SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
During the early manifestation of peripheral facial paralysis, VZV specific IgA antibodies were detected in the serum in a single case. In similar cases, this serological parameter should be tested for causal diagnosis in connection with early Aciclovir therapy.
Neither clinical examination nor electrical or radiological investigations were able to predict, pre-operatively, the malformatory or traumatic etiology in 9 cases of neonatal facial paralysis. Surgical exploration demonstrated that the paralysis was due to trauma in 3 cases and to malformations in the other 6. Exploration of the intrapetrous portion of the facial nerve in these 9 cases was not satisfactory, as in 6 patients nerve agencies was detected. Simultaneous investigation of the parotid region in 5 of these 6 infants demonstrated absence of the intraparotid part of the facial nerve. When confronted with a spontaneously non-regressive facial paralysis in a neonate, and when doubt persists after radiological and electrical examinations, the intraparotid portion of the facial nerve should be explored in the stylomastoid region. Its absence suggests agenesis of the nerve, and makes intramastoid exploration of no value.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The purpose of this study was to standardize and evaluate the results of evoked electromyography (EEMG) in normal patients and in patients with acute idiopathic facial paralysis. A comparison of the amplitude of response to EEMG from one side of the face to the other in 288 normal patients yielded a great variability in results. The amplitude difference was not greater than 50%, and therefore a difference of less than 50% was considered normal. Test-retest variability of the percentage difference in amplitude in 10 subjects showed a 10% variation in seven patients and up to a 20% variation in the remaining three patients. Fifty patients with acute idiopathic facial paralysis were seen within 14 days of onset. A favorable prognosis was based on an EEMG amplitude of more than 25% of the normal side. With this criterion EEMG was accurate in predicting complete recovery in 36 (92%) of 39 patients. When EEMG was 25% of normal or less, incomplete recovery occurred in 9 (82%) of 11 patients. The response was 0% to 10% in six patients; four had a poor recovery and the remaining two had a fair recovery. The technique, interpretation of results, avoidance of pitfalls, and shortcomings of this test are discussed.
The treatment of 100 cases of acute stage peripheral facial paralysis with electro-acupuncture has indicated that, with the stimulation intensity and time interval strictly controlled, electro-acupuncture is effective. Suitable wave forms and electric intensity, as well as proper needling techniques and controlled duration of the stimulation according to experimental experience have yielded high therapeutic effects without aggravation of symptoms.
A shift from subjective scales to objective measures of facial paralysis requires physical models against which to validate and calibrate the new objective techniques. The purpose of this report was to demonstrate such a model and to test the capacity of an objective computer system to accurately measure physical change. The physical model consisted of an advancing edge of a spreading gelatin film. The model was measured in submillimeter increments. Concurrent measurements were made using the computed system. Ten trials were conducted. The objective system proved to be exquisitely sensitive (0.03 mm) and highly correlated with the physical criterion model (Pearson's product moment correlation coefficient [r]=0.9849). Sensitive and calibrated objective methods of analysis of facial motion are crucial to the design of clinical trials, clinical studies of nerve regeneration, and comparisons of reanimation techniques.
The face proclaims to the world an individual's identity and as such is the most conspicuous part of his anatomy. No wonder, then, that idiopathic facial paralysis is a frightening experience for the patient. Ever since it was first noted, all manners of measures have been used to bring about early and full recovery. Unfortunately, none of these treatments is effective. Following Rothendler's case description in 1951, a multitude of papers have appeared, evaluating the effectiveness of steroids in idiopathic facial paralysis. This article evaluates 92 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. But several less valid prospective and retrospective studies have suggested that steroid treatment is beneficial. The definitive, statistically valid study of the benefits of steroids in treating has yet to be performed. Until then steroid treatment of this condition will continue to be controversial.
A group of 95 patients with facial paralysis in the neonatal period are presented. In 74 patients it was believed to be secondary to trauma associated with pregnancy and delivery, and in 21 to be secondary to congenital lesions. The cause, extent, and clinical course of the paralyses are discussed. A classification is outlined to help in organizing a logical and systematic evaluation plan for these patients. Patients may be divided into four groups based on the time they are seen after birth, whether the nerve is stimulable, or whether the nerve loses its stimulability. On the basis of this classification, electromyogram studies, and roentgenographic findings, a presumptive diagnosis may be made and a treatment plan formulated. The treatment plan is based on the diagnosis, facial nerve excitability testing, and degree of deformity present. If there is evidence of facial nerve disruption, a facial nerve exploration is indicated. In congenital cases, reanimation procedures may be necessary.
The authors introduce the use of a disposable stapler to create a stable muscle end in transferring a free neurovascular muscle segment for the treatment of facial paralysis. This procedure allows the firm fixation of the fragile soft end of a muscle transferred to the nasolabial region of a paralyzed face, and avoids adhesion and tethering of the muscle end to the skin, which may result in inaccurate positioning of a newly-created nasolabial fold and an asymmetrical smile. Transection and hemostasis at both ends of the harvested muscle segment also can be achieved simultaneously. Although the disposable stapler incurs additional cost, it can greatly improve the result of a free neurovascular muscle transfer for the treatment of facial paralysis, as well as simplify harvesting of the muscle segment. No complications and problems have been encountered in stapling the muscle.
A case of peripheral facial palsy revealing a recent HIV infection is reported. Facial paralysis is frequent in HIV patients. Its etiology depends on the stage of the disease. At all stages, Bell's palsy is the most important cause and can reveal the seropositivity. Among the other HIV otoneurological manifestations, hearing loss is frequent and of multiple origins. It is associated with early abnormal auditory brainstem responses. Vestibular dysfunction in HIV infection mostly concerns advanced stages of the disease even though early pathologic electrophysiologic findings are noted.
Peripheral nerve lesions are one of the most frequent causes of chronic incapacity. Upper or lower limb palsies due to brachial or lumbar plexus injuries, facial paralysis and nerve lesions caused by systemic diseases are one of the major goals of plastic and reconstructive surgery. However, the poor results obtained in repaired peripheral nerves during the Second World War lead to a pessimist vision of peripheral nerve repair. Nevertheless, a well understanding of microsurgical principles in reconstruction and molecular biology of nerve regeneration have improved the clinical results. Thus, although the results obtained are quite far from perfect, these procedures give to patients a hope in the recuperation of their lesions and then on function. Technical aspects in nerve repair are well established; the next step is to manipulate the biology. In this article we will comment the biological processes which appear in peripheral nerve regeneration, we will establish the main concepts on peripheral nerve repair applied in facial paralysis cases and, finally, we will proportionate some ideas about how clinical practice could be affected by manipulation of the peripheral nerve biology.
A case is described of a primary neuroblastoma of the facial nerve in a 13-year-old boy presenting with a recurrent facial paralysis. This tumour was excised preserving the nerve and followed with post-operative radiotherapy. The pathology of the tumour is described and facial nerve tumours briefly discussed as a cause of facial palsy. There have been no other cases of a primary neuroblastoma of the facial nerve arising at this site reported in the last 20 years.
Reanimation of a spontaneous and synchronous smile, and sufficient depressor mechanism of the lower lip presents a surgical challenge in facial paralysis. Hypoglossal-facial nerve crossover and cross-facial nerve grafting are the best options if the mimetic muscles around the mouth are still viable in patients in whom the facial nerve was sacrificed at the brainstem. Although good muscle tone and facial motion have been obtained by hypoglossal-facial nerve crossover, smile is dependent on conscious tongue movement. Cross-facial nerve grafting provides a voluntary and emotion-driven smile, but requires two coaptation sites, which leads to substantial axonal loss and a long regeneration time. This method was not successful in activating the depressor mechanism. The first stage is the classic "baby-sitting" procedure, in which the bulk of the mimetic muscles was maintained by the rapid reinnervation of the hypoglossal-facial nerve crossover during the regeneration period of the cross-facial nerve graft, and temporalis muscle transfer to the eyelids is performed. During the second stage, the cross-facial nerve graft that used the thickest zygomaticobuccal branch on the healthy side was coapted with the corresponding branches on the paralyzed side. The hypoglossal-facial nerve crossover continued to innervate the depressor muscles. Good spontaneous smile and sufficient depressor mechanism were achieved by cross-facial nerve grafting and hypoglossal-facial nerve crossover respectively, and these techniques are demonstrated by the authors clinically and electrophysiologically.
Extratemporal involvement of the seventh cranial nerve is often secondary to a tumor of the parotid gland. We describe six patients who had facial paralysis associated with an occult malignant neoplasm of the parotid gland. Initial evaluations in these patients, including computed tomography and magnetic resonance imaging, provided no evidence of a parotid tumor. Four of the six patients had a progressive triad of ear pain, facial paralysis, and sensory loss in the second and third divisions of the trigeminal nerve. This pattern indicates a high probability of a malignant lesion of the parotid gland, even in the presence of normal findings on noninvasive studies.
We describe a case of facial paralysis in a 19-month-old male recently diagnosed with acute otitis media. Results of his physical examination was remarkable for left-sided peripheral facial nerve palsy with an associated middle ear infection. Physicians should understand the etiology, pathophysiology, treatment options, and prognosis of facial palsy in association with otitis media.
Bilateral traumatic facial paralysis is a very rare clinical condition. Abducens palsy, associated with bilateral traumatic paralysis, is even rarer and has not been well described in the literature. In this report, a 24-year-old male, who developed immediate bilateral facial and right abducens paralyses following a motor vehicle accident, is presented. The patient was referred for neurotologic evaluation 22 days after the injury. Electroneurography (ENoG) demonstrated 100 per cent degeneration at the first examination and, correspondingly, electromyography showed no regeneration potentials. Using high-resolution computed tomography (HRCT), a longitudinal fracture on the right and a mixed-type fracture on the left were identified. The patient had good cochlear reserve on both sides. The decision for surgery was based not on ENoG, because of the delayed referral of the patient, but on the HRCT, which showed clear fracture lines on both sides. The middle cranial fossa approach for decompression of the right facial nerve was performed on the 55th day following the trauma, and a combined procedure using the middle cranial fossa and transmastoid approaches was applied for decompression of the left facial nerve on the 75th day following the trauma. On the right, there was dense fibrosis surrounding the geniculate ganglion and the proximal tympanic segment whereas, on the left, bone fragments impinging on the geniculate ganglion, dense fibrosis surrounding the geniculate ganglion, and a less extensive fibrotic tissue surrounding the pyramidal segment were encountered. There were no complications or hearing deterioration. At the one-year follow up, the patient had House-Brackmann (HB) grade 1 recovery on the right, and HB grade 2 recovery on the left side, and the abducens palsy regressed spontaneously. The middle cranial fossa approach and its combinations can be performed safely in bilateral temporal bone fractures as labyrinthine sparing procedures if done on separate occasions.