Auditory evoked blink reflex and posterior auricular muscle response: Observations in patients with HFS and PFS

Journal of Electromyography and Kinesiology 20 (2010) 508–512

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Auditory evoked blink reflex and posterior auricular muscle response: Observations in patients with HFS and PFS Meral E. Kızıltan, Aysßegül Gündüz *, Rahsßan Sßahin I.U. Cerrahpasa Medical School, Department of Neurology, Istanbul, Turkey

a r t i c l e

i n f o

Article history: Received 17 January 2009 Received in revised form 21 June 2009 Accepted 27 July 2009

Keywords: Hemifacial spasm Postparalytic facial syndrome Blink reflex Auditory blink reflex Posterior auricular muscle response

a b s t r a c t Our goal was to investigate the characteristics of the auditory brainstem reflexes in patients with hemifacial spasm (HFS) and postparalytic facial syndrome (PFS). The spasm activities and responses by supraorbital and auditory stimuli were recorded from the orbicularis oculi, the posterior auricular and the mentalis muscles in 27 HFS and 21 PFS patients. The results were compared with those of 20 controls. Blink reflex (BR) was obtained by supraorbital stimulation in normal controls and on both sides of HFS and PFS patients whereas sound evoked bilateral auditory blink reflex (ABR) in 96.3%, 90.5% and 100%, respectively. Both BR and ABR showed synkinetic spread on symptomatic sides in all patients. The posterior auricular muscle response (PAMR) was observed bilaterally in 59.3%, 42.9% and 75.0% of groups, respectively. However, there was no synkinetic spread of PAMR. Since PAMR does not show synkinetic spread even in the presence of synkinetic spread of ABR and BR, we may suggest that a distal origin may be responsible of the synkinetic spread, or PAM is probably governed by a smaller nucleus in the brainstem. Thus it may be speculated that its excitability is insufficient to stimulate the ABR nucleus, whereas the reverse process is possible. Ó 2009 Elsevier Ltd. All rights reserved.

1. Introduction The auditory and supraorbital electrical stimuli produce reflexive closure of the eyelids by contraction of orbicularis oculi (O.oc) muscle (auditory blink reflex [ABR] and blink reflex [BR], respectively). ABR is a teleceptive reflex which occurs by contraction of bilateral O.oc muscles (Esteban, 1999) and has an onset latency of between 23 and 63 ms (Rushworth, 1962; Shahani and Young, 1973) whereas BR has two components. Characteristically, a supraorbital electrical stimulus on trigeminal nerve (V1) induces two recordable responses in the O.oc muscles: an early one, the socalled R1, ipsilateral to the stimulated side, and a later one, the R2, which is bilaterally expressed (Esteban, 1999). Besides the ABR, auditory stimulation also results in a response over the posterior auricular muscle (PAM), which is another muscle innervated by the facial nerve (O’Beirne and Patuzzi, 1999). So-called posterior auricular muscle response (PAMR) has a peak latency of 12–13 ms and is suggested as an unbiased electrophysiological method for determination of auditory sensitivity (Purdy et al., 2005).

* Corresponding author. Address: I.U. Cerrahpasa Medical Faculty, Department of Neurology, 34098 K.M. Pasa, Istanbul, Turkey. Tel.: +90 212 4143162; fax: +90 212 6330176. E-mail address: [email protected] (A. Gündüz). 1050-6411/$ - see front matter Ó 2009 Elsevier Ltd. All rights reserved. doi:10.1016/j.jelekin.2009.07.009

The hemifacial spasm (HFS) and postparalytic facial syndrome (PFS), which are appropriate prototype diseases to study brainstem reflexes, share some similar clinical and electrophysiological characteristics. Electrophysiological characteristics include spasms of facial muscles on symptomatic side, presence of responses on facial muscles that are not involved in the formation of the BR (Eekhof et al., 2000; Oge et al., 2005). This involvement refers to the lateral spread or synkinesia (Kimura et al., 1975; Auger, 1979). We also observed and previously reported the synkinetic spread of spasm activity and BR to PAM in HFS patients (Kiziltan et al., 2006). In this study, we investigated the characteristics of the ABR and the PAMR in patients with HFS and PFS and aimed to further enlighten the characteristics of the PAMR reflex pathway. 2. Patients and methods HFS patients of 27 (11 males, 40.7%) and 21 PFS patients (5 male, 23.8%) were included in the study. The mean ages in two groups were 54.1 ± 14.8 and 46.2 ± 15.4 years, respectively. They were compared to age-matched 20 healthy volunteers (8 males, 40%) (mean age: 46.3 ± 10.3). The duration of symptoms varied between 6 months to 20 years in HFS patients and 1–38 years in PFS patients. Among patients with HFS, four had tortuous vertebral and/or basilar artery, one Arnold–Chiari malformation, another one an arachnoid cyst and in four other patients one artery

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(anterior inferior cerebellar artery or vertebral artery) showed proximity to facial nerve. The PFS patients participating in the study did not have any intracranial lesions which may cause facial paralysis and only one patient had a history of herpes simplex skin lesions which accompanied paralysis. Ten patients with PFS had some weakness in the previously paralyzed side, which was quite mild in five of these patients, and two patients had grade 3 symptoms observed by House–Brackmann scaling system (House and Brackmann, 1985). The auditory thresholds were determined prior to electrophysiological investigations and they were estimated to be below 25 db in all patients and participants. In all patients, the botulinum toxin treatment followed the electrophysiological investigations. We studied blink reflexes using standard techniques (Kimura, 2001). The first step in an examination was voluntary recording of EMG activity (Neuropack Sigma MEB-9100, Nihon Kohden Medical, Tokyo, Japan) from the O.oc, the PAM and the mentalis muscle (MM) in order to detect any spasm activity or its spread, if any. The Ag–AgCl pair of cutaneous recording electrodes were placed on bilateral O.oc, bilateral PAM and the MM on midline. The ground electrode was placed on the sternum. The second step of the examination consisted of a classical stimulus–response recording: the BR was obtained by stimulating with a bipolar electrode supraorbitally. Similar to recordings from O.oc, the recording electrode was placed on the lower eyelid with a reference electrode located on the lateral orbital margin. The recordings from PAM were made in accordance with previously published reports (O’Beirne and Patuzzi, 1999). Briefly, the active electrode was placed on the surface of the skin directly overlying the PAM, and the reference electrode was placed on the pinna. The responses and the spasm activities were recorded while patients remained in sitting position with their eyes slightly closed. A single electrical stimulus of 0.2 ms duration and with an intensity three times that of R2 threshold was applied percutaneously to supraorbital nerve at its exit from the supraorbital foramen. The intensity of this stimulus was progressively increased until a value comparable to intensities of stimuli which provoke movement on the healthy side was reached.

A

For auditory stimulations, the monophasic 100 ls click auditory stimulus produced by Neuropack Sigma MEB-9100, Nihon Kohden Medical, Tokyo, Japan was delivered bilaterally through earphones as five bursts, with an intensity of 105 dB and at random intervals of 2–5 min. Its rise time was 1 ms and it consisted of two stimuli at an interval of 3 ms. The monitor and analysis times were adjusted as 20 ms and 30 ms, respectively. The filter settings were 2 kHz high cut and 20 Hz low cut. The bilateral non-rectified recordings were obtained after each stimulus. The onset latencies from first deflections and the lateral spread of the reflex activity to other muscles supplied by the facial nerve were recorded and measured. The analysis was composed of three or four consecutive reflex responses with shortest latencies. In the literature, generally the peak latencies used for PAMR in normal individuals are 12–13 ms. However, since we measured distal latencies of initial deflection for other reflexes, we used distal latency of initial deflection for PAMR. For responses on muscles other than O.oc, early response was defined as responses with latencies in the range of early blink reflex R1 response of O.oc ± 2SD and late response as responses with latencies in the range of late blink reflex R2 response of O.oc ± 2SD. Statistical analysis: We compared the latencies and the occurrence rate of responses in HFS and PFS groups and in healthy subjects. The analyses of data obtained were performed using the SPSS 11.5 statistical software package. The response rates were analysed by Fisher exact test or chi-square test. The response latencies were determined either by one way anova or t-test, based on suitability. A p-value of <0.05 was considered statistically significant. 3. Results The supraorbital electrical stimulation elicited early (R1) and late responses (R2–R2c) over O.oc (BR) in all three groups as well as over symptomatic sides in HFS and PFS patients. The latencies and amplitudes of the R1 and R2 responses did not differ between HFS, PFS and control groups (p1 = 0.346 and p2 = 0.376, respectively). The supraorbital stimulation also produced early and late

Left O.oc Left PAM

B

Right O.oc

Right PAM MM C

Left O.oc B

D

Left PAM Right O.oc Right PAM MM Fig. 1. (A) BR and synkinetic involvement with right supraorbital stimulus in a patient with right HFS. (B) BR and synkinetic involvement with right supraorbital stimulus in a 32-year-old woman with right PFS. (C) ABR and synkinetic involvement, and PAMR in a 38-year-old woman with right HFS. (D) ABR and synkinetic involvement in a 31-yearold woman with right PFS. (O.oc, orbicularis oculi; BR, blink reflex; ABR, auditory blink reflex; PAM, posterior auricular muscle; PAMR, posterior auricular muscle response; MM, mentalis muscle).

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Table 1 Latencies and response rates obtained by supraorbital electrical stimulation. HFS side

PFS side

Normal controls

p

RR (%)

Latency (ms)

RR (%)

Latency (ms)

RR (%)

Latency (ms)

RR (%)

Latency (ms)

R1 R2 R2C

100 100 100

10.2 32.1 32.1

100 100 100

10.7 31.9 31.7

100 100 100

10.2 33.5 33.3

>0.05 >0.05 >0.05

0.346 0.376 0.475

PAM Early Late

100 100

10.1 38.9

100 100

10.0 31.6

0 0

– –

0.000 0.000

0.867 0.104

MM Early Late

100 100

12.4 34.8

100 100

12.4 32.3

0 0

– –

0.000 0.000

0.994 0.226

HFS, hemifacial spasm; PFS, postparalytic facial syndrome; PAM, posterior auricular muscle; MM, mentalis muscle; RR, response rate.

Table 2 Latencies and response rates obtained by auditory stimulation. HFS side

PFS side

Normal controls

p

RR (%)

Latency (ms)

RR (%)

Latency (ms)

RR (%)

Latency (ms)

RR (%)

Latency (ms)

O.oc Early Late

0 96.3

– 36.5

0 90.5

– 35.0

0 100

– 34.5

– 0.324

– 0.756

PAM Early Late

59.3 44.4

10.3 40.3

42.9 47.6

10.3 31.7

75 0

9.5 –

0.112 0.827

0.546 0.098

MM Early Late

0 48.1

– 38.2

0 71.4

– 33.0

0 0

– –

– 0.105

– 0.280

O.oc, orbicularis oculi; ABR, auditory blink reflex; PAM, posterior auricular muscle; PAMR, posterior auricular muscle response; MM, mentalis muscle; RR, response rate; HFS, hemifacial spasm; PFS, postparalytic facial syndrome.

responses both over PAM and MM on symptomatic sides in patients with HFS and PFS (Fig. 1A and B). These early and late responses were in the range of R1 and R2 latencies, respectively (Table 1). There were no early or late responses from PAM or MM in the control group (p = 0.000). A bilateral response was obtained from O.oc following auditory stimulation (ABR) in 20 (100%) healthy volunteers, in 26 (96.3%) HFS patients, and in 19 (90.5%) PFS patients. There was no habituation of the ABR responses by repeated stimuli. A late reflex response of PAM on symptomatic side was obtained in 12 HFS (44.4%) and 10 PFS (47.6%) patients and a similar response of MM on symptomatic side was observed in 13 (48.1%) HFS and 15 (71.4%) PFS patients. The latencies were similar to that of ABR. There were no late responses from PAM and MM in normal controls. There were sound evoked early bilateral responses from PAM in 15 (75%) healthy controls, 16 (59.3%) HFS patients and 9 (42.9%) PFS subjects. We did not observe early responses over O.oc or MM in any group (Fig. 1C). The latencies and amplitudes of ABR or PAMR showed no differences in three groups (pL1 = 0.756 and pL2 = 0.546; pA1 = 0.702 and pA2 = 0.374, respectively). The response rates and latencies evoked by auditory stimulation are presented in Table 2. 4. Discussion We studied reflexes evoked by supraorbital electrical and auditory stimuli in muscles innervated by the facial nerve. Both components of BR were elicited in all patients. The involvement of lower facial muscles on symptomatic sides, which is not observed in control groups, can be attributed to lateral spread or synkinesia similar to that reported in the literature (Kimura et al., 1975; Auger, 1979). This involvement is not observed in healthy subjects. Although several studies have already shown that stimulation of the facial

nerve may produce stable muscle responses on PAM (De Meirsman et al., 1980), this muscle is not involved in BR formation. We have observed synkinetic involvement of PAM, similar to what we previously reported (Kiziltan et al., 2006). The presence of ABR in normal subjects has been established (Rushworth, 1962) and in our study, ABR was obtained bilaterally in all three groups. All subjects in our study had ABR latencies in the normal range (Rushworth, 1962; Shahani and Young, 1973). The ABR also spreads to MM or PAM in most of the patients with HFS or PFS, but it did not spread in control subjects or on healthy sides among patient group (Fig. 1C and D). Some authors believe that ABR is the initial response of startle response, which originates in O.oc and proceeds to the masseter, sternocleidomastoid, and the muscles of the upper and lower limbs, whereas others suggest that the startle response actually originates at a relatively longer latency and merely overlaps with ABR (Brown et al., 1991; Chokroverty et al., 1992). There are three differences to help differentiation of startle response and synkinetic spread. Firstly, the ABR latencies and the latencies of muscular responses in our study were shorter than those anticipitated in startle response. Latencies of startle responses in lower facial muscles are expected to be longer than upper muscle group in contrary to our findings. Secondly, startle response habituates by repeated stimuli whereas responses of other facial muscles in our patient group persisted without any latency or amplitude change. Lastly, startle response develops bilaterally whereas we obtained responses from other facial muscles on only symptomatic sides. These characteristics led us to consider them as synkinetic spread rather than startle responses. Therefore, it seems that both BR and ABR show synkinetic spread. Since it is known that very strong wind, cold weather, and sometimes the emotional state of a person may trigger spasms and such spasm activities may be observed in all muscles innervated by the facial nerve, synkinetic spread by auditory stimulation

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is reasonable. However, the PAMR which is reported to possibly share the same reflex pathway with the ABR (Hori et al., 1986; Patuzzi and O’Beirne, 1999) did not exhibit any synkinetic spread to lower facial muscles or to O.oc. The PAMR is easily measured and has previously been suggested as a screening test for newly developed conditions of deafness; but it is not commonly used due to personal variations among individuals, as is described by Picton et al. (1974) and Cody and Bickford (1969)). However, it was obtained in all of our groups consistently. Owing to those observations, we may have some suggestions for the reflex pathways or generation of disease process. Primarily, we should accept that the possibility of a difference in ABR and PAMR pathways which is yet unknown may be the cause. However, if we neglect this possibility, this observation may have important impact from the point of pathogenesis. As known, there are two hypotheses for the pathogenesis of HFS: a peripheral nerve hypothesis and a central or ‘‘nucleus” hypothesis. (1) An abnormal cross-transmission (ephaptic transmission) between the facial nerve fibers at the site of vascular compression or where the nerve is injured; the site generally suggested being the pontocerebellar angle (Nielsen, 1984a,b; Nielsen, 1985; Ravits and Hallett, 1986; Tankéré et al., 1998); (2) Hyperactivity in the facial nucleus (Møller, 1987): peripheral injury to the facial nerve induces a functional reorganization of synapses within the facial nucleus which is associated with a general hyperexcitability of its whole motoneuronal pool. This in turn would result in abnormal cross-transmission at the origin of the abnormal response (Møller, 1987; Møller and Jannetta, 1986). There are similar explanations for PFS, one being a defective nerve regeneration, and the other the hyperexcitability of facial nucleus and/or brainstem reflex circuits (Kimura et al., 1975; Ferguson, 1978). O.oc weakening increases the excitability of supraorbital evoked blinks and decreases the threshold for evoking blinks on the side ipsilateral to weakening. The changes in threshold indicate an adaptive increase in the ability of trigeminal sensory stimuli to engage motor activity, i.e. motor learning (Evinger and Manning, 1988). O.oc weakening primarily modifies trigeminal sensory–motor circuits ipsilateral to facial nerve transsection (Schicatano et al., 1997). However, there is also some proof that facial motoneurons are hyperexcitable in essential HFS. It is likely that extrinsic irritation of the facial nerve at the posterior fossa generates an antidromic bombardment of inputs to facial motoneurons, causing excitability changes and spontaneous or reflex firing of motoneurons after a ‘‘kindling” effect (Martinelli et al., 1983; Møller, 1991; Valls-Solé, 2007). Therefore in both HFS and PFS, hyperexcitability of facial nuclei and circuits of BR is suggested (Valls-Sole and Tolosa, 1989; Syed et al., 1999; Oge et al., 2005). In the case of either theory, any stimulus which activates a muscle innervated by the facial nerve should result in the activation of other muscles. In HFS, a third more distal mechanism has recently been suggested: a repetitive firing of facial nerve terminal axons in periorbital region (Montero et al., 2007). The findings that PAMR does not show synkinetic spread even in the presence of synkinetic spread of ABR and BR decreases the possibility of cross-transmission hypothesis in our patients. Nevertheless, more distal origin for abnormal firing is still possible. Since facial nerve branch to PAM is the most proximal, any abnormal firing around the periorbital region may affect the PAM. The anatomical and histological studies showed that there is musculotopic organization of the facial motor nucleus, and that there are some peculiarities in terms of the relative size of each column, which might be related to the functional and behavioral importance of each muscle in the particular context of various species (Sherwood, 2005). Horta-Júnior et al. reported a clear musculotopic organization in the facial nucleus, with individual muscles being innervated by longitudinal functional columns of motoneurons in C. Alpella primate (Horta-Júnior et al., 2004). Since other

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species, including humans have similar features, social and functional requirements may result in the enlargement of the associated motor column. Therefore, the PAM which is rudimentary in humans probably has a smaller motor column and we may speculate that it may be too weak to stimulate O.oc motoneuron while the reverse is possible. In conclusion, our findings may indicate that either more distal origin may be responsible for the synkinetic spread or PAM is probably governed by a smaller nucleus in the brainstem and so it may be speculated that its excitability is insufficient to stimulate the ABR nucleus, whereas the reverse process is possible. References Auger RG. Hemifacial spasm: clinical and electrophysiologic observations. Neurology 1979;29(9 Pt. 1):1261–72. Brown P, Rothwell JC, Thompson PD, Britton TC, Day BL, Marsden CD. New observations on the normal auditory startle reflex in man. Brain 1991;114(Pt. 4):1891–902. Chokroverty S, Walczak T, Hening W. Human startle reflex: technique and criteria for abnormal response. Electroencephalogr Clin Neurophysiol 1992;85(4): 236–42. Cody DT, Bickford RG. Averaged evoked myogenic responses in normal man. Laryngoscope 1969;79(3):400–16. De Meirsman J, Claes G, Geerdens L. Normal latency value of the facial nerve with detection in the posterior auricular muscle and normal amplitude value of the evoked action potential. Electromyogr Clin Neurophysiol 1980;20(6):481–5. Eekhof JL, Aramideh M, Speelman JD, Devriese PP, Ongerboer De Visser BW. Blink reflexes and lateral spreading in patients with synkinesia after Bell’s palsy and in hemifacial spasm. Eur Neurol 2000;43(3):141–6. Esteban A. A neurophysiological approach to brainstem reflexes. Blink reflex. Neurophysiol Clin 1999;29(1):7–38. Evinger C, Manning KA. A model system for motor learning: adaptive gain control of the blink reflex. Exp Brain Res 1988;70(3):527–38. Ferguson JH. Hemifacial spasm and the facial nucleus. Ann Neurol 1978;4(2): 97–103. Hori A, Yasuhara A, Naito H, Yasuhara M. Blink reflex elicited by auditory stimulation in the rabbit. J Neurol Sci 1986;76(1):49–59. Horta-Júnior JA, Tamega OJ, Cruz-Rizzolo RJ. Cytoarchitecture and musculotopic organization of the facial motor nucleus in Cebus apella monkey. J Anat 2004;204(Pt 3):175–90. House JW, Brackmann DE. Facial nerve grading system. Otolaryngol Head Neck Surg 1985;93(2):146–7. Kimura J. Electrodiagnosis in diseases of nerve and muscle: principles and practice. 3rd ed. New York: Oxford University Press; 2001. Kimura J, Rodnitzky RL, Okawara SH. Electrophysiologic analysis of aberrant regeneration after facial nerve paralysis. Neurology 1975;25(10):989–93. Kiziltan M, Sahin R, Uzun N, Kiziltan G. Hemifacial spasm and posterior auricular muscle. Electromyogr Clin Neurophysiol 2006;46(5):317–20. Martinelli P, Gabellini AS, Lugaresi E. Facial nucleus involvement in postparalytic hemifacial spasm? J Neurol Neurosurg Psychiatry 1983;46(6):586–7. Møller AR. Hemifacial spasm: ephaptic transmission or hyperexcitability of the facial motor nucleus? Exp Neurol 1987;98(1):110–9. Møller AR. The cranial nerve vascular compression syndrome: II. A review of pathophysiology. Acta Neurochir (Wien) 1991;113(1–2):24–30. Møller AR, Jannetta PJ. Physiological abnormalities in hemifacial spasm studied during microvascular decompression operations. Exp Neurol 1986;93(3): 584–600. Montero J, Junyent J, Calopa M, Povedano M, Valls-Sole J. Electrophysiological study of ephaptic axono–axonal responses in hemifacial spasm. Muscle Nerve 2007;35(2):184–8. Nielsen VK. Pathophysiology of hemifacial spasm: I. Ephaptic transmission and ectopic excitation. Neurology 1984a;34(4):418–26. Nielsen VK. Pathophysiology of hemifacial spasm: II. Lateral spread of the supraorbital nerve reflex. Neurology 1984b;34(4):427–31. Nielsen VK. Electrophysiology of the facial nerve in hemifacial spasm: ectopic/ ephaptic excitation. Muscle Nerve 1985;8(7):545–55. O’Beirne GA, Patuzzi RB. Basic properties of the sound-evoked post-auricular muscle response (PAMR). Hear Res 1999;138(1–2):115–32. Oge AE, Yayla V, Demir GA, Eraksoy M. Excitability of facial nucleus and related brain-stem reflexes in hemifacial spasm, post-facial palsy synkinesis and facial myokymia. Clin Neurophysiol 2005;116(7):1542–54. Patuzzi RB, O’Beirne GA. Effects of eye rotation on the sound-evoked post-auricular muscle response (PAMR). Hear Res 1999;138(1–2):133–46. Picton TW, Hillyard SA, Krausz HI, Galambos R. Human auditory evoked potentials. I. Evaluation of components. Electroencephalogr Clin Neurophysiol 1974;36(2):179–90. Purdy SC, Agung KB, Hartley D, Patuzzi RB, O’Beirne GA. The post-auricular muscle response: an objective electrophysiological method for evaluating hearing sensitivity. Int J Audiol 2005;44(11):625–30. Ravits J, Hallett M. Pathophysiology of hemifacial spasm. Neurology 1986;36(4): 591–3.

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Meral E. Kızıltan is a professor of Neurology at the Cerrahpasa Medical faculty of Istanbul University. She was educated between 1970 and 1976 and then progressed at the same institute. Her main area of interest EMG, clinical neurophysiology, electrophysiological aspects of movement disorders and diabetic neuropathies.

Aysßegül Gündüz was born in 1980 in Istanbul, Turkey. She graduated from Istanbul University Cerrahpasa School of Medicine in 2003. She completed her education in neurology residency at the same faculty between 2003 and 2008. Since then she was working as a neurologist in a state hospital. Her areas of interest are clinical neurophysiology and movement disorders.

Rahsßan S ß ahin was born in 1974 in Istanbul, Turkey. She graduated from Istanbul University Cerrahpasa School of Medicine in 1998. She completed her education in neurology residency at the same faculty between 1999 and 2004. Since then, she has been working as a general neurologist at various hospitals’ neurology departments. She was interested in neuromuscular diseases and clinical neurophysiology.