Peripheral Facial Nerve Research Articles

Effect of high dose steroid therapy for peripheral facial nerve palsy

Effect of high dose steroid therapy for peripheral facial nerve palsy

Bell’s palsy: a manifestation of prediabetes?

Idiopathic peripheral facial nerve palsy or Bell's palsy (BP) is the most common cause of facial nerve palsy. To evaluate the role of glucose metabolism abnormalities in BP. We identified 148 patients with unilateral BP and 128 control subjects. In all we evaluated glucose level at fasting and after a 2-h oral glucose tolerance test (2h-OGTT). In addition we determined insulin resistance (IR), by HOMA-index. Patients and controls were divided in to two groups, according to their Body Mass Index (BMI). Following a 2h-OGTT, the prevalence of glucose metabolism abnormalities was significantly higher in patients with BP than in controls (P < 0.001). Impaired glucose tolerance (IGT) was found in 57 (38%) patients and in 23 (18%) controls, while a new-diagnosed DM (NDDM) was found in 29 (19%) patients and in 8 (6%) controls. The IR was significantly increased only in BP patients with BMI ≥ 24.9 (P = 0.005). BMI, waist circumference, blood pressure, tryglicerides, serum lipid, drugs use were not significantly different between patients and controls. In this study we found that prediabetes is frequently associated with facial palsy. We propose to perform a 2h-OGTT in patients with peripheral facial palsy and normal fasting glycaemia. HOMA-index should be evaluated in obese facial palsy patients.

Peripheral Facial Nerve Paralysis After Upper Third Molar Extraction

Peripheral facial nerve paralysis (PFNP) after mandibular interventions has been reported in the literature. In most cases, paralysis begins immediately after the injection of the mandibular anesthesia, and duration of facial weakness is less than 12 hours. However, there are few documented cases of PFNP after maxillary dental or surgical procedures. A variety of mechanisms have been associated to PFNP, including viral reactivation, demyelination, edema, vasospasm, and trauma. The purpose of this presentation was to report a rare case of facial paralysis that occurred after an upper third molar extraction. The cause of the PFNP and the importance of the multidisciplinary approach in the management are emphasized.

A case of middle-ear angiosarcoma

Middle-ear angiosarcoma is a rare malignant tumor that requires early diagnosis to allow satisfactory removal. The objective of the present study was to describe and discuss the diagnosis and treatment of this rare malignant middle-ear tumor. A 12-year-old girl was admitted for a left retroauricular mass and a budding left external auditory canal tumor without associated peripheral facial nerve palsy. CT scan showed a mastoid-region tumor extending to the external auditory canal with mastoid and occipital bone-loss. Tumor removal used a retroauricular approach. Postoperative diagnosis was of angiosarcoma. At 12 months' regular follow-up, there were no signs of local recurrence. Middle-ear angiosarcoma is a rare tumor, in which diagnosis is late because early symptoms are not specific. A multidisciplinary approach is essential for efficient management.

Peripheral facial nerve communications and their clinical implications

The facial nerve (CN VII) nerve follows a torturous and complex path from its emergence at the pontomedullary junction to its various destinations. It exhibits a highly variable and complicated branching pattern and forms communications with several other cranial nerves. The facial nerve forms most of these neural intercommunications with branches of all three divisions of the trigeminal nerve (CN V), including branches of the auriculotemporal, buccal, mental, lingual, infraorbital, zygomatic, and ophthalmic nerves. Furthermore, CN VII also communicates with branches of the vestibulocochlear nerve (CN VIII), glossopharyngeal nerve (CN IX), and vagus nerve (CN X) as well as with branches of the cervical plexus such as the great auricular, greater, and lesser occipital, and transverse cervical nerves. This review intends to explore the many communications between the facial nerve and other nerves along its course from the brainstem to its peripheral branches on the human face. Such connections may have importance during clinical examination and surgical procedures of the facial nerve. Knowledge of the anatomy of these neural connections may be particularly important in facial reconstructive surgery, neck dissection, and various nerve transfer procedures as well as for understanding the pathophysiology of various cranial, skull base, and neck disorders.

Un cas d’ophtalmoplégie horizontale bilatérale : le syndrome 1+1

Oculomotor deficiencies in multiple sclerosis (MS) are frequently characterized by internuclear ophthalmpoplegia or isolated abduction or adduction palsies. Complete unilateral conjugate gaze paralysis and the "one and a half" syndrome are rare. Complete bilateral horizontal gaze paralysis has been exceptionally reported. Here, we describe an unusual oculomotor paralysis as a suspected first event of MS. A 24-year-old woman with an uneventful medical history presented for sudden onset of binocular diplopia. On examination, abduction and adduction saccades were impossible, whereas vertical eye saccades and convergence were normal. Oculocephalic reflex failed to improve horizontal eye movement. No nystagmus and no other sign of brainstem dysfunction were observed. Visual acuity was 4/10 in the right eye and 6/10 in the left eye. A sign of Marcus Gunn was noted in the right eye. Blood samples and cerebrospinal fluid were normal, no oligoclonal bands were detected. Visual evoked potentials were significantly impaired in both eyes and argued for bilateral optic neuritis. Brain MRI scans showed white matter T2-hypersignal abnormalities, which fulfill Barkhof criteria for MS. A small symmetric lesion was noted in the posterior part of the medial pontine tegmentum. As a first episode of MS was suspected, treatment with methylprednisolone 1000 mg/d for 3 days was started, and was followed by complete recovery of eye movements and visual acuity after 3 weeks. To our knowledge, only two cases of complete horizontal bilateral ophthalmoplegia have been reported in the literature. Both were associated with peripheral facial nerve palsy as a first event in MS. In our case report, we describe for the first time a complete bilateral horizontal ophthalmoplegia with no other brainstem dysfunction. By analogy with the "one and a half" syndrome, such complete horizontal gaze paralysis could be named a "one and one" syndrome and seems to be specifically related to a first event of MS.

Post-traumatic peripheral facial nerve palsy: surgical and neuroradiological consideration in five cases of delayed onset

The facial nerve is frequently injured after head trauma with or without temporal bone fractures. Computed tomography (CT) is the best procedure for detecting the fracture line at the level of the facial nerve canal and for assessing any associated lesions within the temporal bone. Magnetic resonance (MR) is required if there is a facial nerve paralysis, unexplained by CT findings. We present five cases of delayed post-traumatic facial nerve palsy without evidence of temporal bone fractures on CT, thus studied on MR. MR was essential for diagnosing the nerve impairment. Neuroradiological findings, clinical presentation, and electrodiagnostic tests influenced the management of the patients.

Early and reliable detection of herpes simplex virus type 1 and varicella zoster virus DNAs in oral fluid of patients with idiopathic peripheral facial nerve palsy: Decision support regarding antiviral treatment?

Idiopathic peripheral facial nerve palsy has been associated with the reactivation of herpes simplex virus type 1 (HSV-1) or varicella zoster virus (VZV). In recent studies, detection rates were found to vary strongly which may be caused by the use of different oral fluid collection devices in combination with molecular assays lacking standardization. In this single-center pilot study, liquid phase-based and absorption-based oral fluid collection was compared. Samples were collected with both systems from 10 patients with acute idiopathic peripheral facial nerve palsy, 10 with herpes labialis or with Ramsay Hunt syndrome, and 10 healthy controls. Commercially available IVD/CE-labeled molecular assays based on fully automated DNA extraction and real-time PCR were employed. With the liquid phase-based oral fluid collection system, three patients with idiopathic peripheral facial nerve palsy tested positive for HSV-1 DNA and another two tested positive for VZV DNA. All patients with herpes labialis tested positive for HSV-1 DNA and all patients with Ramsay Hunt syndrome tested positive for VZV DNA. With the absorption-based oral fluid collection system, detections rates and viral loads were found to be significantly lower when compared to those obtained with the liquid phase-based collection system. Collection of oral fluid with a liquid phase-based system and the use of automated and standardized molecular methods allow early and reliable detection of HSV-1 and VZV DNAs in patients with acute idiopathic peripheral facial nerve palsy and may provide a valuable decision support regarding start of antiviral treatment at the first clinical visit.

Acute Ophthalmoparesis Associated with Human Parvovirus B19 Infection

Parvovirus B19 infection (PVB19) has been linked with a broad spectrum of clinical syndromes. In addition to erythema infectiosum and asymptomatic infection, other less common manifestations include transient aplastic crisis in patients with hemoglobinopathies, pure red cell aplasia and pancytopenia in immunocompromised persons, nonimmune hydrops fetalis, chronic arthritis, myocarditis, and hepatitis. Only 19% of patients had peripheral nervous system damage, mainly including brachial plexitis and carpal tunnel syndrome. Two cases of cranial nerves palsies have been described in children in the literature, including one case of peripheral facial nerve palsy and one case of velopalatine hemiparalysis. We report the first case of acute ophthalmoparesis associated with PVB19 infection. We present a 40-year-old man with PVB19 with acute sixth cranial nerve palsy, diagnosed on the basis of serology and polymerase chain reaction carried out both on serum and cerebrospinal fluid. Clinicians should be aware of this possible clinical presentation.

Frequency and Location of Synkineses in Patients With Peripheral Facial Nerve Paresis

Synkinesis is an involuntary movement accompanying a voluntary one. These unintentional movements are caused by an undifferentiated regeneration of the facial nerve that occurs after being compressed or partially damaged. Synkinesis can affect eating, drinking, and speaking and can be socially distressing because of facial asymmetry and disruption of intended emotional expressions. This study aims to describe the frequency and location of synkinesis in patients with peripheral facial nerve paresis. Patients were observed on video and analyzed using a standardized Synkinesis Scoring Form. Five voluntary expressions, derived from the Sunnybrook Facial Grading Scale, were tested: brow lift, eye closure, smile, snarl, and lip pucker. The Kruskal-Wallis test, 95% confidence intervals, and analysis of variance were used to analyze data. Patients with a facial nerve paresis (n = 103) were observed, and all showed synkineses. Lifting-mouth-corner-synkinesis coupled to voluntary brow lift movements (89%) or eye closure (85%) occurred most frequently. The voluntary movement lip puckering evoked the most synkineses of the eye (narrowing, 82%). During all voluntary expressions lifting-brow-synkineses occurred the least (17%). A significant effect for sex and age (p < 0.05) was found but not for side and duration of the paresis (p > 0.05). Mouth-corner-synkinesis is most common in brow lift and eye movements, whereas eye synkinesis is coupled to mouth movements. These are important facts for rehabilitation of facial nerve pareses, to refine and intensify the inhibition and control of synkineses so that facial symmetry and expressions may improve.

Incomplete Facial Nerve Palsy: New Lessons from Activated Orbicularis Oculi Muscles

Motor nerve conduction studies (MNCS) and blink reflexes (BR) were done on a 42-year-old female patient who presented with peripheral facial nerve palsy (PFNP); these investigations were done while she had her facial muscles relaxed ("A"), and contracted ("B"). While in the "A" state, MNCS of the facial nerves had prolonged latency and low amplitude and R3 of the blink reflex was absent in the affected side; an early contralateral R1 response was recorded on the unaffected side. In state "B," the third silent period was "prolonged" on the affected side and absent on the unaffected one. This is an illustrative case of a variant of facial nerve palsy in humans.

Analiza morfologii potencjałów słuchowych z pnia mózgu u pacjentów z samoistnym obwodowym porażeniem nerwu twarzowego

Idiopathic facial nerve paresis still remains a challenge for laryngologists and neurologists. The etiology of idiopathic peripheral facial nerve paresis has not been explained so far. There is a group of patients that complain about coexisting hearing abnormalities. Analysis of audiological abnormalities in patients with idiopathic peripheral facial nerve paresis on the basis of pure tone audiometry and auditory brainstem responses. The retrospective analysis of 35 patients, aged under 40 years, with idiopathic peripheral facial nerve paresis hospitalised in Department of Otolaryngology of Warsaw Medical University-Poland (2004-2009). Control group consisted of age-matched, 23 healthy subjects. Each patient underwent audiometric evaluation that included pure tone audiometry and auditory brainstem responses. Statistical analysis was performed with Student's t-test. In the analysed group of 35 patients (17 male + 18 female), age ranged 13-40 years (mean 26.7 +/- 7.1) significantly prolonged latencies of wave III and V and III-V and I-V intervals in comparison with control group where observed (p < 0.05). We found also that 48.6% patients with idiopathic peripheral facial nerve paresis had high-frequency hearing loss. The auditory brainstem responses in this study showed an association between retrocochlear pathology of the auditory system and idiopathic peripheral facial nerve paresis. Further investigations are necessary to estimate the etiopathology of these coexisting abnormalities.

Congenital bilateral parotid gland agenesis in Klinefelter syndrome

Bilateral parotid gland agenesis is a rare clinical entity and it's an etiopathogenesis remains obscure. The literature contains no reports of the co-existence of bilateral parotid gland agenesis and Klinefelter syndrome. The condition is usually asymptomatic and causes asymmetry in the head and neck areas. Its diagnosis is generally made in the light of accompanying developmental anomalies. Herein we report the clinical and radiological findings of a 17-year-old male with Klinefelter syndrome accompanied by unilateral peripheral facial nerve paralysis and isolated congenital bilateral parotid gland agenesis.

Etiology of Aseptic Meningitis, Peripheral Facial Nerve Palsy, and a Combination of Both in Children

A variety of microorganisms have been shown to cause peripheral facial nerve palsy (PFNP) and/or aseptic meningitis in children. Clinical findings and history may help to predict the specific etiology of these entities. Children > or =12 months old hospitalized at the University Children's Hospital Basel, Switzerland, from 2000 to 2005 with clinical signs of PFNP and/or aseptic meningitis were studied retrospectively. History, clinical, and laboratory findings were evaluated using analysis of variance with Bonferroni (Dunn) correction. Of 181 patients, 123 (68%) had aseptic meningitis, 28 (15%) had PFNP, and 30 (17%) had a combination of both. PFNP with aseptic meningitis was associated with Borrelia burgdorferi (Bb) infection in the majority of patients (73%) compared with 11% and 9% of patients with PFNP or aseptic meningitis, respectively. The majority of patients with aseptic meningitis without PFNP had enterovirus infection (63%). In patients with aseptic meningitis, mean leukocyte counts in cerebrospinal fluid (CSF) were higher with enterovirus (565/microL) compared with Bb infection (191/microL; P < 0.01) or unknown causes (258/microL; P < 0.01). Further, CSF mean mononuclear cell proportion was higher in patients with Bb (89%) than in those with enterovirus infection (51%; P < 0.01) or unknown causes (60%; P < 0.01). Mean time interval between onset of disease and admission to hospital showed significant differences between Bb (7.6 days) and enterovirus infection (2.8 days; P < 0.01) or unknown causes (2.0 days; P < 0.01). Time interval between onset of disease and hospital admission and CSF characteristics can contribute to distinguishing the etiology of aseptic meningitis with or without PFNP. As expected, the most common etiology for aseptic meningitis with PFNP was Bb infection whereas enterovirus infection was the predominant cause for aseptic meningitis alone.

The Management of Peripheral Facial Nerve Palsy

Conservative management of idiopathic or herpetic acute peripheral facial palsy (herpes zoster oticus, HZO) often leads to a favorable outcome. However, recent multicenter studies have challenged the necessity of antivirals. Whereas large numbers of patients are required to reveal statistical differences in a disease with an overall positive outcome, surprisingly few studies differentiate between patients with paresis and paralysis. Analyzing our own prospective cohort of patients and reviewing the current literature on conservative treatment of Bell's palsy and HZO, we reveal the importance of initial baseline assessment of the disease course to predict the outcome and to validate the impact of medical treatment options. STUDY DESIGN AND DATA SOURCE: Prospective analysis of consecutive patients referred to 2 tertiary referral centers and research on the Cochrane Library for current updates of their previous reviews and search of MEDLINE (1976-2009) for randomized trials on conservative treatment of acute facial palsy were conducted. One hundred ninety-six patients with Bell's palsy or HZO were followed up prospectively until complete recovery or at least for 12 months. The numeric Fisch score (FS) was used to classify facial function, and patients were separated between incomplete palsy (=paresis) and complete paralysis. Electroneuronography (ENoG) was used to further subdivide patients with paralysis. The treatment protocol was independent of the ongoing investigation including prednisone and valacyclovir in most patients. A total of 250 previous studies on facial palsy outcome were evaluated regarding their distinction between different severity scores at baseline and its impact on treatment outcome. Trials not making the distinction between paresis and paralysis at baseline and with an insufficient follow-up of less than 12 months were excluded. In the Bell's and HZO paresis group, all except 1 patient recovered completely, most of them within 3 months, independent of the treatment regimen. In the Bell's paralysis group, 38 patients (70%) recovered completely after 1 year, including 94% of patients with a denervation by ENoG of less than 90%. Thirty percent of Bell's paralysis patients recovered incompletely, revealing the worst outcome in patients with a 100% denervation on ENoG. None of the 4 patients with HZO and ENoG denervation of more than 90% recovered to normal facial function. We found a highly significant difference regarding the time course and final outcome in patients with incomplete palsies versus total paralysis; however, only 3 of 250 studies make this distinction. The time course for improvement and the extent of recovery is significantly different in patients presenting with an incomplete facial nerve paresis compared with patients with a total paralysis. Whereas the term "palsy" includes both entities, the term "paralysis" should only be used to describe total loss of nerve function. Patients with incomplete acute Bell's palsy (paresis) should start to improve their facial function early (1-2 wk after onset) and are expected to recover completely within 3 months. These patients do not benefit from antiviral medications and most likely do not profit from systemic steroids. Mixing patients with different severity of palsies will always lead to controversial results.

Chirurgische Korrektur des paralytischen Lagophthalmus

Impairment of the peripheral or central part of the facial nerve causes an ipsilateral peripheral facial nerve paresis. It is quite a common syndrome and affects 20-35 persons per 100,000 per year in Western Europe and the United States. A possible complication of facial palsy is paralytic lagophthalmos with aesthetic and functional impairment for the patient. Beside primary nerve reconstructive procedures plastic-reconstructive procedures play a major role in correcting paralytic lagophthalmos. The eyebrow, upper and lower lids, medial and lateral lid angle as well as the lacrimal system need to be seen as functional units and can be corrected with local surgical procedures. Restoration of eye closure is the most important goal in treating the affected eye. Due to the significant aesthetic limitations and resultant psychological stress for the patient cosmetic aspects must be included in the surgical concept.

Two Tolosa-Hunt Syndrome Accompanied By Peripheral Fasial Nerve Paralysis

Tolosa-Hunt syndrome is characterized of a painful ophthalmoplegia and is usually markedly responsive to corticosteroid therapy. In 2004 the re-defined diagnostic criteria of Tolosa-Hunt syndrome by International Headache Society the imaging findings have very important place. Cranial imaging demonstrates the contrast enhancement of cavernous sinus and orbital apex related to inflammation. We represented two case reports of Tolosa-Hunt syndrome. The cranial nerve involvement of 3., 4., 6., and first and the second branches of 5. were observed in both cases. One week later left peripheral facial nerve paralysis is added to the clinic in one of the cases. After excluding other diagnosis IV pulse steroid therapy is given and had fine response.

Periphere Fazialisparese mit Krusten an der Ohrmuschel und Bläschen am Gaumen. Der pädiatrische PRAXIS-Fall.

Ramsay Hunt syndrome (RHS) is defined as a peripheral facial nerve palsy accompanied by an erythematous vesicular rash on the ear (zoster oticus) and hard palate. It is known that varicella zoster virus (VZV) causes RHS. History and neurological examination remain the mainstay of diagnosis. Prednisolone and acyclovir/valacyclovir is helpful in RHS when given within three days of onset. We report on a 14-year-old boy who had RHS accompanied by meningitis. Polymerase chain reaction identified VZV in exudates from the geniculate zone of the ear, the hard palate and in the CSF.

Presumed Metastasis of Breast Cancer to the Abducens Nucleus Presenting as Gaze Palsy

A 51-year-old woman with breast cancer presented with progressive diplopia. Neuro-ophthalmologic examination revealed right gaze palsy and peripheral facial nerve palsy. Brain magnetic resonance imaging (MRI) was normal. However, two months later a repeat brain MRI revealed an enhancing round nodular mass at the right facial colliculus of the lower pons, at the location of the abducens nucleus. Localized metastasis to the abducens nucleus can cause gaze palsy in a patient with breast cancer.

Peripheral facial nerve axotomy in mice causes sprouting of motor axons into perineuronal central white matter: Time course and molecular characterization

Generation of new axonal sprouts plays an important role in neural repair. In the current study, we examined the appearance, composition and effects of gene deletions on intrabrainstem sprouts following peripheral facial nerve axotomy. Axotomy was followed by the appearance of galanin+ and calcitonin gene-related peptide (CGRP)+ sprouts peaking at day 14, matching both large, neuropeptide+ subpopulations of axotomized facial motoneurons, but with CGRP+ sprouts considerably rarer. Strong immunoreactivity for vesicular acetylcholine transporter (VAChT) and retrogradely transported MiniRuby following its application on freshly cut proximal facial nerve stump confirmed their axotomized motoneuron origin; the sprouts expressed CD44 and alpha7beta1 integrin adhesion molecules and grew apparently unhindered along neighboring central white matter tracts. Quantification of the galanin+ sprouts revealed a stronger response following cut compared with crush (day 7–14) as well as enhanced sprouting after recut (day 8 + 6 vs. 14; 14 + 8 vs. 22), arguing against delayed appearance of sprouting being the result of the initial phase of reinnervation. Sprouting was strongly diminished in brain Jun-deficient mice but enhanced in alpha7 null animals that showed apparently compensatory up-regulation in beta1, suggesting important regulatory roles for transcription factors and the sprout-associated adhesion molecules. Analysis of inflammatory stimuli revealed a 50% reduction 12–48 hours following systemic endotoxin associated with neural inflammation and a tendency toward more sprouts in TNFR1/2 null mutants (P = 10%) with a reduced inflammatory response, indicating detrimental effects of excessive inflammation. Moreover, the study points to the usefulness of the facial axotomy model in exploring physiological and molecular stimuli regulating central sprouting. J. Comp. Neurol. 518:699–721, 2010. © 2009 Wiley-Liss, Inc.