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PubMed2006

[Microsurgical anatomy of the facial nerve trunk in facial-hypoglossal nerve anastomosis].

OBJECTIVE: To study the microsurgical anatomy of the facial nerve (FN) trunk and provide some important morphometric data about facial-hypoglossal nerve anastomosis (FHA). METHODS: Bilateral microsurgical dissection was performed on the heads of 9 cadavers fixed with formalin with three different methods. In the first method, the posterior belly of the digastric muscle was used as a mark, and the FN trunk was identified on the medial side of this muscle. In the second method, dissection was initiated at the parotid gland, the FN trunk was identified at its entrance into the parotid gland. In the third method, the styloid process was identified and traced back to the stylomastoid foramen (SMF). The FN trunk was identified on its emergence from the SMF. In every dissection, the whole FN trunk was exposed; its diameter and depth at the the SMF and its length were measured; its relationship, with other structures was studied. RESULTS: The FN invariably emerged from the cranial base through the SMF. Its diameter upon its emergence from the foramen was 2.57 +/- 0.60 mm. The mean minimal distance of the FN trunk from the skin surface in this area was 22.62 +/- 2.88 mm. The length of the FN trunk was 15.71 +/- 1.97 mm. The distance between the bifurcation and the mastoidale was 18.20 +/- 4.41 mm. The distance between the bifurcation and the mandibular angle was 39.91 +/- 8.38 mm. The distance between the mastoidale and the SMF was 17.91 +/- 2.68 mm. The branches from the FN trunk proximal to its bifurcation were the posterior auricular nerve, the digastric muscle nerve and the stylohyoid muscle nerve. CONCLUSION: The third method to expose the FN trunk on its emergence from the SMF is safe and reliable. It is feasible to use only part of the hypoglossal nerve fibers for anastomosis with the FN trunk.

Adult↗
PubMed1994

Neonatal facial nerve defect.

Facial paralysis in the newborn may be caused by trauma associated with delivery or by lesions secondary to congenital developmental anomalies. We previously reported the absence of the facial nerve in the horizontal segment of the temporal bone on both sides in a patient with Mobius' syndrome, usually classified as a nuclear developmental defect. In this study we report the findings from 7 additional temporal bones with similar abnormalities. A study of 42 temporal bones from infants with various congenital anomalies revealed nine temporal bones in which the facial nerve disappeared mid-way through the course of the temporal bone. Some of the nerve fibers suggested regeneration after necrotic lesions induced during the perinatal period.

Axons↗
PubMed1996

Intracanalicular and intratemporal facial nerve schwannomas.

Facial nerve schwannomas can mimic acoustic neuromas. We report herein two cases: a purely intracanalicular and an intratemporal facial nerve tumor extending into the internal auditory canal and the cerebellopontine angle. These tumors have to be suspected in patient with small-size tumors presenting with facial paralysis. We advocate translabyrinthine or middle fossa approach to facilitate nerve anastomosis. The establishment of the correct properative diagnosis is difficult, but the patient must be warned about the impossibility of preserving the facial nerve in these tumors.

Case Reports↗
PubMed2006

Graphic-visual adaptation of House-Brackmann facial nerve grading for peripheral facial palsy.

OBJECTIVE: To determine if the diagram with schematic drawings of the face based on House-Brackmann facial nerve grading scale can be of easier use than the original grading scale for facial palsy patients. STUDY DESIGN: Prospective case study of 32 patients with facial palsy. SETTING: Tertiary referral center-university hospital. PATIENTS: Patients with different degrees of acute peripheral facial palsy from any cause. MAIN OUTCOME MEASURES: The patients were photographed and then classified by degree of facial palsy through analysis of the pictures. At first, three of the authors individually utilised the original classification described by House-Brackmann facial nerve grading and then, after 7 days, they employed the illustration table proposed. After 30 days, the same methods were again used by the same authors for both House-Brackmann facial nerve grading and the illustration table. RESULTS: The analysis of the obtained data reveals that the classification described by House and Brackmann (Otolaryngol. Head Neck Surg. 1985;93:146) presents several items to be evaluated, making it difficult to use and demanding greater time for correct application. On the contrary, the proposed illustration table allows faster evaluation and easier memorisation, not being subject to possible interpretation or translation mistakes, as illustrations are a universal language. Neither method presented absolute reproducibility, however, we found slightly larger concordance indexes among the authors for the proposed illustration table. We noticed average values of reproducibility were approximately 65% in the House-Brackmann classification, and 75% in the evaluation using the diagram of the schematic drawings. CONCLUSIONS: The authors concluded that the illustration table could be utilised in substitution for the original description of House-Brackmann facial nerve grading; they also concluded that the illustration table allows faster evaluation and easier memorisation.

Facial Muscles↗
PubMed2003

Facial nerve schwannoma.

Facial nerve schwannomas are clinically challenging tumors. This is a case study of a young woman with an extensive facial nerve schwannoma. The clinical presentation, radiographic diagnosis, pathological confirmation, and treatment options for this relatively rare tumor are discussed.

Adult↗
PubMed1989

Magnetically evoked facial nerve potential.

Facial nerve stimulation by electrical current is painful and tends to discourage serial studies. Transcutaneous magnetic stimulation of the facial nerve is painless, easily reproducible, and elicits facial muscle responses identical to electrical stimulation.

Electromyography↗
PubMed1995

Hemihypoglossal-facial nerve anastomosis in treating unilateral facial palsy after acoustic neurinoma resection.

Eight patients underwent hemihypoglossal-facial nerve anastomosis (anastomosis of a split hypoglossal nerve to the facial nerve) for treatment of unilateral facial palsy. All patients previously had undergone resection of a large acoustic neurinoma and the facial nerve had been resected at that time. The interval between tumor resection and hemihypoglossal-facial nerve anastomosis ranged from 1 to 6 months, with an average of 2.1 months. Postoperative recovery of facial movement was good in all cases during an average follow-up period of 4.2 years. In all eight patients, the degree of hypoglossal nerve atrophy on the operated side was graded mild or moderate, but not severe. It was concluded that hemihypoglossal-facial nerve anastomosis results in good facial reanimation as long as the procedure is performed early after the onset of facial palsy and that this procedure may reduce the degree of hemiglossal atrophy in comparison with classic hypoglossal-facial nerve anastomosis.

Adult↗
PubMed2004

New one-stage nerve pedicle grafting technique using the great auricular nerve for reconstruction of facial nerve defects.

A new one-stage nerve pedicle grafting technique, employing a vascularized great auricular nerve graft, was used to repair a facial nerve defect. The facial nerve of a 39-year-old woman with facial schwannoma was resected, and an island vascularized great auricular nerve graft from the ipsilateral side was transferred to bridge a 4 cm long defect of the buccal branch. Postoperatively, rapid nerve sprouting through the vascularized nerve graft and excellent facial reanimation were obtained within 6 months after surgery. This method in one-stage using a vascularized nerve graft is technically easy, requires a short operating time, has minimal donor-site morbidity, and leads to successful nerve regeneration postoperatively.

Adult↗
PubMed1989

Total facial nerve decompression for recurrent facial paralysis: an update.

Recurrent facial paralysis (RFP) is a rare disorder that in some individuals may lead to worsening sequelae. Melkersson-Rosenthal syndrome is a variant of RFP that is associated with recurrent facial edema. In the past, decompression of the mastoid segment of the facial nerve has not been successful in preventing recurrences. In 1981 we began performing total facial nerve decompression for RFP and in 1986 reported its efficacy in one patient with Melkersson-Rosenthal syndrome and in another in whom both nerves were decompressed for alternating bilateral paralysis. An additional four cases with 3 to 8 years of followup demonstrate no recurrences in any patient. Total facial nerve decompression for RFP in selected patients appears efficacious in preventing recurrences. Decompression will remain investigational until further followup is obtained. Furthermore, its salutary effect should not be extrapolated to Bell's palsy without further study.

Adolescent↗
PubMed1996

Nimodipine accelerates axonal sprouting after surgical repair of rat facial nerve.

Facial-facial anastomosis (FFA), i.e., suture of transected facial nerve, was performed in adult Wistar rats. For 10-112 d post-operation (DPO), half of the animals received standard food (placebo) and half received food pellets containing 1000 ppm nimodipine, a Ca2+ channel blocker. The time course of mimetic reinnervation between these two groups was compared by counting all retrogradely labeled motoneurons after injection of horseradish peroxidase (HRP) into the whiskerpad. In unoperated animals, injection of HRP labeled 1280 +/- 113 motoneurons. After FFA, this number dropped to zero, and the first HRP-labeled facial motoneurons reappeared in both placebo- and nimodipine-treated animals at 14 DPO. The treatment with nimodipine yielded two beneficial effects. (1) It accelerated axonal sprouting until 28 DPO. Whereas the number of HRP-labeled cells in the placebo group was 171 +/- 9 (mean +/- SD) at 16 DPO, 372 +/- 43 at 21 DPO, and 636 +/- 187 at 28 DPO, the number of sprouted motoneurons in nimodipine-treated rats was twice as high: 386 +/- 34 at 16 DPO, 620 +/- 28 at 21 DPO, and 756 +/- 257 at 28 DPO. (2) Nimodipine reduced the polyneuronal innervation of the target muscles. Whereas the number of HRP-labeled cells in the placebo group increased to 1430 +/- 36 at 56 DPO and 1600 +/- 31 at 112 DPO, the number of labeled motoneurons in nimodipine-treated rats remained almost within the normal range: 1315 +/- 31 at 56 DPO and 1354 +/- 33 at 112 DPO.

Anastomosis, Surgical↗
PubMed1985

Facial nerve recording from the eardrum: a possible method for evaluating idiopathic facial nerve paralysis.

A noninvasive technique has been developed for recording from the the facial nerve within the fallopian canal. Following transcutaneous stimulation of the nerve on the face, an antidromic nerve potential can be detected with electrodes placed on the eardrum and enhanced by the technique of averaging. In studies conducted on cats and normal human subjects it has been determined that the primary recording site of the nerve potential is along the tympanic segment of the nerve just distal to the geniculate ganglion. Disturbances in nerve conduction caused by an experimental lesion produced changes in the recorded nerve potential. Thus it seems likely that this technique could assess a developing lesion in a patient with idiopathic facial nerve paralysis. A more accurate and earlier prognosis could be obtained than with conventional peripheral nerve testing techniques, since the severity of the developing lesion itself could be assessed.

Animals↗
PubMed1988

Electronmicroscopic observation of the human facial nerve.

The facial nerves of Bell's palsy, Ramsay-Hunt's syndrome and traumatic facial palsy patients were studied using a transmission electron microscope. Changes were a proliferation of the collagen fibres, the degeneration of the Schwann cell, and a loosened or deteriorated myelin sheath. These changes differ considerably between individuals. Changes also vary in one subject. The cause and severity of the lesion, the duration of the palsy and the location of biopsy are possibly responsible for this phenomenon.

Adult↗
PubMed1998

Infantile cortical hyperostosis and facial nerve palsy.

Facial nerve palsy was diagnosed in a 13-month-old child with infantile cortical hyperostosis. Facial palsy preceded the roentgenographic evidence of mandibular hyperostosis but there was concurrent evidence of hyperostosis of multiple other bones. This case exemplifies the importance of maintaining a high index of suspicion for infantile cortical hyperostosis in infants and children presenting with facial swelling and facial nerve palsy.

Facial Paralysis↗
PubMed1997

Differential diagnosis of facial nerve palsy.

Facial nerve palsy is the most frequent neurological presentation of sarcoidosis. It occurs with equal frequency on the right or left side, and equally unilateral or bilateral. When bilateral facial palsy develops in a young adult, sarcoidosis is the most likely cause. In our series of 147 patients with ocular sarcoidosis, facial palsy occurred in 12 per cent and parotid gland enlargement in 10 per cent. Resolution of facial palsy is complete in 80 per cent of patients. It does not recur, unlike orofacial granulomatosis in which facial palsy tends to be recurrent. The differential diagnosis is large (Table I) and needs full investigation in order to provide a better understanding of the treatment and prognosis. A 7-point scheme of management is set out for the patient with idiopathic facial nerve palsy.

Adult↗
PubMedDate not supplied

Degeneration and regeneration processes in experimental facial nerve paralysis.

Facial nerve paralysis was provoked by compression of its extratemporal portion in rabbits and the degeneration and regeneration of the nerve fibres was studied ultrastructurally. The compression was removed to study the regenerative process in one group of animals. Axonal and myelin degeneration were the first events seen as a collagen tissue proliferation from the endoneurium and perineurium. Ultimately all the nerve was transformed into fibrous tissue. The myelin was disintegrated by Schwann's cells without any macrophagic activity. The regeneration process begins by the axons, that are orientated towards Büngner's bands of remnants of the Schwann's cells, in which a new myelin sheath appears. Schwann's cells play an important role, in both the degeneration and the regeneration process. The final aspect of the regenerated fibres is similar to normal but they contain more collagen tissue, thinner myelin sheaths, and a greater proportion of unmyelinated fibres.

Animals↗
PubMed1993

Chronic electrical stimulation of the facial nerve causes signs of facial nucleus hyperactivity.

The proximal segment of the facial nerve in rats was stimulated electrically daily for a duration of 2-10 min. After 4-8 weeks of such stimulation, 12 of 18 rats developed abnormal muscle responses that could be demonstrated by recording the electromyographic response from lower face muscles (the mentalis muscle) while the temporal branch of the facial nerve was being stimulated electrically. This abnormal electromyographic response consists of activity that appears in the latency range 6.5-15 ms. In addition, these chronically stimulated rats developed signs of facial synkinesis on the side that had been chronically stimulated. This could be demonstrated by recording electromyographic activity when the blink reflex was being elicited by electrical stimulation of the ophthalmic nerve. Rats in which electrodes had been implanted but which had not been stimulated did not develop any abnormal electromyographic activity. The abnormal electromyographic activity that could be recorded in rats that had been stimulated chronically could not be recorded 4-8 weeks after the stimulation had been terminated. We interpret these results to indicate that chronic electrical stimulation of the facial nerve can render the facial motonucleus hyperactive, and that the signs of this hyperactivity (abnormal muscle response and synkinesis) are similar to those typically seen in patients with hemifacial spasm. We thus presume that these results support the hypothesis that it is the irritation of the facial nerve from a compressing blood vessel that causes the facial nucleus to become hyperactive in patients with hemifacial spasm.

Animals↗