Prevention of denervated muscle atrophy with accelerated nerve‐regeneration by babysitter procedure in rat facial nerve paralysis model
Kazuki HashimotoHajime MatsumineHironobu OsakiYoshifumi UetaWataru KameiMari ShimizuKaori FujiiYosuke NiimiMariko MiyataHiroyuki Sakurai
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Abstract Purpose The “babysitter” procedure is a reconstruction technique for facial nerve complete paralysis and uses the movement source from the healthy facial nerve with a cross‐nerve graft. First, an end‐to‐side neurorrhaphy is performed between the affected facial nerve trunk and hypoglossal nerve for continuously delivering stimuli to the mimetic muscles for preventing the atrophy of mimetic muscles. Despite favorable clinical results, histological and physiological mechanisms remain unknown. This study attempted to establish a model for the “babysitter” procedure and find its efficacy in rats with facial nerve complete paralysis. Materials and Methods A total of 16 Lewis rats were used and divided into 2 groups; cross nerve graft ( n = 8) and babysitter groups ( n = 8). The facial nerve trunk was transected in both groups. Babysitter group underwent a two‐stage procedure. Cross nerve graft group underwent only the transfer of nerve graft from the healthy side to affected side. The animals were assessed physiologically by compound muscle action potential (CMAP), and the regenerated nerve tissues were evaluated histopathologically at 13 weeks after surgery. Results Facial nucleus stained with retrograde tracers proved the re‐innervation of affected facial muscle by the babysitter procedure. In CMAP, the amplitude of babysitter group was significantly higher than that of the cross‐facial nerve graft group ( p < .05). Histological examination found a significant difference in myelin g‐ratio between two groups ( p < .05). Conclusion This study investigated the “babysitter” procedure for rat facial nerve palsy. Babysitter procedure shortened the denervation period without mimic muscle atrophy.Keywords:
Muscle Atrophy
Facial paralysis
Sir:FigureFacial paralysis reanimation is influenced by several factors, of which denervation time and muscle atrophy are of high relevance. Thus, for paralysis of short duration (<6 months), cross-facial nerve grafting is recommended because it achieves a harmonious and synchronous smile with the nonparalyzed side, although contraction may be weak. For cases between 6 months and 2 years, in which cross-facial nerve grafting alone is not advisable because of the high risk of developing irreversible muscle atrophy while the axons reach the paralyzed side, Terzis introduced the “baby-sitter” procedure, with very good results.1 Finally, longstanding cases (i.e., >2 years) are best treated with muscle transfers. In our experience with treating facial paralysis, we have come to observe that gender also plays an important role in reanimation. We have seen that women defend better from injury and thus are more resistant than men to denervation and muscle atrophy. Several studies performed in animals have demonstrated that female subjects resist neural injury better and regenerate faster than male subjects.2,3 Sex hormones (i.e., progesterone) might be key in this phenomenon. These observations have led us to modify our standard protocol in facial paralysis reanimation and perform techniques indicated for palsy of short duration (i.e., cross-facial nerve grafting) in women with longstanding disease (facial paralysis for >3 years), achieving good functional and aesthetic results and a high grade of patient satisfaction. The case illustrated is a 28-year-old woman with a history of left facial paralysis secondary to resection of an acoustic neurinoma with whom we consulted for smile reanimation 4½ years later. Physical examination revealed complete facial paralysis with asymmetry at rest and on activity, lack of definition of the nasolabial fold, and no commissural excursion of the left side. A baby-sitter procedure with fibers from the right hemihypoglossal nerve with a nerve graft coapted to an ipsilateral zygomatic branch was performed together with cross-facial nerve grafting. On follow-up, the patient presented adequate excursion of the right commissure with acceptable symmetry in repose and smiling. The patient was very satisfied with the results obtained and refused to undergo connection of the cross-facial nerve graft (Fig. 1).Fig. 1: The patient shown had complete left facial paralysis secondary to resection of an acoustic neurinoma. Four and a half years later, a baby-sitter procedure was performed together with cross-facial nerve grafting. The patient was very satisfied with the results obtained from the first operation and refused to undergo connection of the cross-facial nerve graft. Preoperative views show the patient at rest (above, left) and while smiling (above, right). Two-year postoperative views show the patient in repose (below, left) and while smiling (below, right).Apart from resisting neural insult better, we have also observed that after reanimation with nerves other than the facial nerve (i.e., muscle transfer neurotized to the masseteric nerve), women develop brain plasticity to a greater extent than men. In our experience, most of (and only) our female patients reanimated with nerves other than the facial (masseteric nerve) learn to dissociate the movement of smile from the one that the donor nerve was originally serving. Elbert et al. have stated that brain plasticity develops in response to practice of behaviorally relevant actions.4 Furthermore, several studies have shown that women smile more than men in a wide variety of social circumstances.5 Thus, it is likely that the higher motivational drive of women toward smiling makes them more prone to develop cortical plasticity after reanimation. Finally, based on our clinical observations and the experimental data available, we believe that gender is an important factor to consider in the treatment algorithm of facial paralysis. Diego Marre, M.D. Bernardo Hontanilla, M.D., Ph.D. Department of Plastic and Reconstructive Surgery, Clinica Universidad de Navarra, Navarra, Spain DISCLOSURE There was no source of funds supporting this work. The authors have no financial interest in the methodology described. PATIENT CONSENT The patient provided written consent for the use of her images.
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Herpes zoster may, in some instances, cause motor paralysis as well as the usual sensory and cutaneous manifestations. It is suggested that the presence of electromyographic denervation potentials be used as the criterion of muscle paresis in order to avoid mistaking atrophy of disuse for true lower motor neuron disease. Use of the proper physical therapy procedures hastens the recovery of function and may serve to retard denervation atrophy and fibrosis in patients with muscle paralysis.
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Abstract Numerous causes of peripheral facial nerve paralyses have been described; however, none has satisfactorily explained the genesis of the most common type of paralysis, Bell's palsy. Two patients undergoing an experimental embolization of vascular intracranial tumors suffered a total peripheral facial nerve paralysis when occlusion of the middle meningeal artery had been accomplished. It is speculated that this paralysis resulted from ischemia of the horizontal portion of the facial nerve, an observation that has not previously been described and that might be applicable as well to the etiology of Bell's palsy.
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The facial nerve coursing through the temporal bone provides a challenge to the otologic surgeon. Advances in surgical instrumentation and refinements of surgical strategies enable the otologist to uncover the entire course of the facial nerve safely from brainstem to its exit from temporal bone. The most common cause of facial nerve paralysis is Bell's palsy, followed by traumatic facial paralysis, herpes zoster oticus, and intratemporal tumous lesion. The surgical approaches to the injured facial nerve depend on its causes. Acute, severe facial nerve paralysis caused by viral infection or trauma can be managed by early use of transmastoid approach, middle cranial approach, or combined approach. In case of intratemporal benign tumor with favorable facial function, great care must be taken not to damage the facial nerve with nerve preservation technique. However, in malignant tumor with favorable facial function, the priority must be placed on the complete resection than to the facial nerve preservation. In consideration of selecting surgical technique of facial nerve paralysis reconstruction, clinician must find out the cause, degree and duration of paralysis for the appropriate technique.
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Clinical studies were performed on 325 patients with Ramsay Hunt syndrome who were treated in the Facial Nerve Clinic at Ehime University Hospital between 1976 and 1995. The clinical manifestations of Ramsay Hunt syndrome were various. Three major symptoms, auricular vesicles, facial paralysis and vestibulo-cochlear dysfunction, were found in 57.6% of the patients although these symptoms did not always appear simultaneously. Auricular vesicles appeared before (19.3%), during (46.5%), or after (34.2%) the onset of facial paralysis. Hearing loss was observed subjectively in only 20% but objectively in 48.2% of the patients. Hearing loss appeared before (34.3%), during (34.3%), or after (31.3%) the onset of facial paralysis. Complete recovery from facial paralysis was achieved in 52.4% of the patients. Good recovery of the facial nerve function was achieved in patients who had zoster vesicles or vestibulo-cochlear dysfunction preceding the development of facial paralysis. Complete recovery of hearing was also achieved in 45.4% of the patients, and the recovery was better in patients having light hearing loss, less than 35dB. The patients younger than 16 years old showed better recovery from both facial paralysis and hearing loss than the patients older than 60 years. Glossopharyngeal nerve or vagal nerve paralysis concomitant with facial paralysis was found in 8 (2.5%) patients. The outcome of glossopharyngeal nerve paralysis was good but that of the vagal nerve was poor.
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Abstract A group of 32 patients with severe facial paralysis from 2 to 30 years and of different etiologies were studied. Various degrees of nerve and muscle atrophy were noted in this group. A new concept relative to the status of the paralyzed face, its nerve and muscle system and their capacity for rehabilitation was acquired. The treatment of long‐standing paralysis has been relegated to fascial stripping, muscle slings, tarsorrhaphies and face‐lift operations. This investigation indicates that the situation is not totally irreversible. The determinant factors are the number of surviving axones and the viability of the facial muscles supplied by them. Regardless of the electrical testing, the facial nerve never totally disappears nor do the facial muscles. On surgical exploration, the facial nerve and the posterior belly of the digastric muscle were always recognizable in varying degrees of atrophy and fibrosis. A range of 20‐90 percent of normal size was noted. Electron microscopy of the nerve and muscles demonstrated axone degeneration still taking place and muscle fibers present in cases 20‐30 years post injury to the nerve. The degree of atrophy and fibrosis was dependent upon the length of the paralysis. It was also noted that the degree of severity was less as the site of injury became more peripheral. This was probably related to the rich extratemporal nerve interconnections from the sympathetics, cervical plexus, and cranial nerves V and IX. These findings verified the existence of a subliminal system which is non‐functional, but in certain instances had the potential for rehabilitation. Some of the most interesting aspects of facial rehabilitation in longstanding facial paralysis are beginning to unfold themselves in the recognized potential of a regrowth of axones in a depleted but not annihilated facial nerve system by nerve crossover and nerve grafting techniques. When the peripheral facial nerve system is absent, nerve implantation into the residual mimetic muscles or transposed masticatory muscles is indicated. The introduction of masticatory muscles into the face to accommodate this neural regrowth, when mimetic muscle potential remains subclinical, adds a new neuromuscular facility in the rehabilitation.
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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.
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The authors evaluated magnetic resonance (MR) images obtained with intravenously administered gadolinium in ten patients who had facial paralysis and no facial nerve tumor. In patients with either Bell palsy (four patients) or facial paralysis after temporal bone surgery (six patients), intratemporal facial nerve enhancement was seen. Facial nerve enhancement on MR images proved to be a nonspecific finding.
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