Cause Of Facial Palsy Research Articles

Bell's Palsy in Children-A Pedodontist's Perspective

Bell’s palsy (spontaneous idiopathic facial paralysis), is one of the most common pathology affl icting the facial nerve which has a sudden onset. Bell’s palsy is the most common cause of facial paralysis, involving per cent of facial palsies, when other causes have been eliminated. It has an incidence of 11–40 Garg KN, Gupta K, Singh S, Chaudhary S. Bell’s Palsy : Aetiology, Classifi cation, Differential Diagnosis and Treatment Consideration : A Review. www.journalofdentofacialsciences.com, 2012; 1(1): 1-8 per 100,000 per year, and most commonly occurs in females in their teens and twenties. The occurrence of Bell ’s palsy in children is a comparatively rare event and resolves uneventfully. The child patient with Bell ’s palsy presents a unique case scenario where the emotions of the family and the child have to be dealt and managed in an effi cacious and sensitive manner. The distribution is almost equal in the thirties, with a slight predominance in males over 40. Untreated Bell’s palsy leaves some patients with major facial dysfunction and a reduced quality of life, which may include physical, emotional and psychological issues. It is essential to rule out other causes of facial paralysis before making defi nitive diagnosis, which implies the intervention. An assessment of severity with an overview of management is presented in this review.

Facial Palsy Complicated by Masked Otomastoiditis in A 3-Month-Old Infant

BackgroundThe most common cause of facial palsy is idiopathic or Bell's palsy. Although uncommon in the postantibiotic era, otomastoiditis should receive more attention as a cause of facial palsy, especially in young children. Delay of identification and treatment may result in permanent neurological sequelae. ObjectivesTo describe a 3-month-old infant eventually diagnosed with masked otomastoiditis with initial presentation of facial palsy. Case ReportWe report a case of facial palsy complicated by masked otomastoiditis in a 3-month-old male infant. The facial palsy completely recovered after parenteral antibiotics and myringotomy. ConclusionWe use this case to emphasize that otomastoiditis should be considered in the differential diagnosis of young children with facial palsy. Diagnosis may be difficult as signs and symptoms of otitis media in young children are often nonspecific and subtle, particularly in infants. Early diagnosis and careful investigation of middle ear regions should be performed to avoid permanent sequelae.

Functional outcome of the facial nerve paralysis after late surgical decompression in otic capsule-sparing fracture

AbstractTemporal bone fracture (TBF) following head trauma is a well-known cause of facial nerve paralysis (FNP) and almost 22% of all skull fractures are TBF. It has been estimated that 25–70% of TBF are associated with FNP and otic capsule-violating fracture of the petrous portion of the temporal bone is more commonly associated with FNP, although otic capsule-sparing fracture is more common. (a) The incidence of FNP is reported to be 10–25% of otic capsule-sparing fracture. (b) With otic capsule-sparing fractures, FNP is often delayed 2–3 days, and is incomplete and temporary, with good recovery during a period of 6–8 weeks. Most clinicians seldom consider a surgical intervention in delayed FNP; however, surgical exploration may be required for complete recovery. The optimal timing for surgical exploration of traumatic FNP to best preserve facial function is currently controversial. Decompression surgery still has a beneficial effect if performed within 14 days of injury. However, late exploratory surgery is recommended in patients who do not experience recovery of facial nerve function, patients who cannot be operated on early, and who present 1–3 months after TBF with more than 95% denervation on electroneurography. Here, we report a case of delayed-onset FNP of otic capsule-sparing fracture with an excellent outcome after late surgical decompression at 6 months after trauma.

Peripheral presentation of central facial palsy

Facial nerve palsy in children may be congenital or due to neoplastic, infectious or traumatic conditions. Although idiopathic (Bell’s palsy) facial nerve palsy is the most commonly encountered cause, facial nerve palsy may be the fi rst and only symptom of a severe underlying condition. Previous studies on pediatric populations have reported on a tumor cause of facial nerve palsy in 2%-12% of cases. One of the most important pitfalls for a clinician is to assume that a child with facial nerve palsy has Bell’s palsy and does not need complete and comprehensive evaluation for other etiologies. A case is described of an infant with oculocutaneous albinism who presented with persistent fi ndings of peripheral facial palsy in whom the cause was belatedly identifi ed as a brain tumor following magnetic resonance imaging. The most striking feature in our patient was the peripheral presentation of central facial nerve palsy, and if the magnetic resonance imaging had not been obtained, a potentially serious diagnosis may have been missed. Complete medical history and detailed physical examination should be obtained for every patient presenting with peripheral facial palsy, particularly in infants where cranial tomography or magnetic resonance imaging may be warranted to avoid misdiagnosis.

Microbiologic Findings in Acute Facial Palsy in Children

Microbiologic causes of facial palsy in children were investigated. Prospective clinical study. Tertiary referral center. Forty-six children aged 0 to 16 years with peripheral facial palsy. Paired serum samples and cerebrospinal fluid were tested to find indications of microbes associated with facial palsy. The microbes tested were herpes simplex virus 1 and 2, varicella-zoster virus, human herpesvirus-6, Mycoplasma pneumoniae, Borrelia burgdorferi, influenza A and B virus, picorna, cytomegalovirus, parainfluenza virus, respiratory syncytial virus, coxsackie B5 virus, adenovirus, and enterovirus, Chlamydia psittaci, and Toxoplasma gondii. Besides the routine tests in clinical practice, serum and cerebrospinal fluid samples were tested with a highly sensitive microarray assay for DNA of herpes simplex virus 1 and 2; human herpes virus 6A, 6B, and 7; Epstein-Barr virus, cytomegalovirus, and varicella zoster virus. Incidence for facial palsy was 8.6/100,000/children/year. Cause was highly plausible in 67% and probable in an additional 11% of cases. Borrelia burgdorferi caused facial palsy in 14 patients (30%), varicella zoster virus in 5 (11%) (one with concomitant adenovirus), influenza A in 3 (6%), herpes simplex virus 1 in 2 (4%) (one with concomitant enterovirus), otitis media in 2 (4%), and human herpesvirus 6 in 2 (4%). Mycoplasma pneumoniae, neurofibromatosis, and neonatal age facial palsy affected 1 child (2%) each. Microbiologic etiology association of pediatric facial palsy could frequently be confirmed. Borreliosis was the single most common cause; hence, cerebrospinal fluid sampling is recommended for all pediatric cases in endemic areas. Varicella zoster virus accounted for 11% of the cases, being the second most common factor.

Ramsay Hunt Syndrome in a Girl With Acute Lymphoblastic Leukemia During Maintenance Therapy

A 5-year-old girl with precursor B-cell acute lymphoblastic leukemia developed peripheral-type right facial palsy and very faint erythema on her right pinna during maintenance therapy. Acyclovir was started for possible zoster infection. The following day, vesicles appeared and a diagnosis of Ramsay Hunt syndrome was made. Prednisolone was started on day 5 after onset. Her facial palsy recovered within 6 months. Ramsay Hunt syndrome is a rare cause of facial palsy in patients with acute lymphoblastic leukemia, and this is the first case report. Preemptive therapy with acyclovir before the development of vesicles should help the patient recover from facial palsy.

Pattern of facial palsy in a typical Nigerian specialist hospital

Data on incidence of facial palsy is generally lacking in Nigeria. To assess six years' incidence of facial palsy in Murtala Muhammed Specialist Hospital (MMSH), Kano, Nigeria. The records of patients diagnosed as facial problems between January 2000 and December 2005 were scrutinized. Data on diagnosis, age, sex, side affected, occupation and causes were obtained. A total number of 698 patients with facial problems were recorded. Five hundred and ninety four (85%) were diagnosed as facial palsy. Out of the diagnosed facial palsy, males (56.2%) had a higher incidence than females; 20-34 years age group (40.3%) had a greater prevalence; the commonest cause of facial palsy was found out to be Idiopathic (39.1%) and was most common among business men (31.6%). Right sided facial palsy (52.2%) was predominant. Incidence of facial palsy was highest in 2003 (25.3%) and decreased from 2004. It was concluded that the incidence of facial palsy was high and Bell's palsy remains the most common causes of facial (nerve) paralysis.

Facial Palsy and Nystagmus after Transvenous Embolization of a Carotid Cavernous Fistula

Facial Palsy and Nystagmus after Transvenous Embolization of a Carotid Cavernous Fistula

İki Çocukta Ramsay Hunt Sendromu

Cranial facial nerve palsy is uncommon in childhood. Diagnostic studies in children and adults have provided convincing evidence that reactivation of varicella-zoster virus (VZV) may lead to cranial nerve VII palsy, which is the most common cause of facial palsy in childhood. Careful physical examination especially detailed ear examination is very important when VZV reactivation is suspected. Early treatment with acylovir therapy may improve the recovery rate of facial nerve palsy. In a study of 28 patients for whom treatment with acyclovir and prednisone was initiated within 3 days after the onset of facial paralysis, the recovery from paralysis was complete in 21 (75%), whereas complete recovery was achieved in only 7 out of 23 patients (30%) for whom treatment was initiated more than 7 days after the onset (30%). The difference betwwen the two groups in terms of facial nerve recovery was significant. The aim of this case report is to emphasize the importance of careful examination and early initiation of therapy in suspected cases of Ramsay Hunt syndrome.

Progressive Facial Palsy With Ipsilateral Fasciculation and Sensory Neuropathy

Progressive Facial Palsy With Ipsilateral Fasciculation and Sensory Neuropathy

Successful response of non-recovering Ramsay Hunt syndrome to intravenous high dose methylprednisolone

Ramsay Hunt syndrome (RHS) is a frequent cause of facial palsy. It is a consequence of the infection of geniculate ganglion by herpes zoster or herpes simplex virus. In the lack of randomized controlled trials, RHS is empirically treated by a combination therapy of antiviral agents and steroids given orally. However, RHS has, per se, a poorer prognosis than idiopathic facial palsy (Bell's palsy).We describe a case series of two patients with RHS unsuccessfully treated with antiviral drugs and oral corticosteroids, showing an almost complete recovery after late administration of intravenous (i.v.) high dose methylprednisolone. Both patients had all recognized negative prognostic factors including age of onset, a high grade facial weakness, absence of R1 and R2 response at blink reflex test, and in the first case, the involvement of greater superficial petrosal nerve.We propose that i.v. high dose methylprednisolone should be considered, even as a late treatment option, in patients with RHS non recovering after standard antiviral and oral steroid therapy as well as presenting clinical features suggestive of a poor prognosis.

A rare cause of facial nerve palsy in children: Hyperostosis corticalis generalisata (Van Buchem disease). Three new pediatric cases and a literature review

Differential diagnosis of facial nerve palsy in children is extensive. We report on three pediatric cases presenting with facial nerve palsy caused by hyperostosis corticalis generalisata (Van Buchem disease). This autosomal recessive disease is characterized by progressive bone overgrowth, with narrowing of the neuroforamina in the skull causing cranial neuropathies. These three new cases of Van Buchem disease are of interest because of exceptionally early presentation of symptoms. Furthermore, this is the first report describing bilateral papilledema in a child with Van Buchem disease. Head computerized tomography (CT) scan revealed thickened calvarium, skull base and mandible in all three children, with narrowed facial nerve canals. Bone mineral density (BMD) was markedly increased at all measured points and biochemical markers of bone formation were significantly elevated. Diagnosis of Van Buchem disease was genetically confirmed. The cases are unique in that these are the first well-documented pediatric cases of Van Buchem disease.

Facial Reanimation After Facial Nerve Injury Using Hypoglossal to Facial Nerve Anastomosis: The Gruppo Otologico Experience

To evaluate the results of facial nerve reanimation after facial nerve injury by means of hypoglossal to facial nerve anastomosis. Retrospective case review. Private neuro-otologic and cranial base quaternary referral center. Sixty patients underwent hypoglossal to facial nerve anastomosis for facial nerve reanimation between April 1987 and December 2010. Only forty patients completed a minimal follow up of 24months at the time of evaluation and were included in the study population. Facial nerve paralysis was present for a mean duration of 11.3months (range 2-42months) and all the patients had a HB grade VI prior their surgery. Final facial nerve motor function. The most common cause of facial paralysis was vestibular Schwannoma surgery. All the patients achieved a postoperative HB grade III or IV after a mean follow-up time of 20months. The facial movements were detected after a period that ranged from ranged from 5 to 9months. Only 4 patients suffered from difficulties during eating and drinking and three of them had associated lower cranial nerve deficit. Despite the various techniques in facial reanimation following total facial nerve paralysis, the end to end of hypoglossal to facial nerve anastomosis remains one of the best treatments in cases of viable distal facial stump and nonatrophic musculature.

Paraganglioma of the facial nerve, a rare differential diagnosis for facial nerve paralysis: case report and review of the literature

This report describes a rare case of histopathologically confirmed glomus facial tumor. The role of imaging in the differential diagnosis is discussed and therapeutic options are evaluated, along with a review of the previous literature on glomus facial tumors. A 39-year-old male patient presented with total peripheral facial nerve paralysis. He underwent radical tumor resection and facial nerve grafting for a histopathologically confirmed paraganglioma of the facial nerve. He is now tumor-free after a 4-year follow-up period, and the functional outcome after primary nerve grafting is satisfactory. Facial nerve paragangliomas are a rare cause of facial nerve paralysis. Early imaging using computed tomography and magnetic resonance imaging is essential to clarify the differential diagnosis and assess the location and extent of the tumor. Precise pathological diagnosis requires additional targeted immunohistochemical examinations. The treatment of choice in patients with preoperative facial nerve paralysis is radical tumor resection with nerve reconstruction.

Clinical Management of Microstomia Due to the Static Treatment of Facial Paralysis and Oral Rehabilitation With Dental Implants

Facial-nerve paralysis is seldom seen and may occur because of a broad spectrum of causes. The most commonly seen cause of facial paralysis is the Bell palsy; iatrogenic causes and tumors are relatively rare. Facial asymmetry, drooling, garbled speech, and difficulty in feeding: all adversely affect the psychosocial conditions of the patients. Fascial and tendon sling procedures may be performed for the static treatment of the unilateral permanent facial paralysis. These techniques are used both for the correction of the asymmetry of the face, especially by providing static support for the corner of the mouth, and to prevent drooling. Microstomia after a sling procedure is not a previously observed complication in the literature. A patient is presented with the surgical management of the complication of microstomia that had risen because of a static treatment of his unilateral facial paralysis via a tendon that passes circularly through his orbicularis oris muscle. Oral rehabilitation thereafter was maintained with the support of dental implants and fixed prosthodontics. The most efficient treatment protocol was decided with an interdisciplinary consultation of the oral and maxillofacial surgeon, the plastic surgeon, and the prosthodontist.

Dermoid cyst in the facial nerve—A unique diagnosis

Facial nerve paralysis in children may occur as a complication of infections, trauma, or rarely from benign or malignant tumors of the facial nerve. We present the first reported case of a dermoid tumor in the facial nerve causing facial paralysis in a child. Case report at a tertiary Children's Hospital. A 9-month-old was referred to our institution for evaluation of persistent, complete right sided facial paralysis three months after receiving a diagnosis of Bell's palsy. A workup at our institution including MRI and CT revealed marked widening of the facial canal in the mastoid segment consistent with facial nerve schwannoma or hemangioma. Surgical exploration via mastoidectomy and facial nerve decompression revealed keratinous material containing hair that had fully eroded the facial nerve, disrupting it completely. The entire tumor was removed along with the involved segment of facial nerve, and the missing facial nerve segment was cable grafted. Histological examination of the tumor confirmed a ruptured dermoid cyst in the facial nerve. Facial nerve tumors are rare causes of facial paralysis in children, accounting for fewer than 10% of cases of facial paralysis in the pediatric population. Dermoid cyst can occur throughout the head and neck region in children, but a dermoid tumor in the facial nerve has not been described in the literature prior to this report. This represents a new and uncommon diagnostic entity in the evaluation of facial nerve paralysis in children. Appropriate imaging studies and pathology slides will be reviewed.

Facial Nerve Palsy in Children

Generally, the cause of facial palsy in children is more varied than in the case of adults. Birth trauma is one of them, but reports on this are few. It is possible that the palsy resolved spontaneously before the medical examination. We met with a case of birth trauma caused by forceps delivery. The female patient suffered severe facial nerve palsy and right ear bleeding after arrival. We report herein on the case and our clinical examination of facial nerve palsy in children at the local mainstay hospital. We reviewed 37 cases, ranging in age from 0 to 15 years, who demonstrated facial palsy at Niigata Prefectural Central Hospital between April 1998 and March 2008. The most common causes of facial palsy in children were Bell’s palsy (24 patients, 65%), followed by birth trauma (4 patients, 11%) and Hunt syndrome (3 patients, 8%). Of the 37 patients, 34 were followed up until their recovery or for longer than 6 months. One patient with a cerebellopontine angle tumor improved, another patient with congenital facial palsy remained unchanged, and the remaining 32 patients recovered completely. In 4 cases of birth trauma, the palsy resolved spontaneously within sixty days.

A case of middle-ear cavernous lymphangioma with facial palsy

Only a few benign tumours of the middle ear have been reported to lead to the development of facial palsy. Here, we describe a patient with middle-ear cavernous lymphangioma and facial palsy. Single case study. A 61-year-old man presented with left-sided hearing impairment and incomplete left facial palsy. A tumour was confirmed to be occupying the epi- to mesotympanum and to be joined to the facial nerve. The tumour was removed along with facial nerve tissue, which was resected at its horizontal portion, and the remaining facial nerve was fixed by end-to-end anastomosis. Complete facial paralysis occurred after the operation, but the patient's House-Brackmann grade gradually improved to grade III. Post-operative histopathological examination revealed infiltration of the lymphangioma into the facial nerve tissue, together with mild neural atrophy of the facial nerve. These findings suggested that tumour invasion was the cause of facial palsy in this patient.

Isolated facial palsy as a hallmark of CSF overdrainage in shunted intracranial arachnoid cyst

An 18-year-old man with an intracranial arachnoid cyst (Fig. 1) and existing cysto-peritoneal shunt for 10 years was admitted to our department because of orthostatic headache, nausea and vomiting. Neurological examination was inconspicuous. The shunt was ligated because of an assumed CSF overdrainage. Clinical symptoms persisted, so that magnetic resonance (MR) imaging as well as lumbar puncture were performed, without signs of an increasing intracranial pressure. Myelocisternography excluded CSF leakage. However, this investigation showed just a partial disabled shunt. In a second surgery the shunt was completely ligated. Intermittent diplopia occurred and neuro-ophthalmological examination revealed papilledema. MR imaging indicated an increasing arachnoid cyst and optic nerve sheath dilation, compared to the pre-operative MRI. The patient underwent a shunt revision and an adjustable valve with an opening pressure >140 mmH2O on the left side was implanted. Subsequently, diplopia, papilledema, and headaches disappeared. Two days postoperatively, the patient developed an isolated mild facial palsy on the right side (opposite to the site of the arachnoid cyst; House–Brackmann grade II) as well as headaches. Opening pressure of the valve was decreased to >120 mmH2O and the headaches disappeared. Nevertheless, the facial palsy on the right side aggravated (House–Brackmann grade III) and additionally appeared on the left side (House–Brackmann grade II). MR imaging showed a reduction of the arachnoid cyst and diminished optic nerve sheaths compared to the previous MRI. The opening pressure was readjusted again to >140 mmH2O. After readjusting the opening pressure, bilateral facial palsy was regressive and disappeared within a few days. The patient showed no clinical signs of increasing intracranial pressure and was discharged with no neurological deficits. Possible other causes of facial palsy (meningitis, viral, borreliosis, etc.) were excluded.

Facial Nerve Paralysis After Cervical Traction

Cervical traction is a frequently used treatment in rehabilitation clinics for cervical spine problems. This modality works, in principle, by decompressing the spinal cord or its nerve roots by applying traction on the cervical spine through a harness placed over the mandible (Olivero et al., Neurosurg Focus 2002;12:ECP1). Previous reports on treatment complications include lumbar radicular discomfort, muscle injury, neck soreness, and posttraction pain (LaBan et al., Arch Phys Med Rehabil 1992;73:295-6; Lee et al., J Biomech Eng 1996;118:597-600). Here, we report the first case of unilateral facial nerve paralysis developed after 4 wks of intermittent cervical traction therapy. Nerve conduction velocity examination revealed a peripheral-type facial nerve paralysis. Symptoms of facial nerve paralysis subsided after prednisolone treatment and suspension of traction therapy. It is suspected that a misplaced or an overstrained harness may have been the cause of facial nerve paralysis in this patient. Possible causes were (1) direct compression by the harness on the right facial nerve near its exit through the stylomastoid foramen; (2) compression of the right external carotid artery by the harness, causing transient ischemic injury at the geniculate ganglion; or (3) coincidental herpes zoster virus infection or idiopathic Bell's palsy involving the facial nerve.