Introduction
Hemifacial spasm results from the compression of the facial nerve root usually by
cerebellar arteries, but sometimes major blood vessels, such as the vertebral and
basilar arteries, may also cause hemifacial spasm. In hemifacial spasm, compression
of the facial nerve fibers by a tortuous/ectatic vertebral artery (VA) is relatively
common.[1]
[2]
[3]
[4]
[5]
[6]
[7] Dilation and elongation of the vertebral and basilar arteries with significant tortuosity
is usually called megadolichovertebrobasilar anomaly, dolichoectasia of the vertebrobasilar
artery, vertebrobasilar dolichoectasia, or vertebrobasilar artery tortuosity. It can
manifest as intracranial hemorrhage, obstructive hydrocephalus, ischemic strokes,
spastic tetraparesis, trigeminal neuralgia, hemifacial spasm or vagoglossopharyngeal
neuralgia.[8]
[9]
[10] In such cases, complete decompression of the cranial nerve roots is very difficult
and complicated, since the walls of a compressing vessel are rigid and sometimes densely
atherosclerotic. Therefore, neurovascular decompression may be accompanied by several
complications and recurrence of symptoms. Various modifications in the surgical technique
of vascular decompression are used in these cases of tortuous vertebrobasilar artery
(TVBA), from the placement of metal implants (between the nerve root and the rigid
vessel) to adhesive fixation of the displaced vertebrobasilar artery.[1]
[2]
[3]
[4]
[5]
[6]
[7]
[11]
[12]
[13]
[14]
[15]
[16]
[17]
[18]
[19]
[20]
[21]
[22]
[23]
[24]
[25]
[26]
In the present paper, we describe a new technique to sling a TVBA to the petrous dura
for microvascular decompression (MVD) in a patient with hemifacial spasm caused by
a TVBA.
Operative Techniques
Under general anesthesia with endotracheal intubation, the patient was positioned
in ‘three quarter prone’ by keeping the left side up. Nerve monitors were put in position.
A left-sided retromastoid retrosigmoid lateral suboccipital craniotomy was performed.
The dura was opened under the operating microscope. Upon exploration of the left cerebellopontine
angle, a large tortuous VA was found. The artery was impinging and compressing the
entry/exit zone of the 7th and 8th nerve complex ([Fig. 2] & [3]). There were thick and tight arachnoid bands attaching the artery to the nerve complex
and the pons, which were released by sharp microdissection. The dissection started
just above the lower cranial nerves and ascended progressively (using the bottom-up
technique) to free the entry/exit zone of the 7th and 8th nerves. The arterial walls
were thick and rigid but not atherosclerotic. The compressing portion of the VA was
free of branches and could easily be mobilized from the nerve entry/exit zone with
a microdissecting instrument, but it returned to a point close to its original position
after the removal of the dissecting instrument.
Fig. 2 Schematic (pencil drawing) perioperative picture of the operative findings, that
is, compression of the root exit/entry zone of the 7th and 8th nerves at the cerebellopontine
angle by the tortuous vertebrobasilar artery (TVBA).
Fig. 3 (A, B, C, D, E and F) Sequential perioperative pictures showing exposure of the compression of the nerve
exit/entry zone (7th and 8th nerves) by the tortuous vertebrobasilar artery (TVBA)
at the left cerebellopontine angle.
Through the upper part of the incision, a 2.5 × 1 cm temporalis fascia free flap was
harvested. After fixation and stabilization of the free flap, a 6–0 prolene suture
was passed through its length several times using the traditional Bengali sewing and
stitching techniques to make embroidered quilts called Nakshi katha ([Fig. 4] & [5]). The ‘prolenated’ (sutured with prolene) fascia was passed around the compressing
portion of the VA. Then, both ends of the fascia were brought together and stitched
to the posterior petrous dura (taking great care not to injure the surrounding neurostructures)
to keep the TVBA away from the 7th and 8th nerves and the pons ([Fig. 6] & [7]). After an arteriopexy, Surgicel (Ethicon, Bridgewater, NJ, US) was placed between
the VA and the nerves. The wound was closed accordingly, without a drain.
Fig. 4 Schematic (pencil) drawing of techniques of ‘prolenation’ of fascia or aponeurosis
for slinging of TVBA.
Fig. 5 (A, B, C and D) perioperative pictures of ‘prolenation’ of temporalis fascia with
6-0 prolene in the techniques of ‘Nokshi katha’ stitching.
Fig. 6 Schematic (pencil drawing) perioperative picture after slinging of TVBA by ‘prolenated’
fascial sling with petrous dura.
Postoperative Course
The patient had no hemifacial spasm immediately after the recovery from the anesthesia,
but he developed facial paresis (Brackmann-House (B&H) grade 2), a more intense tinnitus
(in comparison with the preoperative status), and further hearing deterioration on
the left side.
Three months after the operation, the patient's facial paresis improved to B&H grade1,
and the hearing also improved, but was still worse in comparison with the preoperative
state. Though improved, he had occasional annoying tinnitus.
During the follow-up after 6 months, the patient reported further improvement of the
tinnitus, with less intensity and frequency. The other neurological statuses were
stable, with absence of the Hoffman sign. An MRI scan of the brain showed that the
VA was away from the entry zone of the 7th and 8th nerves ([Fig. 8]).
Fig. 7 (A, B, C, D, E and F) Sequential perioperative pictures showing the slinging of the
tortuous vertebrobasilar artery (TVBA) by a ‘prolenated’ fascial sling to the petrous
dura at the left cerebellopontine angle decompressing the nerve exit/entry zone (of
the 7th and 8th nerves).
During the follow-up after 12 months, the patient had no hemifacial spasm, but a persistent
occasional tinnitus in adoptive form.
Discussion
Hemifacial spasm was first described by Gowers in 1884. It is a segmental myoclonus
of facial muscles innervated by the 7th cranial nerve. This disorder usually presents
in the fifth or sixth decades of life, and occurs almost always unilaterally. Bilateral
involvement can occur rarely. Hemifacial spasm usually starts with short clonic contractions
of the orbicularis oculi, and spreads to other facial muscles over the years (corrugator,
frontalis, orbicularis oris, platysma, and zygomaticus muscles).[27]
[28]
It is believed that irritating stimuli of the 7th nerve nucleus in the pons causes
hyperexcitability of the nucleus, while such irritation to the proximal segment of
the nerve may cause ephaptic transmission within the 7th nerve. Both mechanisms explain
the involuntary rhythmic myoclonus observed in hemifacial spasm.[29]
Tumor, arteriovenous malformation, Paget disease, or other compressive lesions, as
well as stroke, multiple sclerosis and basal meningitis, or other non-compressive
lesions, may present clinically as hemifacial spasm. Most cases are idiopathic, and
are due to compression by aberrant vessels such as the distal branch of the anterior
inferior cerebellar artery or a VA on the root exit zone of 7th nerve in the cerebellopontine
angle.[27]
Injections of botulinum toxin are the initial treatment in most cases of hemifacial
spasm. Transient relief of the spasm lasts for 3 to 6 months, and begins within 3
to 5 days after the injection. Sometimes, it may present some serious complications,
such as ptosis, persistent spasm, diplopia, exposure keratitis/ulcer, facial asymmetry
etc.[27]
[28]
Most of the time, the patients become frustrated with the injection, and want a permanent
solution.
Carbamazepine and benzodiazepines are used in the treatment of non-compressive hemifacial
spasm. In patients who refuse botulinum toxin injections and surgical decompression,
carbamazepine, benzodiazepines, and baclofen may also be used, but this form of treatment
is usually not effective. Surgical treatment is required in cases of compressive lesions.
Microvascular decompression surgery can be an effective treatment for those patients
who do not want/respond to botulinum toxin or have complications after the injection.[27]
[28]
[30]
When the patient is fit for surgery and the cause is compression of the nerve exit
zone by a vascular loop, the definitive choice of treatment should be MVD.
Ectatic vessels can cause hemifacial spasm by compressing the exit zone of 7th nerve.
The MVD of these vessels can have an excellent outcome.[31]
[32]
Fig. 8 Postoperative T2-weighted images of amagnetic resonance imaging scan of the brain
in axial (A, B and C) and coronal (D, E and F) views showing that the left sided tortuous
vertebrobasilar artery (TVBA) was shifted anterio-medially with the free exit/entry
zones of the 7th and 8th nerves.
Cases of apparent idiopathic hemifacial spasm may benefit from surgical exploration
and MVD.
W. Dandy[33] was the first to detect the compression of a thickened vertebrobasilar artery as
a cause of trigeminal neuralgia, though he used the term ‘cirsoid aneurysm’ for the
vessel. E. Campbell and C. Keedy,[34] and W. Gardner and G. Sava[35] described the compression of the nerve root entry zone of the facial nerve caused
by adjacent loops of the tortuous and dilated VA.1The TVBA is more commonly involved in the neurovascular conflict in patients with
hemifacial spasm (14%) than in those with trigeminal neuralgia (2.8–7.7%).[1]
[2]
[4]
[5]
[18]
The patients with vertebrobasilar artery compression were older and predominantly
male, with predominant involvement of the left side of the face and high correlation
with ipsilateral hemifacial spasm and hypertension.[18] The higher frequency of left-sided involvement can be understood by the asymmetric
diameter of the VAs with higher caliber on the ipsilateral side. This branching of
the left VA from the subclavian artery originating directly from the aortic arch is
another important factor that results in more pronounced pulse wave transmission on
the left side as opposed to the right VA originating from the brachiocephalic trunk.
All of these hemodynamic factors result in tortuosity and dolichoectatic changes in
the distal (intracranial) segments of the left VA and the whole vertebrobasilar artery.[1]
[8]
[9]
T. Fukushima operated 1,663 cases of hemifacial spasm, and in 232 (14%) cases, compression
(of the exit zone of the facial nerve) was caused by a tortuous VA.[2] In a study by M. Samii et al,[5] who reported 143 cases of hemifacial spasm, facial nerve compression by the VA was
found in 32 (26.6%) cases; isolated involvement of the VA was found only in 6 (4.2%)
cases; and both the anterior and posterior inferior cerebellar arteries were the culprit
vessels in the rest of the cases. S. Nagahiro et al[4] have observed compression of the facial nerve exit zone by the vertebral artery
in 14 patients out of 68 operated cases with hemifacial spasm, but in 11 of them the
nerve root was also compressed by the cerebellar artery.
The increased frequency of postoperative complications of the cranial nerves is due
to many surgical manipulations for the mobilization and transposition of the major
vessels. Major-vessel displacement is associated with the action of both surgical
instruments and dense arterial structures, changing relationships with adjacent neurostructures
on the surrounding cranial nerves (4th, 6th, 8th, 9th and 10th cranial nerves).[1] Postoperatively, hearing loss, facial weakness, lower cranial nerve dysfunctions,
and ischemic strokes of the medulla oblongata are more common in patients with hemifacial
spasm caused by TVBA compared with patients with compression of the facial nerve by
the cerebellar artery.[1]
[18]
Hemifacial spasm disappears immediately after neurovascular decompression in most
of the cases. In the long-term follow-up, the symptoms recur only in a few cases.
In hemifacial spasm caused by a TVBA or cerebellar artery, the success rate is similar
(in the long-term follow-up), and is close to 90%.[4]
[18]
The primary target of the MVD is to eliminate the pulsating effects of the vessels
at the entry/exit zones of the cranial nerves. The most frequently used technique
is microsurgical interposition, in which a few small synthetic implants, typically
pieces of Teflon (polytetrafluoroethylene) wool, are sequentially placed between the
cranial nerve root and the compressing culprit vessel. This technique has been successfully
used not only in patients with compression caused by cerebellar arteries with relatively
small diameters, but also in cases of compression caused by bigger vessels, such as
a TVBA. However, the use of the microsurgical interposition technique to eliminate
the compression effect caused by big arteries has some limitations and disadvantages.
Apart from the common complications, such as the displacement of the installed implant
and the formation of foreign body granulomas in the postoperative period, the important
characteristic of this method is the necessity to insert a significantly larger-than-usual
amount of implanted material between the cranial nerve and the ectatic vessel. This
MVD technique results in the displacement and deformation of the cranial nerve root
itself, instead of in the retraction/displacement of the major vessel away from the
primary position, due to the high density/thickness of its walls and the high intraluminal
pressure. The interposition technique has a higher success rate regarding the elimination
of trigeminal neuralgia, though there is a higher chance of sensory disturbances on
the face (the effect of partial rhizotomy), but its use in hemifacial spasm may almost
inevitably result in postoperative paresis of the 7th nerve and hearing disturbance.[1]
In order to eliminate the compression of the nerve roots caused by a TVBA, isolation
techniques in combination with the interposition technique are used in many ways.
The isolation technique may be performed by wrapping the nerve roots and/or compressing
vessels with many types of implants (in the form of strips and bands), as well as
by implanting cylindrical and fenestrated aneurysmal clips separating the vascular
and neurostructures from each other. However, this surgical technique is not fundamentally
different from the interposition technique, because the implants are in contact with
the cranial nerve roots, and need a much larger number of surgical manipulations.
Extreme variants of this kind of surgical ‘redundancy’ were shown in a few cases of
MVD in which the titanium implants designed for the fixation of the craniotomy bone
flaps were used to isolate the TVBA from the 5th cranial nerve root.[12]
[24]
The transposition of the arteries involved in the neurovascular decompression with
minimal surgical impact on the neurostructures is the most effective and acceptable
method of MVD. During the operation, after the identification of the culprit vessels
in the entry/exit zones of the corresponding cranial nerve roots, the objective of
the surgery is to mobilize and displace the artery from its original site, and to
place and keep it in the new position. Mobilization and placement of major vessels
away from nerve roots is a complicated operation that requires skill because of the
severe tortuosity and high density of the atherosclerotic walls. Sharp microdissection
of the arachnoid membranes fixing the TVBA to the brainstem should begin below the
level of the affected cranial nerve root. In cases of hemifacial spasm, microdissection
should be started with the separation of the caudal group of cranial nerves. The method
of phased ‘bottom-up’ arachnoid microdissection along the brainstem enables the gradual
mobilization of the TVBA, the assessment of its mobility, and the timely identification
of the entrances of the cerebellar and brainstem arteries hidden by nerve roots.[1]
Implant placement between the brainstem and the artery is technically simple. Numerous
Teflon implants in the form of pellets and lumps to tampon the space formed after
the mobilization of the compressing artery are used by most of the authors, which
gives reliable fixation of the newly formed neurovascular relationships. Muscles,
the fascia, fat, cotton, surgical materials etc. are the other materials that can
be used.[1]
Grigoryan et al,1 in 2016, published a series of MVD associated with vertebrobasilar artery tortuosity
in which the TVBA was mobilized by microdissection of the arachnoid membranes between
the artery and the brainstem and retracted laterally. Then, the TVBA was displaced
away from the brainstem in the caudo-rostral direction. These microsurgical manipulations
resulted in ‘spontaneous’ decompression of the cranial nerve roots without implantation
of prostheses between the vessel and the nerve root entry/exit zone. In most cases
(28 out of 30), they used pieces of muscle and adipose tissue, which were inserted
in a phased manner for the fixation of the displaced artery away from the brainstem.
The placement of tissue autoimplants is easy to perform due to the possibility of
arbitrary modeling of the size of the tissue pieces, and it requires no additional
surgical procedures after the mobilization and displacement of the artery. During
the placement of the implant in the ‘bottom-up’ direction and gradual TVBA retraction
from the brainstem, the mobilized and displaced artery ‘spontaneously’ moves away
from the entry/exit zone of the compressed nerve. Because of the ‘spontaneous’ decompression,
microsurgical manipulation on the cranial nerve roots is not performed, and the implants
are not inserted between the TVBA and the nerves, which avoids the development of
postoperative cicatricial deformity of the cranial nerve fibers. Newly formed neurovascular
relationships are further strengthened with fibrin glue, which preserves the spatial
arrangement of the mobilized and displaced artery until the final fixation of the
TVBA by cicatricial adhesions with the autoimplant and the dura mater. No recurrence
of clinical symptoms was observed in the series.[1]
There are various techniques of microsurgical arteriopexy. Arteriopexy can be performed
using adhesive compositions, ‘suspending loops’ made of synthetic materials, dural
and fascial flaps, microsurgical sutures passed around or through the vascular adventitia,
as well as fenestrated aneurysmal clips.[6]
[11]
[13]
[14]
[15]
[16]
[19]
[20]
[21]
[22]
[23]
[24]
[25]
[26] The double-stick tape technique for the transposition of an offending vessel in
MVD in hemifacial spams was described by Ichikawa et al in 2011.[16]
The use of sling/loop fixation of the artery is the most attractive and reasonable
way of performing neurovascular decompression, since: the success rate is very high;
it eliminates the need to install a large implant; it reduces the chance of developing
aseptic granuloma; and it reduces the chance of postoperative neurological complications
that occur due to the placement of large implants.
However, the implementation of this technique requires the expansion of the surgical
field by increasing cerebellum retraction, and may be accompanied by additional injury
to both nervous and vascular structures, with increased number of postoperative complications.
Additionally, it is a more complicated procedure.[6]
[11]
[13]
[14]
[15]
[16]
[19]
[20]
[21]
[22]
[23]
[24]
[25]
[26]
Ferreira et al, in 2011,[14] described vertebral arteriopexy for MVD of the facial nerve in the treatment of
hemifacial spasm in 6 patients. During the operation, after the identification of
the site of VA compression, the artery was adequately mobilized and displaced for
the decompression. Great actions that require skill were taken to avoid kinking/damage
of the perforating arteries arising from the VA. Two 8–0 nylon microsutures were passed
through to the adventitia of the VA and then through the clival or petrous dura, and
then tied carefully to alleviate compression on the facial nerve. Postoperatively,
all patients had complete resolution of the hemifacial spasm, but one patient suffered
from hearing loss, another developed a postoperative transient unilateral vocal cord
paralysis, and a third patient developed a pseudomeningocele that resolved with the
placement of a lumbar drain.[14]
Lin et al, in 2012,[19] performed vertebral or basilar artery mobilization and transposition using the vascular
sling with a strip of non-absorbable dural tape. The vertebrobasilar artery-sling
complex was then fixed to the petrous dura by an aneurysm clip through the dural bridge.
The direction and angle of traction on the vertebrobasilar artery was adjusted using
different lengths of clip or the horizontal level of the dural bridge. They used this
technique in seven cases with very good results. They concluded it is an easy and
adjustable way to perform MVD safely and effectively.
Here we describe the new modified technique to perform the slinging of a tortuous
and large ectatic VA using the ‘prolenated’ temporal fascial sling on the petrous
dura.
