Original Article
Trigeminal Neuralgia due to Vertebrobasilar Artery Compression
C. Michael Honey and Anthony M. Kaufmann
- OBJECTIVE: Classical trigeminal neuralgia (cTN) is
rarely caused by ectatic vertebrobasilar artery compres-
sion of the trigeminal nerve. These patients present a
surgical challenge and often are not considered for
microvascular decompression (MVD) due to assumed risk.
- METHODS: A review of patients who were surgically
treated by the senior author between 1997 and 2016 with an
admitting diagnosis of cTN was performed. Details of the
surgery were documented, including the technique for
maintaining vascular decompression, complications, and
the length of stay. Clinical follow-up was obtained from
patient charts as well as telephone questionnaires.
- RESULTS: During the 20-year review, 552 patients under-
went MVD for cTN, and 13 (2.4%) had dolichoectatic verte-
brobasilar compressions (10 male, 3 female). The average
hospital length of stay was 2.8 days (range 2e7) with no major
complications. At final follow-up (>2 years), 7 had no pain with
no medications (78%), 2 had persistent pain (22%)—1 of whom
underwent a successful glycerol rhizotomy at 8 months—2
were lost to follow-up, and 2 had surgery within 2 years.
- CONCLUSIONS: Patients with cTN due to a dolichoectatic
vertebrobasilar artery compression present a unique surgical
challenge. Mobilizing the vessel can be difficult because it
may be firm from atherosclerosis, maintaining its separation
from the nerve is similarly difficult, and manipulating the
vessel can be dangerous because of its brainstem perfora-
tors. Our case series provides some evidence to support the
safety and efficacy of MVD for patients with vertebrobasilar
ectasia for those that major surgery is not contraindicated.
Key words
- Ectatic vertebrobasilar
- Microvascular decompression
- Neurovascular compression
- Pain
- Trigeminal neuralgia
Abbreviations and Acronyms
cTN: Classical trigeminal neuralgia
eVB: Elongated vertebrobasilar artery
MVD: Microvascular decompression
WORLD NEUROSURGERY -: e1-e6, - 2018
INTRODUCTION
C lassical trigeminal neuralgia (cTN) is characterized by
stereotyped, paroxysmal, excruciating bouts of unilateral
facial pain triggered by non-noxious stimuli.1-3 The pre-
dominant cause of cTN is vascular compression of the trigeminal
nerve root, the culprit vessel most commonly being the superior
cerebellar artery; however, large veins often are implicated.4-6
Medical management, specifically anticonvulsants, provide the
bedrock of treatment.7 For those patients who do not respond to
medication, surgical avenues exist, including a variety of
destructive procedures or microvascular decompression (MVD).
The latter provides the opportunity for a “cure”— sustained pain
relief, without anesthesia.8-11 Rhizotomies, in contrast, also pro-
vide excellent pain relief although may result in a corresponding
numbness, less longevity of benefit, and a risk of anesthesia
dolorosa.12-14 Deciding on which procedure to perform is done on
a case-by-case basis by carefully balancing patient and surgeon
factors.
A small subset of patients suffers from medically refractory cTN
caused by an elongated vertebrobasilar artery (eVB) compressing
their trigeminal nerve. The prevalence of eVB as an offending artery
in TN has been reported as 2%e7% in past case series that studied
MVD,15-22 and such compression presents a unique surgical chal-
lenge. Mobilizing and maintaining the elongated and often
enlarged dolichoectatic vessel away from the trigeminal nerve root
can be difficult, and associated brainstem perforating vessels
introduce additional challenges.23 The role for MVD in these cases is
not well established, and some neurosurgeons may favor destructive
lesions (e.g., rhizotomy) because of concern it is microsurgically
incurable or presents an undue surgical risk.
We present our experience demonstrating the safety and
effectiveness of MVD surgery for this subset of patients. In addi-
tion, we include an explanation of our technique, which empha-
sizes an extensive dissection and mobilization to transpose the
offending artery away from the nerve.
Department of Surgery, Section of Neurosurgery, University of Manitoba Health Sciences
Centre, Winnipeg, Manitoba, Canada
To whom correspondence should be addressed: C. Michael Honey, M.D.
[E-mail: c.michael.honey@gmail.com]
Citation: World Neurosurg. (2018).
https://doi.org/10.1016/j.wneu.2018.06.145
Journal homepage: www.WORLDNEUROSURGERY.org
Available online: www.sciencedirect.com
1878-8750/$ - see front matter ª 2018 Elsevier Inc. All rights reserved.
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C. MICHAEL HONEY AND ANTHONY M. KAUFMANN
METHODS
A review was performed for all patients who were surgically
treated with MVD by the senior author between 1997 and 2016 with
an admitting diagnosis of cTN. Patients with preoperative neu-
roimaging and intraoperative finding of eVB compression of their
trigeminal nerve root were then identified. Demographics of the
patient cohort were collected, including age, sex, side, duration of
symptoms, previous medical treatments, and medical comorbid-
ities (hypertension, smoking history, hypercholesterolemia, coro-
nary atherosclerosis, stroke, and myocardial infarction). Details of
the surgery were documented, including the technique for main-
taining vascular decompression and the length of hospital stay.
Outcome was reported at the following time points after surgery:
1) 3 months, 2) 1 year, and 3) “long-term” (last contact, >2 years).
Outcome was graded as per the Barrow Neurological Institute Pain
Intensity Scoring Criteria24: grade 1: no pain, no medications;
grade 2: occasional pain, no medications; grade 3: some pain,
adequately controlled with medication; grade 4: some pain, not
adequately controlled with medication; and grade 5: severe pain,
not controlled with medications. All surgical complications were
documented. Patients were contacted by phone for their latest
follow-up.
Operative Technique
A standard retrosigmoid approach was used with the patient in the
lateral position with approximately 15
head flexion, downward
tilt, and contralateral rotation. This brought the retromastoid re-
gion to a horizontal plane. Through a linear incision of approxi-
mately 5e6 cm, bone was exposed and a craniectomy was
fashioned with a high-speed drill and rongeur to expose the edge
of the transverse and sigmoid sinus as usual for superior-lateral
approaches to TN cases. In addition, further bone was exposed
Figure 1. Diagram of surgical exposure. (A) Ectatic
basilar artery seen in contact with cranial nerves (CNs)
VII/VIII caudally and CN V rostrally. (B) Dissection is
initiated distal from CN V to mobilize the large vessel.
(C) Dissection continues proximally to transpose the
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ORIGINAL ARTICLE
TRIGEMINAL NEURALGIA DUE TO VB ARTERY COMPRESSION
to the floor of the posterior fossa, as for cases of hemifacial
spasm, to allow an approach from over the lateral and inferior-
lateral cerebellum. This facilitated exposure of the more prox-
imal eVB from both above and below the VIIeVIII cranial nerve
roots.
After the dura was opened in a D-shaped fashion, reflected
anteriorly over a moist gel foam, exposure of the trigeminal nerve
was achieved over the anterosuperior aspect of the cerebellum.
The petrosal bridging vein and branches were preserved whenever
possible, and the Trigeminal Nerve Root Enrty Zone was visual-
ized on either side of these veins. Distal superior cerebellar artery
exposure was gained over the superior cerebellum. The eVB was
seen compressing and distorting the TNR in all cases. Mobiliza-
tion of this large vessel was initiated as proximally as possible,
through a corridor between the IX and VIIeVIII nerves. Shredded
Teflon felt implants were then placed between the brainstem and/
or cerebellum and eVB to maintain the vessel in its new position.
Continuing superiorly, the eVB was moved further anteriorly to
alleviate compression at the Trigeminal Nerve Root Entry Zone
with additional implants placed as required (Figure 1).
Concurrently, neurovascular decompression from other vessels
also was achieved by mobilization of cerebellar arteries while
veins were similarly mobilized or sectioned after coagulation.
In one case (case 1) where transposition was difficult to main-
tain, a nonfenestrated aneurysm clip was used to maintain
vascular decompression. The ectatic basilar artery was compress-
ing the root entry zone from the inferior aspect. A titanium,
nonfenestrated aneurysm clip was used as a strut. A dural tunnel
was created over the petrous bone and one clip blade passed
through the tunnel and other closing onto it. The projecting end
of the clip beyond (medial) to the tunnel held the mobilized and
transposed basilar artery away from the TNR.
offending vessel away from CN V. Teflon is used to
maintain mobilization. (D) Thorough inspection of CN V
for secondary compression is undertaken. In this case,
the superior cerebellar artery is also meticulously
transposed and rotated as to no longer contact CN V.

C. MICHAEL HONEY AND ANTHONY M. KAUFMANN
Figure 2. (A) Three-dimensional time-of-flight magnetic resonance
angiography anterior projection demonstrating a tortuous ectatic basilar
artery. (B) T2-weighted, axial-view magnetic resonance image of the same
patient showing the ectatic vertebrobasilar artery coursing laterally coming
In 2 cases (cases 5 and 7), it was not possible to thoroughly
mobilize the eVB away from TNR, and shredded Teflon felt was
simply interposed between the nerve and vessel.
Interestingly, brainstem perforators were not found to be a
hindrance to mobilization of the eVB. In cases in which brainstem
perforators were observed coming off the offending vessel, they
too had become elongated and mobilization of the parent vessel
was achieved while avoiding any tension on their perforator
branches. Intraoperative monitoring routinely was used and con-
sisted of brainstem auditory-evoked responses, facial electromy-
ography, and facial motor-evoked potentials.
RESULTS
During the 20-year review, 552 patients underwent MVD for cTN,
and 13 of those (2.4%) had eVB compressions (Supplementary
Table 1). All 13 had follow-up of at least 3 months and were
included in the study. Seven patients had pain distribution along a
single division (V1 14%, V2 43%, V3 43%), and the remainder had
multiple divisions affected. The neuralgia was left sided in 8 pa-
tients (62%) and right sided in the other 5 (38%). MVD was the
first surgical intervention for 11 of 13 patients. Previous surgical
interventions were performed for 2 patients, which included case
3, who received 2 peripheral neurectomies and 2 balloon
compression rhizotomies to no avail before undergoing MVD, and
case 7, who underwent percutaneous glycerol rhizotomy, balloon
compression rhizotomy, and gamma knife rhizotomies before
electing for MVD.
Preoperative hypertension (54%), dyslipidemia (23%), and
smoking (31%) were diagnosed in the cohort. The average age at
surgery was 67.3 years (range 50e78 years). There was a pre-
dominance of male patients (77%) in the cohort. Magnetic
WORLD NEUROSURGERY -: e1-e6, - 2018
ORIGINAL ARTICLE
TRIGEMINAL NEURALGIA DUE TO VB ARTERY COMPRESSION
in contact with and deforming the right trigeminal nerve root entry zone. (C)
T2-weighted, axial-view magnetic resonance image of the same patient
after microvascular decompressive surgery highlighting a decompressed
and uncontacted right trigeminal nerve root entry zone.
resonance imaging was used preoperatively to determine the
relevant clinical anatomy and demonstrated the eVB in all cases.
All patients underwent MVD through a retrosigmoid craniec-
tomy. In 12 cases (92%), the culprit eVB compression was seen at
the proximal trigeminal nerve root entry zone. In 1 patient (case 7),
the eVB compressed the anterior lateral pons, which in turn dis-
torted and compressed the trigeminal root entry zone; mobiliza-
tion of this ectatic artery relieved the direct compression on the
pons and partially decompressed the severely atrophic trigeminal
nerve. Compression from an eVB alone was observed in only 1
patient (8%), whereas the remainder had multiple offending ar-
teries (92%), although the eVB was always most prominent.
Ectatic basilar arteries were involved in 7 of 13 cases (54%) and
ectatic vertebral arteries in the other 6 (46%). In all cases of
vertebral artery compression, the anterior inferior cerebellar artery
also was involved. In cases of basilar artery compression, the su-
perior cerebellar artery was also involved in 5 of 6 cases (83%), the
anterior inferior cerebellar artery in 3 patients (50%), and a large
vein in 2 (25%).
The average hospital length of stay was 2.8 days (range 2e7
days), and there were no major complications. In total, 12 of 13
patients (92%) had hospital stays of less than 3 days, whereas the
single outlier had a week of rehabilitation and homecare planning
related to pre-existing compromised neurologic status from pre-
vious unrelated brainstem stroke. Two patients experienced
transient diplopia resolving by postoperative day 2, and one
experienced transient ipsilateral limb ataxia resolving before
discharge from hospital. Postoperative magnetic resonance im-
aging for these and all patients demonstrated no evidence of injury
or infarction (Figure 2).
All the patients experienced significant pain relief before
discharge from hospital. By the time of the first follow-up at 3
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C. MICHAEL HONEY AND ANTHONY M. KAUFMANN TRIGEMINAL NEURALGIA DUE TO VB ARTERY COMPRESSION

months, only 1 patient had experienced a relapse of grade 4
symptoms (8%), whereas the remainder retained a grade 1 result
(92%). For those 10 patients available to assess at a 1-year follow-
up: grade 1 results had reduced to 8 of 10 patients (80%) and the
remaining 2 (25%) were grade 4 with persistent pain (one of whom
underwent a successful glycerol rhizotomy at 8 months). Two were
lost to follow-up, and one had their surgery performed within the
past year. Follow-up beyond 2 years (range: 2e18 years) was
available for 9 of the patients, and 7 (78%) continued to be grade 1.
Interestingly, the only 2 of the patients in whom culprit neuro-
vascular compression could not be thoroughly achieved at surgery
both failed to have sustained pain relief at 1 year.
DISCUSSION
An eVB was found to be the culprit cause of neurovascular
compression in only 2.4% of patients undergoing MVD for cTN
over the senior author’s 20-year experience. The finding of such
compression was not considered a contraindication to surgery,
and only 2 or 13 patients had undergone previous rhizotomies
before their MVD. Following the technique described in Linskey
et al.’s large series of 31 patients,16 it was possible to mobilize and
transpose the culprit eVB in 11 of 13 cases. Perforating vessels were
not a limiting factor because these vessels were significantly
elongated in parallel to the eVB and thereby allowed for liberal
mobilization of the parent vessel, as previously described.16
Recognition of these perforating arteries is a crucial step in the
operation, as blind manipulation under the assumption of
redundancy may lead to injury.
A standard MVD technique was effective for most cases, which
employed the principle to start away from the maximal point of
compression and then work toward the culprit vessel loop apex.
This required access to the eVB inferiorly, below the VII-VIII nerve
complex, and a slight enlargement of the standard retromastoid
craniectomy used for TN. In 1 case, Teflon implants were not
sufficient to maintain the stiff eVB in its transposed position away
from the TNR, and a clip-strut technique was required. In another
2 cases, the eVB was too stiff and inadequate pre-pontine space
was available to mobilize the culprit away from the TNR and
Teflon was simply interposed between the nerve and vessel; both
these patients failed to have long-term pain relief. Such difficulty
to mobilize such larger culprit vessels has been described previ-
ously.22 In 12 of our 13 cases, concurrent mobilization of the
anterior inferior cerebellar artery, superior cerebellar artery, or
veins were necessary and may have contributed to the rate of
success. Our results have demonstrated that successful MVD for
cTN caused by an eVB is a challenging operation but can be
safe and effective as a cohort from a high-volume experience.
This is in keeping with previous case reports (Supplementary
Table 2).25-34 This has led us to recommend MVD in this rare
condition for those in whom major surgery is not contraindicated.
The alternative to MVD, various rhizotomy techniques have to
be considered in all cases. A report of Gamma Knife rhizotomy for
cases of cTN caused by eVB demonstrated pain relief in 38% of
patients at 2 years.35 In comparison, MVD provided an overall
grade 1 outcome of 78% at 2 years with no significant or lasting
complications in our cohort. Results were even better among
patients in whom there was successful mobilization of the eVB,
with 100% (7/7) grade 1 at 2 years.
Our results show a predominance of male sex, hypertension,
and increasing age in those TN patients with eVB compression.
These are all major factors that play a role in atherosclerosis,
which frequently was observed in the operating theater. It has
been previously argued that the hemodynamic effect of high blood
flow through an atherosclerotic vessel can lead to tortuosity.36,37 In
contrast, some have argued that the compression of the
ventral-lateral medulla by tortuous vessels may play a role in the
development of hypertension38-40 and potentially cerebral blood
flow.41 Our results, although not conclusive, do support the
association of hypertension and tortuosity of the vertebral basilar
system.
Despite these promising results, there are some limitations to
our review. First, despite our case series being the largest since the
original papers from Linskey et al.,16 it remains a single-surgeon
analysis that may lack generalizability. Furthermore, although
follow-up reached 18 years in some cases, we had 2 patients lost to
follow-up.
CONCLUSIONS
It is our opinion that trigeminal neuralgia secondary to eVB
compression is not a contraindication to MVD, in fact, in expe-
rienced hands, MVD is an excellent option for this cohort, with a
78% “cure” at 2 years with no significant morbidity. The rarity and
technical challenge of these cases may argue for their referral to
neurosurgical centers experienced in their treatment.
ACKNOWLEDGMENTS
The authors thank Mr. Jon Stepaniuk for his detailed artwork.

3. Maarbjerg S, Di Stefano G, Bendtsen L, Cruccu G. 6. Matsushima T, Huynh-Le P, Miyazono M. Tri-

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Conflict of interest statement: The authors declare that the
article content was composed in the absence of any
commercial or financial relationships that could be construed
as a potential conflict of interest.
Received 5 March 2018; accepted 18 June 2018
Citation: World Neurosurg. (2018).
https://doi.org/10.1016/j.wneu.2018.06.145
Journal homepage: www.WORLDNEUROSURGERY.org
Available online: www.sciencedirect.com
1878-8750/$ - see front matter ª 2018 Elsevier Inc. All
rights reserved.
www.WORLDNEUROSURGERY.org e5
 ORIGINAL ARTICLE
C. MICHAEL HONEY AND ANTHONY M. KAUFMANN TRIGEMINAL NEURALGIA DUE TO VB ARTERY COMPRESSION

SUPPLEMENTARY DATA

Supplementary Table 1. Clinical Summary of the 13 Patients with TN Secondary to eVB in This Study
Case Age, Affected Affected Compressing Length Outcome Outcome Outcome
No. Years/Sex Side Division Vessel(s) of Stay (3 Months) (1 Year) (Long Term) Morbidity

1 69/M Right V3 BA þ SCA 2 days Grade 1 N/A N/A Minor hypoesthesia

2 61/M Left V2, V3 BA 2 days Grade 1 Grade 1 Grade 1 (3.5 years) Transient left gaze palsy
3 60/M Left V1 VA þ AICA 2 days Grade 1 Grade 1 Grade 1 (5 years) None
4 62/M Right V1, V2 Vert þ AICA þ SCA 3 days Grade 1 Grade 1 N/A Transient nystagmus
5 68/F Right V2 Vert þ AICA 2 days Grade 1 Grade 4 N/A Return of symptoms
6 69/F Left V2 Vert þ AICA þ SCA 2 days Grade 1 Grade 1 Grade 1 (2 years) None
7 78/M Left V2, V3 Pons from ectatic VA 2 days Grade 4 Grade 4 Grade 4 Return of symptoms
8 66/M Right V2 BA þ SCA 3 days Grade 1 Grade 1 Grade 1 (12 years) Minor hypoesthesia, transient ataxia
9 55/M Right V1, V2 BA þ AICA þ SCA 7 days Grade 1 Grade 1 Grade 1 (17.5 years) None
10 50/F Left V3 BA þ SCA N/A Grade 1 Grade 1 Grade 1 (18 years) None
11 50/M Left V3 VA þ AICA þ Vein 3 days Grade 1 Grade 1 Grade 1 (11 years) None
12 65/M Left V2, V3 BA þ AICA þ SCA 3 days Grade 1 Grade 1 Grade 1 None
13 72/M Left V1, V2, V3 BA þ AICA þ Vein 3 days Grade 1 N/A N/A Minor hypoesthesia

TN, trigeminal neuralgia; eVB, elongated vertebrobasilar artery; M, male; BA, basilar artery; SCA, superior cerebellar artery; N/A, not available; VA, vertebral artery; AICA, anterior inferior
cerebellar artery; F, female.

Supplementary Table 2. Literature Review of MVD of eVB for cTN

Reference Procedure(s) Results Morbidity

Linskey et al., 199416 29 MVD 86% grade 1 at 10 years 13 hypoesthesia, 7 transient diplopia, 4 hearing loss
Garcia De Sola and Escosa Bage, 200125 3 MVD 100% grade 1 immediately NR
26
Kraemer et al., 2006 1 MVD 100% grade 1 immediately Transient disequilibrium
Noma et al., 200927 1 MVD 100% grade 1 immediately None
22
El-Ghandour, 2010 10 MVD 80% grade 1 at 7.8 years 2 hypoesthesia, 1 trochlear paresis, 1 mild face weakness
28
Alcala-Cerra et al., 2011 1 MVD 100% grade 1 at 9 years None
Campos et al., 201229 1 MVD NR
30
Gressot et al., 2012 1 MVD 100% grade 1 immediately NR
31
Lin et al., 2012 100% grade 1 at 16e92 weeks 1 hypoesthesia
Yang et al., 201232 10 MVD 100% grade 1 at 3e30 months 1 hypoesthesia
Ma et al., 201333 9 MVD 100% grade 1 at 22 months 3 hypoesthesia, 1 facial palsy, 1 facial spasm
Apra et al., 201734 3 MVD 100% grade 1 at 2 years 2 transient diplopia, 1 transient hypoesthesia, 1 mild ataxia
Our series, 2018 13 MVD 78% grade 1 at >2 years 3 minor hypoesthesia, 2 transient diplopia, 1 transient ataxia

MVD, microvascular decompression; cTN, classical trigeminal neuralgia; eVB, elongated vertebrobasilar artery; NR, not reported.

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