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Degrees of peripheral facial paralysis were assessed by the paralysis score table in a modification of May's method together with the integrated EMG method. Paralysis scores and integrated EMGs from the frontal, orbicularis oculi and orbicularis oris muscles were obtained from 68 patients with facial paralysis. A linear regression analysis was tried in the cases of complete recovery with the following equation: Y = B log X + A, where Y = percentage of paralysis score or integrated EMG, B = recovery rate, A = constant and X = days after onset. The correlation coefficient of paralysis score and the days expressed in logarithmic form was 0.979. The paralysis scores obtained showed good correlation (0.933-0.941) with the value of the integrated EMG. The paralysis score for facial paralysis was thus confirmed by the objective EMG method. Recovery process from facial paralysis can be analysed numerically by the application of linear regression analysis in both methods.
Bilateral facial paralysis(facial diplesia) is often observed in Guillain-Barré syndrome(GBS) and Fisher's syndrome (FS). We tried to observe injured facial nerves using three-dimensional(3-D) MRI in facial diplesia due to GBS and its variants and examined function of blood nerve barrier and clinical use of 3-D MRI for detecting injured facial nerves. In the four patients with GBS and its variants(GBS three cases, FS one case), while routine brain MRI did not show any abnormal findings, contrast-enhanced 3-D MRI revealed Gd-enhancement of the facial nerves. On the other hand, only one case showed visualization using contrast-enhanced 3-D MRI in twelve cases of Bell's palsy. Therefore, it may be presumed that the reason why the significantly higher rate of visualization in facial paralysis in GBS and its variants than in Bell's palsy is attributable to a difference in the mechanism of injury or the extreme seriousness of the disease. In conclusion, the observation of facial nerve using 3-D MRI was very useful to know the condition of the facial diplesia in GBS and its variants.
Facial paralyses in children may be grouped under headings displaying a certain amount of individuality. Chronologically, first to be described are neonatal facial paralyses. These are common and are nearly always cured within a few days. Some of these cases are due to the mastoid being crushed at birth with or without the use of forceps. The intra-osseous pathway of the facial nerve is then affected throughout its length. However, a cure is often spontaneous. When this desirable development does not take place within three months, the nerve should be freed by decompressive surgery. The special anatomy of the facial nerve in the new-born baby makes this a delicate operation. Later, in all stages of acute otitis, acute mastoiditis or chronic otitis, facial paralysis can be seen. Treatment depends on the stage reached by the otitis: paracentesis, mastoidectomy, various scraping procedures, and, of course, antibiotherapy. The other causes of facial paralysis in children are very much less common: a frigore or viral, traumatic, occur ring in the course of acute poliomyelitis, shingles or tumours of the middle ear. To these must be added exceptional causes such as vitamin D intoxication, idiopathic hypercalcaemia and certain haemopathies.
A right facial paralysis led to the discovery of a tumor on the left side of the medulla oblongata. A neurinoma was suspected on MRI and confirmed by surgery and pathological examination. Ultrasonic aspiration was on interest in this case. The mechanism of the facial paralysis is uncertain: ischemia, compression and pure coincidence may be considered.
Facial paralysis in children is a complex condition. It may involve functional issues and always involves esthetic issues. Significant psychosocial problems may arise and family support systems are often necessary. In this brief article the etiology of facial paralysis in children is discussed and the common types described. The philosophical approach to the child and his or her family is emphasized. The timing of surgical intervention is addressed as well as a brief outline of the surgical techniques of cross-face nerve grafting and muscle transplantation. Although these latter procedures have added enormously to our capabilities to deal with this condition, further progress will be necessary through research and clinical ingenuity if we are to restore these children to normality.
Facial paralysis following facial injuries during childhood is rare. The literature is reviewed and the mechanisms of facial nerve injuries are discussed. The case of a five-year-old boy with facial paralysis 48 hours after a condylar fracture is presented. The surgical and conservative treatment of traumatic facial paralysis is discussed.
Facial paralysis, although a rare complication of AIDS related complex (ARC) or AIDS, may well be the presenting symptom of HIV positivity. A case report of facial paralysis followed closely by discovery of HIV positivity is described, along with a pertinent and extensive literature review. Seroconversion to HIV-positive status should be suspected in any high-risk patient presenting with idiopathic facial paralysis. HIV testing should be included in the evaluation of Bell's palsy and other idiopathic forms of facial paralysis in the at-risk patient.
Ever since idiopathic facial paralysis (IFP) was first described, several treatments have been tried in an effort to influence early and full recovery. Unfortunately, none of these treatments was effective. After Rothendler's case description in 1951, a multitude of papers have appeared that evaluate the effectiveness of steroids in idiopathic facial paralysis. My presentation reflects a close evaluation of 94 of these papers. Only a few properly controlled, randomized, prospective studies were available. Their main conclusion was that steroid treatment was not more beneficial than conventional treatment. To the contrary, several other less valid prospective and retrospective studies suggest that steroid treatment is beneficial. The definitive, statistically valid study concerning the benefits of steroids in treatment of idiopathic facial paralysis has yet to be performed. Until then, treatment of idiopathic facial paralysis continues to be controversial.
Reanimation of longstanding facial paralysis is a difficult clinical problem commonly tackled with the method of pedicled muscle flap transfer. The temporalis muscle has been the most popular. In the past, one common problem was that the flap was not long enough to reach parts of the face distant from the affected area. To overcome this disadvantage, we have devised a flap consisting of the pedicled temporalis muscle, temporal fascia and galea together and have achieved good static results in paralyzed faces. From June, 1996 to May, 2003, we used this procedure with 38 longstanding facial paralysis patients (16 male and 22 female); 23 had right-sided and 15 had left-sided facial paralysis. The patients were followed-up over three years. Our results were recorded as "Excellent", "Good", "Fair" or "Poor". Excellent or good results were obtained in 33 patients (87%). In these patients, the static results are very good. The oral commissure on the affected side maintained a favorable position and almost complete symmetry of expression was attained. We have achieved dynamic reconstruction by using a temporalis muscle-galea pedicled flap in 38 longstanding facial paralysis patients. Our results show that this is a good option in treating such patients.
Irreversible facial palsy (IFP) presents a multitude of problems arising from a paretic periorbital and facial complex, the solutions to which cross the spectrum of multiple specialties. The process of facial rehabilitation can be simplified by subdividing the face into functional units. These units consist of the brow complex, the periorbital complex, the midface complex, and the lower face/oral complex. Although all of these units are interrelated and influence each other, careful study of the deformity and symptoms of each unit yields a coherent approach and customized surgical plan. The following provides a complete evaluation method for the surgeon to review and customize an approach to the individual patient's needs and desires. Facial rehabilitation must be tailored to each individual, addressing both functional as well as aesthetic concerns for each facial unit.
Hereditary congenital facial paralysis is rare. This paper presents a pedigree of four generations of a family of about 100 members, nine of whom suffer from congenital facial paresis, three with impaired hearing, and three with both facial paresis and impaired hearing. Heredity is dominant with reduced penetrance.
Patients with facial paralysis have a degree of lagophthalmos and paralytic ectropion. We present our experience in the surgical management of 25 consecutive patients treated for these problems. Paralytic lagophthalmos was corrected using gold weights inserted into the upper eyelid. The advantages and disadvantages of this surgical technique are reviewed. Medial canthoplasty and lateral canthoplasty were performed to rectify paralytic ectropion. Ancillary procedures included browpexy, upper-lid blepharoplasty, and temporalis sling. The results were excellent in 23 of 25 patients and good in the remaining two. After a minimum of 6 months' follow-up, there were no complications. The authors believe that the above procedures will yield consistently excellent cosmetic and functional results in patients with paralysis of the eyelids.
We tested sensory and secretomotor function of the greater petrosal nerve (GPN) by means of electrogustometry (EGM) of the soft palate and Schirmer's tear test in 115 patients (59 males, 56 females) with acute peripheral facial paralysis. Facial paralysis was caused by Bell's palsy in 78 cases, Ramsay Hunt syndrome in 27 cases and zoster sine herpetic lesions in 10. All patients had dysfunction of the stapedial nerve. An electrogustometer was used to test taste (GPN sensory function), and elevation of the threshold by > 6 dB on the affected side was considered abnormal. Schirmer's test was used to evaluate lacrimal (GPN secretomotor) function, which was considered abnormal when tear secretion on the affected side was < 50% of secretion on the non-affected side. Of the 78 patients with Bell's palsy, 28.2% had altered taste on the soft palate (sensory dysfunction) and 10.3% had lacrimal dysfunction, indicating that EGM of the soft palate is more sensitive than Schirmer's test for identifying dysfunction of the GPN in patients with facial paralysis due to Bell's palsy. Of the total of 115 patients, 32 (28%) had taste dysfunction and 9 (28.1%) of these 32 patients also had lacrimal dysfunction. This finding indicates that facial paralysis has different effects on the sensory and secretory nerve fibers of the GPN. The results of Schirmer's test were more closely related to the severity of, and prognosis for, facial paralysis than the results of EGM.
The maximal static response assay of facial motion, described in 1994, enables the simultaneous measurement of multiple facial motions by tracking the positions of specific facial points. While the maximal static response assay provides accurate measurement of facial motion, the analysis of these data lacks the simplicity of a single-number scale such as the House-Brackmann system, a subjective scale traditionally used to classify facial function. The purpose of this study was to develop a simplified numerical index capable of summarizing the data generated by the maximal static response assay in a clinically meaningful way. We also wanted to develop a method whereby only anatomic motion or nonanatomic motion in the paralyzed face could be quantitated. Anatomic motion is the motion of the specific facial points studied by the maximal static response assay that can be attributed solely to the pull of the regional facial muscles that govern the movement of those points. Nonanatomic motion is motion that is secondary to the pull of the unaffected contralateral muscles that is transmitted to the paralyzed hemiface. Thirty-four patients with complete facial paralysis were studied. The maximal static response assay was performed on all patients on presentation to the Facial Nerve Center at the University of Pittsburgh Medical Center or after development of complete facial palsy postoperatively. The data from these patients were compared with maximal static response assay data from 26 unaffected controls. The anatomic index of facial motion and the nonanatomic index of facial motion were calculated for all study participants. The anatomic index of facial motion measures anatomic facial motion, and the nonanatomic index of facial motion measures nonanatomic facial motion. To calculate the anatomic index of facial motion, the vector magnitudes of the supraorbital, infraorbital, and modiolar motions during brow lift, eye closure, and smile are summed. The anatomic index of facial motion represents a ratio of this sum on the affected side to the corresponding sum on the unaffected side using only anatomic motions. The nonanatomic index of facial motion is a similar ratio using nonanatomic motion only (i.e., motions in directions that cannot be produced by the ipsilateral muscles). The anatomic index of facial motion represents a single number that can be used to assess facial motion. The value of the anatomic index of facial motion for patients with complete facial paralysis is 0.07 +/- 0.08. The anatomic index of facial motion for normal individuals is 1.05 +/- 0.13 (p < 0.0001, Mann-Whitney rank-sum test). The nonanatomic index of facial motion in normal individuals is 0.05 +/- 0.08; in patients with complete facial paralysis, it is 0.34 +/- 0.32 (p < 0.0001, Mann-Whitney rank-sum test). During recovery from complete facial paralysis, the anatomic index of facial motion and the nonanatomic index of facial motion each revert steadily toward normal values. The anatomic index of facial motion and the nonanatomic index of facial motion are single numbers based on the maximal static response assay, which quantitatively describes anatomic motion and nonanatomic motion in patients with complete facial paralysis. Although patients with complete facial paralysis have motion on the paralyzed hemiface, the motion is primarily nonanatomic. Both indices can be used to track recovery from complete facial paralysis.
Iatrogenic facial paralysis occurs in less than 4% of major otologic procedures. The prevention of iatrogenic injuries involves study, training and experience. These concepts are carefully woven into residency training, fellowship and, ultimately, into peer review. The reasons for injury may be errors of omission, such as inadequate preparation for the procedure, or errors of commission, such as inadequate surgical exposure. Currently, there appear to be enough surgical cases for training programs and the core training of otolaryngology residents prepares them to handle most facial nerve problems. Included in this article is a more detailed description of the anatomy in and around the facial nerve, particularly in the mastoid, with suggestions on how to avoid problems and reduce injuries.
Facial paralysis (FP) in children is most often idiopathic, however, many diverse and identifiable etiologies exist. Twenty-five cases of children admitted consecutively to the Children's National Medical Center over 8.5 years for the evaluation of FP were reviewed retrospectively. In 21 (84%) of the patients the FP was discovered to be secondary to a specific etiology or associated with a recognizable syndrome. In 7 cases, the FP was an initial manifestation of a serious underlying disorder. Causes of the FP in this series include: otitis media, mastoiditis, temporal lobe abscess, osteopetrosis, both blunt and penetrating trauma, iatrogenic surgical injury, facial burns, cerebellar astrocytoma, leukemia rhabdomyosarcoma, intracerebral arteriovenous malformation, Goldenhar syndrome, and Melkersson-Rosenthal syndrome. Four (16%) patients were diagnosed as having Bell's palsy. Methods of management, including the use of electrodiagnostic testing are described.
Simultaneous bilateral facial paralysis (SBFP) is very rare, but it can present itself as the first complaint in a wide spectrum of diseases and a comprehensive evaluation must be completed. Bilateral Bell's Palsy can be diagnosed only when all other possible causes have been excluded. The prognosis and treatment for SBFP is dependent upon the underlying etiology. We present four cases of SBFP seen in our department which were finally diagnosed as leukemic infiltration, sarcoidosis, Bell's Palsy and demyelinating polyneuropathy (probably Guillain-Barré syndrome). The most important etiologies of the SBFP and the management of this entity are discussed.