Facial Motonucleus Research Articles

Treatment with botulinum toxin improves the hyperexcitability of the facial motoneuron in patients with hemifacial spasm

Botulinum toxin type A (BTX) injection into the orbicularis oculi muscle is an effective treatment for patients with hemifacial spasm (HFS). The objectives of this study were to investigate the effect of this treatment on HFS, in particular the associated hyperexcitability of the facial motor nucleus, and to discuss the potential mechanism of HFS. F waves in the mentalis muscle were examined before, 2 and 6 weeks after the BTX treatment of only the orbicularis oculi muscle in ten patients with HFS. F/M ratio, duration of F waves and frequency of F waves decreased significantly after the BTX treatment compared with those before the BTX treatment. These findings demonstrate that the excitability of the facial motonucleus decreases after BTX treatment of the orbicularis oculi muscle. From these results, we hypothesize that the trigeminal afferent input and the cortical control contribute to the hyperexcitability of the facial motor nucleus in patients with HFS. This warrants further investigation into the pathophysiology of HFS.

Anatomie fonctionnelle du nerf facial

Embryologic individualization of the facial nerve primordium occurs early and emphasizes trigeminofacial connections and variations in the transitional zone (TZ). In the brainstem, the specific nuclei of the facial nerve are located within five columns corresponding to the main functions. Three-quarters of the fibers are of the special visceral efferent group (SVE). Central connections of the facial motonucleus are numerous, particularly with the trigeminal complex but also the cochlear nerves. Only endoneurium surrounds facial nerve fibers in the cerebellopontine angle; central nervous system tissue offers a small extracellular space, lacking collagen and funicular plexus, without epiperineurium: nerve fibers are therefore more susceptible to injury. The segment of a nerve that reveals both CNS and PNS components is referred to as the transition zone. It should be regarded as a "locus minor resistae" because of poor vascularization and CNS myelin deficiency. The acousticofacial reflex is often absent in patients with hemifacial spasm. Early (R1) and late (R2) responses of the trigeminofacial reflex (blink reflex) in patients with hemifacial spasm are of major interest in understanding both peripheral and central mechanisms.

Anoxic persistence of lumbar respiratory bursts and block of lumbar locomotion in newborn rat brainstem–spinal cords

The tolerance of breathing in neonates to oxygen depletion is reflected by persistence of inspiratory-related motor output during sustained anoxia in newborn rat brainstem preparations. It is not known whether lumbar motor networks innervating expiratory abdominal muscles are, in contrast, inhibited by anoxia similar to locomotor networks in neonatal mouse lumbar cords. To test this, we recorded inspiratory-related cervical/hypoglossal plus pre/postinspiratory lumbar/facial nerve activities and, sometimes simultaneously, locomotor rhythms in newborn rat brainstem-spinal cords. Chemical anoxia slowed 1 : 1-coupled cervical and lumbar respiratory rhythms and induced cervical burst doublets associated with depressed preinspiratory and augmented postinspiratory lumbar activities. Similarly, anoxia evoked repetitive hypoglossal bursts and shifted facial activity toward augmented postinspiratory bursting in medullas without spinal cord. Selective lumbar anoxia augmented pre/postinspiratory lumbar bursting without slowing the rhythm. This suggests a medullary origin of both anoxic inspiratory double bursts and preinspiratory depression, but a mixed medullary/lumbar origin of boosted postinspiratory lumbar activity. Lumbar respiratory rhythm is likely to be generated by the parafacial respiratory group expiratory centre as indicated by lack of normoxic and anoxic bursting following brainstem transection between the facial motonucleus and the more caudal pre-Bötzinger complex inspiratory centre. Opposed to sustained respiratory activities, anoxia reversibly abolished non-rhythmic spinal discharges and electrically or chemically evoked lumbar locomotor activities, followed by pronounced postanoxic spinal hyperexcitability. We hypothesize that (i) the anoxia tolerance of neonatal breathing includes pFRG-driven lumbar expiratory networks, (ii) the anoxic respiratory pattern transformation is due to disturbed inspiratory-expiratory centre interactions, and (iii) postanoxic lumbar hyperexcitability contributes to spasticity in cerebral palsy.

Dependence on extracellular Ca2+/K+ antagonism of inspiratory centre rhythms in slices and en bloc preparations of newborn rat brainstem

The pre-Bötzinger Complex (preBötC) inspiratory centre remains active in isolated brainstem-spinal cords and brainstem slices. The extent to which findings in these models depend on their dimensions or superfusate [K(+)] and [Ca(2+)] (both of which determine neuronal excitability) is not clear. We report here that inspiratory-related rhythms in newborn rat slices and brainstem-spinal cords with defined boundaries were basically similar in physiological Ca(2+) (1.2 mm) and K(+) (3 mm). Hypoglossal nerve rhythm was 1 : 1-coupled to preBötC activity in slices and to cervical nerve bursts in en bloc preparations lacking the facial motonucleus (VII). Hypoglossal rhythm was depressed in brainstems containing (portions of) VII, while pre/postinspiratory lumbar nerve bursting was present only in preparations with > 79% VII. preBötC-related slice rhythms were inhibited in 1.5 mm Ca(2+) solution, whereas their longevity and burst rate were substantially augmented in 1 mm Ca(2+). Ca(2+) depression of slice rhythms was antagonized by raising superfusate K(+) to 8-10 mm. This strong extracellular Ca(2+)/K(+) antagonism of inspiratory (motor) rhythms was also revealed in brainstem-spinal cords without VII, while the inhibition was progressively attenuated with increasing amount of rostral tissue. We hypothesize that depression of hypoglossal rhythm and decreased Ca(2+) sensitivity of preBötC rhythm are probably not related to an increased content of rostral respiratory structures, but rather to larger brainstem dimensions resulting in interstitial gradients for neuromodulator(s) and K(+), respectively. We discuss whether block of pre/postinspiratory activity in preparations with < 79% VII is due to impairment of the pathway from preinspiratory interneurons to abdominal muscles.

High Sensitivity to Neuromodulator-Activated Signaling Pathways at Physiological [K+] of Confocally Imaged Respiratory Center Neurons in On-Line-Calibrated Newborn Rat Brainstem Slices

The pre-Bötzinger complex (PBC) inspiratory center remains active in a transverse brainstem slice. Such slices are studied at high (8-10 mM) superfusate [K+], which could attenuate the sensitivity of the PBC to neuromodulators such as opiates. Findings may also be confounded because slice boundaries, drug injection sites, or location of rhythmogenic interneurons are rarely verified histologically. Thus, we first generated PBC slices with defined boundaries using novel "on-line histology" based on our finding that rostrocaudal extensions of brainstem respiratory marker nuclei are constant in newborn rats between postnatal days 0-4. At physiological superfusate [K+] (3 mM), 500- and 600-microm-thick slices with the PBC in the center and the caudal boundary 0.70 and 0.76 mm caudal to the facial motonucleus generated rhythm for >2 and approximately 4 h, respectively. Rhythm was abolished by low nanomolar concentrations of the mu-opiate receptor agonist DAMGO ([D-Ala2, N-Me-Phe4, Gly5-ol]enkephalin). After spontaneous arrest of bursting, rhythm was reactivated at clinically relevant or physiological concentrations by 3,5-dihydroxyphenylglycine, thyrotropin-releasing hormone, or rolipram, each affecting distinct second-messenger pathways. Two-photon/confocal Ca2+ imaging revealed that these agents reactivated the same PBC neurons initially active in 3 mM [K+]. The data show that "calibrated" PBC slices at physiological [K+] generate rhythm with a high sensitivity to neuromodulators for extended time periods, whereas spontaneous "in vitro apnea" is an important tool to study the interaction of signaling pathways that modulate rhythm. Our approaches and findings provide the basis for a pharmacological and structure-function analysis of the isolated respiratory center in a histologically well defined substrate at physiological [K+].

F-waves and facilitated late responses of the mentalis muscle in patients with a cerebrovascular accident

F-waves in the extremities result from the backfiring of antidromically activated anterior horn cells and F-waves of the mentalis muscle can be also elicited after stimulation of the marginal mandibular branch of the facial nerve. In order to investigate the influence of the descending pathway of the excitability of the facial motonucleus, the F-wave of the mentalis muscle and the facilitated late response, which follows F-waves and which seems to be the snout reflex due to their similar latency and habituation, were studied in 11 conscious patients with a hemispheric cerebrovascular accident (CVA) presenting with hemiparesis, and in 10 unconscious patients with CVA or head injury. The duration and the persistence of the F-waves increased significantly statistically on the normal side in the CVA patients compared with those of the palsy side and the normal subjects. In comatose patients the F-waves and the facilitated late response were not elicited. The latency (46.1 ± 13.3 msec) of the facilitated late responses in the unconscious patients tended to increase compared with the latency (36.6 ±4.3 msec) in the conscious patients. These findings suggest that the hyperexcitability of the facial motoneuron is ipsilateral to any hemispheric lesion; the hemispheric lesion exerts a bilateral excitatory influence on the interneuron of the facilitated late response: and that the reticular formation may influence the facial motoneuron and any interneurons concerned in the facilitated late response. F-waves and facilitated late responses should be further examined as neurophysiologically useful diagnostic methods [Neurol Res 2000; 22: 576-582]

Effect of repetitive stimulation on lateral spreads and F-waves in hemifacial spasm

The lateral spread (LS) response, which can be elicited in muscles innervated by other branches of the facial nerve, is electromyographycally specific for patients with hemifacial spasm (HFS), occurring about 10 ms after stimulus. The F-wave in facial muscles, which is a late response that antidromicaly propagates to the facial motonucleus and returns orthodromicaly down the same axon, revealed a trend toward enhancement in patients with HFS. The LSs were facilitated by repetitive stimulation during the microvascular decompression (MVD) operation, which has proved to be a successful treatment, and the F-waves were also facilitated by repetitive stimulation on the spasm side more than on the normal side. Greater facilitation of these responses was in direct proportion to higher stimulation rates and greater numbers of stimulations. The repetitive stimulation of the facial nerve may result in activation of the motoneuron pool and in the lowering of the threshold of somatic membranes. These results support the hypothesis that hemifacial spasm is caused by hyperexcitability of the facial motonucleus, which is increased by antidromic repetitive stimulation.

Abnormal muscle response (lateral spread) and F-wave in patients with hemifacial spasm

In patients with hemifacial spasm (HFS) the spasm is due to cross compression of the facial nerve by a blood vessel and microvascular decompression (MVD) has proved to be a successful treatment. Abnormal muscle response (AMR), which can be elicited by one facial nerve branch stimulation in muscles innervated by other branches of the facial nerve, is specific for patients with HFS, and the AMR consists of a constant response occurring about 10 ms after stimulus and an afterdischarge with long duration (variable response, autoexcitation). The F-wave in facial muscles is a small recurrent discharge that antidromically propagates to the facial motonucleus and returns orthodromically down the same axon. We measured the AMRs and F-waves of facial muscles in HFS patients in order to investigate the relationship of both potentials and the origin of the AMRs. We obtained facial nerve evoked electromyograms from 10 HFS patients. The afterdischarges of the AMRs and the enhanced F-waves were always elicited at the same time by marginal mandibular branch stimulation of the facial nerve. There was a linear correlation between the duration of these two potentials in each case. Between the duration of the afterdischarge of the AMRs elicited in the mentalis muscles by the zygomatic branch stimulation of the facial nerve and that of the F-waves in the mentalis muscles, there was also a linear correlation in 10 cases. These results suggest that the F-wave and the afterdischarge have the same origin and that the AMR is an exaggerated F-wave.

F-wave in patients with hemifacial spasm: Observations during microvascular decompression operations

In patients with hemifacial spasm (HFS), the spasm is due to cross compression of the facial nerve by a blood vessel. There are currently two hypotheses how the cross compression can cause HFS: 1. the spasm is caused by ephaptic transmission and hyperexcitability at the site of compression; and 2. the spasm is caused by hyperexcitability in the facial motonucleus. In peripheral nerves, F-waves, which result from the backfiring of antidromically activated anterior horn cells, have been proposed as indices of anterior horn cell excitability. Enhancement of the F-waves in facial muscles also indicates increased excitability of the facial motonucleus. On the other hand, abnormal muscle response (AMR), which can be elicited by stimulating one branch of the facial nerve and recording electromyographically from muscles innervated by other branches of the facial nerve, is specific for patients with HFS. We have therefore measured the AMRs and the F-waves in the facial muscle of HFS patients under anesthesia in order to investigate the excitability of the facial motonucleus. We obtained facial nerve evoked electromyograms from 14 HFS patients during microvascular decompression (MVD) operation. The F-waves, obtained with surface electrodes from the mentalis muscle, were defined as the second response after the M-wave. The F-waves in facial muscles cannot usually be elicited during surgical anesthesia using inhalation anesthetics. However, the F-waves were elicited on the spasm side in 10 out of 14 patients with HFS and the F-waves disappeared after MVD under anesthesia, as the early responses (R1) of the blink reflex were elicited on the spasm side before MVD under anesthesia. The F-waves elicited during anesthesia were suppressed significantly, compared with those before MVD. These results suggest that excitability in facial motonucleus increased on the spasm side.

Electrophysiological investigation of hemifacial spasm: F-waves of the facial muscles.

In patients with hemifacial spasm (HFS), the spasm is due to cross-compression of the facial nerve by a blood vessel. There are currently two hypotheses for the mechanism of HFS: 1) the spasm is caused by ephaptic transmission and an increase in excitability at the site of compression; and 2) the spasm is caused by hyperexcitability in the facial nerve nucleus. In peripheral nerves, F-waves, which result from the backfiring of antidromically activated anterior horn cells, have been proposed as indices of proximal motoneuron conduction and anterior horn cell excitability. Enhancement of the F-waves indicates increased anterior horn cell excitability. We have therefore measured F-waves in the facial muscle of HFS patients in order to investigate the excitability of the facial nerve nucleus. The authors obtained facial nerve evoked responses from 20 HFS patients before microvascular decompression (MVD), 10 HFS patients after MVD and 10 healthy controls. The F-waves, obtained with surface electrodes from the mentalis muscle, were the second response after the M-wave. On the patient's spasm side, the F-wave duration, F/M amplitude ratio and frequency of F-wave appearance significantly increased compared with those of the normal side or healthy controls; minimum latency and chronodispersion did not significantly differ between these groups. In patients whose spasm disappeared completely following MVD, the abnormal muscle response (lateral spread), which is a characteristic sign of HFS, and the enhancement of the F-wave eventually also disappeared. Because of the correlation between HFS and F-waves, the authors' study supports the hypothesis that the cause of HFS is hyperexcitability of the facial motonucleus.

Recordings from the facial motonucleus in rats with signs of hemifacial spasm

We recorded evoked potentials from the facial motonucleus of rats in response to electrical stimulation of the temporal branch of the facial nerve in which chronic irritation from a blood vessel had caused the development of an abnormal muscle response. The abnormal muscle response that can be recorded from face muscles that are innervated by one branch of the facial nerve in response to electrical stimulation of a different branch is regarded to be a sign of hemifacial spasm. In the recordings from the motonucleus in rats that showed such an abnormal muscle response (model rats) there was a late component at a latency of about 5 msec, in addition to the early component with a latency of 1.5-2.5 msec that is also observed in normal rats. The latency of the electromyographic potentials recorded from the mentalis-orbicularis oris muscles in response to stimulation of the facial motonucleus was about 2 msec. The latency of the abnormal muscle response obtained from the mentalis muscle in the model rats was about 7 msec. This value is close to the sum of the conduction time from the motonucleus to the mentalis muscle (2 msec) and the latency of the late response from the motonucleus (5 msec). Similar results were obtained in rats in which the facial nerve had been chronically stimulated electrically and which had developed an abnormal muscle response. The results of this study further support the hypothesis that the hyperactivity of the facial motonucleus is the pathophysiology of hemifacial spasm.

Facial nerve demyelination and vascular compression are both needed to induce facial hyperactivity: a study in rats.

It is generally assumed that hemifacial spasm (HFS) is caused by vascular compression of the facial nerve at the root exit zone (REZ), but the mechanism for the development of HFS is not known. Evidence has been previously presented that the signs of HFS are caused by hyperactivity of the facial motonucleus that is caused by the irritation to the facial nerve from the vascular contact. This assumption has been supported by the finding that daily electrical stimulation of the facial nerve in the rat facilitates the development of an abnormal muscle response that is a characteristic sign of HFS in man and is an indication of an abnormal cross-transmission that makes it possible to elicit a contraction of muscles innervated by one branch of the facial nerve by electrically stimulating another branch of the facial nerve. In the present study we show that close contact between a peripheral branch of the facial nerve and an artery also facilitates the development of an abnormal muscle response, but only if the facial nerve has previously been slightly injured (by a chromic suture) at the location of the arterial contact. We also show that blocking neural conduction in the facial nerve proximal to the artificial vascular compression abolishes the abnormal muscle contraction, which supports the assumption that the anatomical location of cross-transmission that is causing the abnormal muscle response is central to the vascular compression, most likely in the facial motonucleus. These findings may explain why the facial nerve is only susceptible to vascular compression near its REZ, where an injury to its myelin is more likely to occur than where the nerve is covered with schwann cell myelin.

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.

The cranial nerve vascular compression syndrome: II. A review of pathophysiology

The various hypotheses regarding the pathophysiologies of trigeminal neuralgia and hemifacial spasm are reviewed, and the results of recent physiological studies on the pathogenesis of hemifacial spasm are discussed. Evidence is presented that strongly supports the hypothesis that the symptoms and signs of hemifacial spasm are caused by hyperactivity in the facial motonucleus. Some of the contradictions regarding the prevalence of vascular conflicts in the cerebellopontine angle and the symptoms of vascular compression are discussed, and a hypothesis is presented that assumes that a suitable substrate must be present, in addition to vascular compression of the respective cranial nerve root, for the symptoms and signs of a cranial nerve vascular compression disorder to develop. Finally, it is discussed how this hypothesis can explain some of the differences between the disorders that can be cured by microvascular decompression of respective cranial nerves.

Interaction between the blink reflex and the abnormal muscle response in patients with hemifacial spasm: Results of intraoperative recordings

Patients with hemifacial spasm (HFS) have an abnormal muscle response (AMR) that can be elicited by stimulating one branch of the facial nerve and recording electromyographically from muscles innervated by other branches of the facial nerve. In addition, the R1 component of the blink reflex can be elicited from the affected side in patients with HFS who are undergoing microvascular decompression (MVD) operations under inhalation anesthesia. A synkinetic component of the blink reflex response that corresponds to the R1 component can be recorded from the mentalis muscle. In the present study we show that the blink reflex elicited by electrical stimulation of the supraorbital nerve can suppress the AMR elicited by electrical stimulation of the temporal branch of the facial nerve in patients with HFS when the interval between stimulation of the supraorbital nerve and stimulation of the temporal branch of the facial nerve (interstimulus interval, ISI) is such that the blink reflex response would appear later than the AMR if they had been elicited independently. Within a short range of ISIs the two responses suppress each other either partially or totally. We find evidence that the suppression of the AMR is the result of an interaction in the facial motonucleus. We believe that the results of the present study support the hypothesis that the facial motonucleus is hyperactive in patients with HFS, and we suggest that the AMR is a result of backfiring from the facial motonucleus and that it may thus be an exaggerated F-response.

Recordings from the facial nucleus in the rat: signs of abnormal facial muscle response

On the basis of results of electrophysiological studies in patients undergoing microvascular decompression (MVD) operations to relieve hemifacial spasm (HFS), we have postulated that the abnormal muscle response characteristically found in patients with HFS is the result of irritation of the facial nerve by the blood vessel that is compressing the facial nerve near its exit from the brainstem in these patients. This abnormal muscle response is seen when one branch of the facial nerve is electrically stimulated and recordings are made from muscles that are innervated by other branches of the facial nerve. We further hypothesized that the facial nucleus is hyperactive in patients with HFS and that the spasm and the abnormal muscle response are results of a phenomenon known as "kindling". These hypotheses are supported by recent studies showing that chronic electrical stimulation of the facial nerve trunk in rats near the brainstem results in an abnormal muscle response that is similar to that seen in patients with HFS. In this paper, we present the results of recording from the facial motonucleus in rats that had been subjected to repeated electrical stimulation of the facial nerve. The results indicate that the abnormal muscle response in these rats was caused by changes in the function of the facial motonucleus. We interpret these results as showing that the physiological abnormalities that give rise to the signs of HFS in man are located in the facial motonucleus, and that the changes in the function of the nucleus are produced by chronic antidromic neutral activity resulting from close contact between a blood vessel and the facial nerve.

Hemifacial spasm: results of electrophysiologic recording during microvascular decompression operations.

Electrophysiologic recordings were made from patients with hemifacial spasm (HFS) during microvascular decompression (MVD) operations to see if spasm and synkinesis are caused by ephaptic transmission at the site of lesion (root entry zone [REZ] of the facial nerve). The response from the orbicularis oculi muscle to electrical stimulation of the marginal mandibular nerve had a 2.2-msec longer latency (average of 16 patients) than the sum of the conduction times of the parts of the facial nerve that would be involved if the response was the result of ephaptic transmission at the REZ of the seventh cranial nerve. Similar results were obtained when the zygomatic branch of the facial nerve was stimulated. These results indicate that the facial motonucleus is involved in HFS.

On the origin of synkinesis in hemifacial spasm: results of intracranial recordings.

Recordings were made from facial muscles and the facial nerve near its entrance into the brain stem in patients with hemifacial spasm (HFS). The purpose of this study was to determine if the synkinesis commonly seen in patients with HFS could be linked to ephaptic transmission at the presumed site of the lesion (at the root entry zone (REZ) of the facial nerve). When the mandibular branch of the facial nerve was electrically stimulated, a response could be recorded from the orbicularis oculi muscles during the operation. The latency of the earliest response was 11.03 +/- 0.66 msec (mean response of seven patients +/- standard deviation (SD]. With equivalent stimulation a response could also be recorded from the facial nerve near the REZ; the latency of this response was 3.87 +/- 0.36 msec. Stimulation of the facial nerve at the same location yielded a response from the orbicularis oculi muscle, with a latency of 4.65 +/- 0.25 msec. The latency of the earliest response from the orbicularis oculi muscle to stimulation of the marginal mandibular branch of the facial nerve (11.3 msec) is thus larger than the sum of the conduction times from the points of stimulation of the marginal mandibular branch to the REZ of the facial nerve and from the REZ of the facial nerve to the orbicularis oculi muscle (8.52 +/- 0.38 msec). It is therefore regarded as unlikely that the earliest response of the orbicularis oculi muscle to stimulation of the mandibular branch of the facial nerve is a result of "crosstalk" in the facial nerve at a location near the REZ, and it seems more likely that HFS caused by injury of the facial nerve is a result of reverberant activity in the facial motonucleus, possibly caused by mechanisms that are similar to kindling.

An electromyographic analysis of the temporalis muscle and some of the facial muscles in thumb- and finger-suckers: By Claude Baril, University of Michigan, Ann Arbor, Michigan

Patients with hemifacial spasm (HFS) have an abnormal muscle response (AMR) that can be elicited by stimulating one branch of the facial nerve and recording electromyographically from muscles innervated by other branches of the facial nerve. In addition, the R1 component of the blink reflex can be elicited from the affected side in patients with HFS who are undergoing microvascular decompression (MVD) operations under inhalation anesthesia. A synkinetic component of the blink reflex response that corresponds to the R1 component can be recorded from the mentalis muscle. In the present study we show that the blink reflex elicited by electrical stimulation of the supraorbital nerve can suppress the AMR elicited by electrical stimulation of the temporal branch of the facial nerve in patients with HFS when the interval between stimulation of the supraorbital nerve and stimulation of the temporal branch of the facial nerve (interstimulus interval, ISI) is such that the blink reflex response would appear later than the AMR if they had been elicited independently. Within a short range of ISIs the two responses suppress each other either partially or totally. We find evidence that the suppression of the AMR is the result of an interaction in the facial motonucleus. We believe that the results of the present study support the hypothesis that the facial motonucleus is hyperactive in patients with HFS, and we suggest that the AMR is a result of backfiring from the facial motonucleus and that it may thus be an exaggerated F-response.