Journal of Neurology, Neurosurgery, and Psychiatry 1986;49:58-63

Primary hemifacial spasm: a neurophysiological studyANGEL ESTEBAN,* PEDRO MOLINA-NEGROt

From Section of Clinical Neurophysiology, Hospital Provincial de Madrid, Spain* and Section of ClinicalNeurophysiology and Functional Neurosurgery, Hopital Notre-Dame de Montreal, Canada. t

SUMMARY A series of 53 cases of primary hemifacial spasm have been evaluated by means ofblink reflexes and their results compared with a normal control group. Reflex responses were

obtained by percutaneous electrical stimulus of both the supraorbital nerve (trigemino-facialreflex), and the facial nerve at the stylo-mastoid region (facio-facial reflex). The R2 response was

considered abnormal when its latency was shortened (hyperactivity) or delayed (hypoactivity).Thirty-six out of 53 cases with primary hemifacial spasm showed abnormal responses, with a

combination of facial nerve impairment (delayed R2 in the facio-facial reflex) and trigeminal-facial hyperactivity (shortened R2 in the trigemino-facial reflex). Five cases showed hyperactivityin both the trigemino-facial reflex and the facio-facial reflex reflexes. These results suggest a state

of hyperexcitability, probably at the level of the facial nucleus, combined with a peripheral facialnerve involvement in a high proportion of patients with primary hemifacial spasm.

The physiopathology of primary hemifacial spasm isnot fully understood. A peripheral origin is sug-gested by cases of infection, tumour and vascularlesions at the root of the facial nerve,' -5 and is sup-ported by the favourable results obtained by intra-cranial facial neurolysis.68 This mechanism woulddepend on ephaptic interaction of nerve fibres at thelevel of the lesion.9- 13 A central origin, causingfacial neuron hyperexcitability, in both primary aswell as postparalytic facial spasm, has been claimedfor a long time' 14 15 and also in recent publicatons. 16-23The present study concerns blink reflexes

obtained by trigeminal and facial stimulation in agroup of 53 patients with primary hemifacial spasm.Blink reflexes were abnormal in 36 cases, in theform of either trigemino-facial hyperactivity (19cases) or facial nerve impairment (17 cases). Amongthe former, nine demonstrated both types of disor-der. Based on these results it is suggested that prim-ary hemifacial spasm is the consequence of centralfacial hyperexcitability combined with impairedafferent conduction in the facial nerve.

Material and method

Fifty-three patients with primary hemifacial spasm and 20

Address for reprint requests: Dr Angel Esteban, Section of ClinicalNeurophysiology, Hospital Provincial. C/ Dr Esquerdo, 46 28007Madrid, Spain.

Received 17 July 1984 and in revised form 29 January 1985.Accepted 8 March 1985

normal controls were studied. The 53 cases of primaryhemifacial spasm were evaluated between 1975 and 1980.The diagnosis was based on the usual clinical criteria.24Fourteen were men and 39 women. The mean age was52-7 years (range 24 to 81) and the mean duration of thesymptoms was 5-7 years (range 3 5 to 50). In 46 cases theabnormal contractions began in the lower eyelid. Radiolog-ical studies excluded an underlying macroscopic pathology.The group of 20 normal controls had a mean age of 45-3years (range 16 to 68).With the patient in the supine position, two subcutane-

ous monopolar needles were inserted in the common por-tion of m orbicularis oculi at the external orbital borderand in m orbicularis oris at the middle of the nasomalarfold. The studies were performed with a Grass electro-myograph. A four-channel memory oscilloscope with vari-able persistence was used for the recording. Once the suit-able image was selected, a polaroid camera was used toobtain a permanent record.A blink reflex can be obtained following stimulation of

cranial nerves other than the well-known trigemino-facialreflex. A facio-facial reflex was described by one of us(PMN) at the III International Symposium of Facial NerveSurgery held in Zurich in 1976.25 The same reflex has beenstudied further in different pathologies, either peripheral26or central.27 For the trigemino-facial reflex the cathode waslocated on the supraorbital nerve at its exit from the orbitalsquiggle and the anode on the forehead, at the furthestpoint away from the medical line. For the facio-facial reflexthe cathode was applied near the stylomastoid foramen infront of the mastoid process and behind the ear lobe, withthe anode in a relatively posterior-inferior position. A con-stant current stimulator was used to deliver monopolarsquare waves of 0-2 ms duration and intensity of approxi-mately twice the threshold for each reflex. This was

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Primary hemifacial spasm: a neurophysiological study

Table 1 Trigemino-facial and facio-facial reflexes and M potential in primary hemifacial spasm (mean ± 1 SD)

Trigemino-facial reflex Facio-facial reflexRI R2 R2 M

Latency Latency Dif Lat. Amplitude Duration Latency Dif Lat. Latency

Involved side 10-3 + 1.0 28-7 ± 7-4t 2-4 ± 4-2t 05 ± 0.5 46-6 ± 12-4t 33-7 ± 8-3t 5 4 ± 5-7f 2-5 ± 0-4Uninvolved side 10-1 ± 0-8 31-1 ± 4-4 05 + 4-2* 0-4 ± 0 3 40-4 ± 10-6 32-3 ± 7-4* 1-9 + 4-7* 2-5 ± 0-4Normal controls 10-4 ± O*5 31-4 ± 2-3 1-2 ± 1-8 0-5 ± 0-3 38-5 ± 11-5 28-7 ± 2-5 3-9 ± 2-9 2-6 ± 0-4

p < 0-05, when compared with normal values.tp < 0-05, when compared with uninvolved side and normal values.

Table 2 Trigemino-facial response in 19 cases ofprimary hemifacial spasm with latencies smaller than 26 ms (mean +I SD)

Latency Dif Lat. Amplitude Duration

Involved side 20-7 + 1-7* (1) 6-2 + 3.9* (2) 0-7 ± 0-6* 55.3 ± 7-4* (3)Uninvolved side 30-8 ± 5-7 -1.1 + 4-7 0 3 ± 0-2 40-8 ± 11-8

*p < 0-01, when compared with uninvolved side.I A 20 ms arbitrary value was taken when RI and R2 responses were without interruption (14 cases).2 Non evaluated when RI and R2 responses were without interruption.3 60 ms maximal value.

achieved more frequently with an intensity of 10-15 mAfor the trigemino-facial reflex and around 30 for the facio-facial reflex. The stimulation intensity was maintainedunchanged on both sides and its frequency was low andirregular, about one shock every five seconds to avoidhabituation.The direct motor potential (M) was obtained in m.

orbicularis oculi with a supramaximal stimulation of thefacial nerve at the stylomastoid foramen exit. Theresponses were simultaneously recorded in both m.orbicularis oculi and, in the last 23 cases, in orbicularis orisas well.

In each case a number of superimposed responses werephotographed and the following parameters were assessedaccording to similar criteria previously described:2829 (a)Latency of the ipsilateral early (R1) response oftrigemino-facial reflex and late (R2) responses of thetrigemino-facial reflex and facio-facial reflex. The latencyof the M potential was also analysed. (b) Differentiallatency between the late ipsilateral and contralateralresponses to the stimulus in the trigemino-facial reflex andthe facio-facial reflex. (c) Maximum amplitude from peakto peak of the R2 potential (trigemino-facial reflex) and(d) Maximum duration of R2 potential (trigemino-facialreflex).

It is important to avoid confusion between a reflexresponse and a spontaneous spasm. In cases with continu-ous spasm, it was necessary sometimes to wait more than30 seconds between two stimuli since voluntary contrac-tion of any facial muscle can provoke a spasm. The patientwas asked to maintain the gaze slightly below the horizon-tal plane to avoid contraction of m. frontalis. Relaxation ofthe jaw also was important. The possibility of electricalsynkinesis, manifested by the diffusion of the reflexresponses to the m. orbicularis oris and occasionally to them. frontalis, was evaluated in the last 23 cases of primaryhemifacial spasm.The electromyographical characteristics of the muscular

activity were studied in m. orbicularis oculi in all thepatients and simultaneously in the orbicularis oris in thelast cases of the series.

Statistical evaluation The mean value of the results wasobtained by comparing the studied groups using Student's ttest. Only when p was less than 0 05 was the differenceconsidered significant.

Results

The electromyographical recordings did not showspontaneous denervation activity. The clonic facialcontractions were accompanied by irregular activityapproximately synchronous with the hemifacialmusculature, which frequently led to sustained activ-ity lasting a few seconds. In the interspasm periods,complete electrical silence could be obtained but, onmany occasions, isolated activity was detected.

In the trigemino-facial reflex, the latency of Rlwas normal in all cases. The latency of R2 was shor-tened, the differential latency was lengthened, andthe duration was greater on the hemispasm sidecompared with the healthy side, and compared withthe normal group values (table 1). These differenceswere accentuated in the group of 19 patients thatshowed either a R2 latency response of less than 26ms (lower limit of the normal mean latency plus 2standard deviations) or no separation at all betweenthe Rl and R2 (table 2).A particularly interesting phenomenon was the

frequent anticipation of the R2 response on thepathological side following trigeminal stimulation onthe normal side (fig). In the whole group, this gave amean differential latency value (as compared to the

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Esteban, Molina-Negro

k.

Fig. Rightprimary hemifacial spasm. With the ipsilateral trigeminal stimulus, R2 response follows the RI potential withoutinterruption (top, left). With the left stimulation, the R2 response ofthe pathological side shows a systematic anticipationwith respect to the normal stimulated side (bottom, left). On the right ofthe figure, facio-facial reflex. The R2 responsefollows the direct motor potential when the hemispasm side is stimulated (top). Each record with two superimposed traces.T-FR = trigemino-facial reflex; F-FR = facio-facial reflex; R = right side; L = left side.

healthy side) which was less than normal (p < 0-05),and which even produced a negative mean value inthe latency subgroup in which the latencies were lessthan 26 ms (tables 1 and 2). In six cases the R2latency was longer than 36 ms (normal mean plus 2standard deviations).The late response of the blink reflex, provoked by

facial stimulation, did not show any difference inlatency between the affected and the healthy sides.Both sides, nevertheless, showed a lengthening (p <0.05) with respect to the normal mean value (table1). The latency of the R2 response was greater than34 ms (above the normal mean value plus 2 standarddeviations) or it was not obtained on the pathologi-cal side in 27 of the 42 cases studied. In 13 cases,this finding was present on both sides. In contrastfive cases showed an abnormally short latency and,at times, the response followed the direct motorpotential without interruption (fig). Frequently, thedifferential latency could not be obtained from thepathological side because of the absence of con-

tralateral response ( 15 out of 33) and its mean valueshowed an increase (p < 0.02) with respect to thatobtained from the unaffected side (table 1).Twenty of the last 23 cases in this series, studied

since 1978, showed a spread of the reflex responsesto the m. orbicularis oris and the m. frontalis.

Classification of the blink reflexes in primaryhemifacial spasm (table 3).Based on the results obtained by comparison bet-ween trigeminol-facial and facio-facial reflexes, aneurophysiological classification of primary hemifa-cial spasm is proposed. A group of 36 patients(group A) showed alterations in one or both reflex-es. A hyperactive trigeminol-facial R2 response witha latency shorter than 26 ms was found in 19 cases(group Al). This was associated with a facio-facialreflex response which was also hyperactive (latencyshorter than 20 ms) on five occasions (group Ala);normal facio-facial reflex response occurred inanother five cases (group Alb), and a delayed

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Primary hemifacial spasm: a neurophysiological studyTable 3 Blink reflexes in 53 cases ofprimary hemifacial spasm

Trigemino-facial reflex Facio-facial reflex

A. Abnormal 1. Hyperative (19) a. Hyperactive (5)36 cases (68%) b. Normal (5)

c. Impaired (9)2. Normal (11) Impaired (11)3. Impaired (6) Impaired (6)

B. Normal17 cases (32%)

Number of cases within brackets.

response (latency longer than 34 ms) or absence ofpotential in nine cases (group AMc). This samefacio-facial reflex impairment was found to beassociated with some normal trigemino-facial reflexin 11 cases (group A2) and with signs of lesions(latency of trigemino-facial reflex R2 longer than 36ms) in the remaining five cases (group A3).

In group B, the blink reflex responses were nor-mal. In this group, nevertheless, 11 cases corres-ponded to the first of the series which were notevaluated with respect to the facio-facial reflex. Itwas precisely this reflex in the remaining 42 caseswhich showed signs of lesion on 26 occasions (62%),signs of hyperactivity on five occasions (12%) andwas normal on 11 (26%).

Discussion

The results of previous studies on the blink reflexesin primary hemifacial spasm have been contradic-tory. Abnormally prolonged responses have beendescribed,30 as well as a premature response on thepathological side when stimulating the healthyone,3 ' and normal latencies with spread of theresponses to the m. orbicularis oriS.32 33 Besides theclassical trigeminol-facial reflex, we included in ouranalysis of the primary hemifacial spasm the blinkreflex obtained by facial nerve stimulation at thestylomastoid region. In this reflex both afferent andefferent branches belong solely or mainly to thefacial nerve.2527

In primary hemifacial spasm, differences werefound between the affected and healthy sides andalso in relation to the normal control group. Thelatency of the R2 response of the trigemino-facialreflex was shorter while the R2 of the facio-facialreflex was delayed. These abnormalities were foundin isolation or combined in 36 cases (group A),while 17 cases (group B) did not show such altera-tions. In group A, depending on the association ofother changes in both reflexes, various subdivisionscan be considered (table 3).As in other studies,3233 synkinesias were found

following electrical stimulation, with spread of reflexresponses (trigemino-facial reflex and facio-facial

reflex) to muscles which do not normally show them;in our cases, not only to m. orbicularis oris but alsoto m. frontalis. Their incidence was high, (20 casesfrom the 23 studied), and their presence, which canvary from one moment to the next in the samepatient,33 probably represents the lowest level offacial hyperexcitability. In some of the cases in ourseries, such synkinesias were the only sign oftrigeminal-facial hyperexcitability.Many cases of primary hemifacial spasm have

been described with various macroscopic pathologi-cal processes in the posterior fossa.2 35636 Suchpatients together with experience in the surgicaltreatment of primary hemifacial spasm by facialdecompression in its petrous canal'0 and, morerecently, by freeing the nerve from abnormal vesselsin the ponto-cerebellar angle,6-8 has given credenceto the concept of ephaptic transmission at a com-pressive lesion in aetiology of hemispasm.'03' Thefacial synkinesis in primary hemifacial spasm hasbeen similarly interpreted.33From a clinical point of view, an ephaptic mechan-

ism does not explain various aspects of primaryhemifacial spasm: its onset and its almost regularpredominance at the m. orbicularis oculi, its cir-cumscribed persistence in that muscle over a periodof years, the influence of emotional tension on itsintensity and, at times, on its provocation, and itsoccasional appearance during sleep. It is almostimpossible to believe that such a topographicallyvariable cause as an arterial loop in the pon-tocerebellar angle38 or an expansing process, sys-tematically injures the same portion of facial nervefibres (those supplying the m. orbicularis oculi) asthere is apparently no somatotopic arrangement ofthe facial nerve trunk.3940 The characteristicsdescribed in experimental ephaptic interaction"4 42such as the need for a prior stimulus for thepathological discharge, the exclusive transmission ofmotor fibres to sensory fibres, and the need for con-tact between adjacent damaged fibres, do not pro-vide a satisfactory explanation of all the known clin-ical phenomena of primary hemifacial spasm.22

In 14 cases in our series in group Al, with signs oftrigeminal-facial hyperexcitability (tables 2 and 3),

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the R2 potential followed the Rl potential withoutinterruption. Also, in many of them the lateresponse on the hemispasm side appeared beforethat of the unaffected one following stimulation ofthe latter (fig). If the first fact could be explained bya post-discharge of the early potential after the firstactivation wave arrived at the pathological nervearea, the second circumstance would necessarilyrequire a prior level of hyperexcitability in the reflexarc, that is probably in the facial nucleus itself. Thiscould explain the lower values of differential latencyon the hemispasm side as compared with the healthyone (table 1).We think that facial hemispasm, independent of

its initial cause, should be considered a pathologicalincrease of the blink reflex which, under normalconditions, is restricted to the m. orbicularisoculi.3343 However, Kugelberg44 has observed that,on certain occasions, a sufficiently strong stimulus orstate of high emotional tension can cause the blinkreflex in normal subjects to spread to other facialmuscles. The progressive increase of facial nuclearexcitability in hemispasm would cause a decrease inthe reflex threshold, by any of its afferent roots. Thiswould express itself initially as a localised and trans-itory contraction at the palpebral level, which wouldgo on increasing in intensity and spread towardsother facial territories. Gowers,'4 who clearly antici-pated this concept, explained that the usual onset ofthe hemispasm in m. orbicularis oculi is due to thefact that "The motor mechanism of this muscle ismore sensitive, in consequence of its energetic reflexaction" .

In our primary hemifacial spasm series it has beendemonstrated that, together with the signs oftrigeminal-facial hyperactivity, in some cases signsof a lesion coexist in facial conduction. The mechan-ism by which a facial peripheral lesion can reach thepoint of causing an increase in the excitability of itsown nucleus is speculative at the present time.Experimental evidence suggests that an efferentfibre lesion4546 as well as deafferentation47 can giverise to secondary hyperexcitability of the corres-ponding motoneuronal pool, probably through aninterneuronal reorganisation. We cannot exclude,however, the possibility that an afferent irritativemechanism exists as well. The reflex origin of prim-ary hemifacial spasm elaborated by Hunt' was sup-ported by the observations of Rushworth,48 and wasthe theoretical basis of treatment by section of the n.intermedius.63649The possibility of hyperexcitability of the facial

neurons due to a lesion of afferent facial fibres issupported by the presence of bilateral delayed R2responses following stimulation of the facial nerveon the affected side in 25 cases of our series. A

Esteban, Molina-Negro

preliminary analysis of the anatomical findings dur-ing exploration of the cerebello-pontine angle andof the results of facial decompression from arterial,venous or arachnoidal structures, shows that thosewith obvious anatomical abnormalities and betterresults after surgery belong almost exclusively to thisparticular group.

AddendumWhen this paper had been submitted to publicationthe works of Nielsen5' 52 about the pathophysiologyof hemifacial spasm became known to us. In theaffected side of 62 consecutive patients studied hefound an increased latency of the Rl component ofblink reflex with normal latency of R2 and a highamplitude on both responses. An afteractivity usu-ally appeared after the R2 potential and, sometimes,after Rl. He unfortunately did not make simultane-ous recording on both sides in order to measure thedifferential latency. These results persuade him tofavour the theory of the ectopic excitation andephaptic transmission in a facial nerve lesionalthough, as he states, "hyperexcitability of thefacial nucleus could also play a role in thepathophysiology of hemifacial spasm".

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