Repair of the facial nerve in traumatic facial palsies; results of decompression, nerve suture, and nerve grafting in one hundred twenty-seven cases.
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Although there have recently been numerous reports of enhanced MRI in patients with facial palsy, the mechanism of enhancement remains largely unknown. In the present study, animal models with experimentally induced facial paralysis were prepared, and the vascular permeabilities of normal and damaged facial nerves were assessed using Evans blue albumin (EBA) as a tracer. The Gd-DTPA contents in normal and compressively damaged facial nerves were also investigated. The following results were obtained: 1. In the normal intratemporal facial nerve, EBA remained in the vessels, and did not leak into the endoneurium. In contrast, vascular permeability was very high in the epineurium and the geniculate ganglion which showed leakage of large amounts of EBA from vessels. 2. At the site of compression in the damaged nerve, EBA leakage was also seen in the endoneurism, indicating accentuated vascular permeability. This accentuation of vascular permeability shifted toward the distal side. However, no EBA leakage was seen on the side proximal to the site of compression. 3. Significantly higher Gd-DTPA contents were obtained in the facial nerve on the paralytic side than in that on the normal side (p < 0.001). As for differences between the distal and proximal sides, the distal side had a significantly higher Gd-DTPA content (p < 0.01). Assessment of vascular permeability with EBA revealed accentuated vascular permeability on the side distal to the site of compression. These results showed the presence of a blood nerve barrier (BNB) in the facial nerve.(ABSTRACT TRUNCATED AT 250 WORDS)
Intraoperative facial nerve monitoring provides a potentially useful adjunct to recent surgical advances in neurotology and neurosurgery. These measures further aid the surgeon in preserving facial nerve function by enhancing visual identification with electrical monitoring of mechanically evoked facial muscle activation. Facial nerve monitoring in neurotologic surgery may achieve the following goals: (1) early recognition of surgical trauma to the facial nerve, with immediate feedback made available to the surgeon through monitoring of mechanical activation; (2) assistance in distinguishing the facial nerve from regional cranial nerves and from adjacent soft tissue and tumor with selective electrical stimulation; (3) facilitation of tumor excision by electrical mapping of portions of tumor that are remote from the facial nerve; (4) confirmation of nerve stimulability at the completion of surgery; and (5) identification of the site and degree of neural dysfunction in patients undergoing nerve exploration for suspected facial nerve neoplasm or undergoing decompression in acute facial palsy. This paper provides an overview of intraoperative facial nerve monitoring principles and methodology and reports a recent clinical investigation that demonstrates the utility of facial nerve monitoring in translabyrinthine acoustic neuroma surgery.
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Facial hyperkinesias are a common side effect of hypoglossal-facial nerve anastomoses. We report a patient whose facial hyperkinesias were suppressed by botulinum toxin injections a treatment recently introduced in the therapy of craniocervical dystonias. EMG studies are used to document the effect of botulinum toxin on the facial hyperkinesias as well as on voluntary muscle activation.
In the medical treatment of facial nerve paralysis a large number of different techniques have been developed to restore the function of the facial nerve. These include (a) the ipsilateral nerve grafting (e.g., partial hypoglossal-facial, spinal accessory-facial, partial glossopharyngeal-facial), (b) crossfacial nerve grafting and (c) temporal muscle flaps or even free muscle transfers. None of these techniques uses the masseteric nerve as a graft for reconstruction of the facial nerve. This preliminary report deals with the anatomical basis, which could lead to a new technique. The masseteric nerve leaves the infratemporal fossa through the mandibular notch, accompanied by the masseteric artery. At this level the nerve consists in nine of 36 cases studied of only one branch (25.0%), in 17 cases of two branches (47.0%), in nine cases of three (25.0%), and in the remaining case of four branches (2.8%). There are three main reasons for considering the masseteric nerve as a possible donor for at least the orbicular branch of the facial nerve: (1) The approach to the mandibular notch is quite simple; (2) since the nerve consists of two or more branches in 75.0% of the cases, severe dysfunction of the masseter muscle should not occur; (3) if there is complete denervation of the masseter muscle, its function may be taken over by the temporalis muscle.
OBJECTIVE: To investigate regeneration of the mimic musculature after delayed facial nerve repair. MATERIALS AND METHOD: In 30 rats the facial nerve on the right side was resected and immediately repaired with an end-to-end anastomosis. The entire levator labii muscle was removed on the right side and histochemically and morphometrically analyzed at 7, 14, 21, 28, 90 and 180 days after immediate nerve repair. In a further 20 rats, reinnervation was performed after 4 weeks in a further operation and the muscle was assessed at 14, 28, 90 and 180 days. Seven muscles of four normal rats were used as controls. RESULTS: Three muscle fiber types could be identified by comparative histochemical analysis of two enzymes of succinate dehydrogenase (SDH) and m-ATPase: oxidative glycolytic (FOG) fibers, fast glycolytic (FG) fibers and intermediate muscle fibers that were designated SDH-INT. The number of fibers and the frequency distribution of single-fiber cross-sectional areas were determined for each type of fiber. No significant difference in the cross-sectional area of all fiber types was noted after 180 days when comparing immediate and delayed end-to-end sutures. In contrast, comparison of the fiber-type composition showed a significant increase in the number of FG fibers in the delayed suture, at the expense of FOG fibers. After immediate reinnervation the muscle approximately attained its natural fiber-type composition, whereas after delayed reinnervation the muscle showed an overall loss of oxidative capacity and differentiation towards phasic activity. CONCLUSION: Changes in fiber-type composition following delayed nerve suture are irreversible and have specific effects on the precise function of the muscle. Immediate nerve repair improves axonal reinnervation.
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The facial nerve of the albino rat was compressed by inserting a thin nylon thread in the facial canal. After a survival period of 1-60 days, the animal was perfused with Ringer's solution followed by a 2% periodate-lysine-paraformaldehyde fixative. Frozen sections from the brain stem containing the facial motor nucleus (FMN) were obtained and stained for OX-42 (against CR3 antigen), OX-18 (against Class I MHC antigen), OX-6 (against Class II MHC antigen) and GFAP (anti-glial fibrillary acidic protein). The first glial reaction in the FMN occurred in the microglia which showed a significant increase in the CR3 immunoreactivity within 24 h after compression. Upregulation of the GFAP was not noticed until 2 days after compression. In each case, the staining reaction was initially light, but increased with time and appeared to peak at 3-4 days for OX-42 and 4-5 days for GFAP. The activated microglia first assumed a perineuronal position but were later displaced by the activated astrocytes. The number of stained microglia was noticeably increased and was most likely the result of proliferation of the resident microglia rather than invasion from the blood stream. The increase in the number of GFAP positive cells was most likely the result of more resident astrocytes being activated, as previous studies have shown the absence of mitotic activity of astrocytes after lesion of the facial nerve. In addition to increased CR3 and GFAP activity there was also an upregulation of Class I MHC antigen in the microglia, as revealed by increased immunostaining against OX-18.(ABSTRACT TRUNCATED AT 250 WORDS)
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The facial nerve is protected in parotid surgery by finding the main trunk first and peripherally dissecting free the branches. The most constant landmark is the groove between the mastoid and the bony ear canal. Wide exposure of this groove should be obtained without "tunnelling." The thick (2-3 mm) white trunk is dissected forward using the electric stimulator before cutting parotid tissue. Nerve injury is more common in the peripheral branches. Nerve location in recurrent parotid tumors is more difficult. The main trunk may be found more posteriorly than in the previous surgery, but often peripheral branches must be identified crossing the masseter, facial vessels, or the parotid duct; retrograde dissection to the trunk follows. For proven invading malignancy, the trunk or branches may be sacrificed, but immediate grafting should be attempted usually with the greater auricular nerve.
The facial nerve branch termed Ramus communicans cum nervo glossopharyngeo in the current Nomina anatomica was investigated in 245 Japanese, especially as regards the frequency and pertinence as an approved definition. The communication was found in only 18.8%. It runs, if present, either medially, laterally or through the digastric posterior muscle. Teasing examination reveals that it always originates from the ninth nerve instead of the seventh and that it is destined to the back of the pinna. Its terminal bundle leaves the seventh nerve somewhat distally than the posterior auricular nerve in many examples, but the communication is likely to represent the auricular branch of the ninth nerve. As an offshoot of the seventh nerve, it is ill-defined, and should be affiliated to the ninth nerve in the Nomina anatomica. If it pierces the digastric muscle, half examples certainly give additional innervation to this muscle, but the fundamental disposition of the communication itself is not affected.
Facial nerve injury is one major morbidity of surgery performed along the course of this nerve. Surgeons frequently employ stimulators to identify and protect the nerve. Both disposable devices as well as larger, reusable stimulators are available. Despite their common use, relatively little documentation exists regarding the safety and reliability of these devices. We tested the electrical output of the four disposable, single-use motor nerve stimulators that are marketed in the United States. We found that each produced consistent stimulus output over time. One stimulator slightly exceeded the manufacturer's listed output while three devices produced significantly less voltage and current than specified by the manufacturer.
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