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PubMed2006

Facial paralysis.

Detailed knowledge of embryology, anatomy, and function of the facial nerve is essential in treating the devastating functional, aesthetic, and psychological sequelae of facial paralysis. Two basic factors influence the method of repair and the subsequent outcome of the effort to combat facial paralysis. First is the availability of a viable proximal nerve stump which can be used as the source for motor axons, and which is related to the level of the injury. Second is the duration of the paralysis, which will dictate the possibility of reinnervating the facial muscles. Early restoration of nerve continuity, and therefore reestablishment of the neuromuscular junction and preservation of the function of the facial muscles, lead to superior functional and aesthetic rehabilitation. Secondary reconstruction, after the establishment of atrophy of the motor endplates of the facial muscles, is possible with nerve grafts and microsurgical free functional muscle transfer. These techniques, although not perfect, greatly improve aesthetic balance and alleviate the functional and psychological implications of the paralysis.

Facial Nerve↗
PubMed2006

Bilateral facial paralysis: case presentation and discussion of differential diagnosis.

Bilateral facial paralysis is a rare condition and therefore represents a diagnostic challenge. We report the case of a 34-year-old healthy woman with sequential bilateral facial paralysis as a sole manifestation of sarcoidosis. She initially presented with an isolated left sided Bell's palsy without any symptoms to suggest alternative diagnoses. Within a month there was progression to peripheral facial paresis on the contra lateral side, prompting a diagnosis of Lyme disease. Her physical examination and chest x-ray did not reveal any clinical evidence of sarcoidosis. After failing to respond to an empiric trial of intravenous ceftriaxone for a presumptive diagnosis of Lyme disease, computed tomography scan of the chest was ordered which demonstrated bilateral hilar lymphadenopathy. Bronchoscopic biopsy confirmed a diagnosis of sarcoidosis. The patient then made a complete recovery on steroid therapy. We discuss the differential diagnosis of facial diplegia and focus on the clinical presentation, diagnosis and treatment of neurosarcoidosis.

Adult↗
PubMed1999

[Jugular bulb diverticular and facial paralysis].

The authors report a case where a woman presents a right jugular bulb procidence already known and responsible of a perception deafness. Secondarily, a right facial paralysis is appeared progressively and not regressive even with medical treatment. When the computed tomography as shown an intrapetrous diverticular, the facial paralysis treatment was surgical to decompress the facial nerve. The literature study shoes the rarity of this association facial paralysis and jugular bulb procidence (only two cases), more often responsible of deafness, tinnitus, and vertigo. The diagnosis is given by computed tomography. M.R.I. has not still be evaluated. Then the authors insist on the progressive character of the facial paralysis and on the necessity of a surgical treatment.

Adult↗
PubMed1980

Facial paralysis of neoplastic origin: diagnosis and management.

The individual with a progressive (weeks to months) facial weakness should be considered to have a tumor involving the facial nerve until proved otherwise. All individuals experiencing a facial paralysis must undergo a thorough neurotologic evaluation to establish the etiology. Bell's palsy is a diagnosis by exclusion. While computerized axial tomography (CAT) scans, polytomography and arteriograms are extremely helpful, these studies very often fail to demonstrate intrinsic tumors involving the facial nerve. For this reason all individuals experiencing a progressive facial paralysis should have an exploration of their facial nerve from the internal auditory canal (IAC) through the stylomastoid foramen into the parotid gland. The purpose of this paper is to present a series of cases of facial paralysis having as their etiology intrinsic or extrinsic neoplasms. Clinical patterns are established, diagnostic protocols formulated and the results of surgical management reviewed.

Adolescent↗
PubMed1996

Acute otitis media and facial paralysis in children.

We reviewed 10 children who presented with facial paralysis after the onset of acute otitis media. The objective of the study was to examine the outcome of facial paralysis in children with acute otitis media treated without facial nerve decompression. Two groups were identified: 8 patients with incomplete paralysis and 2 with complete paralysis. Seven of the 8 patients with incomplete paralysis had rapid return of function after myringotomy and intravenous antibiotics. The eighth patient had delayed recovery requiring 9 months before complete return of function. The 2 patients with complete paralysis required mastoidectomy to control otorrhea and fever after initial myringotomy and antibiotics. Both patients had a prolonged recovery requiring 3 and 7 months for complete recovery. Patients with incomplete paralysis generally show rapid improvement following wide myringotomy and antibiotic treatment. A more protracted recovery may be expected in patients with complete paralysis; excellent return of function is expected when mastoidectomy without facial nerve decompression is employed.

Acute Disease↗
PubMed2005

Varicella-zoster virus reactivation is an important cause of acute peripheral facial paralysis in children.

BACKGROUND: Reactivation of herpes simplex virus type 1 is thought to be a major cause of adult idiopathic peripheral facial paralysis or Bell's palsy. However, few studies have examined the pathogenesis of this condition in children. Serologic assays and polymerase chain reaction (PCR) analysis of paired sera and saliva samples were used here to investigate the causes of acute peripheral facial paralysis in pediatric patients. METHODS: A total of 30 children with acute peripheral facial paralysis were recruited. Paired sera were assayed for evidence of herpesvirus, mumps virus or Borrelia infection. PCR was used to detect herpes simplex virus type 1 and varicella-zoster virus (VZV) DNA in saliva samples. RESULTS: Ramsay Hunt syndrome with accompanying zoster lesions was diagnosed clinically in 2 patients, and VZV reactivation was confirmed serologically. VZV reactivation in the absence of zoster (zoster sine herpete) was diagnosed in 9 patients with either serologic assays or PCR. Thus VZV reactivation was demonstrated in 11 of 30 (37%) patients. The prevalence of VZV reactivation among patients between 6 and 15 years of age was significantly higher than in those younger than 5 years of age (53% versus 9%, P = 0.023). CONCLUSIONS: Our data indicate that VZV reactivation is an important cause of acute peripheral facial paralysis in children, especially those between 6 and 15 years of age.

Adolescent↗
PubMed2006

Facial paralysis as a presenting symptom of leukemia.

Facial paralysis may occur as a complication of central nervous system leukemias in children, but it is rarely a presenting symptom. This report describes an 8-month-old child who presented with peripheral facial palsy, failure to thrive, anemia, and otitis media. Antibiotic and steroid treatment led to an improvement in the clinical condition, but not the paralysis. At readmission 3 weeks later, physical examination revealed bluish, firm, palpable masses on the scalp and facial areas, and laboratory and imaging studies confirmed the diagnosis of acute myeloid leukemia. This case should alert physicians to consider hematologic malignancies in children with facial paralysis.

Acute Disease↗
PubMed1999

Effect of nerve repair after unilateral partial facial paralysis on craniofacial growth and development.

The effect of partial transection, coaptation, and freezing of the left facial nerve on craniofacial growth and development was investigated. Twelve-day-old New Zealand White rabbits were randomly assigned to four groups: control group (n = 15), nerve ablation group (n = 15) with a surgically induced partial facial paralysis, nerve coaptation group (n = 15) with a surgically induced partial facial paralysis treated by immediate microsurgical nerve coaptation, and nerve freezing group (n = 13) with a freezing-induced partial facial paralysis. All animals were operated on at the age of 12 days; follow-up evaluations were performed at the ages of 2 months (end-point prepubertal growth) and 6 months (full grown). Computerized dorsoventral roentgencephalometric analysis and computer tomographic three-dimensional volumetric measurements were performed at both ages. Roentgencephalometric analysis revealed that the growth disturbances of the nerve ablation group and the nerve coaptation group were analogous. In contrast, in the nerve freezing group, hardly any growth disturbances as compared with the control group were seen. The CT volume measurements revealed a significant left-right difference in maxillary volume at the ages of 2 and 6 months in the nerve coaptation group as compared with the control group. Muscle histomorphometric analysis revealed a shift in muscle fiber composition in the nerve coaptation group and the nerve freezing group, with an increase of type I fibers at the cost of type IIA fibers. This shift was significantly less pronounced in the latter than in the former. Nerve histomorphometric analysis revealed a significant increase in the number of nerve fibers in the nerve coaptation group as compared with the control group. In the nerve freezing group, the increase in the number of nerve fibers was not significantly different as compared with the control group and the nerve coaptation group. Both the equivalent diameter and the myelin area were equally reduced in the nerve coaptation and nerve freezing groups. Thus, the nerve coaptation group and the nerve freezing group did not differ significantly in the extent of nerve recovery, although they differed in the extent of muscle recovery. The extent of muscle recovery, in turn, was related to the extent of abnormal craniofacial growth and development. Indeed, the growth and development were hardly abnormal in the nerve freezing group and as abnormal as after untreated paralysis in the nerve coaptation group. Therefore, factors related to nerve regeneration, other than those assessed by nerve histomorphology, were considered to be responsible for these differences between both groups. The duration of the denervation time was regarded to be considerably shorter in the nerve freezing group than in the nerve coaptation group, resulting in the observed improved muscle recovery. The difference in the degree of axonal malalignment between both groups was considered to be negligible, because of the tolerance toward axonal malalignment at neonatal age.

Animals↗
PubMed2006

[Facial paralysis after temporal bone trauma].

OBJECTIVES: To evaluate functional outcome in 64 cases of facial paralysis following temporal bone fracture and discuss decisive arguments leading either to medical treatment or surgical management. METHODS: Sixty-four patients suffering from post-traumatic facial paralysis were managed between 1995 and 2003: 38 (59%) were given medical treatment and 26 (41%) underwent surgery. A combined middle fossa and transmastoid approach was mostly used (58%). Electrophysiological testing and CT scan results were the main points of the decision algorithm. RESULTS: Electroneuromyography seems to be the most accurate exploration for guiding treatment. Good results (grades I to II on the House and Brackmann scale) were obtained in 63% of cases after medical management and in 39% of cases after surgical treatment. Grades III or IV were obtained in 13% of medically-treated patients and 42% of surgically-treated patients. CONCLUSION: Management of facial paralysis following temporal bone fracture in accordance with electrophysiological testing (evoked EMG) together with CT scan findings enabled accurate indications for surgical treatment. A good grade I or II result can be expected after medical management. A grade III is at best reached after nerve anastomosis.

Adolescent↗
PubMed2003

Ceramic representations of facial paralysis in ancient Peru.

OBJECTIVE: To provide interested scholars with a historical perspective of facial paralysis as interpreted by the ceramists of the ancient Moche culture. METHODS: The authorities and curators of the Museo Arqueológico Rafael Larco Herrera, and the Museo Nacional de Arqueología, Antropología e Historia del Perú, in Lima, Perú, provided photographs of some of the more salient examples of facial paralysis in their Moche ceramic collections. Four of these were selected for inclusion in this article. CONCLUSION: Moche pathologic portraits establish a unique point of reference in the history of facial paralysis and its sequelae. They stand alone as a prehistoric record of this disorder, unsurpassed until the appearance of Bell's work and illustrations.

Ceramics↗
PubMed1997

Neurophysiological evaluation of acute facial paralysis in children.

Objective evaluation of facial nerve paralysis represents a unique challenge to the clinician. Electroneurography (ENoG) and the acoustic reflex (AR) have been widely used as neurophysiological tests in an assessment of facial nerve function. However, ENoG or AR alone does not suffice diagnostic and prognostic purposes of facial function evaluation in children. To further investigate the diagnostic aspects of facial nerve paralysis, the prognostic value of AR and ENoG, and the time course of the disease in pediatric population, a series of 30 children with acute facial paralysis were investigated by correlation of findings from video-taped House-Brackmann facial grading system. AR and ENoG. The results showed that AR was absent or abnormal for thresholds in 68.2% of patients with Bell's palsy and normal middle ear function. Shorter duration and higher percentage of recovery were found in the children with a normal AR than those with an abnormal AR. Three children showed an abnormal tympanogram and hearing loss associated with acute facial paralysis. These findings should alert the clinician to the presence of a specific, treatable disease in the evaluation of Bell's palsy. The percentage of electroneurographic response varied with different days after onset. ENoG showed minimal responses at weeks 1 3 after onset of Bell's palsy in most patients. The study of the time-course in the children with Bell's palsy demonstrated a functional gap in the early (< 1 week) and late clinical stage (after 6 weeks) of the disease, suggesting that ENoG predicted well only during weeks 1-4 after onset. In general, ENoG showed a good recovery in children, however, recurrent Bell's palsy becomes a concern. The need for neurophysiological follow-up for possible incomplete recovery of the facial nerve is emphasized. It is recommended that AR and ENoG should be included in the diagnostic workup when evaluating pediatric facial function.

Acoustic Impedance Tests↗
PubMed2005

[Clinical observation on double moxibustion at Yifeng (TE 17) combined with electroacupuncture for treatment of facial paralysis].

OBJECTIVE: To compare clinical therapeutic effects of double moxibustion at Yifeng (TE 17) combined with electroacupuncture. and simple electroacupuncture on facial paralysis. METHODS: Eighty-seven cases of facial paralysis were randomly divided into a treatment group (n = 47) treated by double moxibustion at Yifeng (TE 17) combined with electroacupuncture, and a control group (n = 40) treated by simple electroacupuncture. Their therapeutic effects were investigated after 30 days. RESULTS: The total effective rate was 100.0% in treatment group and 87.5% in the control group with a significant difference between the two groups (P < 0.05). CONCLUSION: Double moxibustion at Yifeng (TE 17) combined with electroacupuncture in clinical therapeutic effect on peripheral facial paralysis is superior to simple electroacupuncture.

Acupuncture Points↗
PubMed2002

Facial paralysis caused by malignant skull base neoplasms.

OBJECT: Bell palsy remains the most common cause of facial paralysis. Unfortunately, this term is often erroneously applied to all cases of facial paralysis. METHODS: The authors performed a retrospective review of data obtained in 11 patients who were treated at a university-based referral practice between July 1988 and September 2001 and who presented with acute facial nerve paralysis mimicking Bell palsy. All patients were subsequently found to harbor an occult skull base neoplasm. A delay in diagnosis was demonstrated in all cases. Seven patients died of their disease, and four patients are currently free of disease. CONCLUSIONS: Although Bell palsy remains the most common cause of peripheral facial nerve paralysis, patients in whom neoplasms invade the facial nerve may present with acute paralysis mimicking Bell palsy that fails to resolve. Delays in diagnosis and treatment in such cases may result in increased rates of mortality and morbidity.

Adenocarcinoma↗
PubMed2002

Facial paralysis caused by malignant skull base neoplasms.

OBJECT: Bell palsy remains the most common cause of facial paralysis. Unfortunately, this term is often erroneously applied to all cases of facial paralysis. METHODS: The authors performed a retrospective review of data obtained in 11 patients who were treated at a university-based referral practice between July 1988 and September 2001 and who presented with acute facial nerve paralysis mimicking Bell palsy. All patients were subsequently found to harbor an occult skull base neoplasm. A delay in diagnosis was demonstrated in all cases. Seven patients died of their disease, and four patients are currently free of disease. CONCLUSIONS: Although Bell palsy remains the most common cause of peripheral facial nerve paralysis, patients in whom neoplasms invade of the facial nerve may present with acute paralysis mimicking Bell palsy that fails to resolve. Delays in diagnosis and treatment in such cases may result in increased rates of mortality and morbidity.

Adenocarcinoma↗
PubMed2000

Temporalis muscle transfer for facial paralysis: a further refinement.

Facial nerve paralysis can occur due to failure of the central driving mechanism (nuclear or supranuclear pathology), failure of the conduit between the brainstem and the peripheral musculature (the facial nerve), or failure of the peripheral end organ (the neuromuscular system). Where the peripheral neuromuscular system fails, the options for dynamic reanimation include a regional muscle transfer driven by another ipsilateral cranial nerve, or a free muscle transfer driven by the contralateral facial nerve. Temporalis muscle transfer is an example of regional muscle transfer and has been used since early in the twentieth century. A further refinement, involving mobilization of the coronoid process of the mandible in continuity with the insertion of the temporalis muscle via a nasolabial fold approach, using fascial strips to re-create movement around the mouth, is presented.

Adult↗
PubMed1995

Free vascularized double muscle transplantation for the treatment of facial paralysis.

Two cases of free neurovascular double muscle transplantation for facial paralysis are reported, with detailed descriptions of the operative technique and follow-up study. The latissimus dorsi muscle segment is placed between the nasolabial fold and the zygoma to substitute for the zygomatic and levator labii muscles, while the serratus anterior muscle segment is placed between the lower lip and the mandibular margin to substitute for the depressor labii muscles. The thoracodorsal nerve is sutured to the stump of the cross-face nerve graft, and the lateral thoracic nerve is sutured to a part of the hypoglossal nerve. The procedure is able to restore a relatively symmetrical smile, especially in patients with a full denture smile. The satisfactory results of this procedure are expected to lead to new prospects in the treatment of facial paralysis.

Adult↗
PubMed1984

[Treatment of peripheral facial paralysis with ultrasound].

In a survey on the onset of peripheral facial paralysis, the roll of hypertension in the stylomastoid canal compressing the facial nerve is underlined. Intracanalicular hypertension is due to edema resulting from capillary vasodilatation, secondary to anoxia due to a regional vasospasm. When return channels of local circulation are blocked, the edema is further stabilized. Consequent nervous blockage however, very often does not go beyond the functional level; prompt recovery in the majority of cases after hypertension is averted, confirms this assertion. Nevertheless, current treatments seem to have little effect on Bell's palsy. In the present experiment, daily ultrasound irradiations of the mastoid process were tried on 30 cases of peripheral facial paralysis. Results give evidence that this therapy has particular efficiency when applied early in the course of the paralysis, before the onset of Wallerian degeneration. Integral cure or nearly complete recovery was attained before the 20 th sitting in 14 cases out of 15 patients where treatment was begun before the 8 th day of paralysis. The efficiency of ultrasound therapy proved to be less marked when applied with delay or applied on subjects with unhealthy systemic condition. Improvement in some of these cases was evident though and dependent on the presence and quantity of nervous fibres having escaped Wallerian degeneration.

Adolescent↗
PubMed1982

[Palliative surgery for facial paralysis].

Palliative surgery in patients with facial paralysis can be a useful temporary measure before nerve recuperation occurs, or a definitive procedure in cases with permanent loss of the effector muscle. Valid results can be obtained in the periorbital region by performing an external blepharorraphy, together with various static or dynamic procedures for louvering of the upper eyelid. The fascia lata is usually employed to obtain suspension, reequilibrium of soft tissues being ensared by lifting and localized cutaneous resections. Marked hyperactivity on the apposing side can be reduced by selective neurectomies.

Eyelids↗