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Diagnostic utility of Freyss motor examination, House–Brackmann

grading, topognostic tests, and electrophysiological assessments for
unilateral peripheral facial nerve disorder
To cite this article: W Alviandi et al 2018 J. Phys.: Conf. Ser. 1073 022025

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The 2nd Physics and Technologies in Medicine and Dentistry Symposium IOP Publishing
IOP Conf. Series: Journal of Physics: Conf. Series 1073 (2018)
1234567890 ‘’“” 022025 doi:10.1088/1742-6596/1073/2/022025

Diagnostic utility of Freyss motor examination,

House−Brackmann grading, topognostic tests, and
electrophysiological assessments for unilateral peripheral
facial nerve disorder

W Alviandi1*, A Iswara1, B Bramantyo1 and M Hakim2

1
Department of Otolaryngology, Faculty of Medicine, Universitas Indonesia, Jakarta, 10430,
Indonesia
2
Department of Neurology, Faculty of Medicine, Universitas Indonesia, Jakarta, 10430,
Indonesia

*E-mail: widayat_alviandi@yahoo.com

Abstract. Unilateral peripheral facial nerve disorder is most often idiopathic, and the
determination of the cause may be necessary to guide appropriate treatment. There is no
standard diagnostic test for determining the cause or location of the lesion; therefore,
clinicians may rely on a variety of diagnostic methods such as the Freyss system of motor
examination, House−Brackmann grading, topognostic tests (Schirmer, stapedius reflex,
gustatometry), and electrophysiological investigations (nerve conductivity, blink reflex, needle
EMG). However, few studies have directly compared the suitability of these different
diagnostic methods according to disease characteristics (severity, onset, etc.). This descriptive
cross-sectional study compared results using these diagnostic modalities among 44
consecutive patients. There was a significant concordance (Kappa R = 0.5, p < 0.05) between
the Freyss motor system examination results and House−Brackmann scoring for 32 patients
with chronic onset and moderate-to-severe damage. Alternatively, there was poor agreement
(Kappa R = 0.011, p = 0.935) between topognostic and electrophysiological investigation for
determining lesion location. In 13 patients with chronic onset and moderate-to-severe damage,
lesion location could not be determined based on electrophysiology, while topognostic
examination was able to determine the location for both acute- and chronic onset cases. For
lesions that cannot be assessed by electrophysiology, Freyss and House−Brackmann motor
tests can be used for diagnoses and prognosis.

1. Introduction
Peripheral facial nerve disorder is the most common form of unilateral facial paralysis, and most cases
exhibit acute onset of unknown cause. The incidence is 20−30 cases per 100,000 people per year with
a peak incidence between 20 and 40 years of age. Only a small percentage requires surgical treatment.
During the acute phase, surgical indications are not dependent on etiology, but are rather dependent
on the potential for functional recovery [1-4]. Finsterer reported that 60%−80% of facial peripheral
neurological disorders are idiopathic (Bell’s palsy) [3]. This disorder can also recur in about 4%−14%
of reported cases. The incidence does not differ between sexes but the risk is 3.3 times higher in
pregnant women (usually in a third trimester) compared to non-pregnant women.
The electrodiagnosis of facial nerve disorders is achieved by well-established electrophysiological
examinations that aim to determine the severity of nerve dysfunction. In 1962, Campbell introduced a
nerve excitability test (NET) that has proven useful for prognosis in cases of facial paresis with

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The 2nd Physics and Technologies in Medicine and Dentistry Symposium IOP Publishing
IOP Conf. Series: Journal of Physics: Conf. Series 1073 (2018)
1234567890 ‘’“” 022025 doi:10.1088/1742-6596/1073/2/022025

various etiologies [5]. The current electrophysiological examinations used routinely for peripheral
facial nerve examination include the NET, nerve conduction velocity (NCV), electromyography
(EMG), maximal stimulation tests, needle electromyography (needle EMG), and blink reflex test [6-
10].
Another type of routine examination is the topognostic test, which aims to determine the lesion
location based on loss-of-function pattern. These tests include the Schirmer examination, stapedial
reflex, and gustatometry. Each method has its own advantages and limitations, and, currently, there is
no single examination that can determine the etiology and prognosis of all patients with facial nerve
disorders [1,2,6-10].
Currently, there is no international consensus for the use of a specific examination system;
therefore, some institutions and countries have developed their own grading systems for facial nerve
motor function. The Freyss system was introduced in 1973 by Sjarifuddin at the Department of
Otolaryngology Faculty of Medicine-Cipto Mangunkusumo Hospital, Indonesia, and is still used
today by the Neurology Department of Faculty of Medicine-Cipto Mangunkusumo Hospital to assess
peripheral facial nerve disorders of various etiologies [11].
In 2006, the Department of Otolaryngology Faculty of Medicine-Cipto Mangunkusumo Hospital
conducted a comparative study on the scalability of facial nerve motor function scores between the
Freyss System and House−Brackmann grading scale, another metric used routinely in the clinic. The
results indicated the equivalence of both examination systems for light and moderate facial paresis
(i.e., degree I−III with motor function of more than 66.8% according to the Freyss system and
House−Brackmann degree I−III), but not for the more severe cases (degrees IV−VI). Therefore, we
conducted a comprehensive comparison of several systems among the same patients with a wide
range of severities and etiologies.

2. Methods
This study was conducted using cross-sectional descriptive methods to assess the concordance among
the Freyss system, topognostic battery, House−Brackmann grading, and electrophysiological
investigation (nerve conductivity, needle EMG, EMG, and blink reflex) according to Cohen’s kappa
test of inter-rater agreement. The research was conducted by the neurotology clinic of the Department
of Otolaryngology and polyclinic of EMG (peripheral nerve) Department of Neurology Faculty of
Medicine-Cipto Mangunkusumo Hospital starting in August 2012 and continuing until sufficient
numbers of patients were examined (within 10 months).
The inclusion criteria were the diagnosis of unilateral facial paresis/paralysis with fast or slow
onset caused by various etiologies, 17−59 years of age, and willing to undergo the indicated series of
examinations (with signed approval letter). The exclusion criteria were refusal to participate in the
study, unconsciousness at presentation, central facial paralysis, and bilateral peripheral facial
paralysis.

3. Results
The research cohort of 44 patients included a higher proportion of males than females (25 vs. 19).
Patients ranged in age from 17 to 59 years with the largest proportion in the 40−49 year age range (18
patients, 40.9%). Paralysis was on the left side in 25 subjects (56.8%) and the right side in 19 subjects
(43.2%). All the cases were slow onset (chronic) and the most common etiological classification was
idiopathic (17 patients, 38.6%).
Table 1 presents the inter-rater agreement between two ENT specialists using the Freyss
and House− Brackmann systems. Using both systems, the most common classification was degree V
(House−Brackmann: 15 patients, 34.1%; Freyss: 23 patients, 52.3%) and there was good inter-rater
agreement for Degrees I and VI (no cases) as well as Degrees II and IV, for which the proportions
were nearly equal. However, there was poor agreement for Degrees III and V.

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The 2nd Physics and Technologies in Medicine and Dentistry Symposium IOP Publishing
IOP Conf. Series: Journal of Physics: Conf. Series 1073 (2018)
1234567890 ‘’“” 022025 doi:10.1088/1742-6596/1073/2/022025

Table 1. Inter-rater agreement using house−brackmann and freyss systems.

House−Brackmann n (%) Freyss n (%)

Degree I 0 (0.0) Degree I 0 (0.0)
Degree II 12 (27.3) Degree II 13 (29.5)
Degree III 10 (22.7) Degree III 3 (6.8)
Degree IV 7 (15.9) Degree IV 5 (11.4)
Degree V 15 (34.1) Degree V 23 (52.3)
Degree VI 0 (0.0) Degree VI 0 (0.0)

Table 2 presents an overview of the topognostic examination results for the same 44 patients. Of
the idiopathic cases, the lesions were most often suprageniculate (7 of 17 patients, 41.2%). In
infection-related cases, about half of the lesions were suprastapedial-suprageniculate (5 of 9, 55.6%).
In trauma-related cases, most were infrastapedial-supracordal, while in malignancy-related cases most
were suprageniculate (5 of 9, 55.6%).

Table 2. Overview of topognostic test results.

Etiology T
Schirmer Stapedial Reflex Gustatometry Total
N Abn N Abn N Abn
Idiopathic 7 (41.2) 10 (58.8) 6 (35.3) 11 (64.7) 3 (17.6) 14 (82.4) 17 (100)
Infection 5 (55.6) 4 (44.4) 3 (33.3) 6 (66.7) 3 (33.3) 6 (66.7) 9 (100)
Trauma 5 (55.6) 4 (44.4) 7 (77.8) 2 (22.2) 5 (55.6) 4 (44.4) 9 (100)
Malignancy 2 (22.2) 7 (77.8) 4 (44.4) 5 (55.6) 2 (22.2) 7 (77.8) 9 (100)
N: Normal, Abn: Abnormal

Table 3 presents the lesion locations as determined by electrophysiological examination. Of the 17

idiopathic cases, 12 could be classified as proximal or distal (6 patients in each group, 35.3%). Most
of the lesions related to infection and trauma were localized (7 of 9), with more than half classified as
distal (4 in each group, 44.4%), while only 5 of 9 lesions were localized in malignancy-related cases
by electrophysiology, all of which were distal. Thirteen cases could not be localized by
electrophysiological examination. The topognostic tests on these 13 subjects revealed 8 with
suprageniculate lesions, one with a suprastapedial-infrageniculate lesion, one with an infrastapedial-
supracordal lesion, and three with infracordal lesions.

Table 3. Overview of topognostic and electrophysiological test results.

Electrophysiological
Etiology Cannot be Topognostic test
Proximal Distal
determined
Idiopathic 6 (35.3) 6 (35.3) 5 (29.4) 1 (7.6)
Infection 3 (33.3) 4 (44.4) 2 (22.2) 1 (7.6)
Trauma 3 (33.3) 4 (44.4) 2 (22.2) 3(23.1)
Malignancy 0 (0,0) 5 (55.6) 4 (44.4) 8 (61.5)

Table 4 presents the electrophysiological measurements of NCV, blink reflex time, and Needle
EMG. The median R1 value for the entire group was prolonged (12.81 [range, 4.67− 55.50]), as was
the median R2 (34.17 [23.80−64.00]), while R2C latency was actually shorter than normal (36.41
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The 2nd Physics and Technologies in Medicine and Dentistry Symposium IOP Publishing
IOP Conf. Series: Journal of Physics: Conf. Series 1073 (2018)
1234567890 ‘’“” 022025 doi:10.1088/1742-6596/1073/2/022025

[0.80 to 56.0]). Needle EMG revealed spontaneous activity on the paresis side in 14 subjects
(31.8%). Normal recruitment features were found in 35 of 44 subjects (79.5%) and reduced
recruitment was found in 9 subjects (20.5%).

Table 4. Results of electrophysiological screening.

Side of Facial Paresis

Speed of Nerve Conductivity
Latency (ms) *
Median`(Min−Max)
Total Paresis side 3.28 (0−9.10)
Right 3.18 (0.0−1.76)
Left 3.38 (0−9.10)
Amplitude (µV mV)
Total Paresis side 1.17 (0−5.35)
Right 1.59 (0.0−5.35)
Left 1.88 (0.0−5.91)
Blink Reflex (ms)
*(Median, Min−Max)
Paresis side R1, All patients 12.81 (4.67−55.50)
R1 Right-side paresis 12.08 (4.67−55.50)
R1 Left-side paresis 12.50 (7.50−24.33)
Paresis side R2, All patients 34.17 (23.8−64.0)
R2 Right-side paresis 34.17 (23.8−64.0)
R2 Left-side paresis 35.33 (24.5−50.0)
Paresis side R2C, All patients 36.41 (0.80−56.0)
R2C Right-side paresis 40.08 (24.75−55.50)
R2C Left-side paresis 36.00 (0.80−56.0)

Needle EMG (n%)

Recruitment
Normal 35 (79.5)
Abnormal 9 (20.5)
Spontaneous activity
Normal 30 (68.2)
Abnormal 14 (31.8)

Cohen’s test for probability of matches (Kappa) indicated a highly significant concordance
between the Freyss system motor examination and the Seddon class electrophysiological examination
for diagnosis of moderate-to-severe facial nerve damage (Kappa R = 0.50 and p < 0.001). There was
also a moderately significant concordance between Brackmann−House system motor examination and
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The 2nd Physics and Technologies in Medicine and Dentistry Symposium IOP Publishing
IOP Conf. Series: Journal of Physics: Conf. Series 1073 (2018)
1234567890 ‘’“” 022025 doi:10.1088/1742-6596/1073/2/022025

the Seddon classification for moderate-to-severe facial nerve damage (Kappa R = 0.43 with p = 0.05).
In contrast, there was no significant relationship between electrophysiological examination and
topognostic tests for lesion location (Kappa R = 0.011 and p = 0.935). Nerve conduction latency
cannot be used when damage is permanent or the degree of damage is moderate-to-severe. In this
cohort, lesion location could not be determined in 13 patients by electrophysiological examination.
Alternatively, the topognostic test revealed the location in these patients as detailed above (Table 3).

4. Discussion
This study involved 44 patients with facial paresis/paralysis of various etiologies examined by
multiple modalities to assess concordance and the most appropriate for specific conditions. The
demographic distribution (25 men and 19 women, median age 40.9 years with most between 40−49
years) is consistent with Alberton’s report of high Bell’s palsy risk at around age 40 [15]. Volk et al
[1] and Thai [16] estimated an incidence of 20 to 30 cases per 100,000 annually with highest
incidence between 20 to 40 years of age, while Finsterer reported highest incidence rate in the age
range 15−45 years, with no difference in affected side [3]. Thus, the cohort examined here appears
representative of the patients studied in other regions. All the study subjects presented with slow
onset, indicating permanent moderate-to-severe facial nerve damage as the possibility of recovery
(regeneration) drops substantially by 9 weeks after onset [12-14]. Micro-anatomic studies have
concluded that nerve damage occurring in patients with slow onset (> 3 months) has likely reached
the axon due to intraneural pressure, damaging the epineurium and possibly the perineurium and
endoneurium. Axonal damage will impede the healing process, which can be rated by Freyss and
House-Brackmann systems [13].
The most common etiological classification in this cohort was idiopathic (38.6%), while
malignancy (scarring cell carcinoma of the ear canal) was deemed the cause in 9 patients (20.5%), and
infection in 9 patients (20.5%) including chronic suppurative otitis media in 6 (15.9%), sine herpete in
2 (4.5%) and otitis external (OE) malignancy in one (1.2%). Of the 9 cases attributed to trauma
(20.5%) which 4 experienced temporal trauma (9.1%), 3 surgery trauma (6.8%), and 2 facial trauma
(4.5%). Volk et al. [1] and Junior et al [10] reported that 60%−75% of unilateral peripheral facial
nerve paresis cases are idiopathic (Bell's palsy), while the common known causes were accidental
trauma, herpes zoster, otitis media, surgical trauma, and Schwannoma. Ozgur et al. reported an even
higher prevalence of idiopathic cases (85%) [2]. Thus, although there were substantially fewer
idiopathic cases, the distribution of etiologies in this cohort resembles that of previous studies. Further
study is required to assess whether this reflects a true population difference or selection bias.
Based on NCV and amplitude examinations, conduction block was common in this cohort.
Poernomo reported normal values of 10 ms for R1, 30 ms for R2, and 41 ms for R2C latency [17]. In
eye-blink examination, median ipsilateral R1 for the entire group was 12.81 ms [4.67−55.50],
ipsilateral R2 when on the right side was 34.17 ms (23.80−64.00), and contralateral R2C for right-
side paresis was 36.41 ms (0.80−56.0). Thus, this cohort demonstrated prolonged R1 and R2 latencies
but normal R2C latency. The R1 and R2 latencies are usually abnormal in peripheral facial nerve
paresis compared to the normal side. In this study, the healthy side showed an even greater ipsilateral
slow response stimulus (R2) than contralateral side (R2C) did. When connected with the side of
paresis will give opposite response results. The latencies of R1, R2, and R2C during ipsilateral and
contralateral stimulation can reveal whether the lesion is in the supraorbital nerve, the facial nerve, the
pons, or the medulla oblongata, or whether it is a diffuse demyelinating lesion. The results of this
study indicate facial nerve lesions based on previous findings that R1 and R2 latencies on the paresis
side are elongated while R2C values are normal in cases of facial nerve damage.
Basuki and Wijaya reported no electrical activity on EMG needle examination at rest in normal
subjects, while nerve/muscle disorders may be accompanied by spontaneous positive sharp wave
(PSW) activity or fibrillation [18]. Spontaneous activity in the form of PSW and/or fibrillation as
measured from the muscle at rest may indicate damage to the muscle due to loss of innervation and/or
primary damage to the muscle itself. In this study, spontaneous activity on the paresis side was found
by Needle EMG in 14 subjects (31.8%). This indicated that 14 patients already had damage to motor
neurons, axons, or muscles. Recognizing the presence of spontaneous activity may assist in diagnosis,
localization of the lesion, and prognosis. Spontaneous localized activity in chronic lesions suggests
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The 2nd Physics and Technologies in Medicine and Dentistry Symposium IOP Publishing
IOP Conf. Series: Journal of Physics: Conf. Series 1073 (2018)
1234567890 ‘’“” 022025 doi:10.1088/1742-6596/1073/2/022025

poorer prognosis because there is no possibility of reinnervation [19,20]. Normal recruitment was
found in 35 subjects (79.5%) and decreased recruitment was found in 14 subjects (20.5%). Thus, in 14
subjects, the number of motor units was already reduced. No increased recruitment was found in this
study.
Electrophysiological examination of the facial nerve using the Seddon classification divided the
cohort into 3 groups: neuropraxia, axonotmesis, and neurotmesis. Twelve patients were diagnosed
with neuropraxia, which is characterized by focal demyelination without axon disturbance. In
neuropraxia case, there is no Wallerian degeneration and ENMG reveals conduction block only in the
damaged segment of the nerve. The other 32 patients were diagnosed with axonotmesis or
neurotmesis. In axonotmesis, there is already damage to myelin and axons, leading to Wallerian
degeneration. In such cases, ENMG revealed conduction block in less than 10 days from onset, while
compound muscle action potential (CMAP) amplitude decreased 30%−50% by day 9 on the
contralateral side and the EMG needle potential was negative (positive sharp wave, fibrillation) with
morphological changes of the motor unit action potential (MUAP) after week 2. In cases of
neurotmesis already involving the myelin layer, axon, and buffer layer (endo-peri-epineurium),
regeneration requires surgery and ENMG will reveal conduction block in less than 10 days and
reduced CMAP amplitude at day 9, while EMG needle examination will show denervation syndrome
accompanied by MUAP changes after week 2. Electrophysiological examination is not influenced by
etiology so no examination characteristics are unique to a specific etiology. However, this modality
describes the current extent of functional damage to the facial nerve. The results of this study suggest
that patients with new/slow onset (under 3 months) and mild degree of neurological damage have better
prognosis than chronic onset patients (over 3 months) with moderate-to-severe neuronal damage.

5. Conclusion
Based on the results of this study, it can be concluded that there is a strong relationship between
Seddon electrophysiological examination and both the Freyss System and House−Brackmann grading
for patients with chronic onset moderate-to-severe facial nerve damage. However, there was no
acceptable concordance between electrophysiology and topognostic testing for determining the
location of the lesion in chronic onset moderate-to-severe cases because of the limitations of latency
and amplitude measurements. Comprehensive multi-modal examination may be necessary for
accurate diagnosis.

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