Electrophysiological Study Electrically Jun

Elicited Blink Reflex in Assessment of

Kimura, MD; Louis T. Giron, Jr, MD; Samuel M. Young,

electrically elicited blink reflex tested serially in 81 patients with Bell palsy. In 56 patients, the reflex returned before excitability of the distal segment of the facial nerve was lost, indicating recovery of conduction across the involved segment before distal degeneration. These patients generally showed a good clinical recovery within a few months after onset. The reflex latency, \s=b\ The

was

however, was considerably prolonged during the first month, suggesting demyelination or other pathologic change. The reflex latency was reduced considerably during the second month and returned to normal levels during the third or fourth months. In the remaining 25 patients, direct response to facial nerve stimulation before reflex became unelicitable responses returned, indicating distal degeneration of the nerve. In this group of patients, clinical recovery was prolonged and generally incomplete.

Palsy

Prognosis

MD

conventional

The peripheral

of Bell

electrodiagnostic

tests used in the evaluation of

facial paresis include, in addition to electromyography,1,2 measurement of nerve excitability and of conduction time in the segment distal to the stylomastoid foramen.3-6 These tests help to detect Wallerian degeneration but fail to reveal the function of the proximal nerve segment, which is primarily affected in Bell palsy.

Other

diagnostic methods, such as stapedial reflex and electrogustometry, are helpful in determining the

location of the lesion but not in assessing the extent of facial nerve involvement.7 In contrast, the blink reflex reflects the conduction of the entire length of the facial nerve, including the involved interosseous portion.8-11 In a preliminary study of four patients, we

Fig 1.\p=m-\Tworight-sided and two left-sided stimulations were delivered in each case to show consistency. In the patient, R, (arrows) and R, (single brackets) were delayed and small on the right side and normal on the left side regardless of side stimulated. This finding indicates a lesion involving efferent arc of reflex (facial nerve) on right side. Normal Control

Bell

Palsy (right)

delayed

Stimulation

Side of

diminished

(Arch Otolaryngol 102:140-143, 1976) normal

normal

normal

diminished

publication Nov 17, 1975. Department of Neurology and the Neurosensory Center, College of Medicine, University of Iowa, Iowa City. Reprint requests to Department of Neurology, University Hospitals, Iowa City, IA 52242 (Dr Kimura). Accepted

for

From the

Stimulation

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0.5mv

10msec

Side

of

Recording

•—· °.o

Paretic Side Healthy Side

14r

Days After

12

Normal Side

Affected Side

Onset

10

1228 33 27 14

il "

Noof Patients Tested

fi ö

fi b

DIRECT RESPONSE sj

4

4===?fc= I

I

ft

I

05mv 5 msec

Stimulation

1st 2™) 3«14th WEEK

YEAR

MONTH

Time After Onset

Fig 3.—Serial changes of R, in 21-year-old man (subject H in Fig 4) with Bell palsy on right side. Two consecutive tracings were recorded on each side to show consistency of R, on a given day. On affected side, R, (single brackets) was present but delayed on fifth day. It was unelicitable on the ninth day but recovered progressively thereafter. Shaded areas indicate normal range (mean ± 3 SD in 83 subjects).

Fig 2.—Serial changes in latency of R, and direct response, comparing affected and normal sides in 56 patients recovering without nerve degeneration. Mean and standard deviation are shown. Of 12, 28, 33, and 27 patients tested during the first three weeks, R, was absent on the paretic side in 3, 12, 11, and 3, respectively. Otherwise, R, was elicited in all patients throughout course.

Response and R, of Blink Reflex in 83 Subjects (166 Responses Considering Both Sides Together)

Table 1.—Normal Latencies of Direct

R, Component

Direct Response _A_

Latency Mean latency, msec Standard deviation, msec Upper limit of normal, mean ± 3 SD (msec)

2.92 0.39

Difference Between Two Sides 0.17 0.17

4.1

Difference Between Two Sides 0.31 0.30

Latency 10.45 0.84

0.7

1.2

13.0

that serial changes of the reflex latencies corresponded well with the clinical course of peripheral facial paresis.11 Although a few confir¬ matory reports have since ap¬ peared,12"15 a large-scale survey of this reflex in Bell palsy is still lacking. In this study, the electrically elicited blink reflex has been tested serially in 81 patients. The time course of progression and recovery of Bell palsy will be described.

reported

METHODS AND NORMAL VALUES

Table 2.—Time Course of Return of R, After Onset of Paresis in 56 Patients Recovering Without Degeneration of Facial Nerve No. of Patients Tested 12 22 17

Patients

Initially

Seen 1-2 days after onset 3-7 days after onset 2nd week after onset

R, First Appeared

on

Paretic Side

2nd Week 3rd Week 4th Week 1-2 Days 3-7 Days After Onset After Onset After Onset After Onset After Onset 1 + 2| 5 + 4* It It 8 + 3*

4 + 2t

6+

1f

12

3rd week after onset

In seven patients, R, was initially present*, then became unelicitable within but appeared againf on subsequent examination.

a

few days,

Recording electrodes were placed on the lateral aspect of the orbicularis oculi muscle and on the nose on the same side, and a ground electrode was placed around the arm. The conduction in the distal segment of the facial nerve was tested by stimulating the nerve just anterior to the mastoid process and recording the direct muscle response from the ipsilateral orbi¬ cularis oculi muscle. The blink reflex was tested by stimu¬ lating the supraorbital nerve at the supraorbital foramen on one side and recording the reflex responses from the orbicularis oculi muscle on both sides simul¬ taneously.11 The blink reflex consisted of two

temporally separate components,

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an

Normal

in 83 Controls

^ (mean+Range 3 S.D.) 77/7\

,_

-

onset 2

10

14

18

22

26

Serial Changes in Each of 11 Patients, A through R, Absent on Affected Side

30 2

Days After Onset

Months After Onset

Fig 4.—Serial changes in difference of R, latency between normal and paretic sides in 11 patients recovering without nerve degeneration (A through K) seen early in course of disease and followed up frequently. Responses from subject are shown in Fig 3. In general, nerve conduction is relatively normal at onset but deteriorates during first week. Shaded area indicates normal range of difference of R, latency between two sides in same individuals (mean ± 3 SD in 83 subjects).

early (R,) and a late (R2) response. Whereas R, was evoked only on the side of stimula¬ tion, R2 was recorded bilaterally with unilateral stimulation (Fig 1). Table 1 summarizes the normal ranges of R, of the blink reflex and the direct response deter¬ mined in 83 healthy subjects, 7 to 83 years of age (mean age, 37 years).

SUBJECTS AND RESULTS

Eighty-one patients with Bell palsy serially tested. Only those patients were included who had uni¬ lateral peripheral facial paresis with¬ were

out any demonstrable cause for neu¬ ropathy. A majority were treated with steroids for two to three weeks after onset. On the basis of serial changes of the direct and reflex responses, the population was divided into two groups: (1) 56 patients (26 male and 30 female patients, with a mean age of 43 years) who had retained excitability of the distal segment until the reflex responses returned, and (2) 25 pa¬ tients (12 male and 13 female patients, with a mean age of 48 years) who lost distal excitability without recovery of

the reflex. Table 2 summarizes the time course of the return of R, after onset of paresis in the first group of 56 patients. The time of initial detection of the return of R„ of course,

depended on how soon after the onset of paresis the patient was first studied. In Table 2, therefore, this group was subdivided depending on whether patients were first seen within two days of onset (12), between the third and the seventh day (22), during the second week (17), or there¬ after (5). In the first group of 56 patients, all the responses obtained during the course of follow-up were pooled and analyzed to determine the average time course of recovery (Fig 2). On the paretic side, R, was elicited in nine of 12 patients during the first two days after onset, in 16 of 28 patients between the third and the seventh day, in 22 of 33 during the second week, and in 24 of 27 during the third week. The reflex was obtained in all the 39 patients seen during the fourth week or thereafter. The latency of R,

substantially greater than normal during the first two days of onset, further increased during the latter was

half of the first week, then remained essentially unchanged up to the fourth week. It then showed a notable reduc¬ tion during the second month and became essentially normal during the third or fourth month. Latencies of R, in individual patients demonstrated a

similar time course, although there was considerable variation among dif¬ ferent subjects (Fig 3 and 4). In 41 of the 56 patients, previously absent R, and R, reappeared at the same time. In 11 others, R2 returned before R,. In the remaining four, R, was first to appear when R2 was still absent or minimal. In general, the latency measurement of R2 was not as useful as that of R, because of the wider range of variability. Nonethe¬ less, analysis of direct and consensual R, was essential in determining the affected portion of the reflex arc.16 In all 81 patients, the efferent arc of the reflex was implicated because ipsilateral but not contralateral R, was delayed or diminished when the affected side was stimulated (Fig 1). In the second group of 25 patients with eventual degeneration of the facial nerve, the direct response on the paretic side became unelicitable dur¬ ing the first week of onset in 18, during the second week in five, and during the third week in two. In two of six patients seen within the first two days after onset, relatively nor¬ mal R, and R, responses on the paretic side were present initially, but not on subsequent examinations a few days later. In the remaining 23 patients, no reflex responses on the affected side could be recorded during the first two months after onset. With regenera¬ tion of the facial nerve, both the direct and reflex responses returned but their latencies were greatly in¬ creased. Patients in the first group generally showed a good clinical recovery within a few months. Of the 56 patients in this group, 21 were followed up beyond two months after onset. The estimated recovery of facial strength was 100% in 17, 75% in three, and 50% in one. In the remaining 35 patients who were followed up less than two months, the strength had returned 100% in 11 when last seen. The even¬ tual outcome was unknown in the other 24 because they were still improving at the time of last exami¬ nation (75% in 15 and 50% in nine). In contrast, none of the 25 patients in the second group showed appreciable re¬ turn of function during the first two months. The ultimate recovery on the

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basis of

regeneration

of the facial

not available at the conclu¬ sion of this study in all but was gener¬ nerve was

ally incomplete.

COMMENT

Clinical observations suggest that Bell palsy progresses during the first few days. This time course, however, has not been critically investigated by electrophysiological methods. In the present series, the reflex responses were nearly normal initially but became unelicitable later on in six of 18 patients seen within the first two days after onset, two of them ulti¬

mately developing

nerve

degenera¬

tion. Average conduction delay reached its peak during the latter half of the first week rather than at onset, then remained essentially unchanged until the end of the fourth week. In seven of 25 patients who later had nerve degeneration, loss of distal nerve excitability occurred at a time later than would be expected follow¬ ing experimental section of the facial nerve.417 Our findings support the idea that conduction across the involved segment further deteriorates during the first week after onset in a considerable number of patients. This possibility should be weighed in assessing the prognosis of Bell palsy. The distal excitability of the facial nerve is substantially reduced in some patients within the first week of

onset.3"6 Whereas this finding indi¬ cates distal degeneration and poor prognosis, the presence of a relatively normal direct response during this period does not preclude late-onset degeneration as mentioned above. The measurement of reflex responses circumvents the pitfall of relying solely on the direct response because it allows detection of the recovery of conduction across the affected seg¬ ment." The return of R, or R, offers a reasonable assurance that remaining axons will survive without undergoing further deterioration. Indeed, none of our patients who had return of previously absent R, experienced sub¬ sequent degeneration of the facial nerve. Even in this group of patients, however, R, is markedly delayed during the first four weeks, suggest¬ ing demyelination or other patholog¬ ical change. An additional inference is that the commonly used term "physi¬ ological or functional block" is inap¬ propriate to describe most cases of the milder form of Bell palsy, despite the absence of axonal degeneration. How soon after the onset of paresis is it possible to detect beginning of recovery by studying the blink reflex? In our series of 56 patients destined to recover without substantial degenera¬ tion, the reflex on the affected side was elicitable in 57% during the latter half of the first week, in 67% during the second week, and in 89% during

the third week. The reflex responses were also present in 75% when seen within two days after onset. Because of possible progression of disease during the first week, however, the presence of the reflex in this period cannot be taken as a sign of recovery. These findings are in fair agreement with those of Penders and Boniver13 and Schenck and Manz.14 We believe that testing of the blink reflex is a useful addition to clinical observations and conventional elec¬ trical studies in predicting the course of recovery in Bell palsy. Serial studies are most helpful since return of the previously absent reflex before the loss of distal excitability is nearly always associated with satisfactory clinical recovery. If the excitability of the facial nerve is lost before the return of the reflex, on the other hand, no recovery is expected within a few months, and the eventual clinical outcome depends on regeneration of the nerve. Recently, there has been renewed controversy concerning sur¬ gical and medical management of Bell palsy.ls-,a The electrically elicited blink reflex may also have practical value in evaluating the efficacy of these modes of therapy.

Maurice W. Van Allen, MD, reviewed the paper. Sheila Mermen, Joanne Nahnsen, and Pam Harnack provided technical assistance.

References 1. Wigand ME, Spreng M, Bumm P, et al: Electronic evaluation of electromyograms in facial nerve paralysis. Arch Otolaryngol 95:324\x=req-\ 330, 1972. 2. Steidl L: Prognosis and course of Bell's palsy: II. Electromyographic study. Arch Psychiatr Nervenkr 216:323-341, 1972. 3. Taverner D: Electrodiagnosis in facial palsy. Arch Otolaryngol 81:470-477, 1965. 4. Campbell EDR: A simple prognostic test in facial palsy. J Laryngol 77:462-466, 1963. 5. Laumans EPJ: Nerve excitability tests in facial paralysis. Arch Otolaryngol 81:478-488, 1965. 6. Yanagihara N, Kishimoto M: Electrodiagnosis in facial palsy. Arch Otolaryngol 95:376-382, 1972. 7. Alford BR, Jerger JF, Coats AC, et al: Diagnostic tests of facial nerve function. Otolaryngol Clin North Am 7:331-342, 1974. 8. Rushworth G: Observation on blink reflexes.

J Neurol Neurosurg Psychiatry 25:93-108, 1962. 9. Gandiglio G, Fra L: Further observation on facial reflexes. J Neurol Sci 5:273-285, 1967. 10. Bender LF, Maynard FM, Hastings SV: The blink reflex as a diagnostic procedure. Arch Phys Med Rehabil 50:27-31, 1969. 11. Kimura J, Powers M, Van Allen MW: Reflex response of orbicularis oculi muscle to supraorbital nerve stimulation. Arch Neurol 21:193-199, 1969. 12. Penders CA, Delwaide PJ: Int\l=e'\r\l=e^\tde I'exploration du r\l=e'\flexede clignement en cas de paralysie faciale. Electromyography 11:149-156, 1971. 13. Penders CA, Boniver R: Exploration \l=e'\lectrophysiologique du r\l=e'\flexede clignement dans la paralysie faciale a frigore. ORL 34:17-26, 1972. 14. Schenck E, Manz F: The blink reflex in Bell's palsy, in Desmedt JE (ed): New Developments in Electromyography and Clinical Neuro-

physiology. Basel, Switzerland,

S Karger, 1973, vol 3, pp 678-681. 15. Marinacci AA: Orbicularis oculi (blink) reflex in Bell's palsy. Bull Los Angeles Neurol Soc 38:126-137, 1973. 16. Kimura J: The blink reflex as a test for brain-stem and higher central nervous system function, in Desmedt, JE (ed): New Developments in Electromyography and Clinical Neurophysiology. Basel, Switzerland, S Karger, 1973, vol 3, pp 682-691. 17. Gilliatt RW, Taylor JC: Electrical changes following section of the facial nerve. Proc R Soc Med 52:1080-1083, 1959. 18. Adour KK, Wingerd J: Idiopathic facial paralysis (Bell's palsy): Factors affecting severity and outcome in 446 patients. Neurology 24:1112-1116, 1974. 19. Study casts doubt on efficacy of corticosteroids against Bell palsy, MEDICAL NEWS. JAMA 232:1203-1204, 1975.

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Electrophysiological study of Bell palsy: electrically elicited blink reflex in assessment of prognosis.

The electrically elicited blink reflex was tested serially in 81 patients with Bell palsy. In 56 patients, the reflex returned before excitability of ...
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