43(3):319-323,2002

CLINICAL SCIENCES

Blink Reflex in the Prediction of Outcome of Idiopathic Peripheral Partial Facioparesis:

Follow-up Study

Ivan Mikula, Snje´ana Miškov, Ru´ica Negovetiæ, Vida Demarin

Department for Neurology and Clinical Neurophysiology, Sisters of Mercy University Hospital, Zagreb, Croatia

Aim. To determine the value of the blink reflex as a predictor of outcome of idiopathic peripheral partial facial paresis.
Methods. The study included 30 patients suffering from acute idiopathic peripheral facioparesis and 30 age- and
sex-matched healthy controls. Patients with symptomatic disease were excluded on the basis of neuroradiologic and
laboratory findings. We stimulated the supraorbital foramen and recorded the evoked response from both orbiculares
oculi muscles. We measured the ipsilateral early phasic component (R1) and bilateral late tonic component (ipsilateral
R2 and contralateral R2’) immediately, and a week and 6 months after the first test.
Results. In the acute phase of idiopathic peripheral partial facioparesis, the blink reflex showed slightly prolonged la-
tencies and greatly reduced amplitudes of both R1 and R2 and the normal latencies and amplitudes of R2’. All subjects
showed clinical symptoms and typical electromyographic (EMG) changes, whereas 24 had blink reflex abnormalities.
One week after the onset, all patients were still symptomatic and showed EMG changes, but blink reflex abnormalities
remained in only 11 patients. Six months after the onset, 21 patients became asymptomatic and showed no EMG
changes, 7 had no clinical symptoms but showed chronic neurogenic EMG changes, whereas 2 showed both clinical
symptoms and EMG changes. Blink reflex abnormalities were observed in 6 patients. The amplitudes of R1 immedi-
ately and one week after the onset were the best predictors of residual motor deficit.
Conclusions. Blink reflex is a useful tool for follow-up and recovery prognosis in patients with partial idiopathic
facioparesis, especially in the early recovery phase.
Key words: blinking; electromyography; facial muscles; facial paralysis; nervous system physiology; reflex

Blink reflex can be elicited by either electrical or
magnetic stimulation of the supraorbital nerve (1,2),
and the responses of bilateral orbicularis oculi mus-
cles can be recorded. The ipsilateral early blink com-
ponent (R1) can be observed together with an ipsila-
teral early eye movement at a latency of 10-15 ms. Bi-
lateral late components (R2, R2’) can be observed at
40-70 ms (3). R3 component has also been described
and considered nociceptive (4). Studies of the blink
reflex provide useful information on neurophysio-
logic status of the trigeminal and facial nerves (5), the
brainstem, and the cranial end of the cervical seg-
ment of the spinal cord (6), and show a high level of
correlation with magnetic resonance imaging (MRI)
findings (7).
The test is particularly useful in Bell’s palsy pa-
tients with hemifacial spasm and synkinesis (8,9). It
can demonstrate hyperexcitability of central motor
neurons and its return to normal level after recovery
(10). It can also indicate the quality of lower brain
functions, such as feeding (11,12). Blink reflex laten-
cies are prolonged and amplitudes decreased in pe-
ripheral facial palsy, some polyneuropathies (e.g., dia-
betic and uremic), Guillain Barre’s syndrome (13,14),
Behcet’s disease (15), Chiari II malformation (16), and
Wallenberg’s syndrome (17). R2 time can be used to
diagnose demyelinating diseases (18). Absence of the
blink reflex has been demonstrated in Holmes-Adie
syndrome (19). Dysfunction of small afferent fibers of
the trigeminal nerve is frequent in patients with dia-
betic and other sensory polyneuropathies (20). Habit-
uation of blink reflex and occurrence of the late R3
component are found in psychotic disorders and mi-
graine (21,22). Blink reflex has also been used for fol-
low-up after a cross facial nerve graft (23). Blink reflex
can be inhibited by anti-migraine drugs, sumatriptan
and zolmitriptan (24). Excess thyroid hormone inhib-
its the blink response (25), as well as clonidine (26)
and tension headache (27). Its parameters can also be
modified by a pre-pulse caused by somatosensory in-
puts (28,29). Teeth clenching facilitates blink reflexes
(30). The facilitation of the blink reflex and the ap-
pearance of R3 are also seen in tetanus and stiff per-
son syndrome (31). The same effect may be observed
contralaterally to the affected side in patients with pe-
ripheral facial palsy when the affected side is stimu-
lated (32).

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Mikula et al: Blink Reflex and Facial Palsy Outcome
Although the blink reflex has been accepted as a
valuable diagnostic tool, there have been no studies
on specific parameters of the blink reflex, describing
which of the parameters are diagnostically useful and
prognostically valuable, in which cases, and when.
In our clinical practice we have observed that pe-
ripheral facial paresis inhibits the blink reflex and that
its recordable abnormalities precede other clinical
and neurophysiologic changes. These abnormalities
seem to correlate with the disease outcome, or more
specifically, with the residual motor deficit.
In this study we assessed the value of the blink
reflex as a predictor of the outcome of idiopathic peri-
pheral partial facial paresis. We aimed to determine
the applicability of several blink reflex parameters in
the prediction of residual motor deficit, such as laten-
cies and amplitudes of ipsilateral R1 and R2 compo-
nents, and contralateral R2’ component.
Subjects and Methods
Subjects
The study comprised 30 patients (17 men and 13 women;
mean age 37.7±7.2 years) diagnosed with idiopathic peripheral
facial paresis according to the International Classification of the
Diseases (ICD-X) criteria (an abrupt, isolated, unilateral, periphe-
ral facial paralysis without detectable cause). The patients were
included in the study within 3 days after the onset of the disease.
Patients suffering from tumors, diabetes, thyroid disease,
and other neuropathies or taking medications that could affect the
test results (clonidine, sumatriptan or zolmitriptan) were excluded
from the study (7 subjects: 3 with diabetes, 1 taking sumatriptan,
1 with neurofibromatosis, 1 with neurinoma of the statoacoustic
nerve, and 1 with Melkersson-Rosenthal syndrome).
The control group comprised 30 age- and sex-matched
healthy controls (17 men and 13 women, mean age 35.2±8.1
years).
The symptomatic disease was ruled out by means of thor-
ough disease history taking and neurological examination, as
well as by specific laboratory and radiological tests. Laboratory
findings (sedimentation rate, complete blood count, and differen-
tial white blood cell count) showed no sign of an inflammatory
disease, blood glucose was normal, as well as serum electrolytes,
triiodothyronine (T3), thyroxin (T4), thyrotropin (TSH), serum
gamma-gluttamyl-transpeptidase (SGGT), serum glutamic-oxalo-
acetic-transaminase (SGOT), and serum glutamic-pyruvic-trans-
aminase (SGPT). X-ray examination of the paranasal sinuses and
pyramids gave normal findings. Computerized tomography (CT)
of the brain, with special consideration to basal structures,
showed no pathology.
Methods
Recordings were made with the Medelec “Sapphire” equip-
ment (Old Woking, Surrey, UK) via cup electrodes located over
both orbiculares oculi muscles (active electrode above the lateral
and reference electrode above the lower part of the muscle) and
one non-cephalic ground electrode located over the left wrist.
The supraorbital foramen was stimulated with a single stim-
ulus of 15-20 mA (sweep 100 ms, division 10 ms, gain 5 mV).
The evoked response was recorded from both orbiculares oculi
muscles. The amplitudes and latencies of ipsilateral early phasic
component (R1) and bilateral late tonic components (R2, R2’)
were measured at the first negative peak.
The measurements were made in the acute phase of the ill-
ness and repeated 1 week and 6 months after the onset of symp-
toms. All patients began taking oral prednisone (80 mg/day)
within 3 days after the onset of disease. The initial dose of predni-
sone was administered for a week and then tapered gradually
over the following week. The results were compared with those
of the age and sex-matched normal controls (volunteers among
the hospital staff and students). Due to the generally unpleasant
nature of electrical stimulation, only a single testing was per-
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Croat Med J 2002;43:319-323
formed on subjects from the control group. All the participants
gave their informed consent.
Statistics
Median, minimum, and maximum values of amplitudes
and latencies were calculated for the blink reflex components R1,
R2, and R2’ in the two groups of subjects (patients being tested
three times and the controls only once).
As the data were not normally distributed, non-parametric
Wilcoxon Mann Whitney’s test on ranks was used to determine
significant differences between the patient and control group
(p<0.05). The C5.0 algorithm was used to determine the input
variables on the basis of which the patients divided in two groups
according to the residual motor deficit (recovered and non-recov-
ered) could be discriminated.
Results
Median values of amplitudes (mV) of both
ipsilateral components R1 and R2 were lower in pa-
tients suffering from idiopathic peripheral facial pare-
sis, especially in the acute phase, than the median val-
ues of amplitudes of contralateral R2’ component,
which were similar to those in the control group (Fig.
1). Median values of latencies (ms) of both ipsilateral
components R1 and R2 were higher in patients with
idiopathic peripheral facial paresis, especially in the
later phases, whereas the latencies of contralateral
R2’ component showed values similar to those in the
control group (Fig. 2).
Wilcoxon Mann Whitney’s test on ranks showed
that the patients differed significantly from the control
group, both in the amplitudes and latencies. Signifi-
cant differences were found between the amplitudes
of R1 components measured in patients immediately
after the onset of disease and a week later, and those
measured in healthy controls. Significant differences
were also found between the amplitudes of R2 com-
ponent measured in patients immediately after the
onset of disease and a week later, and those measured
in healthy controls. Six months after the onset, the dif-
ferences ceased to be significant. R2’ amplitude val-
ues in patients never differed significantly from those
measured in the control group (Fig. 1). The latencies
of R1 and R2 components immediately after the on-
set, and especially after a week, differed significantly
Figure 1. Median and minimum and maximum values of
amplitudes (mV) of blink reflex components R1, R2, and
R2’ immediately after the onset of the disease (open circle)
and a week (closed circle) and six months after (open
rhomb) the onset, compared with amplitude values of the
control group (closed rhomb). Asterisk indicates p<0.05 vs
controls, Wilcoxon Mann Whitney’s test.
Mikula et al: Blink Reflex and Facial Palsy Outcome
from those of normal controls. The latency values mea-
sured six months after the onset of the disease did not
differ significantly from those of normal controls, and
neither did R2’ latencies (Fig. 2).
Figure 2. Median and minimum and maximum values of la-
tencies (ms) of blink reflex components R1, R2, and R2’ im-
mediately after the onset of the disease (open circle) and a
week (closed circle) and 6 months after (open rhomb) the
onset, compared with latency values of control group
(closed rhomb). Asterisk indicates p<0.05 vs controls,
Wilcoxon Mann Whitney’s test.
Clinical symptoms and neurogenic EMG
changes were found in all patients in the acute phase
of disease, whereas blink reflex abnormalities were
observed in 24 of them. A week after the onset, all
symptoms and EMG changes were still present in all
patients, but the latency and amplitude abnormalities
of R1 and R2 remained in only 11 out of 30 patients.
Six months after the onset of symptoms, 21 patients
became asymptomatic and their EMG showed no
changes, 7 had no clinical symptoms, but the chronic
neurogenic EMG changes were observed, whereas 2
showed the residual weakness of the facial muscles
and the signs of denervation in EMG. Blink reflex ab-
normalities, especially the decrease of the R2 ampli-
tude, were observed in 6 patients (Fig. 3).
120
100
80
Percent
60
40
20
0
immediately 1 week after 6 months after
Figure 3. Presence of symptoms (%) on physical examina-
tion (open columns), electromyography findings (closed
columns), and blink reflex abnormalities (gray columns) in
patients with idiopathic peripheral facial paresis at different
time points after the onset of disease.
Twenty-one patients showing neither the resid-
ual motor deficit nor chronic neurogenic EMG
Croat Med J 2002;43:319-323
changes recovered from the disease, whereas the re-
maining 9 did not. The C5.0 algorithm was used to
determine the input variables that differed between
the recovered and non-recovered patients (Fig. 4).
The decision tree calculation showed that the ampli-
tudes of R1 immediately (accuracy 83.3%) and a
week after the onset (accuracy 90.0%) were the best
classifiers for predicting the residual motor deficit.
Accuracy calculation remained stable after the
cross-validation testing of classifiers. The decision
tree calculation showed that the amplitudes of R1 im-
mediately and a week after the onset were the best
classifiers for predicting the residual motor deficit.
Decision tree:
£0.09: non-recovered (4/12)
R1 amplitude immediately
>0.09: recovered (1/18)
(a) (b) classified as
--- ---
17 4 (a): class recovered
1 8 (b): class non-recovered
Evaluation on training data (30 cases):
Decision tree
---------------------
Groups Errors accuracy 83.3% (80% after cross-validation)
2 5 (16.7%)
£0.09: non-recovered (0/6)
R1 amplitude one week after
>0.09: recovered (3/24)
(a) (b) classified as
---
21
---
0 (a): class recovered
3 6 (b): class non-recovered
Evaluation on training data (30 cases):
Decision tree
---------------------
Groups Errors
accuracy 90% (90% after cross-validation)
2 3 (10%)
Figure 4. The decision tree for the amplitudes of R1 imme-
diately and a week after the onset of disease as classifiers for
predicting the residual motor deficit. Sample divided in two
groups according to the residual motor deficit (group a – re-
covered, group b – non-recovered), number and percent-
age of prediction errors, accuracy calculation and cross-val-
idation testing of classifiers.
Discussion
In patients with idiopathic facial paresis in the
acute phase, the blink reflex showed slightly pro-
longed latencies and severely reduced amplitudes of
both R1 and R2 on the afflicted side and the normal
latencies and amplitudes on the contralateral side,
proving the dysfunction in the efferent part of the re-
flex cycle. All patients had clinical symptoms, and
their EMG revealed acute neurogenic changes.
Twenty-four patients showed blink reflex abnormali-
ties. Both the axon damage and (less pronounced)
conduction block were significant in this phase.
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Mikula et al: Blink Reflex and Facial Palsy Outcome
These findings were concordant with those of Eekhof
et al (8) and Calleja et al (13). A week after the onset of
the disease, all patients were still symptomatic and
there were changes in their EMG findings, but the la-
tency and amplitude changes of R1 and R2 remained
in only 11 patients. It should be emphasized that the
conduction velocities – indicators of a conduction
block – were significantly changed at the time,
whereas the reduction of amplitudes – indicators of
an axonal damage – was not so pronounced any lon-
ger. However, the amplitudes were still significantly
lower than those measured six months after the onset
or in the group of healthy controls. To our knowl-
edge, this is the first report on the blink reflex after a
week of follow-up. Celik et al (9) investigated the dis-
ease 3 weeks after the onset and had similar findings.
In our study, 21 patients become asymptomatic 6
months after the onset of symptoms, and their EMG
showed no changes; 7 had no clinical symptoms, but
the chronic neurogenic EMG changes could have
been observed; and 2 showed the residual weakness
of the facial muscles and the signs of denervation in
EMG. Blink reflex abnormalities, especially the de-
crease of the R2 amplitude, were observed in 6 pa-
tients, 4 of them in the group with EMG changes and
no clinical symptoms and 2 of them in the group with
both EMG changes and clinical symptoms. The pa-
tients showing residual clinical and EMG changes
were those 11 who still had blink reflex abnormalities
a week after the onset of symptoms. These findings
are concordant with most clinical investigations deal-
ing with the residual impairment after the chronic
course of idiopathic peripheral facial paresis
(14,17,18).
In conclusion, the blink reflex is a valuable tool
for follow-up and recovery prognosis of the partial id-
iopathic facial paresis, especially in the early recov-
ery phase and when combined with EMG and
neurography of the facial nerve. Furthermore, ampli-
tudes of ipsilateral R1 and R2 components could be
used as the primary predictive factors in the earliest
course of illness. R1, and particularly R2 latency,
should assume that role in later phases of the disease,
but not sooner than a week after the onset.
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Received: April 5, 2001
Accepted: April 19, 2002
Correspondence to:
Ivan Mikula
Department for Neurology
Sisters of Mercy University Hospital
Vinogradska cesta 29
10000 Zagreb, Croatia
ivan.mikula@zg.tel.hr

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