microvascular decompression surgery: surgical principles and technical nuances based on 4000 cases
TRANSCRIPT
Microvascular decompression surgery:surgical principles and technical nuancesbased on 4000 cases
Jun Zhong, Jin Zhu, Hui Sun, Ning-Ning Dou, Yong-Nan Wang,Ting-Ting Ying, Lei Xia, Ming-Xin Liu, Bang-Bao Tao, Shi-Ting Li
Department of Neurosurgery, Xinhua Hospital (The Cranial Nerve Disease Center of Shanghai), Shanghai JiaoTong University School of Medicine, China
Background: As an etiological treatment of trigeminal neuralgia (TN) and hemifacial spasm (HFS),microvascular decompression (MVD) has been popularized around the world. However, as a functionaloperation in the cerebellopontine angle (CPA), this process can be risky and the postoperative outcomesmight not be good enough sometimes.Objective: In order to obtain a better result with less complication, this surgery should be further addressed.Methods: With experience of more than 4000 MVDs, we have gained knowledge about the operativetechnique. Through abundant intraoperative photos, each step of the procedure was demonstrated indetail and the surgical strategy was focused.Results: The principle of MVD is to separate the nerve-vessel confliction rather than isolate it withprostheses. A prompt identification of the conflict site is important, which hinges on a good exposure. Asatisfactory working space can be established by an appropriate positioning of the patient’s head and aproper craniectomy as well as a rational approach. A sharp dissection of arachnoids leads to a maximalvisualization of the entire intracranial course of the nerve root. All the vessels contacting the trigeminal orfacial nerve should be treated. Intraoperative electrophysiological mentoring is helpful to distinguish theoffending artery for hemifacial cases.Conclusion: MVD is an effective treatment for the patient with TN or HFS. Immediate relief can be achievedby an experienced neurosurgeon with good knowledge of regional anatomy. A safe surgery is the tenet ofMVD, and accordingly, no single step of the procedure should be ignored.
Keywords: Microvascular decompression, Surgical technique, Hemifacial spasm, Trigeminal neuralgia
IntroductionTrigeminal neuralgia (TN) and hemifacial spasm
(HFS) account for the majority of cranial nerve
diseases.1 The compression of the V or VII cranial
nerve root by vessel(s) has been believed to be the
etiology. It was hypothesized that an ephaptic
transmission occurred between those individual nerve
fibers or the excitability threshold of the neuron
dropped following the vascular compression of
the nerve root.2–7 Our preliminary study implied that
the autonomic nervous system in the adventitia of the
offending vessel may contribute to the disorder.7,8
Carbamazepine may relieve the symptoms for the
patients with TN or HFS in the early stage of the
disease.9–12 When patients are weaned off medications,
they may try balloon techniques,13 glycerol injections,14
stereotactic radiosurgery with Gamma Knife,15 or
Botox injections.2 Nevertheless, in spite of being less
invasive, all these above modalities are destructive at
the cost of partial nerve function loss and may leave
facial numbness or palsy.9,16–22 However, as a non-
destructive surgery, microvascular decompression
(MVD), has nowadays become the most effective
remedy for TN or HFS since it was first introduced
by Dandy in 193423 and then popularized by
Janetta.24 Although the efficacy of MVD has been
reported to be more than 90%,18 not all institutes
reported perfect and consistent results.25–27 To date,
we have performed 4000 MVDs in China.18 Most of
the surgeries were performed in recent years, and the
relief rate is increasing continuously while the
complication is decreasing. Therefore, we believe
that, theoretically, as soon as the offending vessel(s) is
(are) removed away from the nerve, the symptoms of
Correspondence to: Shi-ting Li, Department of Neurosurgery, XinhuaHospital (The Cranial Nerve Disease Center of Shanghai), Shanghai JiaoTong University School of Medicine, Shanghai 200092, China. Email:[email protected]
882� W. S. Maney & Son Ltd 2014DOI 10.1179/1743132814Y.0000000344 Neurological Research 2014 VOL. 36 NO. 10
the patient should be gone immediately. The
improvement mainly depends on the surgeons’
understanding, experience, and technical nuances.
An unsuccessful MVD may be largely attributable to
misidentification of the culprit vessel. Although it was
claimed that endoscopy offers enhanced visualization
to identify offending vessels,28 it remains to be a sort
of assistance to MVDs. However, a good working
space may finally be obtained anyway with a fine
dissection. Apart from a meticulous manipulation
under microscope, a successful MVD depends on
many other factors, including approach, craniect-
omy, positioning, and so on. Therefore, every single
step of the process needs to be emphasized in order to
achieve an excellent postoperative outcome. In this
paper, we would like to present our experience with
emphasis on surgical principles and technical nuances
rather than postoperative outcomes, which have been
mentioned much in our previous papers.27
ImagingPreoperative imaging study is used for exclusionof mass lesions rather than identification of theoffending vesselThe disease is diagnosed in the light of the character-
istic symptom, while iconography is a supplementary
entity that is valuable in finding secondary TN or
HFS. Magnetic resonance imaging (MRI) with three-
dimensional time-of-flight (3D-TOF) sequence is recom-
mended, which may provide accurate information on
the relative locations of the nerve and the vessel
(Fig. 1A). Our previous study has observed that a
tortured vertebrobasilar artery deviated to the sympto-
matic side in 86.4% of HFS patients (Fig. 1B).29
However, this phenomenon is not so common in TN
patients. Actually, the main function of MRI is to
exclude the neoplasmal pathologies in the cerebellopon-
tine angle (CPA), e.g., meningiomas, acoustic neuromas,
cholesteatomas, etc. The occurrence of these neoplasms,
which in all intracranial tumors mentioned above, were
Figure 1 Preoperative magnetic resonance imagings (MRI). (A) MRI with three-dimensional time-of-flight (3D-TOF) sequence
showed an artery contacting the left facial nerve root. (B) A tortured vertebrobasilar artery deviated to the symptomatic side in a
hemifacial case. (C) It was a case of secondary hemifacial spasm (HFS). The space of left cerebellopontine angle (CPA) was
bigger with different signal intensity compared to the right side, which delineated a cholesteatoma.
Zhong et al. Microvascular decompression surgery
Neurological Research 2014 VOL. 36 NO. 10 883
about 13–26%,30 8–10%,31 and 3–10%,32 respectively,
according to the literature. It should be noted that
cholesteatoma is apt to be missed in the imaging before
posterior fossa exploratory surgery (Fig. 1C).33 Com-
puted tomography (CT) scan is an alternative when
MRI is not applicable because of metal implants.
IndicationsMicrovascular decompression is appropriate formost TN or HFS patientsGenerally, MVD is indicated for all the patients
suffering from drug-resistant TN or HFS as long as
their general conditions do not contraindicate general
anesthesia. Drug-resistant TN or HFS is defined as
uncontrolled pains or spasms when more than
1200 mg per day of carbamazepine is needed or
unacceptable complications occur. We would like to
point out that old age is not a contra-indication for
MVD surgery. Instead, it is much easier to operate on
old patients because of wide subarachnoid space as a
result of brain atrophy; only those with decompen-
sated dysfunction of vital organs (heart, lungs,
kidneys, or liver) should be evaluated cautiously. In
our cohort, the patient age at the time of surgery
ranged from 8 to 93 years without significant
difference in gender and side; the length of sympto-
matic illness ranged from 3 months to 22 years. We
suggest performing the surgery in the early stage
before the patient’s quality of life is awfully
influenced. Especially for those undernourished
because of reduced eating to avoid an attack of
severe pain induced by oral movement, a prompt
surgery is encouraged.
PositionA proper positioning contributes to a satisfactoryexposureGeneral anesthesia is the best option for MVD
patients. We place the patient in a park bench
position (3/4 lateral prone decubitus). This position
is superior to supine or full prone position because it
obviates the need to turn the patient’s head into an
uncomfortable position and therefore decreases the
risk of postoperative neck pain. This is especially
important for obese patients who usually have
generous supraclavicular fat pads. It is necessary to
point out that the contralateral shoulder should be
close to the edge of the bed so that the surgeon can
easily reach the surgical site. Meanwhile, the ipsilat-
eral shoulder should be slanted forward and pulled
away from the head by a shoulder belt so as to create
a satisfactory working space, which facilitates the
instruments getting in and out of the surgical field. A
fixation frame is used to hold the patient’s head stable
and make it possible to apply the retractor system
when necessary during the surgery, though we have
not used it even in cases of secondary TN or HFS
resulting from CPA masses since 2010, when we
began to choose an oblique position for the patients’
head (Fig. 2A). This inclined position with the
patient’s head turning back 15–20u from the level
surface facilitates the cerebellum to fall away under
its own gravity from the petrosal bone and obviates
the need of retractors (Fig. 2B). Actually, a good
exposure is achieved by rational positioning rather
than retracting. Brain relaxation methods such as
mannitol/hypertonic saline/hyperventilation are unne-
cessary in MVD surgeries, especially in old patients,
since cerebrospinal fluid (CSF) removal from the
cisterns works well. For TN cases, if a very steep
tentorium was showed after dural opening, the rostral
end of the table could be lowered a bit.
As the approach trajectory is somewhat different
between TN and HFS, the patient’s position varies
accordingly. As the cranial nerve VII is behind the
VIII in the surgical field, the axis of the head should
be placed 15–20u downward to expose the proximal
aspect of the facial nerve in HFS cases (Fig. 2C). In
TN cases, the axis is level.
IncisionThe incision is not ‘the smaller, the better’, buttoo large is not actually good for exposureDespite transversal, arc, or reverse ‘U’ shape incisions
having been reported,34 we choose a vertical linear
incision. It is laterally parallel to the hairline and
crosses the inion-zygomatic line with 1/3 above and 2/
3 below for TN cases and a bit lower for HFS cases
(Fig. 3). Nowadays, we have adopted a mastoid
retractor to hold the incision and no scalp clip is
needed. Owing to the limitation of the retractor’s
open angle, a longer than 7 cm incision is not really
necessary. To save a good blood supply, undue
coagulation should be avoided and a quick retraction
of the incision is recommended.
CraniectomyThe craniectomy should be as lateral as possibleA craniectomy of 3 cm in diameter is enough for
most cases. The edge of the sigmoidal sinus should be
exposed for both the TN and HFS cases to ensure an
ideal surgical corridor. Particularly, the craniectomy
should be rostral enough to the transverse sinus for
TN cases while low enough to expose the caudal
nerves for HFS cases. To avoid dural sinus injury, we
prefer craniectomy with pneumatic drill and Kerrison
rongeur to craniotomy with milling cutters. Bone
dust and chips were preserved for the later cranio-
plasty. The bone over the sigmoid sinus should be
removed in small pieces. Bone wax is effective for
homeostasis at the edge of dural sinuses. To obtain a
good working angle, the mastoid antrum could be
opened if necessary, but it should be immediately
waxed to prevent infection and CSF leak.
Zhong et al. Microvascular decompression surgery
884 Neurological Research 2014 VOL. 36 NO. 10
Figure 2 Positioning. (A) The patient is placed in a 3/4 lateral prone decubitus position with the ipsilateral shoulder slanted
forward (%a) and pulled away from the head. The patient’s head is turned back 15–20u from the level surface (%b). (B) The
sketch exhibits the benefits of an inclined head position. It offers a bigger visualizable area (B) than a flat position (A) does.
Zhong et al. Microvascular decompression surgery
Neurological Research 2014 VOL. 36 NO. 10 885
DurotomyThe dural opening is tailored to a maximalexposure of the conflict siteThe dural opening is tailored to the anatomy of each
case to allow a maximal exposure, which differs
between TN and HFS cases. We prefer to make a
wide ‘Y’ shape cutting with its tip pointing to the
junction of the transverse and sigmoid sinus for TN
cases, while to the lower outer quadrant in the
surgical area for HFS cases. The end of the durotomy
should be 1–2 mm away from the bone edge, so that a
gutter is built along the edge of craniotomy after the
dura flap is reflexed, which maintains the surgical
filed clear from potential outside bleeding. After the
dural mater is sutured back with double knotting, the
suture thread remains in place (without cutting off),
which facilitates tightening when necessary during the
procedure. This pattern of dural opening leaves the
majority of the dura on the cerebellum, which avails
the protection of the cerebellar hemisphere during the
process. To avoid shrinkage of the dura due to the
heat generated by the operating microscope’s lamp
aimed at the surgical field during the intradural
portion of the operation, pieces of wet gelforms are
placed over the dura.
ExposureA good exposure is obtained by sharpmicrodissection as well as proper positioningand craniectomy rather than harsh retractionWith analysis of our data, we found that approxi-
mately 4.5% of the patients had no symptomatic
relief postoperatively,18 and the main reason of
a failed surgery was that the exact offending vessel(s)
was(were) not recognized or the neurovascular con-
tact site was inaccessible intraoperatively. So we
believe a full exposure of the trigeminal or facial
nerve root is the key to obtaining a good result.
Usually, an unhurried suction drainage of CSF and
an ample adhesiolysis are effective enough to achieve
brain relaxation and no mannitol or lumbar puncture
is needed for most of the cases. We do not use
retracting blades because a narrow suction tube allows
more mobility and can actually afford more working
space than a wider spatula does during the operation at
a moment when a specific area is dissected. As a matter
of fact, with a good knowledge of the regional
anatomy, one does not have to visualize the whole
area of CPA while operating at a particular site (but
those surrounding structures should always be in
mind). Basically, an alternate use of a pair of the
microinstruments, i.e., a Fukushima teardrop suction
tube, a microscissors, a microdissector, and a bipolar
coagulation forceps, are enough to complete all the
intracranial manipulation. Instead of the ordinary
gun-shape forceps, a self-irrigating bipolar forceps
can keep the cottonoid over the cerebellum moist all
the time and avoid cerebellar contusion. The action
of clamping an artery should be avoided, which may
cause vasospasms. In that way, one can achieve more
effective exposure with less manipulation of the
cerebellum (Fig. 4).
Figure 3 Incision. A 7-cm vertical linear incision paralleling
laterally to the hairline is made. It crosses the inion-
zygomatic line with 1/3 above and 2/3 below for trigeminal
neuralgia (TN) cases and a bit lower for hemifacial spasm
(HFS) cases. This picture exhibited a trigeminal case.
Owing to its own gravity, the cerebellum falls away from the petrosal bone and provides more working space (D) than a flat
position (C) does. (C) For hemifacial cases, the axis of the head should be tilted down slightly, so that the facial nerve (VII) can
be easily seen from behind the acoustic nerve (VIII) (c1). Otherwise, it would be mostly covered by the VIII (c2).
Figure 4 Exposure. With a proper positioning and an
appropriate craniectomy, a satisfactory exposure is estab-
lished using a sharp microdissection of arachnoids. This was
a right trigeminal case. The complete intracranial course of
the trigeminal nerve root (V) from pons to Meckel’s cave was
visualized.
Zhong et al. Microvascular decompression surgery
886 Neurological Research 2014 VOL. 36 NO. 10
ApproachA caudorostral approach is suggestedFor TN cases, the protection and management of
petrosal veins (PV) poses the main challenges and
risks during the operation.35,36 In early cases, we
approached the trigeminal nerve from the super-
olateral aspect of the cerebellum, and PV were
obstructing the access path. We used to sacrifice the
petrosal vein or its branches to prevent unintention-
ally tearing at its entry to the superior petrosal sinus,
which is disastrous and difficult to manage. In that
case, compression with gelfoam is the only way for
homeostasis, while coagulation only makes things
worse. However, when a gelfoam is used to cover the
bleeding point, working space becomes narrower and
the following process can be very difficult. Our
previous study showed that sacrifice of the petrosal
vein may lead to a risk of delayed intracerebellar
hemorrhage, which was fatal unless timely identified
and treated.37 To detour off PV, we suggest a new
entry corridor. Recently, we started to select a
caudorostral approach (via cerebellar fissures),
through which the root entry/exit zone (REZ) of
trigeminal nerve could be accessed directly without
sacrifice of PV (Fig. 5a).
For HFS cases, the dissection should also start
from the lower cranial nerves with sharp opening of
the surrounding arachnoid, while the cerebellum is
superomedially retracted by a suction tube. The
retraction is most effective when it is parallel to the
VII/VIII cranial nerves. Arachnoid membrane over
the VII/VIII nerve complex is then cut with micro-
scissors, while the cerebellum is further retracted
medially until the pontomedullary sulcus is visualized
(Fig. 5B). The REZ of nerve VII is anterior and
slightly inferior to nerve VIII and may be directly
visualized upon gentle elevation of nerve VIII using a
fine dissector.
Identification of the Neurovascular ConflictionA full-way inspection of the nerve root increasesthe chance to find the culpritApart from I and II, the other cranial nerves are
composed of a central nervous system segment and a
peripheral nervous system segment. The central
segment has a structure similar to that of white
matter of the brain, consisting of parallel traveling
nerve fibers. It lacks funicular structure and is less
vascularized. Conversely, the winding density in the
peripheral segment is greater than in the central
segment, consisting of undulating nerve fibers, which
creates a more elastic and firmer structure. As a
result, the peripheral segment of the nerve is more
resistant to compression. The central segments of the
12 cranial nerves differ in length. Basically, motor
nerves have a shorter central segment than sensory
nerves.38 As the central segment of the trigeminal
nerve is longer than that of the facial nerve, logically,
the TN patients have more chances of lateral conflic-
tion than HFS patients.39–42 Hence, TN patients have
more chances of lateral confliction (Fig. 6A) than HFS
patients (Fig. 6B), which is in accordance with our
data (Table 1) as well as others.43 The neurovascular
confliction of TN patients is relatively complicated,
and a superior cerebellar artery (SCA) along the
shoulder of the REZ compressing the caudal side of
the trigeminal nerve ventromedially is common.9,19,44
The possibility of multiple offending vessels (arterial
and/or venous loops) should be excluded with careful
inspection (Fig. 6C). In our series, venous compres-
sion is not rare in TN patients.45 For HFS cases, the
very medial location of the contact site increases the
risk/chances of being missed by a poor exposure and
may thus lead to unsuccessful decompression and
failure of MVD. In accordance with others,46–50 we
found that the most frequent offending vessel was the
anterior inferior cerebellar artery (AICA) followed by
posterior inferior cerebellar artery (PICA) or vertebral
artery.41 Sometimes, the culprit could be those
Figure 5 Approach. A caudorostral approach is appropriate
for both hemifacial and trigeminal cases. (A) To detour off
petrosal veins (PV), dissection begins from petrosal fissure
and then extends rostrally for trigeminal cases. (B) For
hemifacial cases, dissection begins from caudal cranial
nerves and then extends rostrally.
Zhong et al. Microvascular decompression surgery
Neurological Research 2014 VOL. 36 NO. 10 887
arterioles (Table 2) (Fig. 6E). Mobilization of the
arterial loop often discloses a site of discoloration (or
even an indent) along the nerve, which confirms that
the intended pathology is found and predicts a good
outcome postoperatively (Fig. 6D).36 Accordingly, for
TN patients, we would check the entire root from pons
distally, while focusing on the medial portion of the
facial nerve for HFS patients. Nevertheless, to achieve
Figure 6 Identification of the offending vessel. (A) For trigeminal cases, the neurovascular conflict could be anyway along the
nerve root. In this case, the trigeminal nerve (V) was compressed rostrally by superior cerebellar artery (SCA) in cisternal
portion, which was separated by Teflon (T). (B) For hemifacial cases, the offending artery (*) is often discovered in the axilla
(caudal root exit zone) of the hemifacial nerve (VII). (C) Sometimes the nerve is compressed by multiple vessels. In this case, the
trigeminal nerve (V) was compressed by the SCA rostrally and by petrosal veins (PV) dorsally. (D) Sometimes an indent or
discoloration could be found in the nerve when an arterial loop is removed, which confirms that the intended pathology is found
and is predictive of a good outcome postoperatively. (E) Arterioles could also be the culprit. Note that one (a) of the arterioles
had been separated by Teflon in this left hemifacial case. These arterioles (a) looked redder in color compared to those veins
around under microscope. REZ: the root entry zone of trigeminal nerve; AICA: anterior infracerebellar artery; VIII: the
vestibulocochlear nerve; IX-X-XI: caudal cranial nerves.
Zhong et al. Microvascular decompression surgery
888 Neurological Research 2014 VOL. 36 NO. 10
a high cure rate, it is recommended that the whole
intracranial nerve course be a thorough exposed.
DecompressionThe principle of MVD is separation of the nerve–vessel confliction rather than isolation withprosthesis between themAs a matter of fact, a skillful driving of a micro-
dissector in assistance with a fine suction tube by the
operator’s two hands are enough to complete the
decompression process, including removal of the off-
ending vessel(s) and placement of Teflon felts piece by
piece, and no other instruments controlled by a third
hand are needed in such a small room. Moving the
vessel with forceps is not recommended. The sub-
stance of decompression should be separation of the
neurovascular confliction rather than isolation with
prosthesis between the nerve and the vessel (Fig. 7).
Actually, the role of the Teflon is to keep the
offending vessel from rebounding, and therefore it
is unnecessary to be always put at conflict site.
Intraoperative MonitoringElectrophysiological monitoring could be used topredict a satisfactory decompression for HFScasesElectrophysiological monitoring has been routinely used
in our department for years, and it has been proved to be
a good way to predict the results for HFS cases. Short
acting neuromuscular junction blocking medications
were used for intubation. No additional paralytic agent
was administered during electromyography (EMG)
monitoring. Our published data demonstrated that the
abnormal muscle response (AMR) vanished after the
decompression in 93.9% of the relieved HFS patients,51
which was in accordance with others.52 However, AMR
is not always reliable.53,54 Recently, we also stimulated
the offending artery directly during the operation for
HFS cases and achieved a wave analogous to the AMR
(Fig. 8). We named this new wave as ‘Z–L response’,which could only be recorded at the offending artery
and disappeared immediately after the decompression.7
To record the Z–L response, the same needle
electrodes as used in AMR recording is used. The
reference electrodes are inserted into the frontal
muscle, and the recording electrodes are inserted into
the orbicularis oculi, orbicularis oris, and mentalis
muscles. A non-invasive concentric electrode is
placed on the offending artery wall near the
compression site before it is detached from the facial
Table 1 The conflict site in our series
Cases REZ (%) non-REZ (%)
TN 52 48HFS 93 7
REZ: root entry/exit zone; non-REZ: the lateral (cisternal)segment of trigeminal or facial nerve root; TN: trigeminalneuralgia cases; HFS: hemifacial spasm cases.
Figure 7 Decompression. The substance of microvascular
decompression (MVD) process should be separation of the
neurovascular conflict rather than isolation with prosthesis
between them. This was a left trigeminal case. (A) The
superior cerebellar artery (SCA) was identified as the culprit,
which contacted with trigeminal nerve (V) rostrally. (B) The
offending artery (SCA) was separated from the nerve (V). In
case of rebound, a Teflon wadding (T) was placed between
them. Notice that the Teflon was not placed at the original
conflict site (*). It may work anyway as long as it could keep
the vessel from rebounding. VIII: the vestibulocochlear
nerve; PV: petrosal vein.
Table 2 The offending vessel(s) in our series
SCA (%) AICA (%) PICA (%) VA (%) Arterioles (%) Vein(s) (%)
TN 41 33 9 7 8 35HFS 0 36 52 9 13 1
TN: trigeminal neuralgia; HFS: hemifacial spasm; SCA: superior cerebellar artery; AICA: anterior inferior cerebellar artery; PICA:posterior inferior cerebellar artery; VA: vertebral artery; REZ: root entry/exit zone. Sometimes, more than a single vessel accounted forthe confliction.
Zhong et al. Microvascular decompression surgery
Neurological Research 2014 VOL. 36 NO. 10 889
nerve, and a square impulse (2 mA 6 0.2 ms) is
delivered. Z–L response monitoring is useful when an
AMR is not recorded before decompression or
persists after all vascular compressions are properly
treated. It could help neurosurgeons to determine the
real culprit when multiple offending vessels exist.
Accordingly, we suggest monitoring both AMR and
‘Z–L response’ during the MVD for HFS cases.
ClosureThe dura should be closed in a watertightpatternAt the end of the operation, the surgical field should
be well irrigated with 37uC normal saline to assure
that there is no bleeding as well as to vent air.
Meanwhile, attention should be paid to make sure the
implanted Teflon is stable under the flow of CSF.
Before dural closure, it is suggested to place a whole
piece of wet gelfoam over the cerebellum, which
prevents epidural hemorrhage from assessing to the
subdural space as well as protects accidental injury to
the brain tissue while suturing. In order to prevent
CSF leakage, the dura should be closed with stitch as
tight as possible. The operator should begin the stitch
process from the lowest level while the assistant is
pulling the suture thread, which will protect blood
inflow from outside. Sometimes, it is difficult to
complete a watertight closure due to dura defect. In
our series, this situation used to occur in 25%
proximately, but it reduced to 10% after we adopted
the following measurements: (1) no dural coagulation
was used; (2) dura mater was quickly sutured back as
soon as it was opened; (3) wet gelforms were inserted
between the dura and the craniotomy rims. Besides,
we would use a muscle patch to repair in case of a
defect. Then, the dura is sealed with glue and covered
by an artificial dura plus bone chips to reconstruct
the normal anatomy. Finally, the muscles, subcuta-
neous tissues and the scalp are sutured layer by layer.
No drainage is required (Fig. 3).
ComplicationsGenerally, those complications caused by serious organic
lesions, such as cerebellar hemorrhage, abrupt hydro-
cephalus, facial palsy and numbness16,17,19–22,55–58
(Table 3) can be avoided by an experienced operator.
However, those mild complications, e.g., dizziness,
disequilibrium, nausea, and vomit, may still occur in
some cases (Table 4).9,16 It might be attributable to
cerebellar laceration or pneumocrania. Therefore, a good
approach with gentle sharp dissection is very important,
which avoids undue retraction of the cerebellum.
Meanwhile, a thorough irrigation with warm normal
saline before tying the last suture of the dura stitch (which
should be in the highest position) should not be ignored.
Occasionally, an ipsilateral facial palsy or lip herpes may
occur a couple of days postoperatively for HFS or TN
cases, respectively.
Management of Failed MVDsWe have analyzed failed MVDs and found the main
reason for the failure was misidentification of the
offending vessel followed by insufficient decompres-
sion (Table 5).35,41 It was generally caused because a
Figure 8 Electrophysiological monitoring. For an abnormal
muscle response (AMR) wave to be monitored exclusively in
patients with hemifacial spasm (HFS), electrophysiology has
been widely employed to predict a satisfactory decompres-
sion. Recently, we also stimulated the offending artery
during the operation for HFS cases and achieved a wave
analogous to the AMR. It could only be recorded at
the offending artery and disappeared immediately after the
decompression. In this case, the offending artery and the
conflict site was finally proved to be the anterior infracer-
ebellar artery (AICA) in the cisternal segment of the facial
nerve. Notice that the facial nerve was not visualized in this
picture due to the positional block of the acoustic nerve (VIII).
Table 3 Postoperative malaises
Items Literatures (%) Our data (%)
Face paresthesia 1–359,16,18,56,63 6.7Nausea/vomit 1–28.29 15.2Hearing change 0.87–169,16,18,56 2Headache 28.29 22.3Dizziness/vertigo 0.89–28.29,16,17 18.2Herpes labialis (TN) 1.99 2.1Balance disorder 118 1
TN: trigeminal neuralgia.
Table 4 Complications of microvascular decompressions(MVDs)
Items Literatures (%) Our data (%)
Cerebrospinalfluid (CSF) leak
0.89–1316–20,55,56,64,65 1.3
Incisional infection 3–755 0.4Meningitis 0.6–9.29,16,17,55, 0Brain infarctions 0.69 0.2Pulmonary embolism 0.69 0Facial palsy 0.6–8.79,17–22,57,58,66 0.7Deafness 0.89–8.216,17 0.9Cerebellar edema 555 3.2Hydrocephalus 4.655 2.1Cerebellar mutism 1.255 0.1Mortality 0–2.616,18,19 0.13
Zhong et al. Microvascular decompression surgery
890 Neurological Research 2014 VOL. 36 NO. 10
good anatomical angle had not been obtained during
the operation. It may happen when PV blocked the
surgical way or even when arteries were attached the
petrosal bone and made it very difficult to remove
the cerebellum (Fig. 9). As TN or HFS is a functional
rather than life-threatening disorder, we regard
‘safety’ as the priority of MVD. In case of difficult
exposure, we would end the operation if an apparent
offending vessel has been identified at the most
haunted site, especially when a dent has been
observed at the contact point (Fig. 7D). For those
patients who do not improve at all after the surgery,
we would review the operative video records care-
fully. As long as we find that not all the entire
intracranial root of the nerve has been exposed, we
would communicate with the relatives as well as the
patient. If the patient is ready to take the risk that
arises from additional exposure, we would redo
MVD. We are not against the possibility of ‘delayed
relief’ mentioned by many authors, especially in HFS
cases.59 However, we do not think it may happen in
patients whose symptom were completely unim-
proved or even deteriorated. It might happen when
multiple vessels are involved. Once the larger
involved artery is isolated, the symptoms may
marginally improve as the main problem has been
solved. For the smaller vessel, a little movement may
allow the lesions at the interfaces to repair over time.
With the restoring of both the epineurium and
adventitia, the nerve may finally be isolated from
the vessel. Therefore, if the patient hopes for an
immediate cure and there is a chance for it, why do
we still ask him or her to suffer while anxiously
expecting a possible relief? Our philosophy looks like
a sort of Eastern view–‘Middle Way’, but it does give
the patient more choice. With this surgical strategy,
we have achieved a good postoperative outcome with
very low incidence of complications.36,45,60–62
Disclaimer Statements
Contributors Dr Zhong and Dr RLi performed all the
MVD surgeries. The others assisted the operations
and collected data; Dr Zhong finished the manu-
script; and Dr Li supervised all the work.
Funding This study was supported by Science & Tech-
nology Committee of ShanghaiMunicipal (124119a0800)
and Education Commission of Shanghai Municipal
(10YZ42).
Table 5 Comparison of surgical findings between primary and reoperative MVDs in HFS patients (adapted from Ref. 41)
Patients
1st MVD 2nd MVD
The failure reasonof the 1st MVD
Offendingartery(ies)
Conflictsite (zone)
Severity ofcompression
Offendingartery(ies)
Conflictsite (zone)
Severity ofcompression
1 VA z PICA 2 and 3 Indentation VA z PICA 2 and 3 Indentation Teflon was not enough2 VA z AICA 3 Indentation AICA 4 Contact Zone 4 missed3 AICA 3 Indentation AICA 4 Contact Zone 4 missed4 AICA 2 and 3 Indentation AICA 4 Deviation Zone 4 missed*5 AICA 2 and 3 Indentation AICA 4 Deviation Zone 4 missed*6 AICA 2 and 3 Contact AICA 4 Contact Zone 4 missed#7 AICA 2 and 3 Contact AICA 4 Deviation Zone 4 missed*8 VA z AICA 2 and 3 Indentation AICA 2 Indentation Incomplete decompression‘9 AICA 2 and 3 Contact AICA 4 Deviation Zone 4 missed*
MVD: microvascular decompression; VA: vertebral artery; PICA: posterior inferior cerebellar artery; AICA: anterior inferior cerebellarartery.*AICA went through between facial and acoustic nerves.#A vein went through between facial and acoustic nerves.‘decompression between AICA and the nerve was not enough.Zone 1: where the nerve emerges to the brainstem surface from the parenchymal and goes through the pontomedullary sulcus; Zone2: where the root attaches to the surface of the pons; Zone 3: where it is gradually transiting to be narrower, which corresponds to theObersteiner–Redlich zone (the traditional REZ); Zone 4: where the nerve fibrins separates from the brainstem and extends to theinternal meatus.
Figure 9 An unsatisfactory exposure due to individual
anatomical difference. This was a left HFS case. The medial
portion of the facial nerve could not be exposed because the
anterior infracerebellar artery (AICA) was attached to the
petrosal bone (*) and made the retraction of cerebellar
hemisphere impossible. V: trigeminal nerve; VIII: the vesti-
bulocochlear nerve; IX: glossopharyngeal nerve.
Zhong et al. Microvascular decompression surgery
Neurological Research 2014 VOL. 36 NO. 10 891
Conflicts of interest None.
Ethics approval This study was approved by the
Ethics Committee of XinHua Hospital, Shanghai
JiaoTong University School of Medicine.
Reference1 Yang K-H, Na J-H, Kong D-S, Park K. Combined hyperactive
dysfunction syndrome of the cranial nerves. J KoreanNeurosurg Soc. 2009;46:351–4.
2 Rosenstengel C, Matthes M, Baldauf J, Fleck S, Schroeder H.Hemifacial spasm: conservative and surgical treatment options.Dtsch Arztebl Int. 2012;109:667.
3 Kuroki A, Møller A. Facial nerve demyelination and vascularcompression are both needed to induce facial hyperactivity: astudy in rats. Acta Neurochir (Wien). 1994;126:149–57.
4 Wu Y, Davidson AL, Pan T, Jankovic J. Asian over-representation among patients with hemifacial spasm comparedto patients with cranial-cervical dystonia. J Neurol Sci.2010;298:61–3.
5 Love S, Coakham HB. Trigeminal neuralgia pathology andpathogenesis. Brain. 2001;124:2347–60.
6 Devor M, Seltzer Z. Pathophysiology of damaged nerves inrelation to chronic pain. In: Wall PD, Melzack R, editors.Textbook of pain, Vol. 4. London: Churchill Livingstone; 1999.p. 129–64.
7 Zheng X, Hong W, Tang Y, Wu Z, Shang M, Zhang W, et al.Sympathetic nerves bridge the cross-transmission in hemifacialspasm. Neurosci Lett. 2012;517(1):52–5.
8 Zhou QM, Zhong J, Jiao W, Zhu J, Yang XS, Ying TT, et al.The role of autonomic nervous system in the pathophysiologyof hemifacial spasm. Neurol Res. 2012;34:643–8.
9 Oesman C, Mooij JJ. Long-term follow-up of microvasculardecompression for trigeminal neuralgia. Skull Base. 2011;21:313.
10 Espay AJ, Schmithorst VJ, Szaflarski JP. Chronic isolatedhemifacial spasm as a manifestation of epilepsia partialiscontinua. Epilepsy Behav. 2008;12:332–6.
11 Perkin G, Illingworth R. The association of hemifacial spasmand facial pain. J Neurol Neurosurg Psychiatry. 1989;52:663–5.
12 Lemos L, Alegria C, Oliveira J, Machado A, Oliveira P,Almeida A. Pharmacological versus microvascular decompres-sion approaches for the treatment of trigeminal neuralgia:clinical outcomes and direct costs. J Pain Res. 2011;4:233.
13 Campos WK, Linhares MN. A prospective study of 39 patientswith trigeminal neuralgia treated with percutaneous ballooncompression. Arq Neuropsiquiatr. 2011;69:221–6.
14 Wang X, Zhou C, Guang-Jian S, Min-Hui X, Guang-Xin C,Yong-Wen Z, et al. Long-term outcomes of percutaneousretrogasserian glycerol rhizotomy in 3370 patients withtrigeminal neuralgia. Turk Neurosurg. 2011;21(1):48–52.
15 Lee JK, Choi HJ, Ko HC, Choi SK, Lim YJ. Long termoutcomes of gamma knife radiosurgery for typical trigeminalneuralgia-minimum 5-year follow-up. J Korean Neurosurg Soc.2012;51:276–80.
16 Gunther T, Gerganov VM, Stieglitz L, Ludemann W, Samii A,Samii M. Microvascular decompression for trigeminal neur-algia in the elderly: long-term treatment outcome andcomparison with younger patients. Neurosurgery. 2009;65:477–82.
17 Illingworth R, Porter D, Jakubowski J. Hemifacial spasm: aprospective long-term follow up of 83 cases treated bymicrovascular decompression at two neurosurgical centres inthe United Kingdom. J Neurol Neurosurg Psychiatry.1996;60:72–7.
18 Zhong J, Li S-T, Zhu J, Guan HX, Zhou QM, Jiao W, et al. Aclinical analysis on microvascular decompression surgery in aseries of 3000 cases. Clin Neurol Neurosurg. 2012;114:846–51.
19 Jagannath PM, Venkataramana NK, Bansal A, RavichandraM. Outcome of microvascular decompression for trigeminalneuralgia using autologous muscle graft: a five-year prospectivestudy. Asian J Neurosurg. 2012;7:125.
20 Jeon C-J, Kong D-S, Lee J-A, Park K. The efficacy and safetyof microvascular decompression for hemifacial spasm in elderlypatients. J Korean Neurosurg Soc. 2010;47:442–5.
21 Han J-S, Lee J-A, Kong D-S, Park K. Delayed cranial nervepalsy after microvascular decompression for hemifacial spasm.J Korean Neurosurg Soc. 2012;52:288–92.
22 Kim HJ, Park YS, Ryu JS, Huh R, Han I, Shin DA, et al.Intraoperative facial electromyography and brainstem auditoryevoked potential findings in microvascular decompression forhemifacial spasm: correlation with postoperative delayed facialpalsy. Stereotact Funct Neurosurg. 2012;90:260–5.
23 Dandy WE. Concerning cause of trigeminal neuralgia. Am JSurg. 1934;24:447–55.
24 Jannetta PJ, McLaughlin MR, Casey KF. Technique ofmicrovascular decompression: technical note. NeurosurgFocus. 2005;18:1–5.
25 Kondo A. Microvascular decompression surgery for trigeminalneuralgia. Stereotact Funct Neurosurg. 2001;77:187–9.
26 Park JS, Kong DS, Lee JA, Park K. Hemifacial spasm:neurovascular compressive patterns and surgical significance.Acta Neurochir (Wien). 2008;150:235–41.
27 Zhong J. An ideal microvascular decompression techniqueshould be simple and safe. Neurosurg Rev. 2012;35:137–40.
28 Ishimori T, Nakano S, Kagawa M, Yokoe K, Togami T,Asakura H. Virtual endoscopic images by 3D FASE cisterno-graphy for neurovascular compression. Magn Reson Med Sci.2003;2:145–9.
29 Guan HX, Zhu J, Zhong J. Correlation between idiopathichemifacial spasm and the MRI characteristics of the vertebralartery. J Clin Neurosci. 2011;18:528–30.
30 Zimny A, Sasiadek M. Contribution of perfusion-weightedmagnetic resonance imaging in the differentiation of meningio-mas and other extra-axial tumors: case reports and literaturereview. J Neurooncol. 2011;103:777–83.
31 Palmisano S, Schwartzbaum J, Prochazka M, Pettersson D,Bergenheim T, Florentzson R, et al. Role of tobacco use in theetiology of acoustic neuroma. Am J Epidemiol. 2012;175:1243–51.
32 Albera R, Canale A, Piumetto E, Lacilla M, Dagna F.Ossicular chain lesions in cholesteatoma. Acta Otorhino-laryngol Ital. 2012;32:309.
33 Ilıca AT, Hıdır Y, Bulakbası N, Satar B, Guvenc I, Arslan HH,et al. HASTE diffusion-weighted MRI for the reliable detectionof cholesteatoma. Diagn Interv Radiol. 2012;18:153.
34 Cohen-Gadol AA. Microvascular decompression surgery fortrigeminal neuralgia and hemifacial spasm: nuances of thetechnique based on experiences with 100 patients and review ofthe literature. Clin Neurol Neurosurg. 2011;113:844–53.
35 Li S, Hong W, Tang Y, Ying T, Zhang W, Li X, et al. Re-operation for persistent hemifacial spasm after microvasculardecompression with the aid of intraoperative monitoring ofabnormal muscle response. Acta Neurochir (Wien).2010;152:2113–8.
36 Zhu J, Li ST, Zhong J, Guan HX, Ying TT, Yang M, et al.Role of arterioles in management of microvascular decompres-sion in patients with hemifacial spasm. J Clin Neurosci.2012;19:375–9.
37 Zhong J, Li S, Xu S, Wan L, Wang X. Management of petrosalveins during microvascular decompression for trigeminalneuralgia. Neurol Res. 2008;30:697–700.
38 De Ridder D, Moller A, Verlooy J, Cornelissen M, De RidderL. Is the root entry/exit zone important in microvascularcompression syndromes? Neurosurgery. 2002;51:427–33; dis-cussion 433–4.
39 Katusic S, Beard CM, Bergstralh E, Kurland LT. Incidence andclinical features of trigeminal neuralgia: Rochester, Minnesota,1945-1984. Ann Neurol. 1990;27:89–95.
40 Auger RG, Whisnant JP. Hemifacial spasm in Rochester andOlmsted County, Minnesota, 1960 to 1984. Arch Neurol.1990;47:1233–4.
41 Zhong J, Zhu J, Li ST, Li XY, Wang XH, Yang M, et al. Ananalysis of failed microvascular decompression in patients withhemifacial spasm: focused on the early reoperative findings.Acta Neurochir (Wien). 2010;152:2119–23.
42 Zhong J, Li ST, Zhu J, Guan HX. Is entire nerve rootdecompression necessary for hemifacial spasm? Int J Surg.2011;9:254–7.
43 Katusic S, Beard CM, Bergstralth E, Kurland LT. Incidenceand clinical features of trigeminal neuralgia, Rochester,Minnesota, 1945-1984. Ann Neurol. 1990;27:89–95.
44 Prieto R, Pascual JM, Yus M, Jorquera M. Trigeminalneuralgia: assessment of neurovascular decompression by 3Dfast imaging employing steady-state acquisition and 3D time offlight multiple overlapping thin slab acquisition magneticresonance imaging. Surg Neurol Int. 2012;3:50.
45 Zheng X, Feng B, Hong W, Zhang W, Yang M, Tang Y, et al.Management of intraneural vessels during microvascular
Zhong et al. Microvascular decompression surgery
892 Neurological Research 2014 VOL. 36 NO. 10
decompression surgery for trigeminal neuralgia. WorldNeurosurg. 2012;77:771–4.
46 Kawashima M, Yamada M, Sato S, Oka H, Fujii K,Matsushima T. Hemifacial spasm caused by vascular compres-sion of the distal portion of the facial nerve associated withconfiguration variation of the facial and vestibulocochlearnerve complex. Turk Neurosurg. 2009;19:269–75.
47 Campos-Benitez M, Kaufmann AM. Neurovascular compres-sion findings in hemifacial spasm. J Neurosurg. 2008;109:416–20.
48 Sindou M. Microvascular decompression for primary hemi-facial spasm. Importance of intraoperative neurophysiologicalmonitoring. Acta Neurochir (Wien). 2005;147:1019–26.
49 Yamashita S, Kawaguchi T, Fukuda M, Watanabe M, TanakaR, Kameyama S. Abnormal muscle response monitoring duringmicrovascular decompression for hemifacial spasm. ActaNeurochir (Wien). 2005;147:933–8.
50 Polo G, Fischer C, Sindou MP, Marneffe V. Brainstemauditory evoked potential monitoring during microvasculardecompression for hemifacial spasm: intraoperative brainstemauditory evoked potential changes and warning values toprevent hearing loss-prospective study in a consecutive series of84 patients. Neurosurgery. 2004;54:97.
51 Ying T-T, Li S-T, Zhong J, Li XY, Wang XH, Zhu J. The valueof abnormal muscle response monitoring during microvasculardecompression surgery for hemifacial spasm. Int J Surg. 2011;9:347–51.
52 Fukuda M, Oishi M, Takao T, Hiraishi T, Sato Y, Fujii Y.Monitoring of abnormal muscle response and facial motorevoked potential during microvascular decompression forhemifacial spasm. Surg Neurol Int. 2012;3:118.
53 Joo W-I, Lee K-J, Park H-K, Chough CK, Rha HK.Prognostic value of intra-operative lateral spread responsemonitoring during microvascular decompression in patientswith hemifacial spasm. J Clin Neurosci. 2008;15:1335.
54 Hatem J, Sindou M, Vial C. Intraoperative monitoring of facialEMG responses during microvascular decompression forhemifacial spasm. Prognostic value for long-term outcome: astudy in a 33-patient series. Br J Neurosurg. 2001;15:496–9.
55 Dubey A, Sung W-S, Shaya M, Patwardhan R, Willis B, SmithD, et al. Complications of posterior cranial fossa surgery – aninstitutional experience of 500 patients. Surg Neurol. 2009;72:369–75.
56 Jellish WS, Benedict W, Owen K, Anderson D, Fluder E, SheaJF. Perioperative and long-term operative outcomes after
surgery for trigeminal neuralgia: microvascular decompressionvs percutaneous balloon ablation. Head Face Med. 2008;4:11.
57 Dannenbaum D, Kuzmina E, Lejeune P, Torrie J, Gangbe M.Prevalence of diabetes and diabetes-related complications inFirst Nations communities in Northern Quebec (EeyouIstchee), Canada. Can J Diabetes. 2008;32:46–52.
58 Kalkanis SN, Eskandar EN, Carter BS, Barker FG II.Microvascular decompression surgery in the United States,1996 to 2000: mortality rates, morbidity rates, and the effects ofhospital and surgeon volumes. Neurosurgery. 2003;52:1251–62.
59 Goto Y, Matsushima T, Natori Y, Inamura T, Tobimatsu S.Delayed effects of the microvascular decompression on hemi-facial spasm: a retrospective study of 131 consecutive operatedcases. Neurol Res. 2002;24:296–300.
60 Zheng X, Hong W, Tang Y, Ying T, Wu Z, Shang M, et al.Discovery of a new waveform for intraoperative monitoring ofhemifacial spasms. Acta Neurochir (Wien). 2012;154:799–805.
61 Yang XS, Li ST, Zhong J, Zhu J, Du Q, Zhou QM, et al.Microvascular decompression on patients with trigeminalneuralgia caused by ectatic vertebrobasilar artery complex:technique notes. Acta Neurochir (Wien). 2012;154:793–7;discussion 797.
62 Zhong J, Zhu J, Li ST, Guan HX. Microvascular decompres-sions in patients with coexistent hemifacial spasm andtrigeminal neuralgia. Neurosurgery. 2011;68:916–20; discussion920.
63 Rhee DJ, Kong DS, Park K, Lee JA. Frequency and prognosisof delayed facial palsy after microvascular decompression forhemifacial spasm. Acta Neurochir (Wien). 2006;148(8):839–843.
64 Hyun SJ, Kong DS, Park K. Microvascular decompression fortreating hemifacial spasm: lessons learned from a prospectivestudy of 1,174 operations. Neurosurg Rev. 2010 Jul;33(3):325–34; discussion 334. doi: 10.1007/s10143-010-0254-9. Epub 2010Mar 27.
65 Park JS, Kong DS, Lee JA, Park K. Intraoperative manage-ment to prevent cerebrospinal fluid leakage after microvasculardecompression: dural closure with a ‘‘plugging muscle’’method. Neurosurg Rev. 2007 Apr;30(2):139–42; discussion142. Epub 2007 Jan 13.
66 Barker FG, Jannetta PJ, Bissonette DJ, Larkins MV, Jho HD.The long-term outcome of microvascular decompression fortrigeminal neuralgia. N Engl J Med. 1996 Apr 25;334(17):1077–83; discussion 142. Epub 2007 Jan 13.
Zhong et al. Microvascular decompression surgery
Neurological Research 2014 VOL. 36 NO. 10 893