Severe Facial Palsy Research Articles

Assessment of airway the MOUTH concept

kg of propofol and 0.2 mcg/kg Department of Anesthesiology and Intensive Care, of sufentanilwere administered intravenously (IV) for induction of GA. The patient has been ventilated twice by facemask and trachea immediately intubated. Anesthesiawas maintainedwith nitrousoxide50%in oxygenand sevoflurane. In postanesthesia care unit, a left peripheral facial paralysis was noted. An emergent brain computed tomography (CT) scan was normal. Oral prednisolone was introduced after neurologist’s assessment. The patient was discharged on day 2. One year after, hemifacial spasms and synkinesis were still observed.A 47-year-old woman 2.presented with a postcoital headache with loss of consciousness. A brain CT scan revealed a subarachnoid hemorrhage (ruptured basilar artery aneurysm). On emergency, an external ventricular drain was inserted and aneurysm was occluded by coiling. Patient’s trachea was extubated on day 10. Right labial herpes lesions appeared on day 21 and were treated by topical application of acyclovir. Five days after, a ventriculoperitoneal shunt was inserted because of a persistent hydrocephalus. Induction of GA was performed with propofol (2.5 mg/kg), sufentanil (0.3 mcg/kg) and cisatracurium (0.15 mg/kg) IV. The patient’s lungs was ventilated by facemask and trachea intubated without difficulty. Anesthesia was maintained with sevoflurane without nitrous oxide. After tracheal extubation, a right peripheral nerve palsy was noted. Intravenous acyclovir and methylprednisolone were administered for 10 days. Six months later, a severe facial palsy was still present.These cases are highly suggestive of associations between IFP and GA.In demyelinating disorders, such as multiple sclerosis, GA has been implicated in causing disease exacerbation.

重篤な外傷性顔面神経麻痺に対して動的顔面神経再建術を施行した1例

Various methods are used for reconstruction in patients with traumatic facial palsy. We describe facial nerve dynamic reconstruction for severe traumatic facial palsy in a 42-year-old man. His face was cut by an electric lawn mower. Two years later, a hypoglossal nerve-facial nerve anastomosis was peformed to treat facial nerve palsy. We used the great auricular nerve for bypass grafts, and jump grafts for end-to-end anastomoses with the facial nerve and with the hypoglossal nerve. Seven months after reconstructive surgery, facial palsy had improved to grade III according to the House-Brackmann method.

Clinical manifestations and prognosis of patients with Ramsay Hunt syndrome

PurposePatients with Ramsay Hunt syndrome have a poorer prognosis than those with Bell palsy despite the use of various treatment modalities. We compared the clinical characteristics, treatment methods, and outcomes in patients with Ramsay Hunt syndrome and Bell palsy. Materials and MethodsPatients with Ramsay Hunt syndrome were compared with patients with Bell palsy treated using oral steroids and with those treated with both steroids and an antiviral agent. Functional recovery of the facial nerve was scored according to the House-Brackmann grading system. Patients were followed up until recovery or for 3 months. Recovery rates in each group were assessed by age, sex, and initial and last House-Brackmann grade. ResultsCompared with patients with Bell palsy, those with Ramsay Hunt syndrome were generally younger, had initially more severe facial palsy, and a lower recovery rate. Various factors including initial House-Brackmann grade, starting time to treatment, age, comorbid disease, electroneurography, and electromyography showed some correlations with prognosis in all groups. The addition of antiviral agents to an oral steroid regimen did not improve the recovery rate of patients with Bell palsy. ConclusionPatients with Ramsay Hunt syndrome have a poorer prognosis than do those with Bell palsy.

Long‐Term Effect of Prednisolone on Functional Blink Recovery after Transient Peripheral Facial Motor Paralysis

To determine the functional recovery in patients with severe transient peripheral facial motor paralysis (Bell palsy). Prospective controlled trial. Academic medical center. Blink recovery was studied in 2 groups of severely affected Bell palsy patients during a follow-up period of 84 weeks. The patients in one group received prednisolone within the first week after the onset of symptoms. No medication was given to the other group. A control group of healthy subjects was also included. Simultaneous orbicularis oculi muscle activity and eyelid kinematics were recorded by surface electromyographic (EMG) recording and eyelid search coils, respectively. At the beginning of the paralysis, very little integrated orbicularis oculi muscle activity and eyelid movement was measured at the palsied side of the face. Thirteen weeks later, the integrated orbicularis oculi EMG and functional blink recovery gradually improved until 39 weeks. Beyond, only the integrated orbicularis oculi EMG slightly increased. At 84 weeks, the integrated orbicularis oculi EMG was significantly larger in the prednisolone group compared with the control group. The integrated EMG of the nonmedicated group recovered to normal values. Curiously enough, the functional blink recovery at the palsied side remained reduced to 64% compared with the healthy controls in the prednisolone-treated group and to 36% in the nonmedicated group. The authors demonstrate that prednisolone significantly increased the orbicularis oculi muscle activity and significantly improved functional blink recovery in severely affected Bell palsy patients. However, the increase of muscle activity was insufficient to restore functional blinking to normal values.

Non-accidental caustic ear injury: Two cases of profound cochleo-vestibular loss and facial nerve injury

Non-accidental caustic injury is a rare form of child abuse usually secondary to forced ingestion. Caustic injury to the ear most commonly arises from battery lodgement in the external canal. This case series represents the first report of non-accidental caustic injury to previously normal ears resulting in profound sensorineural hearing loss, vertigo with horizontal canal hypofunction and in one patient a severe facial nerve paralysis. Both patients required blind-end sac closure of the injured ear and one required sural nerve interposition combined with transfer of the masseteric branch of the trigeminal nerve to the ipsilateral facial nerve.

Periocular Cosmesis & Facial Dynamic Procedures

AbstractPurpose To present Periocular Cosmesis & Facial Dynamic Procedures, that can be performed in severe and refractory facial nerve palsy cases.Methods Didactic course lectureResults Facial reanimation using dynamic procedures is a multidisciplinary rehabilitative type of management which may be undertaken in longstanding and severe facial nerve palsy. This management includes facial nerve repair, facial nerve substitution and temporalis muscle transfers. Peri‐ocular aesthetic issues need to be addressed in severe and refractory facial nerve palsy cases. Brow lift, midface lift and facial lift can be performed to improve functionality and cosmesis.Conclusion These procedures can provide a moderate to significant degree of improvement in facial nerve functionality and periocular cosmesis

Facial Nerve Decompression Surgery with Gelatin Containing bFGF

Objective: Basic fibroblast growth factor (bFGF) promotes the regeneration of denervated nerves. Our experimental study suggested that bFGF-impregnated biodegradable gelatin hydrogel facilitates regeneration of the facial nerve in guinea pigs due to the sustained release of bFGF. Clinically, this therapeutic regimen may be useful for facial nerve decompression surgery. Method: Twenty-five patients with severe facial paralysis were treated with the new procedure. The facial nerve was decompressed tympanic and mastoid portions via mastoid. A bFGF-impregnated biodegradable gelatin hydrogel was placed around the exposed nerve. Regeneration of the facial nerve was evaluated once per month by observing the facial movement. Results: Patients were followed until complete recovery occurred, or for more than 6 months in cases with a poor prognosis. All patients with severe Bell’s palsy and Ramsey Hunt syndrome showed early recuperation and milder sequelae compared to conventional decompression surgery. Recovery from the palsy was defined as House-Brackmann grading 1 and 2. The rates of recovered patients with novel surgery and conventional surgery were 92.0% (n = 25) and 70.7% (n = 58), respectively; the former was significantly better than the latter ( P < .05). Conclusion: This is the first study to reveal the efficacy of a bFGF-impregnated biodegradable gelatin hydrogel as a drug-delivery medium in the paralyzed facial nerve surgery. Advantages of this decompression surgery are low risk of hearing impediment and long effective period after onset of paralysis.

Hepatocyte growth factor incorporated into herpes simplex virus vector accelerates facial nerve regeneration after crush injury

Hepatocyte growth factor (HGF) promotes regeneration of the central nervous system, but its effects on the peripheral nervous system remain unclear. This study was conducted to elucidate the effect of HGF on regeneration of the murine facial nerve after crush injury. To do so, a replication-defective herpes simplex virus vector that incorporated HGF was prepared (HSV-HGF). The main trunk of the facial nerve was compressed by mosquito hemostats, and HSV-HGF, control vector or medium was then applied to the compressed nerve. We found that mice in the HGF group required significantly fewer days for complete recovery from nerve compression. Furthermore, the amplitude of the evoked buccinator muscle compound action potential increased following HSV-HGF application. HGF expression in and around the compressed nerve was demonstrated by enzyme-linked immunoassay and immunohistochemistry. In addition, HSV-HGF introduction around the damaged nerve significantly accelerated recovery of function of the facial nerve. These data suggest a possible role of HGF in promoting facial nerve regeneration after nerve damage. Furthermore, this viral delivery method may be applied clinically for many types of severe facial palsy during facial nerve decompression surgery.

Intraoperative continuous monitoring of evoked facial nerve electromyograms in acoustic neuroma surgery

Preservation of facial nerve function is one of the most important goals in acoustic neuroma surgery. We have been using intraoperative continuous monitoring of evoked facial nerve electromyograms (EMGs) since 1997 in acoustic neuroma surgery. We therefore investigated surgically treated patients to clarify the usefulness of this monitoring, and to determine safety criteria for preserving facial nerve function. This intraoperative continuous monitoring of evoked facial nerve EMG is a method for checking the EMG evoked by continuous direct electrical stimulation of the facial nerve during tumor excision. The greatest advantage of this method is the ability to identify changes in EMG in real time. We retrospectively investigated 216 patients with surgically treated acoustic neuroma to identify correlations between parameters in this monitoring and postoperative facial nerve function immediately and 1year after surgery. In these patients, the functional preservation rate of the facial nerve (House and Brackmann grade 1 or 2 at 1year after surgery) was 98.6% with a 98.2% mean tumor resection rate. Amplitude preservation ratio correlated significantly with facial nerve function both immediately and 1year after surgery. To avoid severe facial nerve palsy, a warning criterion of amplitude preservation ratio >50% appears useful. Postoperative course of facial nerve function appears predictable using intraoperative continuous monitoring of evoked facial nerve EMGs. This monitoring is useful to increase the tumor excision rate while avoiding severe postoperative facial nerve palsy in acoustic neuroma surgery.

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.

Progressive external ophthalmoplegia as initial manifestation of sporadic late-onset nemaline myopathy

Sporadic late-onset nemaline myopathy (SLONM) is a rare disease and typically presents in patients older than 40 years with slowly progressive weakness in a limb-girdle distribution and unremarkable family history [1, 2]. Serum creatine kinase is usually normal, and electromyography may show myopathic changes. Nemaline rods in affected muscle fibers are considered the histopathological hallmark of nemaline myopathy and are mainly found within the sarcoplasm, inside of myonuclei, or both [3]. Ocular involvement has never been described in a patient with SLONM. We report a patient with SLONM suffering from prominent involvement of external ocular muscles. A 60-year-old female patient was reexamined for a chronic progressive oculopharyngeal syndrome that was present for 6 years. Initial symptoms were double vision and ptosis, followed by weakness of eye-closure. Two years after the onset of symptoms, she presented an exclusive picture of external ophthalmoplegia. During the following years she was unable to open or close her eyes voluntarily, lost her ability to whistle or smile, developed a hoarse voice and swallowing difficulties. There was no diurnal variation of symptoms, or fatigability. Family history for neuromuscular diseases was unremarkable. On examination she had complete bilateral ptosis and palsy of extraocular muscles, while pupillar size and pupillar reactions to light and accommodation were normal. She had a myopathic face with atrophy of masseter and temporalis muscles, severe bilateral facial palsy, and severe dysphonia. Strength was MRC grade 4 for neck flexion, head rotation, and neck extension. Further neurological examination was normal, notably fundoscopy and proximal and distal limb strength. Laboratory examinations provided normal values for standard parameters, serum creatine kinase, a comprehensive panel of autoimmune antibodies, including antibodies against acetylcholine receptor or muscle-specific kinase, anti-HIV 1/2 antibodies, and p24 antigen. Serum ACE, soluble Interleukin-2 receptor levels, serum and urine calcium levels, and repeated imaging studies ruled out sarcoidosis. Protein electrophoresis and immunofixation did not show any paraprotein, findings that rule out an association with HIV, sarcoidosis, or monoclonal gammopathy, as described in some patients in the literature [4–7]. MRI revealed symmetric atrophy of ocular muscles and fatty degeneration of pterygoideus medialis and masseter muscles, no signs of edema or contrast enhancement. Thorough neuromuscular transmission studies as well as spinal cord and brain imaging were unremarkable. No other organs were involved. Muscle biopsy of the sternocleidomastoideus revealed numerous rods, which appeared to be O. Wengert A. Meisel Department of Neurology, Charite-Universitatsmedizin Berlin, Chariteplatz 1, 10117 Berlin, Germany

Intraoperative Monitoring of Motor Evoked Potential for the Facial Nerve Using a Cranial Peg-Screw Electrode and a “Threshold-level” Stimulation Method

Transcranial motor evoked potential (MEP) for the facial nerve (facial MEP) has been recognized as a good method for quantitative monitoring of facial nerve function in skull base surgery. To improve the feasibility and safety of facial MEP monitoring, a peg-screw electrode and a "threshold-level" method were investigated. From 2007 to 2009, intraoperative facial MEP monitoring with the peg-screw electrode and threshold-level method was successfully achieved in 26 of 29 patients who underwent surgery for the posterior fossa extra-axial tumor. The relationship between the change in the facial MEP threshold level and the postoperative function of the facial nerve was analyzed in 23 patients who had no facial palsy preoperatively. There were no complications associated with facial MEP monitoring. Nine patients who had stable facial MEP threshold had no facial palsy. Fourteen patients who had worsened but measurable facial MEP threshold had mild palsy at discharge. Two of three patients who had severely worsened and unmeasurable facial MEP threshold had severe facial palsy. The change in the facial MEP was well correlated with the postoperative facial function. The peg-screw electrode and threshold-level method are good options for facial MEP monitoring.

Toxina botulínica y parálisis facial. Nuestra experiencia

Introduction and objectives Therapeutic indication of peripheral facial paralysis depends on the degree of nerve injury. Severe facial palsy (electroneuronographic study less than or equal to 10%) leads to healing with sequelae. The sequelae of facial paralysis are contractures, hemifacial spasm and synkinesis.Our purpose was to demonstrate that these patients could benefit from rehabilitation treatment. Methods We present a study of 48 patients with severe peripheral facial paralysis. They were treated from the beginning of reinnervation with botulinum toxin and facial exercises according to the Wisconsin School. Results The subjective efficacy of rehabilitation is high. Conclusions Rehabilitation treatment can inform patients about their chances of recovery, give them control over and quality of facial expression and help to achieve greater facial symmetry. These factors provide better functionality and quality of life.

Herpes simplex virus type 1 and Bell's palsy—a current assessment of the controversy

Bell's palsy causes about two thirds of cases of acute peripheral facial weakness. Although the majority of cases completely recover spontaneously, about 30% of cases do not and are at risk from persisting severe facial paralysis and pain. It has been suggested that herpes simplex virus type 1 (HSV-1) may be the etiological agent that causes Bell's palsy. Although corticosteroid therapy is now universally recognized as improving the outcome of Bell's palsy, the question as to whether or not a combination of antiviral agents and corticosteroids result in a better rate of complete facial recovery compared with corticosteroids alone is now a highly contentious issue. The evidence obtained from laboratory studies of animals and humans that HSV-1 may be linked to facial nerve paralysis is first outlined. The discussion then focuses on the results of different clinical trials of the efficacy of antiviral agents combined with corticosteroids in increasing the rate of complete recovery in Bell's palsy. These have often given different results leading to opposite conclusions as to the efficacy of antivirals. Of three recent meta-analyses of previous trials, two concluded that antivirals produce no added benefit to corticosteroids alone in producing complete facial recovery, and one concluded that such combined therapy may be associated with additional benefit. Although it is probably not justified at the present time to treat patients with Bell's palsy with antiviral agents in addition to corticosteroids, it remains to be shown whether antivirals may be beneficial in treating patients who present with severe or complete facial paralysis.

Botulinum toxin and facial palsy. Our experience

Introduction and objectivesTherapeutic indication of peripheral facial paralysis depends on the degree of nerve injury. Severe facial palsy (electroneuronographic study less than or equal to 10%) leads to healing with sequelae. The sequelae of facial paralysis are contractures, hemifacial spasm and synkinesis. Our purpose was to demonstrate that these patients could benefit from rehabilitation treatment. MethodsWe present a study of 48 patients with severe peripheral facial paralysis. They were treated from the beginning of reinnervation with botulinum toxin and facial exercises according to the Wisconsin School. ResultsThe subjective efficacy of rehabilitation is high. ConclusionsRehabilitation treatment can inform patients about their chances of recovery, give them control over and quality of facial expression and help to achieve greater facial symmetry. These factors provide better functionality and quality of life.

Stereotactic Radiation in the Treatment of Glomus Jugulare Tumors

Introduction: Glomus jugulare tumors are a challenge to treat due to their proximity to the facial nerve and lower cranial nerves. Postoperative deficits may include severe dysphagia, hoarseness, and facial paralysis. To decrease the morbidity from the treatment of glomus jugulare tumors, we have incorporated radiosurgery as either primary treatment or as an adjunct to surgery.

SP124 – The association between severity of facial paralysis and psychosocial consequences

SP124 – The association between severity of facial paralysis and psychosocial consequences

The n10 component of the ocular vestibular-evoked myogenic potential (oVEMP) is distinct from the R1 component of the blink reflex

Bone-conducted vibration (BCV) in the midline at the hairline (Fz), results in short latency potentials recorded by surface electrodes beneath the eyes - the ocular vestibular-evoked myogenic potential (oVEMP). The early negative component of the oVEMP, n10, is due to vestibular stimulation, however it is similar to the early R1 component of the blink reflex. Here we seek to dissociate n10 from R1. Surface potentials were recorded from the infraorbital electromyogram of 10 healthy subjects, 6 patients with bilateral vestibular loss, 2 with unilateral vestibular loss, 4 with facial palsy and 3 with facial and vestibular nerve lesions on the same side. BCV was delivered at Fz, the inion, the glabella or the supraorbital ridge using a tendon hammer or a bone-conduction vibrator. Onset latencies of the n10 evoked by taps at Fz or inion were significantly shorter than the R1 components of blink responses to supraorbital and glabellar stimuli. Upward gaze increased the amplitude of n10 but not R1. The n10 was absent bilaterally in patients with bilateral vestibular loss and beneath the contralesional eye in patients with unilateral vestibular loss, but in both these groups of patients R1 was preserved. In severe facial palsy the R1 component was absent or delayed and attenuated ipsilesionally, but n10 was preserved bilaterally. In subjects with unilateral facial and vestibular nerve lesions (Herpes Zoster of the facial and vestibulocochlear nerves) the dissociation was complete - the ipsilesional R1 was absent or attenuated whereas the ipsilesional n10 was preserved. n10 is distinguished from R1 by its earlier onset, laterality, modulation by gaze position and dissociation in patient groups. The n10 component evoked by BCV at Fz is not the R1 component of the blink reflex.

The benefits of steroids versus steroids plus antivirals for treatment of Bell’s palsy: a meta-analysis

Objective To determine whether steroids plus antivirals provide a better degree of facial muscle recovery in patients with Bell’s palsy than steroids alone.Design Meta-analysis.Data sources PubMed, Embase, Web of Science,...

Facial paralysis after superselective intra-arterial chemotherapy via the middle meningeal artery in maxillary cancer

Previous studies have suggested that the severity of facial paralysis after superselective intra-arterial chemotherapy (SSIAC) is usually mild. Here we present two cases of facial paralysis after SSIAC via the middle meningeal artery (MMA). In case 1, the patient completely recovered from his facial paralysis (to H-B grade I) in 6 months after the onset of paralysis. However, in case 2, his facial movement remained at House-Brackmann (H-B) grade IV with severe synkinesis. We must be careful that SSIAC via the MMA may potentially increase the risk of facial paralysis.