were older, more often presented in summer, more often reported tick bites, more frequently had LB in the past, more often complained of constitutional symptoms and radicular pain, and more often had bilateral palsy and CSF pleocytosis. Among the patients with possible LB and patients with unknown cause of PFP there were no differences in frequency of constitutional symptoms, radicular pain, bilateral palsy or CSF pleocytosis.Presentation in summer, tick bites, constitutional symptoms and radicular pain, bilateral palsy, and CSF pleocytosis strongly suggest borrelial etiology of PFP.