Denervation pattern of three mimic muscles in Bell's palsy.

OBJECTIVE: To explore the presence and grade of denervation in three mimic muscles in facial nerve palsy. METHODS: The frontalis, orbicularis oculi (OO), and mentalis muscles were explored in 54 patients with Bell's palsy, after 30 days from the beginning of symptoms. Concentric needle electromyography, including fibrillation detection, was performed in the three muscles on the affected side. Compound muscle action potentials (CMAP) were recorded on both sides and a CMAP ratio was calculated from each muscle. The House-Brackman scale was used to assess the initial clinical evaluation and the follow-up until recovery. RESULTS: Fibrillation was recorded in 32 patients on the 30th day after the onset and was present in 100% of mentalis and in 90% of frontalis, but in only 34% of OO, a statistically significant difference. The grade of fibrillation in OO was also statistically lower from those in the other two muscles. The 32 patients were grouped according to the presence (A) or not (B) of fibrillation in OO. In group A, CMAP ratios (affected/normal side) did not differ significantly among the three muscles. However, in group B they were significantly greater in OO and frontalis than in mentalis. In between-group comparison, group B muscles had significantly higher CMAP ratios, lower degree of fibrillation, and better functional recovery. CONCLUSION: In facial palsy, the presence and grade of fibrillation in OO are lower than in frontalis and mentalis muscles and prognosis is more favorable for the non-fibrillating OO group of patients.     

Prognostic value of minimal excitability of facial nerve in Bell's palsy.

Nerve excitability is useful for prognosis in Bell's palsy. Minimal excitability values (MEV) were obtained by stimulating the facial nerve and recording the effective current (mA) required to evoke a minimal visible contraction of frontalis, orbicularis oculi, orbicularis oris, and mentalis muscles respectively. Serial MEVs were performed on 100 patients with facial palsy, of whom 87 were followed for six months or to complete recovery; 61 patients were treated with steroids of whom 57 had good recovery. Serial MEVs were not only useful for prognosis, but also helpful in regulating the dosage of prednisone.     

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.     

Blink reflexes and lateral spreading in patients with synkinesia after Bell's palsy and in hemifacial spasm

We compared various electrodiagnostical tests in patients with hemifacial spasm and in patients who developed synkinesia after Bell's palsy. We examined the evoked blink reflexes in the orbicularis oculi (o. oculi) and orbicularis oris (o. oris) muscles in 23 patients with hemifacial spasm (HFS), in 10 patients with synkinesia after Bell's palsy (BPS) and in 22 control subjects. In the patient groups, we recorded synkinesia, latency and amplitude of compound muscle action potential (CMAP) in the mental muscle after stimulation of the facial nerve and we examined electromyographic activity of the o. oculi and mental muscles synchronously. Furthermore, we studied the phenomenon of lateral spreading, also known as ephaptic transmission, between the different facial nerve branches. Patients with BPS had a prolonged R1 latency on the affected side in o. oculi and smaller mental CMAP amplitude as an indication of facial nerve damage and nerve fiber loss. This was not found in patients with HFS, who showed an increased amplitude of the R1 and R2 responses in o. oris. Patients with BPS showed only an increased R1 amplitude in o. oris. All patients had signs of synkinesia. Lateral spreading with different patterns was present in all patients with HFS and in half of the patients with BPS. Latencies of early and late responses showed no differences between HFS and BPS. In addition to alterations in facial nucleus excitability in both conditions, ectopic re-excitation of facial nerve axons in HFS may explain the differences in neurophysiological findings between HFS and BPS patients. A loss of control following synaptic stripping may also be a contributing factor.     

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.     

A new method for measuring compound muscle action potentials in facial palsy: a preliminary study

To establish a simple, reproducible procedure for studying facial motor nerve conduction (MNC), we determined the optimal electrode position to record evoked compound muscle action potentials (CMAPs) from perioral muscles in normal subjects. We examined three new electrode positions in which the electrode connected to the one input of the amplifier was placed on the mental protuberance, and the one connected to the other input was placed on the skin over the orbicularis oris muscle (the philtrum, mouth angle, or lower lip). We then compared the morphology and amplitudes of the CMAPs, right-left differences, and the reproducibility of CMAP amplitudes with recordings taken from the standard electrode position in which one electrode was placed on the nasolabial fold closely lateral to the ala nasi, and the other was placed on the skin over the orbicularis oris. Percutaneous supramaximal electrical stimulation was applied to the main trunk of the facial nerve. All three of the new recording positions showed greater amplitudes and more obvious biphasic CMAPs than the standard method. Positioning the electrode connected to the negative input on the philtrum was optimal in terms of right-left differences and the reproducibility of CMAP amplitudes. Therefore, this midline recording is a simple, reproducible method for calculating the CMAP amplitude ratio. However, prior to clinical use of this procedure, analyses of patients with facial palsy are required.     

Quantitative ultrasonography of facial muscles in patients with chronic facial palsy

Introduction: In this study we introduce quantitative facial muscle ultrasound as a diagnostic tool for patients with chronic unilateral facial palsy. Methods: Muscle area, thickness, and echo intensity of 6 facial muscles (frontalis, orbicularis oculi, orbicularis oris, depressor anguli oris, depressor labii inferioris, and mentalis) and of 2 chewing muscles (temporalis and masseter, as controls) were measured in 20 patients with chronic facial palsy. Results: Aside from 1, all facial muscles were significantly smaller on the paralyzed side. With exception of frontalis and orbicularis oculi muscles, all other facial muscles showed significantly higher echo intensity on the affected side. Muscle size and echo intensity of the chewing muscles showed no side‐to‐side asymmetry. Conclusions: Quantitative ultrasound of facial muscles helps to better characterize their status in patients with chronic facial palsy in the phase of denervation and during regeneration. Muscle Nerve 50 : 358–365, 2014     

Prognosis and course of Bell's palsy

Summary The clinical picture of ischemic palsy of the facial nerve was analyzed by symptoms in 87 patients. The level of the lesion of the facial nerve in the channel was determined by topesthesia. Mutagenic disorder usually causes incomplete or defective recovery. The speed of development of palsy does not affect its course. Retroaural pain has little significance in the prognosis of palsy. Recorvery may be defective even in cases where no pain is present. If the nasopalpebral reflex is absent and Bell's phenomenon is positive in the 3rd week the prognosis is infavourable. In half the patients no precipitating or etiological factor was found.Clinical appraisal was made in five muscles (M. frontalis, M. orbicularis oculi et oris, M. zygomaticus, M. depressor labii inferioris). The patients were divided into three groups according to the degree of their recovery: complete, incomplete and defective recovery. Recovery was defective in elderly patients with vascular hypertension. Voluntary activity in Group 1 (complete recovery) is symmetrical by the 1st–2nd month and in Group 2 (incomplete recovery) by the 5th–7th month; in Group 3 it is permanently insufficient.     

Electrophysiologic findings and prognosis in Bell's palsy

Electrophysiologic investigations were carried out on 45 patients with Bell's palsy at periodic intervals after the onset of paralysis. It was found that there was a good correlation between prognosis in Bell's palsy and the amplitude of evoked motor response obtained after six or more days of clinical paresis. When the average amplitude of evoked motor response was within normal limits (i.e., 504μV or greater), complete recovery with no residual deficits took place two to six weeks after the onset of facial palsy. When the evoked motor response was absent in all three major branches of the facial nerve, indicating complete nerve degeneration, electromyographic signs of recovery were apparent by the third or fourth month after the onset of paralysis. In these cases, recovery was relatively slow and incomplete, with some degree of residual deficit and synkinesis. Maximal return of voluntary facial movement was established 8 to 12 months after the initial symptom. When the mean amplitude of evoked motor response was below the lower limit of normal (i.e., less than 504μV), electromyographic signs of recovery were noted within 1 to 3 months, depending on the amplitude values. The final outcome of this intermediate group was similar, but not identical, to that of the previous group. The prognosis of facial paralysis in Bell's palsy was thus found to be directly related to the mean amplitude of evoked motor response, regardless of the extent of clinical paralysis.     

神经肌电图对特发性面瘫治疗及预后评估的研究

目的探讨神经肌电图(神经电图electroneurography,ENG和肌电图electromyography,EMG)在特发性面瘫治疗及预后评估中的价值。方法采用丹麦生产的keypointⅣ肌电图仪对96例确诊为特发性面瘫的患者进行患侧与健侧ENG、EMG检测,分别记录患侧面神经颞支、颧支、颊支的运动传导潜伏期、波幅以及所支配的额肌、眼轮匝肌、口轮匝肌的肌电图情况,并与自身健侧作对比。结果特发性面瘫患者患侧面神经运动传导潜伏期延长、M波波幅降低,与自身健侧相比,差异有统计学意义(P<0.05)。波幅下降<70%、NCV(神经传导速度)减慢<20%、EMG大致正常的轻度患者,3个月内面肌完全恢复,治愈率100%;波幅下降70%～90%、NCV减慢20%～50%、EMG呈部分神经源性损害的中度患者,3个月内大部分可完全恢复,治愈率87.8%;波幅下降>90%、NCV减慢>50%、EMG呈部分或完全神经源性损害的中重度患者,3个月内面肌完全恢复者为50%;诱发电位消失、NCV引不出、EMG呈完全神经源性损害的重度患者,3个月内面肌完全恢复者为25%。结论 ENG和EMG检测对特发性面瘫的神经损伤、面肌恢复等预后评估有重要价值,能对临床治疗提供客观依据。     

Orbicularis oculi-Reflexe und Summenpotentiale des Orbicularis oris bei idiopathischer Facialislähmung

In 84 patients with idiopathic, clinically complete Bell's palsy the electrically induced blink reflexes with their two components (OOR I and II) were electromyographically recorded on both sides using skin electrodes. In 67 of these patients the evoked responses of the orbicularis oris muscle were also studied. The latencies and amplitudes were measured and related to the clinical outcome of the facial paralysis. The patients were divided into two groups, one with good recovery of the palsy (46 patients), the other with significant residual paresis and/or strong associated movements of the facial musculature (38 patients). In the group with good recovery the following results were obtained: 1. the OOR I remained elicitable or reappeated during the first 12 days after the onset of palsy; 2. the OOR II began to rise during the first 10 days of palsy; 3. the amplitude of the orbicularis oris response did not decrease to below 10%. In the group with poor recovery: 1. both components of the OOR were absent or diminished to below 4% for more than 12 days after the onset of palsy; 2. the latency difference of the OOR I exceeded 8 msec; 3. the amplitude of the orbicularis oris responses decreased to below 10%. Using these criteria it appears to be possible in about 85% of patients to make a prognosis between the 3rd to 5th and the 10th to 12th day after the onset of Bell's palsy.     

Estimation of facial central motor delay by electrical stimulation of the motor cortex of the dog.

Central delay time (CD) has been estimated for activation of limb muscles by electrical or transcranial magnetic coil (TMC) stimulation of motor cortex and ventral root outflow. In the present study, we used surface electrical stimulation of the motor cortex of the right hemisphere to produce evoked compound muscle action potentials (CMAP) from the contralateral orbicularis oris (o.r.), and orbicularis oculi (o.c.), in dogs. Monopolar electrical stimulation of the facial nerve at the cerebello-pontine (CP) angle yielded CMAP activation of ipsilateral facial muscles. These latencies when subtracted from those obtained by direct cortical stimulation established CD for activation of the seventh cranial nerve. Preliminary data with single pulse magnetic stimulation at high outputs (greater than 80%) revealed CMAP with onset latencies similar to the direct facial nerve stimulation at the CP angle by electrical means.     

Evaluation of proximal facial nerve conduction by transcranial magnetic stimulation.

A magnetic stimulator was used for direct transcutaneous stimulation of the intracranial portion of the facial nerve in 15 normal subjects and in patients with Bell's palsy, demyelinating neuropathy, traumatic facial palsy and pontine glioma. Compound muscle action potentials (CMAPs) thus elicited in the orbicularis oris muscle of controls were of similar amplitude but longer latency (1.3 SD 0.15 ms) compared with CMAPs produced by conventional electrical stimulation at the stylomastoid foramen. No response to magnetic stimulation could be recorded from the affected side in 15 of 16 patients with Bell's palsy. Serial studies in two patients demonstrated that the facial nerve remained inexcitable by magnetic stimulation despite marked improvement in clinical function. In the patient with a pontine glioma, the CMAP elicited by transcranial magnetic stimulation was of low amplitude but normal latency. In six of seven patients with demyelinating neuropathy, the response to intracranial magnetic stimulation was significantly delayed. Magnetic stimulation produced no response in either patient with traumatic facial palsy. Although the precise site of facial nerve stimulation is uncertain, evidence points to the labyrinthine segment of the facial canal as the most likely location.     

Investigation of facial motor pathways by electrical and magnetic stimulation: sites and mechanisms of excitation.

A refined technique is described for non invasive examination of the facial motor pathways by stimulation of the extra- and intracranial segment of the facial nerve and the facial motor cortex. Surface recordings from the nasalis muscle rather than from the orbicularis oris muscle were used, since the compound muscle action potential (CMAP) from this muscle showed a more clearly defined onset. Electrical extracranial stimulation of the facial nerve at the stylomastoid fossa in 14 healthy subjects yielded a mean distal motor latency of 3.7 ms (SD 0.46), comparable with reported latencies to the orbicularis oris muscle. Using a magnetic stimulator, transcranial stimulation of the facial nerve was performed. The mechanism of transcranial magnetic facial nerve stimulation was studied using recordings on 12 patients who had facial nerve lesions at different locations, and with intraoperative direct measurements in four patients undergoing posterior fossa surgery. The actual site of stimulation could be localised to the proximal part of the facial canal, and a mean "transosseal conduction time" of 1.2 ms (SD 0.18) was calculated. The cerebrospinal fluid (CSF) played an important role in mediating the magnetically induced stimulating currents. Finally, with transcranial magnetic stimulation of the facial motor cortex, clearly discernible CMAPs could be produced when voluntary activation of several facial muscles was used to facilitate the responses. From this, a central motor conduction time of 5.1 ms was calculated (SD 0.60, 6 subjects).     

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)     

Quantitative ultrasonography of facial muscles

Introduction: There is no standardized method for examination of facial muscles with ultrasound. The purpose of this study was to identify those facial muscles accessible for reliable identification and to provide reference data. Methods: In healthy subjects all facial muscles were screened for visibility, separation from adjacent muscles, and reliability of landmarks. Bilateral scans of reliable muscles were performed in 40 adult volunteers. Results: Six facial muscles were clearly demarcated with ultrasound. These were: frontalis, orbicularis oculi, orbicularis oris, depressor anguli oris, depressor labii inferioris, and mentalis muscles. Cross-sectional area and muscle thickness showed gender differences and were independently related to age for some muscles. A significant left–right side difference was only seen for the orbicularis oculi muscle in women. Conclusions: These data demonstrate the usefulness of ultrasonography to assess facial muscles and provide reference values that can be applied in the clinical setting. Muscle Nerve 47: 878–883, 2013     

Latenzmessungen am N. facialis beim Acusticusneurinom

Zusammenfassung Es wurden bei 28 Untersuchten mit operativ gesichertem einseitigen AN unter röntgenologischer Kontrolle Latenzen am N. facialis gemessen und die Ergebnisse mit den Meßwerten der nicht befallenen Gesichtsseite und mit denen einer Population Gesunder verglichen. Bei 9 Patienten mit AN war das Elektromyogramm negativ, die Latenz nicht verlängert. Bei 19 Patienten mit AN, von denen 8 eine Facialisparese, 11 eine klinisch intakte Gesichtsinnervation aufwiesen, konnte neben dem EMG (17mal positiv) eine signifikante Latenzdifferenz der Tumorseite gegenüber der nicht befallenen Seite und den Latenzen 20 gesunder Versuchspersonen für den M. orbicularis oris von 1,57 msec und für den M. frontalis von 1,52 msec festgestellt werden. Ein signifikanter Unterschied zwischen Patienten mit und ohne klinisch manifeste Facialisparese ergab sich nicht. Eine Latenz von 5,64 msec und länger ist unter Berücksichtigung der angegebenen Methode als pathologisch anzusehen. Auch bei zwei Patienten mit AN ohne elektromyographische Denervierung in der mimischen Muskulatur war die Facialislatenz auf der Tumorseite verlängert; es handelt sich dabei offenbar um eine Zeitfrage.Als Ursache der Latenzverlängerung beim AN wird eine tumorbedingte Markscheiden- und/oder Axonläsion im Porus acusticus internus mit distaler Schädigung angenommen. Mit der vergleichenden Latenzmessung am N. facialis kann eine klinisch latente Facialisparese festgestellt werden. Die Methode eignet sich deshalb neben dem EMG in der Frühdiagnose des AN. Sie war bei unserem Krankengut in 69% der Patienten mit AN positiv.

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Latency measurements of the facial nerve in acoustic neurinomas

Summary The latency of the facial nerve was determined under radiological control in a group of 28 patients with a unilateral acoustic neurinoma. The results are compared with those of the unaffected side and of a group of normal controls. In 9 out of 28 patients with acoustic neurinoma the latency of the facial nerve fell within the normal range. There was no denervation as verified by electromyography. The other 19 patients (8 with and 11 without facial palsy) yielded a significantly prolonged latency of the tumor-bearing side. There was no significant difference in latency between the 8 patients with facial palsy and those without. 17 of the 19 patients showed electromyographical signs of denervation of facial muscles. Mean normal latencies of the M. orbicularis oris and the M. frontalis were 1,57 and 1,52 msec, respectively. By this method a latency of more than 5,64 msec indicates a pathological process of the facial nerve. — Two additional patients without electromyographical signs of denervation also exhibited a prolonged latency. It is assumed that the prolonged latency of the facial nerve due to an acoustic neurinoma is caused by damage to the myelin sheath or the axon. Measuring the facial latency may serve to uncover a clinically inapparent facial palsy. This method together with the EMG which showed positive results in 69% of our patients, may be of aid in the early diagnosis of acoustic neurinomas.

     

Uncrossed cortico-muscular projections in humans are abundant to facial muscles of the upper and lower face,but may differ between sexes

It is a popular concept in clinical neurology that muscles of the lower face receive predominantly crossed cortico-bulbar motor input, whereas muscles of the upper face receive additional ipsilateral, uncrossed input. To test this notion, we used focal transcranial magnetic brain stimulation to quantify crossed and uncrossed cortico-muscular projections to 6 different facial muscles (right and left Mm. frontalis, nasalis, and orbicularis oris) in 36 healthy right-handed volunteers (15 men, 21 women, mean age 25 years). Uncrossed input was present in 78% to 92% of the 6 examined muscles. The mean uncrossed: crossed response amplitude ratios were 0.74/0.65 in right/left frontalis, 0.73/0.59 in nasalis, and 0.54/0.71 in orbicularis oris; ANOVA p>0.05). Judged by the sizes of motor evoked potentials, the cortical representation of the 3 muscles was similar. The amount of uncrossed projections was different between men and women, since men had stronger left-to-left projections and women stronger right-to-right projections. We conclude that the amount of uncrossed pyramidal projections is not different for muscles of the upper from those of the lower face. The clinical observation that frontal muscles are often spared in central facial palsies must, therefore, be explained differently. Moreover, gender specific lateralization phenomena may not only be present for higher level behavioural functions, but may also affect simple systems on a lower level of motor hierarchy.     

Trigemino-facial reflex inhibitory responses in some lower facial muscles

The effects of electrical trigeminal stimulation on activated facial muscles were studied in 20 normal subjects in order to evaluate whether excitatory or inhibitory responses are present and to investigate whether the reflex organization is similar in all the facial muscles. No inhibition was observed in frontalis, orbicularis oculi, orbicularis oris, and mentalis muscles. By contrast, a clear suppression of electromyographic (EMG) activity (late silent period or SP2) was present in the levator labii superioris, depressor anguli oris, and depressor labii inferioris muscles, with a mean latency ranging from 41.8 to 50.2 ms, and a mean duration ranging from 27.5 to 40.9 ms. An early suppression of EMG activity (early silent period or SP1) was observed, with a latency of 16 to 20 ms and a duration of 10 ms, mainly in inferior perioral muscles. Our findings show a selective trigeminal inhibitory influence upon some specific lower facial muscles.     

Electrophysiological study of ephaptic axono-axonal responses in hemifacial spasm

One of the classic features of hemifacial spasm (HFS) is spread of the blink reflex responses to muscles other than the orbicularis oculi. The pathophysiological mechanisms underlying the generation of such abnormal responses include lateral spread of activity between neighboring fibers of the facial nerve and hyperexcitability of facial motoneurons. In this report we present evidence for another mechanism that can contribute to the generation of responses in lower facial muscles resembling the R1 response of the blink reflex. In 13 HFS patients, we studied the responses induced in orbicularis oris by electrical stimuli applied at various sites between the supraorbital and zygomatic areas. We identified responses with two different components: an early and very stable component, with an onset latency ranging from 10.5 to 14.8 ms, and a more irregular longer-latency component. Displacement of the stimulation site away from the supraorbital nerve and towards the extracranial origin of the facial nerve caused a progressive shortening of response latency. These features indicate that, in our patients, the shortest latency component of the orbicularis oris response was likely generated by antidromic conduction in facial nerve motor axons followed by axono-axonal activation of the fibers innervating the lower facial muscles. Our results suggest that motor axono-axonal responses are generated by stimulation of facial nerve terminals in HFS.