Otogenic facial paralysis

Summary The histopathological changes of the facial canal and nerve in facial paralysis due to chronic suppurative otitis madia are described in six temporal bones. Bony destruction of the facial canal was found in its tympanic segment and in its upper mastoid part in all cases, but it was particularly notable in the labyrinthine segment as well. The pathological process, cholesteatoma or granulation tissue surrounding the exposed facial nerve was inflamed in all cases. The affected facial nerve showed degenerative and inflammatory changes throughout its tympanic segment in all cases, but its mastoid segment appeared to be relatively normal. Our findings suggest that facial paralysis occurs us chronic suppurative otitis when the inflammatory process specifically involves the facial nerve trunk.     

Primary and secondary tumors of the facial nerve. A temporal bone study

Of 1400 temporal bones in the collection at the University of Minnesota, Minneapolis, 17 temporal bones from 15 patients were found to have tumors involving the facial nerve. The findings were as follows: one case of facial nerve schwannoma; two cases of invasion of the facial nerve by contiguous tumor; and 14 cases of metastatic tumors involving the facial nerve. Facial nerve paralysis was present in half of the cases (nine of 17). Facial nerve paralysis was present in the case of facial nerve schwannoma, in both cases of invasion of the facial nerve by contiguous tumor, and in six of 14 cases of metastatic tumors involving the facial nerve. The presence of the facial nerve paralysis correlated well with the degree of tumor infiltration into the nerve fibers and the segment of the tumor involvement in the facial nerve. In the patients with metastatic tumors, facial nerve paralysis was a sign of extensive intracranial tumor involvement and was usually accompanied by other cranial nerve palsies, most commonly involving the fifth nerve.     

Histopathological incidence of facial canal dehiscence in otosclerosis

The objective of this study was to evaluate the histopathological incidence of facial canal dehiscence in otosclerosis cases compared with non-otosclerotic controls. 133 temporal bones from 84 otosclerosis (35 unilateral otosclerosis, 49 bilateral otosclerosis) cases were compared to 102 age-matched normal temporal bones from 70 subjects (38 unilateral normal cases, 32 bilateral normal cases). Temporal bones were serially sectioned in the horizontal plane at a thickness of 20 μm, and were stained with hematoxylin and eosin. We evaluated the location and the invasion of otosclerosis to the facial canal and incidence of facial canal dehiscence under light microscopy. Facial canal was subdivided into four portions: (1) the geniculate ganglion, (2) the tensor tympani muscle, (3) the oval window, and (4) mastoid. The incidence of facial canal dehiscence in otosclerosis [66 temporal bones (49.6%)] was significantly lower than normal controls [67 control temporal bones (65.7%)] in the oval window area (P = 0.019). Temporal bones with otosclerotic invasion to the thin bone of the canal were significantly less likely to have dehiscence [10 temporal bones (31.3%)] compared to the otosclerotic bones without invasion [56 temporal bones (55.5%)] (P = 0.025). There was no significant difference in the incidence of facial canal dehiscence between temporal bones with and without otosclerosis in the entire segment of facial nerve. Our findings in this study suggest that otosclerotic lesions have the potential to close dehiscence of the facial canal in the oval window area.     

周围性面瘫41例临床分析

目的 总结周围性面瘫的疗效及治疗体会.方法 回顾性分析我院2004年7月-2009年1月间41例周围性面瘫患者的临床资料,以House-Brackman(HB)分级法作为疗效评估标准.结果 41例患者中Bell面瘫14例,Hunt综合征11例,胆脂瘤型中耳炎致面瘫8例,外伤性面瘫4例,颞骨肿瘤致面瘫4例.治疗前面瘫HB分级Ⅱ级2例,Ⅲ级11例,Ⅳ级13例,Ⅴ级12例,Ⅵ级3例.22例行单纯药物治疗;19例行手术治疗:其中单纯行面神经减压术6例,病变切除+面神经减压术10例,病变切除+面神经移植术2例,病变切除+面神经垂直段切除术1例.治疗后随访8月～4年半,除2例患者面瘫无明显改善外,其他患者均有不同程度的恢复;6例经药物治疗无效的患者经面神经减压术后1例恢复至I级、3例恢复至Ⅱ级、2例恢复至Ⅲ级.结论 周围性面瘫经及时、恰当的药物或手术治疗,大多可获得满意疗效;对于保守治疗无效者,及时果断地行面神经减压术是有效的治疗手段.     

The behavior of the facial nerve in vitamin A and thalidomide induced atresia auris congenita. A microsurgical and histological animal study (author's transl)

Atresia auris congenita may include either a complete or incomplete paralysis of the facial nerve as well as a possible abnormal course of its tympanic segment. Pregnant Wistar rats were given high doses (50,000, 80,000 or 100,000 USP units) of vitamin A and (10,15 or 20 mg) Thalidomide on the 8th, 9th, 10th and 11th days of gestation. The animals were then sacrificed, and the temporal bones and the medulla oblongatas of the fetuses and the adult rats were examined microsurgically and histologically. In contrast to previous reports in the literature, no significantly abnormal courses of the nerve could be found. These findings corresponded to those of 62 endaurally operated human ear malformations. The paralysis of the facial nerve in these patients seems due to a reduced diameter of the nerve and not to a malformation of its nucleus.     

面神经瘤误诊分析

目的总结分析面神经瘤误诊的原因，提高对面神经瘤的认识。方法1993年1月至2006年9月手术治疗的28例面神经瘤患者，11例有误诊的经历。所有患者均行CT或MRI检查、纯音测听，面神经功能的评估采用House-Brackman（HB）系统。结果11例患者被误诊。2例术前被误诊为腮腺肿块，行腮腺浅叶切除术，术中发现肿块来自面神经。4例单侧面神经麻痹长期外院误诊为贝尔面神经麻痹，病史1至8年。由于长期面神经麻痹无好转，行影像学检查发现面神经占位病变。2例复发性面神经麻痹误诊为贝尔面神经麻痹，行影像学检查发现均为面神经膝状神经节占位。1例因左耳渐进性听力下降，体检见外耳道新生物，诊断为外耳道新生物，行活组织检查示神经鞘瘤，进一步影像学检查提示为面神经瘤。1例右耳流脓数年，面神经麻痹1个月。查体示右鼓膜穿孔，CT检查诊断为慢性中耳炎行手术，术中见上鼓室肿块同面神经关系密切，取部分组织送病理，术后病理为面神经鞘瘤。另1例面神经麻痹1年半，CT检查误诊为先天性胆脂瘤，入院后发现乳突肿块同面神经关系密切，MRI证实为面神经肿瘤并且侵及腮腺内面神经。11例均经手术和病理证实。结论面神经瘤较罕见，不为大多数临床耳科医生熟悉，在临床中易被漏诊和误诊。临床中，如贝尔面神经麻痹半年内无好转现象或患者表现为反复面神经麻痹，应行影像学检查排除面神经瘤的可能。如患者出现面神经麻痹，CT示中耳占位并同面神经关系密切时，行MRI检查可同中耳胆脂瘤、肉芽、胆固醇肉芽肿等区分。腮腺肿块同面神经总干关系密切者应警惕面神经可能。     

耳内镜下上鼓室进路面神经水平段及膝状神经节减压术

目的 :探讨耳内镜下经上鼓室进路行面神经锥段、水平段及膝状神经节减压手术的可行性。方法 :对 1 2例外伤性周围性面瘫患者术前采用颞骨薄层CT扫描、流泪试验、镫骨肌反射、味觉试验及听力学检查 ,以明确受损部位。均在耳内镜下经上鼓室进路行面神经锥段、水平段及膝状神经节减压术。结果 :出院时完全恢复面肌功能 (Ⅰ级 ) 6例 (5 0 % )。随访 2～ 1 0个月 ,面肌功能完全恢复者 1 0例 (83 .3 % ) ,面肌功能ⅡⅢ级者 2例(1 6 .7% )。术后听力水平与术前对比 ,无明显变化 8例 ,听力提高 2例 (术前面瘫伴听骨链脱位 ) ,下降 5 1 0dB 2例。结论 :耳内镜下行水平段、膝状神经节减压术 ,可尽量减少对正常组织的破坏 ,进路方便、简捷 ,具有微创的手术效果     

儿童乳突-颞下迷路外面神经减压术8例临床分析

目的 探讨儿童颞骨骨折性面神经麻痹经乳突-颞下迷路外径路面神经减压术的疗效.方法 8例颞骨骨折性面神经麻痹患者分别在病情出现的1个月内,行经乳突-颞下迷路外径路面神经减压术,部分同期行听骨链重建术,随访1～2年,评估听力及面神经功能(H-B)程度.结果 术前H-B Ⅴ级7例、Ⅳ级1例,术后恢复Ⅰ级5例、Ⅱ级3例;术前2...     

经乳突进路面神经减压术治疗中耳胆脂瘤并发面神经损害75例

目的 探讨经乳突进路治疗中耳胆脂瘤导致的面神经损伤的最佳方法和疗效。方法 对由中耳胆脂瘤引起周围性面瘫的75例患者,采取经乳突进路面神经减压术。75例中累及垂直段13例,水平段及锥段36例;膝状神经节22例,膝状神经节及迷路段4例。结果 术后随访1～6个月,通过House-Beckmann面神经分级系统评分,结果为Ⅰ～Ⅴ级。结论 对由中耳胆脂瘤累及面神经所致周围性面瘫,及时采取经乳突进路施行面神经减压术治疗,可取得满意效果。     

Use of a novel ultrasonic surgical system for decompression of the facial nerve

OBJECTIVE: The middle cranial fossa approach has been used to explore and decompress the facial nerve in patients with Bell's palsy and facial nerve tumors. Unfortunately, this approach is technically challenging and has a significant risk of injury to the facial nerve and to the cochleovestibular organs. One way to minimize the risk may be with the use of the Sonopet Omni ultrasonic aspirator (Synergetics Inc., St Charles, MO) instead of an otologic drill. METHODS: In this prospective study using cadaveric temporal bones, a total of 17 temporal bone specimens were used. Seven cadaveric temporal bones were used (4-left, 3-right) for the initial feasibility study. At a second session, an additional 10 temporal bones (5-left, 5-right) underwent decompression of the facial nerve from the fundus of the internal auditory canal (IAC) to the geniculate ganglion (ie, labyrinthine segment). The average time to decompress the labyrinthine segment was measured. The temporal bones were then examined for evidence of any injury. RESULTS: None of the 17 temporal bones showed any sign of injury to the superior semicircular canal or the cochlea. However, one specimen did have penetration of the IAC dura; another specimen did have penetration of the epineurium of the facial nerve. However, in neither case was there any evidence of injury to the facial nerve itself. At the first session, the average time for decompression of the labyrinthine segment was 10 minutes and 12 seconds. At the second session, the average time for decompression was 5 minutes and 0 seconds. CONCLUSION: The ultrasonic surgical system may be used as an alternative to the surgical drill for decompression of the facial nerve. Although a learning curve does exist, as with any new surgical tool or device, our results indicate that the device can be used safely and in a reasonable amount of time. However, before proceeding with intraoperative use of this device for otologic and neurotologic procedures, familiarization is first recommended on cadaveric temporal bone specimens.     

Oval window canal and CT-diagnosis of peripheral pareses of the facial nerve

Computed tomography (CT) has examined 200 patients (400 temporal bones) at the age of 0-74 with unaffected facial nerve and 28 patients with symptoms of peripheral paresis or paralysis of the facial nerve of different genesis. Polyposition CT of the temporal bone is an intravital noninvasive method of the Fallopius' canal visualization. The canal is visualized on the tomograms in 100% cases irrespective of the patients' age. The following causes of n. facialis paresis were revealed: neurinoma of the facial nerve, sarcoma of the temporal bone, destruction of the tympanic canal wall in chronic otitis media, fractures of the temporal bone, malformations of the Fallopius' canal in malformations of the temporal bone, stenosis of the canal in fibrous dysplasia. The above alterations of n. facialis canal determine further therapeutic policy.     

Two cases of intratemporal facial nerve neurilemmomas

The patients with neurilemmomas of the facial nerve within the temporal bone were treated. Although most of cases of the facial nerve neurilemmoma in the temporal bone present with a facial palsy, a few cases have normal facial nerve function and are especially difficult to diagnose preoperatively because of few symptoms. Case 1, a 31-year-old man, developed progressive left facial palsy with protrusion of the posterior wall of the external auditory meatus over a five-month period. Case 2, a 64-year-old man, complained of only fullness and tinnitus of the right ear without any facial nerve symptoms. Polytomography of the temporal bone demonstrated no abnormal findings in both cases. However, computed tomography revealed a soft-tissue density area in the left mastoid cavity with destruction of the posterior wall of the external auditory meatus in case 1. A similar soft-tissue density mass was found in the right tympanic cavity in case 2, suggesting the presence of the tumor in the temporal bone. At operation, the tumors were found to originate from the vertical portion of the facial nerve in both cases. It was assumed that normally existing dehiscences of fallopian canal might account for why some patients have normal facial nerve function.     

Ossification patterns of the tympanic facial canal in the human fetus and neonate

Dehiscences in the bony facial canal are comparatively common in the human adult. The highest incidence occurs in the tympanic segment of the facial nerve near the region of the oval window. Thirty-three fetal temporal bones, ranging from 16 to 40 weeks' gestation, and four from 1, 2, 4 and 12 weeks' postpartum neonates, were studied to evaluate the normal patterns of ossification of the fallopian canal of the tympanic facial nerve segment in the human. The tympanic facial nerve segment elongates threefold during this period (from 1 mm to 3 mm). The ossification starts at 21 weeks' gestation anteriorly from apical otic ossification centers and at 26 weeks from canalicular ossification centers near the stapedius muscle. The ossification proceeds in an anterior-to-posterior direction as two periosteal shelves of bone surround the facial nerve. The superior periosteal bony ledge contributes 75% of the circumference of the fallopian canal. The anterior ossification center forms over 83% of the fallopian canal length. The two centers fuse post partum near the region of the oval window. The anatomic location of the facial nerve, nerve branching, and neural vasculature precede ossification. In 80% of the paired temporal bones, this ossification pattern appears to be symmetrical. The patterns and incidence of bony dehiscences within the tympanic fallopian canal segment can be explained by these observations. This study demonstrates that fallopian canal dehiscences are not congenital anomalies, but variations of normal developmental anatomic processes.     

A pseudo-malignant Warthin's tumor presenting with facial nerve paralysis

Facial nerve paralysis, in association with a parotid mass, is generally considered pathognomonic of malignancy. However, nine cases of paralysis with benign tumors have been reported: four in association with a pleomorphic adenoma, three with a Warthin's tumor and one with an oncocytoma. The details of these cases are described and an additional case of Warthin's tumor causing a facial paralysis is reported. In all four cases of Warthin's tumor the pathology is similar, with inflammation, fibrosis and necrosis, especially in areas surrounding branches of the facial nerve. In view of the 10 cases reviewed herein, it is suggested that the pathology be confirmed at the time of surgery and every effort made to preserve facial nerve function.     

慢性中耳炎并周围性面瘫的临床特点及预后

目的探讨慢性中耳炎（chronic otitis media,COM）并周围性面瘫的临床特点及预后影响因素。方法对42例行手术治疗的COM并面瘫的临床资料进行回顾性总结,分析临床特点及面瘫程度、面瘫病程对手术效果的影响。结果术中发现面神经管破坏最常见部位是鼓室段（88.6%）,共存迷路瘘管10例（28.6%）,共存脑膜暴露13例（37.1%）。不完全面瘫与完全面瘫的术后面神经恢复良好率（HB分级I～II级）无显著性差异,全部病例治疗效果良好率为47.6%。面瘫病程〈1个月者面神经功能恢复良好率显著性高于≥1个月。结论开放式乳突根治术及面神经局部减压术是治疗COM并面瘫的有效术式,手术时机影响术后面神经功能恢复效果。     

Non-recovery animal model of severe facial paralysis induced by freezing the facial canal

ObjectiveSome cases of peripheral facial paralysis are resistant to treatment, thus, a non-recovery model of facial paralysis is needed to develop new treatment strategies for this condition. The purpose of the current study was to develop an animal model of which facial palsy was severe and prolonged.MethodsTen 8-week-old female Hartley guinea pigs weighing between 400 and 500 g were used for the animal model. The vertical segment of the facial canal was accessed via the otic bulla, without removing the bony wall of the facial canal. The canal was then frozen for 5 s using freeze spray. Facial movements, electroneurography (ENoG), histology, and changes in temperature were evaluated.ResultsAll animals exhibited complete facial paralysis immediately after the procedure and recovered gradually, however, not all of them had recovered completely 15 weeks after freezing. The ENoG values one week after freezing for all animals (10/10) were 0%. Histological examination one week after freezing revealed that most of the vertically placed myelinated nerve fibers which had been frozen were remarkably affected and denatured. The number of vertically placed myelinated nerve fibers increased 15 weeks after freezing, but the nerve fibers were smaller than normal nerve fibers and were distorted in shape.ConclusionComplete facial paralysis was induced in Hartley guinea pigs by freezing the facial canal. The behavioral, ENoG, and histopathological data suggest that the facial paralysis was severe and prolonged. This model may assist in developing novel treatment for severe facial palsy and facilitate basic research on facial nerve regeneration.     

Postnatal developmental changes in facial nerve morphology

Accurate measurements of the lengths and angles of the facial nerve were obtained in eight normal human temporal bones of varying ages from 7 days to 76 years. Measurements were made on serial histological sections, using computer-aided three-dimensional (3-D) reconstruction. The most noteworthy of the findings demonstrated that both the mastoid portion of the facial nerve and the segment of the facial nerve between the second genu and the divergence of the chorda tympani nerve lengthened with age. The mastoid segment lengthened more significantly than the latter, indicating the facial canal grows more than the facial nerve in its mastoid portion. This difference in growth rates results in the site of the chorda tympani nerve divergence shifting with age relative to the stylomastoid foramen.     

Dermoid cyst in the facial nerve--a unique diagnosis

Facial nerve paralysis in children may occur as a complication of infections, trauma, or rarely from benign or malignant tumors of the facial nerve. We present the first reported case of a dermoid tumor in the facial nerve causing facial paralysis in a child. Case report at a tertiary Children's Hospital. A 9-month-old was referred to our institution for evaluation of persistent, complete right sided facial paralysis three months after receiving a diagnosis of Bell's palsy. A workup at our institution including MRI and CT revealed marked widening of the facial canal in the mastoid segment consistent with facial nerve schwannoma or hemangioma. Surgical exploration via mastoidectomy and facial nerve decompression revealed keratinous material containing hair that had fully eroded the facial nerve, disrupting it completely. The entire tumor was removed along with the involved segment of facial nerve, and the missing facial nerve segment was cable grafted. Histological examination of the tumor confirmed a ruptured dermoid cyst in the facial nerve. Facial nerve tumors are rare causes of facial paralysis in children, accounting for fewer than 10% of cases of facial paralysis in the pediatric population. Dermoid cyst can occur throughout the head and neck region in children, but a dermoid tumor in the facial nerve has not been described in the literature prior to this report. This represents a new and uncommon diagnostic entity in the evaluation of facial nerve paralysis in children. Appropriate imaging studies and pathology slides will be reviewed.     

Transcranial magnetic stimulation in acute facial nerve injury

OBJECTIVE/HYPOTHESIS: Available electrodiagnostic tests that are used to evaluate facial nerve injury examine the nerve distal to the stylomastoid foramen; because most facial nerve injuries are within the temporal bone, the tests cannot evaluate the nerve at or across the injury site. The interpretation of these tests depends on the predictability (or unpredictability) of distal degenerative process. Transcranial magnetic stimulation may be able to stimulate the nerve proximal to the injury site. The hypothesis of the present study is that in cases of mild traumatic facial nerve injury where axonal integrity is maintained, proximal stimulation of the nerve using higher than normal stimulus intensities to "overcome" the block at the injury site result in recordable facial nerve activity. STUDY DESIGN: A prospective controlled animal study comparing response to transcranial magnetic stimulation of the facial nerve in the following groups: mild injury, severe injury/transection, and control. METHODS: We studied 44 facial nerves in 22 cats. Fifteen nerves were subjected to mild trauma. Five nerves were severely crushed, 2 nerves were completely transected, and 22 nerves were not traumatized. All nerves were examined with the transcranial magnetic stimulation system before the trauma, immediately after the trauma, and at 3, 8, and 12 weeks after trauma. RESULTS: All nerves in the mild and severe trauma groups showed complete clinical paralysis immediately after trauma. The nerves in the mild trauma group showed significant increase in threshold as well as significant increase in latency for recordable facial muscle response to transcranial magnetic stimulation. Thresholds and latencies decreased gradually within 3 to 12 weeks and returned almost to preinjury levels. This paralleled the return of clinical facial muscle movement. In the severe trauma/transection group, the nerves had no facial muscle response to transcranial magnetic stimulation after trauma. Neither facial muscle response to transcranial magnetic stimulation nor facial muscle movements recovered. CONCLUSIONS: In cats transcranial magnetic stimulation can assess the integrity of the facial nerve after trauma and predict its potential for regeneration. This technique can excite the nerve proximal to the injury site and may play a role in the clinical evaluation of the acute traumatic facial nerve paralysis. It can be used immediately after trauma, because it does not depend on wallerian degeneration to occur.     

单纯疱疹病毒性面神经炎的动物模型

目的建立单纯疱疹病毒1型（herpes simplex virustype 1，HSV-1）感染造成的面神经麻痹动物模型，研究HSV-1与面神经麻痹之间的关系。方法Balb／c小鼠66只，切断双侧面神经耳后支，右侧神经断端接种HSV-1，左侧接种胎牛血清作为对照。观察小鼠全身情况、双侧面肌运动的对称性；颞骨连续切片HE染色；颞外段面神经锇酸染色；双侧面神经、脑干、三叉神经节、脊髓行PCR检测HSV-1 DNA片断。结果28只小鼠（42．42％）于接种后2～5d发生右侧面神经麻痹，病程持续3～6d后恢复。38只未发生面神经麻痹。与对侧比较，颞骨连续切片显示面神经麻痹鼠右侧神经肿胀、神经周围问隙变小、炎细胞浸润，面神经横截面秽面神经管横截面积的比值明显变大；颞外段面神经出现神经髓鞘变薄、脱失。面神经麻痹鼠和无面神经麻痹鼠的部分神经组织中检测到HSV DNA。结论在面神经耳后支断端接种HSV-1可以引起小鼠暂时性面神经麻痹，可能是由于病毒逆行转运引起面神经炎，进而神经肿胀受压发生面神经麻痹。