Acta Neurochir (2016) 158:181188
DOI 10.1007/s00701-015-2628-9
CLINICAL ARTICLE - FUNCTIONAL
Does arteriosclerosis contribute to hemifacial spasm?
Miki Ohta 1 & Masahito Kobayashi 1 & Naruhiko Terano 1 & Kenji Wakiya 1 &
Kenji Suzuki 2 & Takamitsu Fujimaki 1
Received: 4 August 2015 / Accepted: 28 October 2015 / Published online: 7 November 2015
# Springer-Verlag Wien 2015
Abstract
Background Hemifacial spasm (HFS) is caused by pulsative
vascular compression of the root exit zone (REZ) of the facial
nerve. However, the mechanism that causes the offending
vessels to compress the REZ has not been clarified.
Elongation of intracranial arteries due to arteriosclerosis is
one possibility, but such arteriosclerotic changes are not ob-
served very frequently among patients with HFS. The aim of
the present study was to investigate whether arteriosclerotic
changes would contribute to the pathogenesis of HFS.
Methods This study included 111 HFS patients, all of whom
were Japanese. The prevalence rates of hypertension, hyper-
lipidemia, and diabetes mellitus were examined as risk factors
of atherosclerosis, and the cardio-ankle vascular index (CAVI)
was measured as an indicator of arteriosclerotic change. The
severity of white matter lesions (WMLs) in HFS patients was
measured by magnetic resonance imaging. These data were
compared with data from healthy Japanese controls.
Results The prevalence rates of the risk factors for atheroscle-
rosis in the HFS patients were not higher than those in the
general Japanese population. The CAVI scores for the HFS
patients were similar to, or lower than those in the healthy
controls for all age groups except 60 to 69-year-old men.
The severity of WMLs in the HFS patients was not signifi-
cantly worse than that in the controls.
* Miki Ohta
m_johta@saitama-med.ac.jp
1
Department of Neurosurgery, Saitama Medical University, 38
Morohongo, Moroyama-machi, Iruma, Saitama 350-0495, Japan
2
Japan Health Promotion Foundation, 1-244 Ebisu, Shibuya-ku,
Tokyo, Japan
Conclusions It is suggested that arteriosclerotic changes are
not involved in the pathogenesis of HFS, and that vascular
compression syndromes are attributable to anatomical features
of the intracranial arteries and facial nerves formed during the
prenatal stage.
Keywords Arteriosclerosis . Cardio-ankle vascular index .
Hemifacial spasm . White matter lesions
Introduction
It is widely accepted that hemifacial spasm (HFS) is caused by
pulsative vascular compression of the root exit zone (REZ) of
the facial nerve [3, 5]. However, the pathogenesis responsible
for compression of the REZ by intracranial vessels remains
unclear. A correlation between this condition and elongation
of the intracranial arteries due to arteriosclerosis has been
speculated because the symptoms usually begin in midlife or
later [10, 11]. Furthermore, previous reports have discussed
hypertension as a risk factor for HFS [6, 7, 23, 30, 31].
Arteriosclerotic changes in the compressing arteries have been
demonstrated intraoperatively and in angiograms of HFS pa-
tients [15]. However, such changes were not always obvious
in our previous operative series of more than 500 HFS pa-
tients, most of whom showed apparently normal compressing
vessels without arteriosclerosis, as revealed using an operating
microscope. In addition, the prevalence of risk factors for
atherosclerosis, such as hypertension, hyperlipidemia or dia-
betes mellitus, was not particularly high in comparison with
that among stroke patients.
Recently, the cardio-ankle vascular index (CAVI) has been
established for evaluation of arteriosclerotic changes. The
CAVI is an index of the overall stiffness of an artery from its
origin on the aorta to the ankle, indicating the degree of
182
arteriosclerosis. The CAVI value increases with age in both
men and women [26], and it has been reported that there is a
convincing relationship between the CAVI value and diseases
resulting from atherosclerosis [9, 16, 20, 28].
In the present study, we investigated the prevalence of hy-
pertension, hyperlipidemia and diabetes mellitus in a cohort of
patients to determine whether arteriosclerosis is a risk factor
for HFS. In addition, the CAVI was measured to evaluate
arteriosclerotic changes in the HFS patients in comparison
with normal controls, and the white matter lesions (WMLs)
in the preoperative magnetic resonance (MR) images were
investigated to estimate consecutive, possible ischemic chang-
es in the brain parenchyma of patients with HFS.
Methods and materials
Clinical materials
This study included 111 consecutive patients who underwent
microvascular decompression (MVD) for HFS at our institu-
tion, Saitama Medical University Hospital, between
May 2012 and February 2014. All of the patients were native
Japanese and resident in Japan. During this period, 113 pa-
tients with HFS had consulted us about MVD and two of them
were excluded as candidates for surgery because of severe
atrial fibrillation and myelodysplasia syndrome. All of the
subjects provided written informed consent before participat-
ing in the study, which had been approved by the institutional
review board of Saitama Medical University. The mean pa-
tient age was 50.7 years (median,50 years; range, 1976 years;
SD,11.9), and 87 (78.4 %) of the patients were women. The
mean age at onset was 43.7 years (median,43 years; range,
1867 years; SD,11.9). Sixty-one patients (55.0 %) had left-
sided HFS. On admission to our institution, five men and
seven women were receiving medication for hypertension,
two men and eight women for hyperlipidemia, and one man
and one woman for diabetes mellitus. The other 92 patients
were not receiving these medications.
In 25 patients (22.5 %), the vertebral artery (VA) was in-
volved as the offending vessel, compressing the REZ of the
facial nerve. In the remaining 86 patients (77.5 %), the poste-
rior inferior cerebellar artery or/and anterior inferior cerebellar
artery compressed the REZ without involvement of the VA or
the basilar artery.
Risk factors for atherosclerosis
To examine if the risk factors for atherosclerosis are also risk
factors for HFS, the prevalence rates of hypertension, hyper-
lipidemia [high low-density lipoprotein (LDL)], and diabetes
mellitus among HFS patients were compared with those in the
general Japanese population, based on data from the National
Acta Neurochir (2016) 158:181188
Health and Nutrition Examination Survey of Japan, 2012 [2].
A total of 12,488 Japanese people (5,026 men and 7,462
women) aged 20-74 years for whom valid information was
available were extracted and used as the general Japanese
population for comparing the prevalence rates of the diseases.
The criteria for these diseases were a history of the following
conditions, or medication for them: hypertension: systolic
blood pressure 140 mmHg and/or diastolic blood pressure
90 mmHg; hyperlipidemia: serum LDL level 140 mg/dl;
diabetes mellitus: HbA1c 6.5 %.
CAVI
In addition to the risk factors for atherosclerosis, CAVI scores,
which reflect arteriosclerotic changes, were also determined in
all patients. The CAVI and blood pressure were measured
within a week before MVD surgery. During CAVI measure-
ment, patients were instructed to relax in a supine position
with cuffs applied to the bilateral upper arms and ankles.
Blood pressure was measured at the bilateral upper brachial
arteries and electrocardiograms were monitored. CAVI was
measured with a VaSera CAVI instrument (VS-1500ATN;
Fukuda Denshi, Tokyo, Japan) using the methods described
previously [27, 29]. Briefly, CAVI was calculated using the
following formula: CAVI=a{(2/P)ln(Ps/Pd)PWV2}+b,
where Ps is the systolic blood pressure, Pd the diastolic blood
pressure, PWV pulse wave velocity, P=Ps - Pd, is the
blood density, a and b are constants. The PWV was calculated
from the vascular length and latency of pulse waves propagat-
ing between the aortic valve and the ankle [27, 33]. The CAVI
values were measured bilaterally in each subject, and the mean
values were used for analysis.
The original control data for the VaSera CAVI instrument
included 69,967 individuals (34,870 men and 35,097 women)
who underwent an annual health check organized by the Japan
Health Promotion Foundation at urban workplaces in Japan
between January 2006 and March 2013. In this study, to ana-
lyze strictly and elucidate the risk factors for HFS, data for
individuals with possible risk factors for atherosclerosis were
excluded from the normal control group when determining the
CAVI. The exclusion criteria were: (1) hypertension with
medication, or a systolic blood pressure of 140 mmHg, or a
diastolic blood pressure of 90 mmHg; (2) hyperlipidemia
with medication, or a serum low-density lipoprotein (LDL)
level of 140, or a serum high-density lipoprotein (HDL) level
<40, or a serum triglyceride level of 150; (3) diabetes
mellitus with medication, or HbA1c 6.5 %, or a casual blood
glucose level of 200 mg/dl; (4) history of a cardiovascular
event, or cerebrovascular event. Finally, the normal control
group from which CAVI data were obtained comprised 28,
350 healthy individuals (10,999 men and 17,351 women)
without hypertension, hyperlipidemia, diabetes or a history
of cardiovascular or cerebrovascular diseases, and the normal
Acta Neurochir (2016) 158:181188
CAVI values were determined on this basis. The mean age of
the normal control CAVI individuals was 43.4 years (median,
41 years; range, 1691 years; SD,12.6).
White matter lesions (WMLs)
MR imaging was performed 710 days before MVD surgery,
using a 1.5-tesla imaging unit (MAGNETOM Sonata;
Siemens, Erlagen, Germany) with a quadrature head coil.
The standardized MR imaging protocol included axial T2-
weighted (repetition time/echo time [TR/TE]=4,000/88 ms)
and T1-weighted (TR/TE=660/14 ms) spin echo, and fluid-
attenuated inversion recovery (FLAIR; TR/TE = 10,000/
99 ms). The severity of WML was classified according to
the rating scale of the Atherosclerosis Risk in Communities
study [32], as follows: grade 0=no white matter signal abnor-
malities; grade 1=a discontinuous periventricular rim or min-
imal Bdots^ of subcortical white matter; grade 2=a thin con-
tinuous periventricular rim or a few patches of subcortical
WMLs; grade 3=a thicker continuous periventricular rim with
scattered patches of subcortical WMLs; grade 4=a thicker,
shaggier periventricular rim with mild subcortical WMLs,
possibly with minimal confluent periventricular lesions; grade
5=mild periventricular confluence surrounding the frontal
and occipital horns; grade 6=moderate periventricular conflu-
ence surrounding the frontal and occipital horns; grade 7=
periventricular confluence with moderate involvement of the
centrum semiovale; grade 8=periventricular confluence in-
volving most of the centrum semiovale; grade 9=all of the
white matter involved. One neurosurgeon and two radiolo-
gists, who were all blind to the patients data, evaluated and
classified the severity of WMLs in the preoperative MR
images.
Statistical analysis
All analyses were performed separately in the groups of men
and women.
The prevalence rates of hypertension, hyperlipidemia and
diabetes mellitus were classified according to age. Fishers
exact probability test was used to compare these prevalence
rates between the HFS patients and the general Japanese
population.
The CAVI data for HFS patients and the normal controls
were also classified by age group and subjected to two-way
analysis of variance (ANOVA) followed by post hoc
Bonferroni/Dunn correction. All results were reported as
meansSDs and grouped according to age. The HFS pa-
tients were divided into two groups according to the
offending vessels, i.e. VA involvement or not, and the
CAVI values were compared between these two groups
using ANOVA. All results were reported as meansSDs
and grouped according to age.
183
Results
Risk factors for atherosclerosis
The prevalence rates of hypertension and hyperlipidemia in
the female patients with HFS were significantly lower than in
the Japanese controls in the age groups of 5069 and 5059
years. In the other age groups of female HFS patients and all
age groups of male patients, there were no significant differ-
ences in the prevalence rates of hypertension, hyperlipidemia,
or diabetes mellitus compared with those among the general
Japanese population (Fig. 1). Thus, the prevalence rates of
these diseases were not high among the HFS patients, but
were rather lower in middle-aged female patients.
CAVI
In the HFS group, the average CAVI score in men and women
was 7.671.47 and 7.341.08, respectively. In the normal
control group, the average CAVI score in men and women
was 7.200.97 and 7.170.89, respectively. CAVI tended to
increase with age in both groups, and in both men and women
(Fig. 2). The CAVI score of 84.7 % for the HFS patients was
lower than the mean+1SD lines, and the CAVI score of
60.4 % for the patients was below the mean of the normal
control group without risk factors for arteriosclerosis. The
patients with VA-involved vascular compression and non-
VA-involved vascular compression are presented separately
in this figure because large vessels, such as the VA, would
be strongly influenced by systemic atherosclerotic changes.
Figure 3 shows the mean CAVI values for the HFS patients
and the normal control group at different ages. For men,
ANOVA revealed a significant effect of Bage^ on the CAVI
score [F(5, 10,918)=13.689, p<0.00001] and also a signifi-
cant interaction between Bage^ and Bgroups^ [F(5, 10,918)=
5.429, p=0.00005], but without any group effect [F(1, 10,
918)=0.740, p=0.390]. Post hoc tests demonstrated that in
the controls the CAVI score increased significantly with age:
in the HFS patients the CAVI score for patients in their 60s
was significantly higher than those for patients in their 30s and
40s, and the CAVI score for those in their 50s was significant-
ly higher than that for patients in their 40s. In addition, the
CAVI scores for male HFS patients aged 6069 years were
significantly higher than those for controls (Fig. 3, left). As for
women, ANOVA revealed a significant effect of Bage^ on the
changes in CAVI score [F(5, 17,401)=37.53, p<0.00001] and
an interaction between Bage^ and Bgroups^ [F(5, 17,401)=
2.255, p= 0.046], but without any group effect [F(1, 17,
401)=0.081, p=0.776]. Post hoc tests showed that in the con-
trols the CAVI score for each age group was significantly
higher than for younger age groups: in the HFS patients the
CAVI score for those in their 60s was significantly higher than
that for patients in their 30s and 40s, and the score for patients
184
Fig. 1 Prevalence rates of hypertension, hyperlipidemia, and diabetes
mellitus. Black columns HFS patients; gray columns data from the
National Health and Nutrition Examination Survey of Japan, 2012;
in their 70s was significantly higher than for patients in their
20s, 30s, 40s and 50s. In addition, the CAVI scores for HFS
patients aged 40-49 years were significantly lower than those
for the controls. These results indicate that CAVI scores in-
creased gradually with age, and that the scores for the HFS
patients were quite similar to those for the controls when com-
pared in each age group, except for male patients aged 6069
years. There was no significant difference in the CAVI values
between patients with non-VA-involved and VA-involved
HFS (data not shown).
Acta Neurochir (2016) 158:181188
asterisksnumbers above columns show the number of people with risk
factors/total number of people; indicate significant differences
White matter lesions
Table 1 shows the prevalence of each grade of WMLs by age
group. Most of the HFS patients preoperative MR images
showed no or only slight WMLs. In total, WMLs were found
in 27 of the 111 HSF patients (24.3 %) and only two (1.8 %)
patients had moderate grade (grades 4 and 5) WMLs. The
prevalence rates among the HFS patients appeared to be al-
most similar to, and not significantly higher than, those in the
general Japanese population (see also BDiscussion^).
Acta Neurochir (2016) 158:181188
Fig. 2 CAVI values for the normal control group and HFS patients. Gray line and gray broken lines indicate the means and standard deviations of the
normal control group. Small and large dots represent non-VA-involved HFS patients and VA-involved HFS patients, respectively
Discussion
Our study analyzed arteriosclerotic changes in patients with
HFS by investigating the prevalence rates of hypertension,
high LDL cholesterol levels, and diabetes mellitus as risk
factors for atherosclerosis, and we also assessed CAVI scores
and the prevalence rates of WMLs as an index of brain arte-
riosclerosis. All of the study results indicated that arterioscle-
rotic changes do not contribute to the pathogenesis of HFS,
especially in individuals younger than 60 years of age.
Among our HFS patients, who were all native Japanese, the
prevalence rates of the risk factors for atherosclerosis were all
similar to, or even lower than, those indicated by data for the
general Japanese population obtained in the national survey of
Fig. 3 CAVI values of the normal control group and HFS patients in each
age group. Left: CAVI values for male controls and HFS patients; right:
those of female controls and HFS patients. Significant differences are
indicated by plus, asterisk and sharp symbols (see text). Black columns
185
Japan. These findings indirectly but clearly indicate that these
diseases are not risk factors for HFS, and that arteriosclerotic
changes in HFS patients are similar to, or even less marked
than those in the general Japanese population.
The CAVI is an index of the overall stiffness of an artery
from its origin on the aorta to the ankle. When the vascular
walls of the aorta and elastic arteries are quite stiff, they do not
cushion the pulsatile flow generated by cardiac beats as effec-
tively [21]. Without this buffering capacity, such pulsations
will extend into the microvasculature, and preferentially into
organs with high perfusion such as the brain and kidneys [21,
22]. In individuals with arteriosclerosis, high pulsation pres-
s u r e a n d f l o w w i t h o u t e n e rg y l o s s w i l l i n d u c e
microhemorrhages and infarcts in these organs [21]. Indeed,
HFS patients; light-gray columns normal control. Data are presented as
meansSD. Error bar for male HFS patients in their 20s is not shown
because there was only one patient
186
Table 1 White matter lesions
(WMLs) in each age group Age (years) Total (n) Grade of WMLs (n)a
0 1
<40 18 18
40-49 34 31
50-59 30 20
60-69 21 13
70 7 2
a
No patient showed WMLs with grade >5
the CAVI score is significantly greater in patients with ische-
mic cerebrovascular disease, such as WMLs, large artery ath-
erosclerosis, and small vessel occlusion [4, 28]. Our CAVI
data for HFS patients, however, revealed no significant differ-
ences between HFS patients and normal controls without risk
factors for atherosclerosis, demonstrating directly that arterio-
sclerotic changes do not form the basis of HFS pathogenesis.
WMLs, sometimes described as leukoaraiosis, are fre-
quently detected in MR images of elderly individuals, but
are especially common in patients with known vascular risk
factors and symptomatic cerebrovascular disease [24]. Since
the pathophysiological mechanism of WMLs is similar to that
of stroke, WMLs have been considered an intermediate sur-
rogate of stroke [8]. Park et al. [25] analyzed the clinical data
and MR images of 1,030 healthy Japanese individuals aged
2878 years (mean age, 52.7 years) and found that the prev-
alence rate of WMLs was 28.8 % (Table 1). The prevalence of
WMLs in our HFS patients did not appear to be higher than,
but rather similar to those in their Japanese population in all
age groups. These findings, together with data for CAVI and
the prevalence rates of hypertension, hyperlipidemia and DM,
demonstrate that arteriosclerotic changes cannot explain the
pathogenesis of HFS.
It has been suggested that HFS patients with VA-involved
compression would show atherosclerotic changes [17, 18].
However, in our present series, there was no significant dif-
ference in CAVI values between patients with VA-involved
compression and those with non-VA-involved compression.
While the CAVI values for HFS patients increased with age,
the changes were quite similar to those observed in normal
controls, and indeed almost all the data for the HFS patients
were within 1 SD, i.e. normal limits. Thus, it appears unlikely
that arteriosclerotic changes contribute essentially to the path-
ogenesis of vascular compression, even in elderly HFS
patients.
While it is widely recognized that the cause of HFS is
vascular compression at the REZ of the facial nerve [1], the
pathogenesis that causes small intracranial arteries to com-
press the REZ has not yet been clarified. A correlation be-
tween vascular compression and arteriosclerosis has been
speculated [10, 13, 31] because the symptoms of HFS often
Acta Neurochir (2016) 158:181188
Overall prevalence rates (%)
2 3 4 5 This study Park et al. [25]
0 0 0 0 0 0.0 3.6
3 1 0 0 0 11.8 12.5
6 3 0 1 0 33.3 29.5
2 4 2 0 0 38.1 49.2
0 4 0 0 1 71.4 81.2
appear in middle-aged or elderly individuals, and the
offending arteries are likely to be elongated and arteriosclerot-
ic. In contrast, different mechanisms such as the involvement
of veins as the offending vessels [19], a thickened arachnoid
surrounding the offending vessels [14], and anatomical varia-
tions at the REZ [12] have been suggested for HFS in the
young, based on observations in case reports. Our study of
the HFS patients has shown that the prevalence of risk factors
for atherosclerosis, the CAVI data and the incidences of
WMLs were similar to or lower than those in the control
group, except for CAVI in 60 to 69-year-old men. These
observations imply that arteriosclerotic changes in elderly
men with HFS would be slightly more marked than those in
normal controls, possibly contributing to the pathogenesis of
vascular compression. However, the number of elderly male
patients in our study was not sufficiently large, and therefore
further study will be required to elucidate the contribution of
atherosclerosis to the pathogenesis of HFS in elderly male
patients. In contrast, patients showing onset of HFS in youth
or middle age would have minimal arteriosclerotic changes,
and the early onset of symptoms in such patients may be
attributable to anatomical features that developed in the pre-
natal stage, resulting in compression of the REZ of the facial
nerves.
A possible limitation of this study is that the HFS patient
population may have included only those who were healthy
enough to be candidates for neurosurgical intervention. In our
series of 113 patients, however, only two were excluded as
surgical candidates because of cardiological or hematological
problems. Furthermore, as a control for the CAVI data, we
analyzed normal, healthy individuals without risk factors for
atherosclerosis, thus successfully avoiding any bias for HFS
patients.
Conclusion
The results of this study support the contention that arterio-
sclerotic changes do not contribute to the pathogenesis of
HFS. Presumably, the anatomical features of the compressing
arteries and the REZ of facial nerves would contribute to the
Acta Neurochir (2016) 158:181188
manifestation of vascular compression syndromes, and any
arteriosclerotic changes that are present in some elderly male
patients may contribute to HFS to some extent.
Acknowledgments We would like to thank Drs. Mamoru Niitsu and
Kaiji Inoue for diagnosis and helpful comments on the MR images of the
patients.
For this work, support was received from a Grant-in-Aid for Young
Physicians from Saitama Medical University Hospital Grant Number 24-
C-1 (Miki Ohta) and the Japan Society for the Promotion of Science
KAKENHI Grant Number 23592105 (Masahito Kobayashi).
Compliance with ethical standards
Conflict of interest None.
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58(Suppl 1):S95S98
188
Comment
Hemifacial spasm due to vascular compression of the facial nerve repre-
sents an important neurologic issue that can be effectively treated by
microvascular decompression. At the time of surgery many surgeons
describe thickened arteries, suggestive of atherosclerotic disease,
compressing the root exit zone. This description has persisted in the
literature for decades with little solid research into this aspect of the
disease.
The authors compared the risk factors hypertension, hyperlipidemia,
and diabetes mellitus as well as cardio-ankle vascular indices (CAVI), a
measure of global atherosclerosis (Izuhara et al. 2008), and cerebral white
matter changes, as a measure of local atherosclerosis (Park et al. 2015), in
a series of 111 patients with hemifacial spasm who had undergone mi-
crovascular decompression, and compared these factors to the healthy
population. They found no significant difference in rates of risk factors
or degrees of local or global atherosclerosis between the hemifacial spasm
population and the healthy population. Arteriosclerosis is often cited as an
etiology for hemifacial spasm and this article provides a fresh perspective
on this assumption (Jannetta 1977; Kondo et al. 1981). The authors con-
firm the findings of the cadaver studies performed by Hosemann (1983).
The authors are to be commended on the fine work in evaluating this
important issue. While their work does not elucidate a definite pathophys-
iologic etiology or risk factor for microvascular compression causing
Acta Neurochir (2016) 158:181188
hemifacial spasm, it does lay the groundwork for further study. Further
investigations of the association between arteriosclerosis and hemifacial
spasm in the elderly population and study of embryological contributions
to the genesis of hemifacial spasm are warranted.
Ryan Hofler
Christopher M. Loftus
IL, USA
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