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PubMed1977

Preoperative facial paralysis in malignant parotid tumours.

Preoperative paralysis of the facial nerve was found in 145 of 1,029 patients with malignant parotid tumours (14%) treated at nine university clinics in Scandinavia. The incidence of facial paralysis varied between the different clinics. A parellelism between the incidence of the facial paralysis and the impairment of the prognosis of the different tumour types is shown. The presence of preoperative facial nerve paralysis in malignant parotid tumours implies a very poor prognosis but the situation is not as hopeless as has been suggested and therefore one must rely on very radical surgery.

Adenoma↗
PubMed1992

Bilateral facial paralysis: a case presentation and literature review.

Bilateral facial paralysis is a diagnostic challenge, which may manifest itself as either a simultaneous or alternating form, occurring in 0.3-2.0% of patients that present with facial paralysis. The differential diagnosis of facial paralysis includes congenital, traumatic, neurologic, infectious, metabolic, neoplastic, toxic, iatrogenic and idiopathic etiologies. While idiopathic facial paralysis is the most common diagnosis, a comprehensive evaluation must be completed prior to this diagnosis in patients with bilateral facial paralysis. A representative case of simultaneous bilateral facial paralysis is presented. The literature is reviewed and discussed. A diagnostic protocol for the evaluation of bilateral facial paralysis is proposed. Bilateral facial paralysis requires a thorough evaluation and may prove to be a diagnostic dilemma.

Aged↗
PubMed1996

A survey of facial paralysis: etiology and incidence.

Facial paralysis has numerous etiologies ranging from the most common, Bell's palsy and trauma, to rare tumors and congenital anomalies. This paper divides the etiologies of facial paralysis into five major classifications: idiopathic, traumatic, infectious, neoplastic and neurologic. The incidence of each of these classifications has been estimated from incidence rate information published in the United States and abroad. Using this information, an estimate of the incidence rate has been determined. This information was previously untabulated, thus making statistical analysis nearly impossible regarding this disorder.

Facial Paralysis↗
PubMed1979

Idiopathic facial paralysis in the dog.

Facial nerve paralysis of acute onset is reported in seven mature dogs, five of which were cocker spaniels. The clinical signs were characterised by ear drooping, lip commissural paralysis, sialosis, and collection of food on the paralysed side of the mouth. All dogs showed absent menace responses and trigeminofacial/acousticofacial reflexes. Horner's syndrome was not present in any dog. In four dogs, bilateral facial paralysis developed. The facial paralysis was unrelated to otitis media. Electrodiagnostic studies revealed denervation potentials and absent evoked muscle potentials. Facial nerve biopsies from two cases showed nerve fibre degeneration and apparent loss of larger diameter myelinated fibres. The condition has been termed idiopathic facial paralysis since the aetiopathogenesis is presently unknown.

Animals↗
PubMed1999

Facial reanimation with jump interpositional graft hypoglossal facial anastomosis and hypoglossal facial anastomosis: evolution in management of facial paralysis.

When viable proximal facial nerve is inacessible, facial nerve paralysis has been classically managed with the hypoglossal facial anastomosis (HFA) for at least the past 70 years. While this procedure has proven its reliability, its problems with hemilingual atrophy (speech deglutition, drooling, mastication), hypertonia, synkinesis, and mimetic deficits indicate the need for a more perfect solution for facial paralysis. The jump interpositional graft hypoglossal facial anastomosis (JIGHFA) along with gold weight lid implantation and electromyographic (EMG) rehabilitation achieves substantial facial reanimation without hemilingual deficits. We present our results in 18 patients who underwent JIGHFA along with gold weight lid implantation and EMG rehabilitation for facial paralysis. These results were compared with those from published series of 30 patients treated with HFA with EMG rehabilitation evaluated with objective (House-Brackmann) criteria. Anonymous retrospective information from questionnaires from 22 of 48 patients who were treated with the classic HFA was also presented. In properly selected patients, the JIGHFA technique is capable of achieving substantial facial reinnervation (House-Brackmann grade III or better) in 83.3% of the patients without hemilingual sequelae which was seen in 45% of the HFA patients. In contrast to the HFA, this procedure can be used by patients with concomitant lower cranial nerve paralysis (except hypoglossal), and bilateral facial paralysis. Hypertonia, synkinesis, and lagophthalmus were less symptomatic in the JIGHFA patients. Mimetic expression was not improved in the JIGHFA population compared with the HFA group.

Adolescent↗
PubMed1988

Electromyographic rehabilitation of facial function and introduction of a facial paralysis grading scale for hypoglossal-facial nerve anastomosis.

For reinnervation of facial paralysis, the XII-VII nerve anastomosis provides tone and mass contraction but rarely allows selective muscle control. The efficacy of EMG rehabilitation was evaluated in 30 patients who had no coordinated control of facial muscles. EMG signals from bilateral homologous facial muscle sites were converted into computer-compatible waveform traces and displayed on a video monitor. This facilitated modification of neuromuscular responses using behavioral shaping techniques. A six-point Facial Nerve Grading Scale was introduced for hypoglossal-facial nerve anastomosis to assess the results of EMG rehabilitation. Rehabilitation lasted from 3 to 18 months. Ten patients (33%) achieved the highest possible grading (II) with symmetry and synchrony of function and spontaneity of expression; 17 (57%) reached grade III, which allowed voluntary control of eye and mouth function; 3 (10%) showed minimal gains. It is suggested that neural plasticity allows therapeutic manipulation of central facilitory and inhibitory mechanisms, and possible unmasking of neural connections between the ipsilateral VII and XII nerve motor nuclei which leads to improved facial function.

Adult↗
PubMed2006

[Clinical analysis of facial nerve decompression on the treatment of facial paralysis].

OBJECTIVE: To study the occasion and curative effect of facial nerve decompression on the treatment of facial paralysis. METHOD: Facial nerve decompression was applied to 57 cases of severe facial paralysis from 1997 -2004 in our hospital. They were divided into two groups: A group received treatment within two months and B group after two months. Their curative effects were compared and the chi2 test between groups was applied. RESULT: The clinical curative ratio of group A was significantly higher than that of group B (P < 0.05). CONCLUSION: To treat facial paralysis, the application of facial nerve decompression at early stage can improve the clinical curative ratio significantly.

Adolescent↗
PubMed1986

Total facial nerve decompression in recurrent facial paralysis and the Melkersson-Rosenthal syndrome: a preliminary report.

Recurrent facial paralysis is an infrequent problem for the otolaryngologist. This paralysis may be associated with the Melkersson-Rosenthal syndrome, a triad of recurrent facial paralysis, relapsing facial edema, and associated fissured tongue. Most patients do not have the accompanying stigmata of this syndrome. This paralysis may occur unilaterally or bilaterally. The usual sequelae of recurrent facial paralysis are progressive synkinesis and increasing residual paresis with each episode, and total facial paralysis may be the final outcome. Two patients, one with unilateral Melkersson-Rosenthal syndrome and the other with a bilateral recurrent idiopathic facial paralysis, were treated with combined transmastoid and middle cranial fossa total facial nerve exposure, decompression, and slitting of the fibrous nerve sheath. Postoperatively they have not suffered from facial paralysis during a follow-up period of three years. It appears that this surgical management safely and effectively prevents recurrent facial paralysis unilaterally or bilaterally, whether or not it is associated with the Melkersson-Rosenthal syndrome. Until further experience with this particular management of recurrent facial paralysis is reported, however, caution should be used in recommending it. Additionally, it should not be assumed from this experience that surgical treatment for idiopathic facial paralysis in Bell's palsy is necessarily implied.

Adolescent↗
PubMed1987

Facial paralysis.

This article discusses peripheral facial paralysis of nontraumatic origin. The term idiopathic facial paralysis is used generically, in place of the often ambiguous term, Bell's palsy, to indicate all types of peripheral facial palsy/paralysis for which no cause is apparent. Included is a brief resumé of the pertinent anatomy and pathophysiology, a synopsis of etiologic considerations, and a discussion of current therapeutic options. This article is aimed at practitioners of otolaryngology, neurology, and neurosurgery with the hope that it will be of value to them in caring for their patients.

Facial Paralysis↗
PubMed2003

Positive effects of mime therapy on sequelae of facial paralysis: stiffness, lip mobility, and social and physical aspects of facial disability.

OBJECTIVE: Evaluation of the effect of mime therapy, a novel therapy combining mime and physiotherapy, for patients with longstanding (at least 9 months) sequelae of unilateral peripheral facial paralysis. STUDY DESIGN: Randomized clinical trial, with the treatment group receiving mime therapy and the control group forming a waiting list. SETTING: Physiotherapy outpatient department of two university medical centers. PATIENTS: There were 50 patients, 21 men and 29 women, with sequelae of facial paralysis and a mean House-Brackmann score of Grade IV. INTERVENTION: Mime therapy, including automassage, relaxation exercises, inhibition of synkinesis, coordination exercises, and emotional expression exercises. MAIN OUTCOME MEASURES: Stiffness of the face, lip mobility (both lip and pout length) and the physical and social index of the Facial Disability Index. RESULTS: Stiffness, lip mobility, and both aspects of the Facial Disability Index improved substantially because of mime therapy. CONCLUSIONS: On the basis of present evidence, mime therapy is a good treatment choice for patients with sequelae of facial paralysis.

Adult↗
PubMed1977

Surgical and nonsurgical management of facial paralysis following closed head injury.

The outcomes of facial nerve decompression, surgical exploration, and nonsurgical treatment for facial paralysis following closed head injury were analyzed in 30 patients with an intact facial nerve, and complete evaluation. Objective evaluation of outcome was achieved by calculation of a Facial Paralysis Recovery Profile and Recovery Index (Profile minus complications). Twelve of 15 patients with incomplete facial paralysis were treated medically. All followed patients with incomplete paralysis and bilaterally equal facial nerve excitability had a Recovery Index of + 10 (complete recovery of function, no complications). Three with partial denervation had a Recovery Profile of + 10 with mild contracture and synkinesis. The average Recovery Profiles for all patients treated by decompression, exploration, or nonsurgically were respectively 4.0, 5.7, and 5.7. The Recovery Indices were +1.8, +3, and +2.7, respectively. Where nerve excitability had become abnormal, facial nerve decompression was of no benefit in traumatic facial paralysis due to closed head injury. Nerve excitability tests of peripheral branches are of great value for prognosis and selection of patients who do not need surgical intervention. Substitution of facial nerve exploration for facial nerve decompression seems reasonable. Polytomography of the facial canal is invaluable in selection of patients for operation.

Adolescent↗
PubMed1983

The facial paralysis prognostic index.

The treatment of facial paralysis requires a reliable estimate of prognosis as well as an accurate diagnosis. Although the majority of patients recover, the degree of subsequent facial function varies. An estimation of the risk of nerve degeneration and subsequent disability is needed to guide therapy and to advise patients. Currently, prognosis is obtained by clinical evaluation of initial signs and symptoms, specific nerve excitability and function testing, and response to medical therapy. This study attempts to identify and quantitate factors that predict the outcome of facial paralysis. In 1214 patients with Bell's palsy, we identified factors associated with a severe course or poor outcome. We analyzed the predictive value of each item in an extensive research protocol, estimating the relative contribution to the total risk of unfavorable outcome by means of multiple regression models. With the use of these data, we have developed the facial paralysis prognostic index (FPPI). The FPPI can assist otologists to more accurately estimate outcome based on physical examination and electrical testing.

Adolescent↗
PubMed2002

[How I treat ... facial paralysis by hypoglosso-facial anastomosis].

Thirteen patients underwent a hypoglosso- or a spino-facial nerve anastomosis between 1990 and 1996. Facial palsy was the result of surgery in 12 cases and of radiosurgery in 1 case. The mean interval between facial palsy and anastomosis was 12 months. Facial nerve function is determined on the basis of clinical examination according to the classification of House-Brackmann and our own evaluation. According to House, 10 patients are classified grade III and 3 grade IV. Our evaluation defines in 10 grade III, 7 good results and 3 fair results. As far as the good results are concerned, the mean interval between palsy and anastomosis is short (< 3 months). The permanent eating and swallowing dysfunctions are consecutive to multiple cranial nerve deficits. The post-paralysis hemifacial spasm is facilitated by prolongated electric stimulations.

Adult↗
PubMed1994

Recurrent lower motor neurone facial paralysis in four successive pregnancies.

Recurrent lower motor neurone facial paralysis in successive pregnancies is a rare phenomenon of which there are few case reports in the literature. There have been two previous reports of recurrent Bell's palsy in two and three successive pregnancies respectively, but it is felt that these should have more appropriately been reported as recurrent lower motor neurone facial paralysis in pregnancy as, by definition, any facial paralysis that recurs should not be classified as Bell's palsy even though Bell himself commented on the association between facial paralysis and pregnancy. We report the first case of recurrent lower motor neurone facial paralysis in four successive pregnancies and review the literature.

Adult↗
PubMed1999

Insulin-like growth factor-I promotes nerve regeneration through a nerve graft in an experimental model of facial paralysis.

Among the pathological sequelae of facial paralysis is a paralytic eye. Apart from the psychological and aesthetic deficits, facial paralysis if left untreated can lead to dryness, ulceration and eventual blindness. Although numerous restorative microsurgical approaches have been introduced to address the sequelae of this problem, complete restoration of function to denervated facial muscles remains elusive.Utilizing the rat model of facial paralysis the present research has as an objective to examine a dual treatment approach. Specifically, this study combined the current microsurgical treatment of the cross-facial nerve graft with local administration of insulin-like growth factor I (IGF-I).The efficacy of this combined approach (cross-facial nerve graft + IGF-I) was assessed in the following ways: (a) behavior measurement of the blink response and (b) histomorphometry light and electron microscopy of the entire nerve graft. These data will help provide insight into the restoration of facial muscle function after trauma and assist in the future development of more potent treatment strategies.7he local adnünistration of IGF-I (50 micro g/ml) to the cross-facial nerve graft was found to restore the blink response faster and to strengthen the degree of eye closure. Light microscopy examination revealed that IGF-I significantly enhanced axonal regeneration within a nerve graft (a 22% increase in the mean number of axons), and increased the mean nerve fiber diameter and myelin thickness. Electron microscopy assessment of the nerve grafts demonstrated that the IGF-I treated grafts possessed a greater density of microtubules, which were evenly distributed within the axoplasm.

Journal Article↗
PubMed2003

Delayed-onset facial paralysis after vestibular neurectomy.

OBJECTIVES/HYPOTHESIS: Delayed-onset facial paralysis (beginning more than 3 d after the procedure) has been described as a complication of many different types of otological procedures. The incidence of this problem in vestibular neurectomy and the relationship to surgical approach are detailed in the study. STUDY DESIGN: Retrospective case review. METHODS: In the setting of a tertiary referral center, vestibular neurectomy was performed in 70 individuals with disabling vertigo unresponsive to medical therapy who elected vestibular neurectomy. The main outcome measure was incidence of delayed onset facial paralysis. RESULTS: Delayed-onset facial paralysis was significantly more common after the middle fossa (18%) and translabyrinthine (11%) approaches compared with the retrosigmoid approach (0%). CONCLUSIONS: Surgical approach influences the incidence of delayed-onset facial paralysis. Measures to prevent this complication such as prophylactic antiviral medication or labyrinthine segment decompression may be considered in middle fossa and translabyrinthine operations.

Adult↗