ORIGINAL ARTICLE
Angiographic manifestations and operative ﬁndings
with 70 cases of hemifacial spasm: relationof common trunk anomalies
Taro Oizumi, Takayuki Ohira1 and Takeshi Kawase1
Department of Neurosurgery, Ise Keio Hospital, Keio University and 1Department of Neurosurgery
School of Medicine, Keio University, Japan(Received for publication on April 8, 2003)

Abstract. The relations between angiographic manifestations and operative ﬁndings of hemifacial
spasm were studied in 70 cases between 1988 and 2001. Vertebral angiography was performed, andTowne, straight AP, and lateral projections were routinely examined. The dominant anterior inferior
cerebellar artery (AICA) directly compressed the facial nerve root exit zone in 26 cases, the dominantposterior inferior cerebellar artery (PICA) in 20, the AICA in 13, the PICA in 2, and the vertebral
artery (VA) in 9. Compression by multiple vessels was observed in 11 cases. Anatomical variations of
the affected AICA and PICA were classiﬁed into 3 groups according to their origins and distributionsof blood supply: normal distribution of AICA and PICA in 18%, common trunk anomaly with dominant AICA (basilar artery origin) in 48% and common trunk anomaly with dominant PICA (vertebral
artery origin) in 34%. Analyses of the angiograms revealed signiﬁcantly increased numbers of common
trunk anomalies compared with cases with normal angiograms. In 18 of the 20 cases of unilateralcommon trunk anomalies, facial nerves were compressed by the dominant artery. Preoperative vertebral angiograms may clarify the offending vessels and their sites in most hemifacial spasm cases, thusincreasing the safety of surgical interventions. (Keio J Med 52 (3): 189–197, September 2003)
Key words: hemifacial spasm, microvascular decompression, vertebral angiogram, common trunk
anomaly

Introduction
Hemifacial spasm is a movement disorder characterized by intermittent, involuntary, irregular, unilateral,
tonic or clonic contractions of muscles innervated by
the ipsilateral facial nerve. In a typical case, the spasm
starts from the orbicularis oculi muscle, buccinator.
Cushing1 ﬁrst suggested the palsies of cranial nerves
could be caused by vascular compression. Vasculararterial compression of the VIIth cranial nerve inpatients with hemifacial spasm was ﬁrst reported byCampbell Keedy.2 In 1962, Gardner and Sava3 proposed vascular decompression for treatment of trigeminal neuralgia and hemifacial spasms. Fifteen years
later, the pioneering work of Jannetta et al.4 provided agreat contribution to understanding the pathophysiological mechanism of this rhizopathy.

The concept of neurovascular decompression for
the treatment of hemifacial spasm is now widely accepted. Recently, in cases of microvascular decompression, some hospitals performed preoperative cerebral
angiography. In our hospital, most patients with hemifacial spasm undergo cerebral angiography to exclude
vascular diseases, and to estimate the operative ﬁndings. In the present study, we understook an anatomical
analysis of compressing arteries, especially for common
trunk anomalies in comparison with operative ﬁndings.
Patients and Methods
Microvascular decompressions and preoperative cerebral angiography were performed between 1988 and2001 in 70 patients with hemifacial spasm. The patientgroup included 45 females (64.3%) and 25 males

Reprint requests to: Dr. Taro Oizumi, Department of Neurosurgery, Ise Keio Hospital, 2-7-28 Tokiwa, Ise city, Mie, 516-0041, Japan, e-mail:taro@taro55.com
189

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a) distance from the clivus

Oizumi T, et al: Angiographical manifestation of hemifacial spasms

14.0 G 1.6 mm (M G SD)b) perpendicular line 5 mm posteriorly from EACc) radius of its area

2.4 G 0.3 mmd) the most medial part from the midline 13.1 G 1.6 mm
A

Fig. 1 Schematic illustration for measurements around the VIIthroot exit zone.

(35.8%), ranging in age from 25 to 74 years (mean age,
50.9 yr). The symptoms were on the left side in 41 cases(58.6%) and right side in 29 cases (41.4%). The mean
duration of symptoms was 5.4 years (range, 1–26 yr).
Cerebral angiography of bilateral internal carotid
arteries and bilateral vertebral arteries was performedby the Seldinger method with stereographic straightanterior-posterior and lateral views. Digital subtraction
was performed in most cases. There were no complications associated with cerebral angiography.
The facial nerve exit zone is present in a circle with aradius of 2.5 mm, and center at the point 14 mm fromthe clivus on the perpendicular drawn from the site 5mm posterior to the opening of the external acoustic
meatus to the anthropologic base line on lateral images.
On frontal images, this zone is present 13 mm from themedian line (Fig. 1).5 Therefore, on vertebral angiograms, the sites of the facial nerve exit zone and thecompressing vessel, and surrounding angioarchitecture
were estimated before operation.
Microvascular decompression was performed in allcases, and the facial nerve exit zone was decompressedby removing the compressing vessel.6,7 After the operation, the anatomical relations of the compressing vessels and area were compared with the angiographic
ﬁndings.

B
Fig. 2 Right vertebral angiogram in a right hemifacial spasm patient.
(A) Straight AP view. (B) Lateral view.

As an example, in the patient shown in Fig. 2, theright side was affected, and the above-described method
and the estimation of the below-described angioarchitecture before operation suggested compression of the
facial nerve exit zone by the metal loop of the dominant
AICA. Fig. 3 shows the operative ﬁndings. As preoperatively estimated, the site of the bifurcation of theinternal auditory artery from the metal loop of the rightdominant AICA compressed the facial nerve exit zone.
As shown in Fig. 4, the site of the compressing vessel
could be determined on vertebral angiograms.
Anatomical Relation of the Cerebropontine
Angle ArteryWe deﬁned the anterior inferior cerebellar artery(AICA) as the artery originating from the basilar artery, and the posterior inferior cerebellar artery (PICA)
as the artery originating from the vertebral artery(VA).8

Keio J Med 2003; 52 (3): 189–197

191

A

Fig. 3 Schematic illustration of an operation in the case of righthemifacial spasm.

B

The AICA generally arises from the basilar artery,runs lateroinferiorly, forming a meatal loop at thelateral end of the pontomedullary sulcus, i.e., aroundthe VIIthVIIIth cranial nerves, and subsequently
divides into the rostral and caudal branches. The rostralbranch runs along the ﬂocculus, reaching the great horizontal ﬁssure, and mainly supplies the cerebellar petrosal surface above the ﬁssure. The caudal branch runsin the direction lateroinferior to the VIIthVIIIth cranial nerves, supplying the cerebellar petrosal surface.9
The PICA originates from the VA, but its subsequent direction varies. When its origin level is high andnear the vertebrobasilar junction, the PICA is associated with the facial nerves in some cases. The PICA
ascends, forms an upward convex loop at the lateralend of the pontomedullary sulcus, approaches theVIIthVIIIth cranial nerves, and posterosuperiorly runs
as the lateral medullary segment, reaching the dorsal
surface of the medulla oblongata.
The distributions of the AICA and PICA in the cerebellum are generally complementary. When the PICA
is hypoplastic, the AICA is well developed, supplying
the original PICA territory. When the PICA is completely absent, the well-developed AICA originates as a

Fig. 4 Right vertebral angiogram. (A) Straight AP view. Anatomicalclassiﬁcation with bilateral dominant AICA. Compressing portion ofright dominant AICA is indicated by an arrow. (B) Lateral view.
Compressing portion is indicated by an arrow.

common trunk (dominant AICA) from the basilar artery, feeding both the original AICA territory (rostralbranch) and PICA territory (caudal branch). In contrast, when the AICA is hypoplastic, the PICA is welldeveloped. When the AICA is completely absent, thewell-developed PICA originates as a common trunk
from the VA (dominant PICA).10–13
Therefore, with these anatomical considerations,images were interpreted, and the site of the facial nerve
origin was estimated based on the positional relation
to the internal acoustic foramen, and the compressing
vessel and vessels running near the compressing vessel
were also evaluated before operation.14,15 In addition,
the presence or absence of common trunk anomalies,
the levels of the origins of the AICA and PICA, theircalibers at the origin, bifurcation site, and the level ofthe cranial loop and the largest caliber of the fourth
segment of the VA were evaluated.

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Oizumi T, et al: Angiographical manifestation of hemifacial spasms

A

A

B

B

Fig. 5 Right vertebral angiogram. (A) Straight AP view. Anatomicalclassiﬁcation with normal distribution of AICA and PICA. Compressing portion of right AICA indicated by an arrow. (B) Lateralview. Compressing portion indicated by an arrow.

Fig. 6 Left vertebral angiogram. (A) Straight AP view. Anatomicalclassiﬁcation with left dominant PICA and right dominant AICA.
Compressing portion of left dominant PICA indicated by an arrow.
(B) Lateral view. Compressing portion indicated by an arrow.

Results
The nerve-compressing vessel was the AICA, PICA
or VA. Patients with compression by veins or withoutcompressing vessels were excluded.
Originating patterns of the AICA and PICA
The originating patterns of the affected AICA andPICA were classiﬁed with consideration of their distribution into 3 types: normal distribution in which the
AICA is present independently of the PICA (Fig. 5);
dominant AICA showing a common trunk of the twoarteries originating from the basilar artery (Fig. 4);
dominant PICA showing a common trunk of the twoarteries originating from the VA (Fig. 6).
Types II and III were deﬁned as common trunk
anomalies. The AICA was present as multiple vessels in

2 patients, of whom 1 with the PICA independent fromthe AICA vessels was considered to have a normal distribution, and the other without a normal PICA who
had one of the AICA vessels as a common trunk wasconsidered to have a dominant AICA. There were 3
patients with the PICA as multiple vessels. All of themwere considered to have the dominant PICA because anormal AICA was absent, and one of the PICA vessels
was present as a common trunk.
Compressing vessel
The compressing vessel was the dominant AICA in
26 patients (37%), dominant PICA in 20 (29%), AICA
in 13 (19%), PICA in 2 (3%), and VA in 9 (13%). Indirect compression by the VA was observed in 2 patients with a dominant AICA, 3 with a dominant PICA,

Keio J Med 2003; 52 (3): 189–197
Table 1

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Operative Findings

Table 3 Common Trunk Anomaly and Compression Vessel (Without direct or indirect VA compression)Compressing vessel

No. of cases

dominant AICA
dominant PICA
AICA
PICA
VA

26 (37%)*20 (29%)**13 (19%)***
2 (3%)
9 (13%)a) Normal Distribution on One Side and Common Trunk Anomaly on
the other Side
Rate of compression vessel
dominant AICA
dominant PICA

13/15 (87%)
5/5 (100%)

Including indirect VA compression * 2 cases, ** 3 cases, *** 6 cases.
b) Cases of Bilateral Common Trunk Anomaly
Table 2 Distribution of HFS and Normal Cases by Common Trunk
Anomaly (Without direct or indirect VA compression)

Normal distribution
dominant AICA
dominant PICA

50 cases of HFS

100 cases of normal 16

9 (18%)
24 (48%)17 (34%)

48%
40%
10%

and 6 with the AICA as the compressing vessel (Table1). Indirect compression by the VA means as follows:
the AICA or PICA is between the VA and the nerve,
they compress the nerve. Furthermore the VA compresses the nerve on that vessel. Direct compression by
the VA means that only the VA compresses the nerve
directly.
Compression vessel in patients excluding those withdirectindirect compression by the VA

Rate of compression vessel
with a large caliber
bilateral dominant AICA
bilateral dominant PICA
dominant AICA and dominant PICA

6/8 (75%)
6/6 (100%)
9/9 (100%)** dominant AICA, 3 cases: dominant PICA, 6 cases.

than that of the contralateral AICA/PICA.
When there were bilateral common trunk anomalies,
the compressing vessel was present on the side showing
a larger caliber at the origin in 6 (75%) of 8 patientswith a bilateral dominant AICA, all 6 with bilateraldominant PICAs, all 9 with dominant AICAs on one
side and dominant PICAs on the other side (compressing vessel: dominant AICA, 3 patients; dominant PICA,
6) (Table 3-b).
Caliber at the origin of the compressing vessel

After excluding 20 patients with directindirect compression by the VA, the compressing vessel was a normal vessel in 9 patients (18%), a dominant AICA in 24(48%), and a dominant PICA in 17 (34%).
One hundred cases of healthy individuals showednormal vessels in 48 patients (48%), dominant AICAs
in 40 (40%), and dominant PICAs in 10 (10%) (Table2).16
Involvement of common trunk anomalies
Of the above 50 patients, 15 had normal distribution
on one side and a dominant AICA on the other. The
compressing vessel was a dominant AICA in 13 (87%)
of the 15 patients and the AICA in normal distribution
in the other 2. In all 12 patients in whom the caliber atthe origin of the dominant AICA was larger than thatof the contralateral AICA/PICA, the dominant AICA
was the compressing vessel.
In all 5 patients with normal distribution on one side
and a dominant PICA on the other side, the dominant
PICA was the compressing vessel (Table 3-a), and thecaliber at the origin of the dominant PICA was larger

The compressing vessel was classiﬁed as the dominant AICA, AICA, dominant PICA, and PICA excluding those associated with indirect VA compression,
VA causing direct compression, and VA causing indirect compression. After excluding patients without acorresponding vessel on the normal side, the caliber
at the origin of the compressing vessel (largest caliberof the fourth segment for the VA) was larger than thatof the corresponding vessel on the unaffected side in 18(86%) of 21 with dominant AICAs as a compressing a
vessel, 5 (71%) of 7 with AICAs, 13 (93%) of 14 withdominant PICA, all 2 with PICAs, 8 (89%) of 9 with
VA, and 10 (91%) of 11 with VAs causing indirectcompression (Table 4).
Levels of the origin and bifurcation of the compressing
vesselFor the AICA, dominant AICA, PICA, and dominant PICA excluding those associated with indirect VA
compression, the levels of the origin and bifurcation
were compared between the compressing vessel and the194
Table 4

Oizumi T, et al: Angiographical manifestation of hemifacial spasms
Caliber of Compression Vessel and Normal Vessel

Compression vessel

Table 6

No. of large caliber
Compression
side

Normalside

18 (86%)5 (71%)
13 (93%)2 (100%)8 (89%)
10 (91%)3 (14%)
2 (29%)
1 (7%)0
1 (11%)
1 (9%)

dominant AICA*
AICA
dominant PICA**PICA
VA (Largest caliber of fourth segment)
VA of indirect compression

Age and Duration

Compression
vesseldominant AICA
AICA
dominant PICA
PICA
VA*

No. ofcases

Mean
age G SD

Mean
duaration G SD
(month)

24
7
17
2
20

51.0 G 11.7
53.3 G 9.4
46.1 G 11.7
36.5 G 16.3
55.4 G 8.2

61.4 G 40.5
14.1 G 89.7
56.8 G 56.6
36.0 G 0.0
53.0 G 29.3

* include indirect compression.

* Excluding 3 cases without AICA on the normal side. ** Excluding 3
cases without PICA on the normal side.

Table 5

The Higher Side of Compression Vessel and Normal Vessel

Compression
vesseldominant AICA*
AICA
dominant PICA**
PICA

Stem

Bifurcation

Compression
side

Normalside

Compression
side

Normalside

11 (52%)4 (57%)
12 (86%)
2 (100%)10 (48%)3 (43%)
2 (14%)0

15 (71%)5 (71%)
13 (93%)2 (100%)6 (29%)
2 (29%)
1 (7%)
0

Table 7

Post-Operative Evaluation

Authors (yearreported)
Oizumi (2003)
Barker (1995) 14
Illingworth (1996) 17
Nagahiro (1997) 18
Samii (2002) 19

No. ofpatients

No. ofMVD

Excelent

Good

Poor

70
612
83
101
143

70
672
86
106
145

96%
84%
92%
85%
91%

1%
7%
3%
8%
2%

3%
9%
5%
7%
8%

* Excluding 3 cases without AICA on the normal side. ** Excluding 3
cases without PICA on the normal side.

corresponding vessel on the unaffected side. When thecompressing vessel was the dominant AICA, its origin
level was higher than that of the corresponding vesselon the unaffected side in 11 (52%) of 21 patients, andits bifurcation level was higher than that of the corresponding vessel in 15 (71%). When the compressing
vessel was the AICA, its origin level was higher thanthat of the corresponding vessel in 4 (57%) of 7 patients, and its bifurcation level was higher in 5 (71%).
When the compressing vessel was the dominant PICA,
its origin level was higher than that of the corresponding vessel in 12 (86%) of 14 patients, and its bifurcationlevel was higher in 13 (93%). Both patients with the
PICA as the compressing level showed higher origins
and bifurcation levels than those of the corresponding
vessel on the unaffected side (Table 5). All 9 patientswith the VA as a compressing vessel and all 11 with the
VA as an indirect compressing vessel showed a higher
level of its cranial loop than that of the corresponding
vessel on the unaffected side.
Mean age and duration until surgery according to thecompressing vessel
In patients with the AICA, dominant AICA, PICA,
or dominant PICA as the compressing vessel exclud-ing those associated with indirect VA compression,
the mean age and mean duration until surgery were51.0 G 11.7 years (mean G SD) and 61.4 G 40.5 months(mean G SD), respectively, in 24 patients with dominant AICAs, 53.3 G 9.4 years and 14.1 G 89.7 months
in 7 with AICAs, 46.1 G 11.7 years and 56.8 G 56.6
months in 17 with dominant PICAs, 36.5 G 16.3 years
and 36.0 G 0.0 months in 2 with PICAs, and 54.4 G 8.2
years and 53.0 G 29.3 months in 20 with VAs including
VAs causing indirect compression (Table 6). The mean
age signiﬁcantly differed (p < 0.01) between patientswith the dominant PICA and VA (including VA causing indirect compression).
Surgical results
Surgical results were classiﬁed according to the postoperative state into: (1) excellent, disappearance ofsymptoms without a decrease in facial muscle power;(2) good, disappearance of symptoms despite a transient decrease in facial muscle power; and (3) poor,
negligible improvement. Excellent results were obtained in 67 (96%) of 70 patients, good results in 1(1%), and poor results in 2 (3%). The 2 patients withpoor results underwent re-operation and showed complete disappearance of spasms (Table 7).14,17–19

Keio J Med 2003; 52 (3): 189–197

195

Discussion
Estimation of the compressing vessel and the incidenceof each vessel causing compression
Preoperative vertebral angiography in patients withhemifacial spasm allows the exclusion diagnosis ofaneurysms and arteriovenous anomalies, and the estimation of the site of the compressing vessel site.
Recntly, MRI has often been used for diagnosis ofhemifacial spasm.20–23 However oblique sagittal gradient echo MRI discriminated between the AICA and
PICA, with a true positive rate of 75.9%.23 The diagnosis of common trunk anomaly is difﬁcult using MRI.
Towne, straight AP, and lateral images were obtained in all patients, and straight AP images were optimal for diagnosis. On Towne images, there were many
overlapping vessels in the cerebellopontine angle, andthe estimation of compressing sites was difﬁcult. On theother hand, magniﬁed stereographic imaging and ﬁlm
subtraction on straight AP images further facilitatedreading. However, for estimating compression sites, notonly subtraction ﬁlms but also evaluation of the positional relation between the vessels and internal acoustic
foramen in negative plates was very useful.
As Table 8 shows, previous studies reported various incidences of each vessel as the compressing vessel.17–19,24 However, the incidence of the AICA was
frequently the highest, followed in order by the PICA
and the VA, which was similar to the present results.
Involvement of common trunk anomalies in hemifacial
spasm
Takahashi,16 who evaluated vertebral angiograms in
100 normal subjects, reported the total, dominant
AICA in 40% and dominant PICA in 10% (50%). In
the present patients with hemifacial spasm excluding
VA compression, the dominant AICA accounted for
48% and dominant PICA for 34% (82%). These percentages were higher than those reported in the normal
subjects by Takahashi. In particular, the dominant
PICA was observed in 10% of the normal subjects but
in 34% of the compressing vessels.
Table 8Compression Vessels

Authors (yearreported)

No. of
cases

AICA

PICA

VA

OthersOizumi (2003)
Huang (1992) 24
Illingworth (1996) 17
Nagahiro (1997) 18
Samii (2002) 19

70
310
89
101
145

56%
56%
16%
51%
66%

31%
39%
55%
19%
19%

13%
4%
9%
29%
4%

0%
1%
20%
1%
11%

When the unilateral dominant AICA/PICA andnormal distribution were observed, the compression
vessel was the dominant AICA in 87% of patients witha dominant AICA and the dominant PICA in 100% of
patients with a dominant PICA. In particular, when thecaliber of the a dominant AICA/PICA was larger thanthat of the AICA/PICA on the unaffected side, thecompression vessel was the dominant AICA/PICA in
100%.
When there were bilateral common trunk anomalies,
the vessel showing a larger caliber at the origin was thecompressing vessel in 75% of patients with a bilateraldominant AICA and 100% in those with a bilateraldominant PICA, and 100% in those with a dominant
AICA on one side and dominant PICA on the other,suggesting the close involvement of the caliber at theorigin.
Therefore, in patients with hemifacial spasm inwhom vertebral angiography excludes the involvementof the VA, when a unilateral dominant AICA/PICA ispresent, there is a strong possibility that this dominantvessel is the compressing vessel. This possibility further
increases when the caliber of this dominant vessel islarger than that of the normal AICA/PICA on the unaffected side.
When bilateral common trunk anomalies are present, it is possible that the vessel with a larger caliber at
its origin is the compressing vessel, particularly in patients with a bilateral dominant PICA and those with adominant AICA on one side and dominant PICA on
the other side.
Considering the presence of a compressing vessel on
the affected side together with the above ﬁndings, thecompressing vessel can be estimated at a relatively highprobability when there is a common trunk.
Calibers of the origin of the compressing vessel and thecorresponding vessel on the unaffected side and the levelsof their origin and bifurcation
When the compressing vessel was the dominant
AICA, AICA, dominant PICA, PICA, VA causing direct compression, and VA causing indirect compression, the caliber of the origin of the compressing vessel(largest caliber of the fourth segment for the VA) was
larger than that of the corresponding vessel on the unaffected side in 86%, 71%, 93%, 100%, 89%, and 91%,
respectively. Thus, the caliber of the origin of each typeof compressing vessels was larger than that of the corresponding vessel on the unaffected side in a very highpercentage of patients.
The origin level of the compressing vessel was higher
than that of the corresponding vessel on the unaffectedside in 52% and 57%, and the bifurcation level of thecompressing vessel was higher than that of the corre-

196

sponding vessel in 71% and 71% of patients with dominant AICAs and AICAs, respectively, as the compressing vessel. Of patients with a dominant PICA and
PICA, 86% and 100%, respectively, showed a higher
origin level of the compressing vessel, and 93% and100%, respectively, showed a higher bifurcation level ofthe compressing vessel than that of the corresponding
vessel on the unaffected side. In the VA, the level of thebent portion was high on the affected side in both direct
and indirect compression.
This may be because vessels with a large caliber atthe origin have lower vascular resistance than narrowvessels and therefore, receive more blood ﬂow, more
readily undergo bendingstretchingdilation, and more
often compress the origin of the facial nerves.25
Comparison of the levels of the origin and bifurcation between the affected and unaffected sides showed
only slight differences for the dominant AICA and
AICA as compressing vessels, which may be due totheir original distribution near the origin of the facial
nerves. However, there was a spatial gap between theorigin of a dominant PICA or PICA and the origin of
the facial nerves above. A dominant PICA or PICA
with its origin and bifurcation at higher levels reduced
the distance to the nerve and may tend to be a compressing vessel. When the compressing vessel was the
VA, its bent portion was often present at a high level,
which may be because the bent portion compresses theorigin of the facial nerves, and its high level reduces thenormally long distance to the facial nerves.
Mechanism of hemifacial spasm and the involvement ofcommon trunk anomalies
In hemifacial spasm, the responsible vessel is normal
or a normal variant in principle. Aged-related vascular bending, stretching, and dilation were suggested to
be involved in the development of nerve compression.
Therefore, hemifacial spasm often occurs after middle
age. In the present study, the mean age of the subjects
was 51 years.
The present results suggested that the vascular architecture itself in addition to age-related arterialchanges is an important factor for the development ofhemifacial spasm. The high incidence of common trunk
anomalies may be due to the complicated arrangement of the main trunk, rostral branch, and caudal
branch near the origin of the facial nerves. Age-relatedchanges in addition to vascular anomalies may induce
nerve compression.
The mean age signiﬁcantly differed (p < 0.01) between patients with a dominant PICA as the compressing vessel and those with a VA (including VA causing
indirect compression). This may be because of the dif-

Oizumi T, et al: Angiographical manifestation of hemifacial spasms

ference in the distance between the compressing vessel
and the origin of the facial nerves. Due to the considerable distance between the VA and the origin of the
facial nerves, a long period is necessary for the development of age-related VA changes that induce spasm.
In contrast, the trunk and branches of a dominant
PICA are present near the origin of the facial nerves
and may more readily induce hemifacial spasm than the
VA even in relatively young people.
Based on the present results, the preoperative estimation of the responsible artery and compression site
may be possible using vertebral angiography in mostpatients. However, in general, cerebral angiography is
not always a safe examination method though no complications were observed in our subjects. When lesions
such as cerebral aneurysm, arteriovenous anomalies,
and tumors are completely excluded by high resolution
CT, 3D CT Angio, MRI, or MRA, cerebral angiography is not always necessary between operation.
However, when an operation is performed without
vertebral angiography, whether the compressing vesselis the AICA or PICA can not be determined in somepatients with complicated vasculature. Janetta et al.4
reported the highest incidence of compression by the
PICA while we observed the highest incidence of compression by the dominant AICA. The results obtainedby Janetta may have been associated with vertebral
angiography performed only in some of the patients.
Many previous studies have shown the highest incidence of AICA as the compressing vessels, followed inorder by the PICA and VA, but some showed thehighest incidence of the PICA (Table 8). Therefore, wereported the results of preoperative vertebral angiography that had been performed at our institution toclarify the pathology of vascular compression of nerves
in hemifacial spasm.
Compared with previous ﬁndings, the postoperative
results in the present study were excellent (Table 7).
We evaluated the association between ﬁndings ofpreoperative vertebral angiography and operative ﬁndings in 70 patients with hemifacial spasm who underwent neurovascular decompression. Straight AP images
were the most useful for interpreting the images. The
compressing vessel was most frequently the group with
AICA, followed in order by the group with PICA and
VA. After excluding VA-associated cases, dominant
AICAs and dominant PICAs accounted for 82% of thecompressing vessels. In the group with the AICA as thecompressing vessels, a dominant AICA was observed in
78%. In the group with the PICA as the compressing
vessels, a dominant PICA was observed in 89%. Whenthe unaffected side showed a normal vascular distribution, the compressing vessel was a dominant AICA in
87% of patients with a dominant AICA and 100% of
patients with a dominant PICA. In most patients, theKeio J Med 2003; 52 (3): 189–197

197

responsible vessel and compression site could be determined by vertebral angiography.
14.

References
15.
1. Cushing H: Strangulation of the nervi abducentes by lateralbranches of the basilar artery in case of brain tumor. Brain 1911;
33: 204–235
2. Campbell E, Keedy C: Hemifacial spasm: a note on the aetiology
in two cases. J Neurosurg 1947; 4: 342–347
3. Gardner WJ, Sava GA: Hemifacial spasm: a reversible pathophysiologic state. J Neurosurg 1962; 19: 240–247
4. Jannetta PJ, Abbasy M, Maroon JC, Ramos FM, Albin MS: Etiology and deﬁnitive microsurgical treatment of hemifacial spasm.
Operative techniques and results in 47 patients. J Neurosurg
1977; 47: 321–328
5. Okamura T, Aoki H, Yanai K, Abe T, Oh M: Radiographic
positions of the cranial nerve root (V, VII–XI) proximal zones
with special reference to microvascular decompression. Neurol
Med Chir (Tokyo) 1983; 23: 776–782 (in Japanese)
6. Jannetta PJ: Microsurgery of cranial nerve cross-compression.
Clin Neurosurg 1979; 26: 607–615
7. Jannetta PJ: Neurovascular compression in cranial nerve andsystemic disease. Ann Surg 1980; 192: 518–525
8. Martin RG, Grant JL, Peace D, Theiss C, Rhoton AL Jr:
Microsurgical relationships of the anterior inferior cerebellar
artery and the facial-vestibulocochlear nerve complex. Neurosurgery 1980; 6: 483–507
9. Matsushima T, Rhoton AL Jr, Lenkey C: Microsurgery of the
fourth ventricle: Part 1. Microsurgical anatomy. Neurosurgery
1982; 11: 631–667
10. Sunderland S: Neurovascular relations and anomalies at the baseof the brain. J Neurosurg Psychiatry 1948; 11: 243–257
11. Lister JR, Rhoton AL Jr, Matsushima T, Peace DA: Microsurgical anatomy of the posterior inferior cerebellar artery.
Neurosurgery 1982; 10: 170–199
12. Carlos R, Fukui M, Hasuo K, Uchino A, Matsushima T, Tamura
S, Kudo S, Kitamura K, Matsuura K: Radiological analysis ofhemifacial spasm with special reference to angiographic manifestations. Neuroradiology 1986; 28: 288–295
13. Baba T, Matsushima T, Fukui M, Hasuo K, Yasumori K, Masuda

16.

17.

18.
19.

20.

21.

22.

23.
24.

25.

K, Kuromatsu C: Relationship between angiographical manifestations and operative ﬁndings in 100 cases of hemifacial spasm
No Shinkei Geka 1988; 16: 1355–1362 (in Japanese)
Barker FG 2nd, Jannetta PJ, Bissonette DJ, Shields PT, Larkins MV, Jho HD: Microvascular decompression for hemifacial
spasm. J Neurosurg 1995; 82: 201–210
Okamura T, Aoki H, Yanai K, Abe T, Oh M: Radiographic
positions of the cranial nerve root (V, VII–XI) proximal zones
with special reference to microvascular decompression. Neurol
Med Chir (Tokyo) 1983; 23: 776–782 (in Japanese)
Takahashi M: The anterior inferior cerebellar artery. In: Newton
TH, Potts DG, eds, Radiology of the Skull and Brain: Angiography, Book 2, St. Louis, Mosby, 1974; 1796–1808
Illingworth RD, Porter DG, Jakubowski J: Hemifacial spasm: aprospective long-term follow up of 83 cases treated by microvascular decompression at two neurosurgical centres in the
United Kingdom. J Neurol Neurosurg Psychiatry 1996; 60: 72–77
Nagahiro S: Pathophysiology and surgical treatment of hemifacial spasm. No Shinkei Geka 1998; 26: 101–111 (in Japanese)
Samii M, Gunther T, Iaconetta G, Muehling M, Vorkapic P,
Samii A: Microvascular decompression to treat hemifacial
spasm: long-term results for a consecutive series of 143 patients.
Neurosurgery 2002; 50: 712–718
Harsh GR 4th, Wilson CB, Hieshima GB, Dillon WP: Magnetic
resonance imaging of vertebrobasilar ectasia in tic convulsif.
Case report. J Neurosurg 1991; 74: 999–1003
Nagaseki Y, Horikoshi T, Omata T, Ueno T, Uchida M, Nukui
H, Tsuji R, Sasaki H: Oblique sagittal magnetic resonanceimaging visualizing vascular compression of the trigeminal or
facial nerve. J Neurosurg 1992; 77: 379–386
Nagaseki Y, Omata T, Ueno T, Uchida M, Ohhashi Y, Kase M,
Nukui H, Tsuji R: Prediction of vertebral artery compression inpatients with hemifacial spasm using oblique sagittal MR imaging. Acta Neurochir (Wien) 1998; 140: 565–571
Pego Reigosa R, Pulpeiro Rios JR: Hemifacial spasm. J Neurol
Neurosurg Psychiatry 1998; 64: 687
Huang CI, Chen IH, Lee LS: Microvascular decompression forhemifacial spasm: analyses of operative ﬁndings and results in
310 patients. Neurosurgery 1992; 30: 53–56
Kondo A, Ishikawa J, Konishi T, Yamasaki T: Mechanismof vascular compression of cranial nerves: role of changes ofvertebro-basilar vasculatures. Neurol Med Chir (Tokyo) 1981;
21: 287–293 (in Japanese)