瞬目反射、面神经电图和面肌肌电图对面神经炎的诊断、治疗和预后的评估

目的 探讨瞬目反射(BR)和面神经电图(ENG)、面肌肌电图(EMG)对面神经炎的诊断、治疗和预后的价值.方法 53例面神经炎患者在发病后1周内首次进行BR检查以及ENG、EMG测定,发病后1,3,6个月重复上述检查.结果 首次检查患侧R1、R2及R2'缺如者23例,其余有30例患侧R1、R2及R2'与健侧相比潜伏期延长,差异有统计学意义(P＜0.01).异常率达91%.37例患侧面神经运动传导与健侧相比潜伏期延长、波幅降低,差异有统计学意义(P＜0.05),异常率为75%.23例患侧出现正锐波、纤颤电位,运动单位电位波幅降低,时限延长,多相渡增多,病理性干扰相.1个月后复查,上述检查完全恢复者26例.3个月后复查完全恢复者42例,6个月后复查完全恢复者51例,2例未恢复者1年后仍遗留有后遗症.结论 BR测定是诊断面神经炎的敏感指标.BR结合ENG、EMG检测能评估面神经炎的病情、疗效及预后.     

神经肌电图对特发性面瘫临床及预后评估的研究

目的 探讨特发性面瘫的神经电图和肌电图的特点及临床意义。方法 采用Sapphire Ⅱ肌电图仪对92例特发性面瘫患者进行病侧和健侧的神经电图和肌电图检查，并对结果进行对比分析。结果 神经电图测提示患侧面神经运动传导潜伏期延长、波幅降低，与健侧比较有极显著差异（P＜0．01）。肌电图检查显示患侧面神经募集减弱，可见有纤颤电位或／和正锐波。结论 神经电图和肌电图有助于特发性面瘫定性及定量诊断，能指导治疗及预后评价。     

脑卒中偏瘫患者的神经电生理研究

目的研究脑卒中偏瘫患者周围神经的神经电生理变化。方法选择南昌大学第三附属医院脑卒中偏瘫患者180例,3～7 d、6个月进行肢体神经传导、针极肌电图、交感神经皮肤反应(SSR)测定。结果 180例患脑卒中偏瘫患者急性期1例检测出双侧腓肠神经传导速度减慢,针极肌电图正常;病程6个月时,56例出现NCV异常,运动神经总异常率为3.6%,感觉神经总异常率6.4%,SCV异常率高于MCV异常率。肌电图:①患侧:21例出现插入电位延长,18例有自发电位;②健侧:4例出现插入电位及自发电位。SSR:脑卒中偏瘫患者急性期、病程6个月时,健侧、患侧SSR潜伏期、波幅与正常值比较差异有统计学意义(P0.05),而健侧潜伏期、波幅及患侧潜伏期、波幅比较差异无统计学意义(P0.05)。6个月与急性期对比,患侧及健侧下肢、健侧上肢潜伏期差异有统计学意义(P0.01),患侧上肢潜伏期及所有肢体波幅差异无统计学意义(P0.05)。结论脑卒中偏瘫患者在病程6个月出现周围神经损害,SCV异常率高于MCV异常率,而在急性期出现SSR抑制、自主神经功能异常。     

13例神经肌炎的临床及肌电图研究

目的:探讨神经肌炎的临床特点以及肌电图(EMG)、神经传导速度(NCV)的诊断价值。方法:分析13例神经肌炎临床表现、EMG、NCV结果。结果:13例患者均以肌肉受累为主要临床表现;11例并发有神经病变的症状及体征。13例患者NCV均有异常。所检测的104根神经NCV异常率为57.7%。F波异常率为26.9%。11例针极EMG呈神经源性与肌源性混合损害,2例呈神经源性损害。结论:EMG、NCV是有价值的电生理诊断方法。确诊神经肌炎需结合临床表现和EMG结果。     

多发性肌炎患者神经电生理特点分析

目的增进对多发性肌炎患者肌电图特点的认识,提高其检查的阳性率。方法对91例多发性肌炎患者进行肌电图(EMG)、神经传导速度测定。结果肌电图异常率为87.9%,肌源性损害者占79.1%,神经源性损害者占8.8%。其中插入电位延长、自发电位的阳性率分别为6%和52%,肱二头肌出现率较高,外展拇短肌出现率最低(p<0.05);运动单位电位(MUP)时限缩短的阳性率为71%,胫前肌出现率最高,外展拇短肌最低(p<0.05);MUP波幅降低的阳性率较低,仅为7%;多相波增多的阳性率为29%,胫前肌出现率最高,股四头肌最低(p<0.05);重收缩时波形异常的阳性率为26%,以股四头肌出现率最高;重收缩时峰值电压降低的阳性率为31%,胫前肌出现率最高,外展拇短肌最低(均p<0.05)。5例患者EMG呈神经源性损害,1例感觉神经传导速度减慢,2例运动神经传导速度减慢。肌电图正常组、肌源性损害组及神经源性损害组患者的病程、年龄无明显差异。结论 EMG对多发性肌炎诊断的阳性率为87.9%,其中以MUP时限缩短出现率最高为71%,其次为自发电位为52%。EMG异常最多见于肱二头肌、股四头肌和胫前肌。     

神经电生理检测在Bell麻痹中的应用

目的探讨神经电生理检测,如瞬目反射(BR)、面神经电图(ENG)、肌电图(EMG)在Bell麻痹患者中的应用价值。方法46例Bell麻痹患者在病程3d内(A组)和>3～10d(B组)分别进行BR、ENG、EMG测定,并于3个月(C组)后复查。结果BR在3d内即出现明显异常;且R1R2R2′消失者预后较差,仅R1R2R2′延长者预后较好。ENG潜伏期延长,波幅下降<70%为轻度损害,3个月内可完全恢复,好转率100%;波幅下降70%～90%为中度损害,3个月内可大部分恢复正常,好转率86.3%;波幅下降>90%为重度损害,预后较差,好转率50%。EMG极早期(3d内)检测无异常,轻收缩有MU者预后较好,无MU者预后差。结论BR检测宜用于早期诊断及鉴别诊断,联合ENG、EMG检测Bell麻痹患者,可全面客观评价面神经损害程度,对估计预后和临床治疗有重要价值。     

脑卒中后偏瘫侧下肢功能与腓神经相关性的临床研究

目的:探讨神经电生理检测在脑卒中单侧偏瘫患者中的临床应用.方法:选取2014年6月～2015年1月在暨南大学附属第一医院东圃康复医学科诊治的脑卒中单侧偏瘫患者40例,对双侧腓神经(包括运动神经和感觉神经)进行神经传导检测,根据病程分为3组:1个月组、3个月组、病程6个月组,同时采用徒手肌力测试量表、改良Ashworth量表与功能性步行量表评定.结果:脑卒中偏瘫患者患侧下肢腓神经与健侧比较均有不同程度的损害.病程1个月组患者腓神经传导速度和波幅降低幅度最大,传导功能最差,与健侧腓神经比较差异有显著意义(P<0.001);病程3个月组患者患侧与健侧腓神经传导波幅比较,差异有显著意义(P<0.02),患侧与健侧腓神经传导速度比较差异有显著意义(P<0.001);病程6个月组患者腓神经传导速度减慢和波幅降低幅度最小,其功能相对好,患侧与健侧腓神经功能比较差异无显著意义(P＞0.05);3组患者腓神经患侧与健侧互相对比分析,潜伏期比较差异无显著意义(P＞0.05).结论:用神经传导作为康复评定脑卒中偏瘫患者患侧下肢腓神经功能情况是一种实用的检测方法,有助于评价腓神经当下的功能情况.     

68例有机磷中毒致周围神经损害的电生理分析

目的观察有机磷中毒的肌电图、神经传导速度改变。方法对68例有机磷中毒患者进行常规肌电图（EMG）及神经传导速度（NCV）测定。结果纤颤电位出现率30％,正向波出现率32％,轻收缩时运动单位电位平均时限延长（57％）,波幅增高（36％）,多相波增多（32％）,重收缩呈单纯相41％,混合相48％。神经传导速度：SCV减慢（24％）,MCV减慢（61％）,远端潜伏期延长（47％）。结论电生理检查对有机磷中毒患者受损肌肉、受损神经、损害性质及预后判断有重要价值。     

42例强直性肌营养不良症(MYD)电生理表现

为了研究探讨MYD患者的电生理特点,本文对42例MYD病人进行了肌电图(EMG)、神经传导速度(NCV)和体感诱发电位(SEPs)检查。结果发现,全部患者均有电肌强直表现,其放电频率以拇短展肌最高。28%的病人发现NCV减慢,以运动神经为主,且早年症状组NCV异常率明显高于成年症状组病人。SEPs异常检出率为24%,且多数合并周围神经损害。结论:42例MYD患者存在着广泛的电生理异常,且早年症状组较成年症状组病人更为常见。     

瞬目反射与面神经运动传导检测在特发性面神经麻痹中的临床应用价值

目的探讨瞬目反射与面神经运动传导在特发性面神经麻痹中的临床应用价值。方法选取特发性面神麻痹患者101例,于发病3~7d内进行瞬目反射(BR)和面神经运动传导(FMC)检测,以评估其与临床表现、面瘫预后的关系。结果 101例患者BR检测均异常,表现为患侧R1、R2、R2'波潜伏期延长或未出波;在比较不同未出波情况的痊愈时间分布时发现,4组(全出波、1个未出波、2个未出波、3个未出波)间痊愈时间分布(P0.05)。101例患者患侧额肌、眼轮匝肌、口轮匝肌M波潜伏期均较对侧延长,差异有统计学意义(P0.05);101例患者患侧M波波幅均有下降,Pearson分析显示痊愈时间与患侧M波下降幅度呈正相关,(r=0.592,P0.05)。按照患侧M波波幅较对侧下降幅度大小,分为50%以下、50%~80%、80%以上3组,3组间痊愈时间分布(P0.05),下降幅度为50%以下组的患者80.4%在1个月内痊愈,下降幅度为50%~80%组的患者56.1%在2个月内痊愈,下降幅度80%以上组的患者77.8%在3个月及以上痊愈。结论特发性面神经麻痹患者患侧BR均异常,BR可作为其诊断的客观、敏感的指标;面神经运动传导检测,患侧M波波幅下降幅度与痊愈时间呈正相关,可客观评估其预后。     

Electrophysiological study of congenital facial paralysis

The common cause of neonatal facial asymmetry is facial nerve paralysis or "asymmetric crying facies syndrome". In the not uncommon later the lower lip, symmetrical at rest, becomes tilted to the so-called normal side when the patient is smiling or crying, as the congenital hypogenesis of sublabial muscles fail to pull down the lower lip in the opposite side. The electrophysiological differentiation between the two diseases has been performed by orbicularis oculi and oris reflexes with mechanically glabellar and supralabial tapping stimulation, respectively, in addition to needle and/or surface EMG recording. In the facial nerve paralysis of the case 1, R1 and R2 were absent in the orbicularis oculi and oris reflexes. EMG activity was completely lacking over the M. orbicularis oculi and oris innervated by facial nerve. On the contrary, the orbicularis oculi and oris reflexes were normal in the asymmetric crying facial of the case 2. EMG activity was absent only in the sublabial muscles including M. depressor anguli oris and/or M. depressor labii inferioris. Furthermore, needle EMG disclosed no spontaneous activity at rest, which was suggestive of no denervation in the sublabial muscles. It was, however, not possible to determine exactly which muscle the needle was inserted, the M. deprossor anguli oris or the M. depressor labii inferioris. The case 3 might be a variant of asymmetric crying facies with hypogenesis of M. orbicularis oris and/or oculi as well as the sublabial muscle, since the latency was normal but the amplitude was significantly attenuated in the components of orbicularis oculi and oris reflexes.(ABSTRACT TRUNCATED AT 250 WORDS)     

Contralateral reinnervation of midline muscles in facial paralysis.

We report on a patient with recovery of activity of the left orbicularis oris and nasalis muscles 3 months after a complete left facial palsy. Stimulation of the affected facial nerve evoked no responses, whereas contralateral facial nerve stimulation showed polyphasic responses with very long latencies in the nasalis and orbicularis oris muscles. Needle electromyography (EMG) revealed abnormal spontaneous activity in the left orbicularis oris muscle. The motor unit action potentials on the left side of the face could be recruited only during marked contraction of the corresponding muscles on the right and were of low voltage and polyphasic ("nascent potentials"). Contralateral reinnervation is probably due to sprouting of terminal branches crossing the midline of the face and innervating bundles of muscle fibers on the affected side. This phenomenon seems unfamiliar to most clinicians. Whether the activity is due to conduction along nerve fibers or muscle fibers crossing the midline is discussed.     

No clinical or neurophysiological evidence of botulinum toxin diffusion to non-injected muscles in patients with hemifacial spasm

Botulinum toxin injected into a muscle may diffuse to nearby muscles thus producing unwanted effects. In patients with hemifacial spasm, we evaluated clinically and neurophysiologically, whether botulinum toxin type A (BoNT-A) diffuses from the injection site (orbicularis oculi) to untreated muscles (orbicularis oris from the affected side and orbicularis oculi and oris from the unaffected side). We studied 38 patients with idiopathic hemifacial spasm. Botulinum toxin was injected into the affected orbicularis oculi muscle alone (at 3 standardized sites) at a clinically effective dose. Patients were studied before (T0) and 3-4 weeks after treatment (T1). We evaluated the clinical effects of botulinum toxin and muscle strength in the affected and unaffected muscles. We also assessed the peak-to-peak amplitude compound muscle action potential (CMAP) recorded from the orbicularis oculi and orbicularis oris muscles on both sides after supramaximal electrical stimulation of the facial nerve at the stylomastoid foramen. In all patients, botulinum toxin treatment reduced muscle spasms in the injected orbicularis oculi muscle and induced no muscle weakness in the other facial muscles. The CMAP amplitude significantly decreased in the injected orbicularis oculi muscle, but remained unchanged in the other facial muscles (orbicularis oris muscle on the affected side and contra-lateral unaffected muscles). In conclusion, in patients with hemifacial spasm, botulinum toxin, at a clinically effective dose, induces no clinical signs of diffusion and does not reduce the CMAP size in the nearby untreated orbicularis oris or contralateral facial muscles.     

Pathophysiology of hemifacial spasm: II. Lateral spread of the supraorbital nerve reflex

The blink reflex was examined in 62 patients with hemifacial spasm. The latency and amplitude of the early (R-1) component of the orbicularis oculi response were increased as compared with the contralateral, unaffected side and controls, p less than 0.001. On the affected side, all patients showed a synkinetic response in the mental muscle, and after-activity and late-activity was observed after the reflex response. These findings indicate lateral spread of impulses to other fibers in the facial nerve (ephaptic transmission) and autoexcitation of fibers. The increased latency indicates a slowing of the nerve conduction in the facial nerve, in keeping with pathologic findings of focal demyelination.     

Reflex excitability of facial motoneurons at onset of muscle reinnervation after facial nerve palsy.

We studied 18 patients with complete unilateral denervation of the facial muscles after idiopathic facial nerve palsy to determine whether motoneuronal excitability is enhanced in the few motor units that are active at onset of muscle reinnervation. The study was carried out between 75 and 90 days after the facial nerve lesion. We used two needle electrodes to record simultaneously the spontaneous and voluntary activity of the orbicularis oris (OOris) and orbicularis oculi (OOculi) muscles, as well as the responses to ipsilateral and contralateral facial and supraorbital nerve stimuli. All patients showed involuntary firing of motor unit action potentials (MUAPs) in at least one of the muscles. Synkinetic activation of motor units in the OOris was induced by spontaneous blinking in all patients, and by inhalation and swallowing in some. Electrical stimulation of the ipsilateral facial nerve induced a direct M response in only 4 patients. In contrast, long-latency reflex responses were induced in both muscles by electrical stimulation of ipsilateral and contralateral facial and supraorbital nerves in all patients, at latencies ranging between 44 and 132 ms. The shape of such MUAP reflex responses was the same as that of the MUAPs seen to fire at rest. These findings provide evidence of enhanced excitability of facial motoneurons in our patients. Such hyperexcitability may be partly responsible for the postparalytic motor dysfunction syndrome that occurs after facial palsy with severe axonal damage.     

Blink reflex in patients with hemifacial spasm. Observations during microvascular decompression operations

The blink reflex cannot normally be elicited during surgical anesthesia using inhalation anesthetics. However, in patients with hemifacial spasm (HFS) the early component of the reflex response (R1) can be elicited on the affected side but not on the unaffected side during such anesthesia. The electromyographic (EMG) response from the mentalis muscle to stimulation of the supraorbital nerve was recorded during microvascular decompression (MVD) of the facial nerve to relieve HFS and compared to the response from the same muscle to stimulation of the zygomatic branch of the facial nerve in four patients. During the operation before the facial nerve was decompressed, contractions in both the orbicularis oculi and the mentalis muscles could be elicited by stimulation of the supraorbital nerve (mean latencies 12.2 +/- 1.9 and 12.9 +/- 2.0 ms, respectively). When the facial nerve had been decompressed the blink reflex could no longer be elicited, and there was no response from the mentalis muscle to stimulation of the zygomatic branch of the facial nerve. Compound action potentials (CAP) recorded from the 7th cranial nerve in response to stimulation of the supraorbital nerve had latencies of 7.5 ms +/- 1.4 ms to the negative peak.     

The role of facial nerve conduction studies and electromyography in predicting the outcome of Bell's palsy

Many electrophysiological tests have been used to determine prognosis and extent of recovery in Bell's palsy but the reliability and sensitivity of the different parameters used is still controversial. We performed bilateral percutaneous facial nerve conduction studies, and volitional needle electromyography on 23 patients within 10–14 days post onset of their Bell's palsy. The following parameters were assessed: denervation and recruitment of the frontalis and orbicularis oris muscles, latency of the compound muscle action potential (CMAP), and CMAP amplitude ratio. The patients were re-examined 6 months later and their recovery graded according to the House-Brackman classification. The CMAP amplitude ratio and the recruitment scores of the frontalis and orbicularis oris muscles were the only parameters to reliably predict outcome (p = 0.016, 0.007 and 0.036, respectively). All patients with a CMAP amplitude ratio above 10% had a complete recovery. Since Bell's palsy is probably caused by herpes simplex virus, the active disease process is completed within 10–14 days; therefore, facial nerve conduction studies and electromyography at that time are appropriate to predict prognosis.