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Vernet's Syndrome After Carotid Endarterectomy

Tomonori Tamaki, Yoji Node, Norihiro Saitoum, Hideto Saigusa, Michio Yamazaki and Akio Morita
PERSPECT VASC SURG ENDOVASC THER 2013 25: 65
DOI: 10.1177/1531003514525476

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525476
research-article2014
PVSXXX10.1177/1531003514525476Perspectives in Vascular Surgery and Endovascular TherapyTamaki et al

Article
Perspectives in Vascular Surgery

Vernet’s Syndrome After Carotid

and Endovascular Therapy
2014, Vol. 25(3-4) 65­–68
© The Author(s) 2014
Endarterectomy Reprints and permissions:
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DOI: 10.1177/1531003514525476
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Tomonori Tamaki, MD1, Yoji Node, MD1,

Norihiro Saitoum, MD2, Hideto Saigusa, MD3,
Michio Yamazaki, MD1, and Akio Morita, PhD3

Abstract
Unilateral paresis of cranial nerves IX to XI is defined as Vernet’s syndrome. We retrospectively assessed cranial nerve
symptoms from the clinical records of 143 carotid endarterectomy patients. A flexible nasolaryngoscope was used to
examine vocal fold movements in 73 patients. If vocal fold paresis (VFP) was confirmed, the patient also underwent
magnifying laryngoscopy (for correct diagnosis of injury to the glossopharyngeal and vagus nerves). It was found from
clinical records that 8 patients (6%) were confirmed to have cranial nerve symptoms corresponding to Vernet’s
syndrome; 7 patients (9 %) had VFP on nasolaryngoscopy. In 2 patients, magnifying laryngoscopy confirmed ipsilateral
VFP, pharyngeal paresis, pharyngeal wall hypesthesia, and ipsilateral pharyngeal wall swelling. These 2 patients also had
symptoms of injury to the accessory nerve. Damage to cranial nerves IX to XI probably occurred in the parapharyngeal
space, based on the existence of posterior pharyngeal wall edema or swelling after carotid endarterectomy.

Keywords
carotid endarterectomy, vagus nerve, parapharyngeal space, cranial nerve, hoarseness

Introduction paid to careful dissection of the nerves around the carotid

During carotid endarterectomy (CEA), dissection is per-
formed in the vicinity of several important nerves. If
nerve injury occurs, it usually affects the vagus nerve, the
hypoglossal nerve, and the marginal mandibular branch
of the facial nerve.1-9 On the other hand, glossopharyn-
geal or accessory nerve injury is an uncommon complica-
tion of CEA because these nerves are remote from the
operating field.10-14 However, we have encountered
patients with ipsilateral paresis of the glossopharyngeal,
vagus, and accessory nerves (Vernet’s syndrome) after
CEA, which was diagnosed by magnifying laryngos-
copy.15 This is the first report of Vernet’s syndrome asso-
ciated with CEA.
Materials and Methods
We performed 223 consecutive CEA procedures in 213
patients over 12 years. There were 188 men and 25
women, with a mean age of 75 years (range = 58-87
years). CEA was performed under general anesthesia
with a medium-sized Portex endotracheal tube. All
patients were treated by the same surgical technique,
which involved dissection of the carotid artery with the
minimum possible injury to any of the cranial and cervi-
cal nerves in the operating field. Special attention was
artery, especially at the sites of proximal and distal clamp-
ing. We used fine needle skin hooks to keep the wound
open instead of self-retaining retractors. An internal shunt
and a Hemashield patchgraft were used in all patients. At
2 to 10 days after surgery, all patients underwent brain
computed tomography or magnetic resonance imaging to
detect postoperative cerebrovascular accidents. Evidence
of a cerebrovascular accident was detected in 5 patients,
who were excluded from this study; 9 patients with mod-
erate to severe wound hematomas were also excluded
from this study.16 In all patients, the absence of carotid
artery or internal jugular vein occlusion was confirmed
by ultrasonography after CEA. We retrospectively inves-
tigated neurological findings related to the glossopharyn-
geal, vagus, and accessory nerves in the clinical records.
There were 143 CEA procedures after which findings
related to these nerves were reported, including
hoarseness, dysphagia, aspiration, abnormal gag reflex,
1
Nippon Medical School Tamanagayama Hospital, Tamashi, Japan
2
Tokyo Rosai Hospital, Ootaku, Japan
3
Nippon Medical School, Bunkyoku, Japan
Corresponding Author:
Tomonori Tamaki, Nippon Medical School Tamanagayama Hospital,
1-7-1 Nagayama, Tamashi, 206-8512, Japan.
Email: tamakito@nms.ac.jp

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66 Perspectives in Vascular Surgery and Endovascular Therapy 25(3-4)
Figure 1.  The left trapezius muscle (black arrow) is weak in
comparison with the right side (white arrow) after left carotid
endarterectomy.
and trapezius muscle weakness. We defined hoarseness
as indicating injury to the vagus nerve or its branches.
Dysphagia and aspiration indicated injury to the glosso-
pharyngeal and/or vagus nerves, whereas impairment of
the gag reflex indicated glossopharyngeal nerve injury.
Weakness of the trapezius muscle indicated accessory
nerve injury.14 We also examined the timing of the onset
of these symptoms after CEA. From 2009, vocal fold
movements were examined in 73 CEA patients by a lar-
yngologist within 2 weeks after the operation using a
flexible nasolaryngoscope (Olympus ENF type P4;
Tokyo, Japan). If vocal fold paresis (VFP) was confirmed
by nasolaryngoscopy, the patient underwent magnifying
laryngoscopy (KG Weerda distending video laryngo-
scope, Karl Storz GmbH and Co; Tuttlingen, Germany)
and electrogustography. These examinations were done
by a laryngologist who was a vocal specialist, at 6 to 8
weeks after CEA. Magnifying laryngoscopy is a tech-
nique in which the vocal folds and pharynx are examined
very closely and contact is made with the pharyngeal wall
and tongue for evaluation of hypesthesia.
Results
Of the 143 CEA patients 8 (6%) had hoarseness, dyspha-
gia, a decreased ipsilateral gag reflex, and trapezius mus-
cle weakness according to their clinical records (Figure
1). These symptoms and findings appeared from 1 to 3
days after CEA. One patient developed aspiration pneu-
monia at 3 days after CEA. He recovered rapidly with
antibiotic therapy and had no further episodes of aspira-
tion. In all the affected patients, these symptoms resolved
within 1 year. Nasolaryngoscopy revealed VFP in 7 (9%)
of the 73 patients examined. Magnifying laryngoscopy
revealed that 2 patients had ipsilateral incomplete VFP,
incomplete pharyngeal paresis, pharyngeal hypesthesia,
ipsilateral hypesthesia of the posterior one-third of the
tongue, and swelling of the posterior pharyngeal wall
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Figure 2.  Ipsilateral posterior pharyngeal wall swelling
(black arrow) just anteromedial to the parapharyngeal space
is detected by magnifying laryngoscopy after left carotid
endarterectomy.
(Figure 2). These 2 patients also showed weakness of the
ipsilateral trapezius muscle. Three other patients only had
incomplete VFP and pharyngeal wall paresis, whereas 2
patients recovered from nerve injury spontaneously
before magnifying laryngoscopy was performed.
Electrogustography revealed normal findings in all
patients. Involvement of other cranial nerves was not
observed. We performed flexible nasolaryngoscopy at
monthly intervals in the 7 patients and found that VFP
recovered between 2 and 11 months after CEA.
Magnifying laryngoscopy was repeated at 1 year after
CEA in 4 patients, and the findings were normal.
Discussion
The major complications of CEA are stroke, myocardial
infarction, and death, whereas cranial nerve injury is usu-
ally considered to be a minor complication.17 The reported
incidence of cranial nerve injury after CEA varies widely
according to the type of study (prospective vs retrospec-
tive) and how carefully injury is investigated.1-9 In sev-
eral studies, the incidence of cranial nerve injury after
primary CEA was reported to range from 3% to 48% and
often involved the vagus nerve, hypoglossal nerve, and
mandibular branch of the facial nerve.1-9 In contrast, glos-
sopharyngeal or accessory nerve injury is uncommon
because these nerves are remote from the CEA operating
field.10-13 In the present series, 8 of 143 CEA patients had
partial injury of the glossopharyngeal, vagus, and acces-
sory nerves. Magnifying laryngoscopy confirmed the
diagnosis of glossopharyngeal and vagus nerve injury in
2 patients. Accordingly, they had Vernet’s syndrome,
which is paresis of cranial nerves IX to XI. Isolated uni-
lateral glossopharyngeal nerve paresis has been reported
to cause deficits ranging from minor swallowing prob-
lems to severe dysphagia and recurrent aspiration.15-18
Tamaki et al 67
Figure 3.  This figure shows the parapharyngeal space
(triangle outlined by dotted lines); cranial nerves IX to XI run
close together. The pharyngeal nerve branches from near the
inferior ganglion of the vagus nerve trunk.
Rosenbloom et al10 reported severe dysphagia and pul-
monary complications resulting from unilateral glosso-
pharyngeal nerve injury after CEA. It is difficult to
diagnose incomplete glossopharyngeal nerve paresis
without performing laryngoscopy.19 Patients generally do
not complain of decreased pharyngeal or glossal sensa-
tion, so it is important to use magnifying laryngoscopy
for correct diagnosis of incomplete glossopharyngeal
nerve paresis. Accessory nerve injury is also a rare com-
plication of CEA, with an incidence of only 0.9% being
reported in the European Carotid Surgery Trial. The
symptoms and signs of accessory nerve damage include
shoulder pain, winged scapula, and weakness of the tra-
pezius muscle. Diagnosis of incomplete accessory nerve
paresis is influenced by how aggressively neurological
findings are investigated. In fact, our patients did not
complain of any symptoms related to the accessory nerve
in daily life. The vagus nerve is the most common and
important cranial nerve to be injured during CEA, with
vagal damage leading to hoarseness, dysphagia, and aspi-
ration.1,3,5,7,20,21 VFP and ipsilateral pharyngeal paralysis
were observed in our patients who had magnifying laryn-
goscopy. These findings indicated that both the pharyn-
geal nerves and the recurrent laryngeal nerve had been
injured, with the probable site of injury being near the
inferior ganglion of the vagal nerve trunk (Figure 3).14,15,20
This ganglion lies within the parapharyngeal space,
which is a location where cranial nerves IX to XI could
be injured together. Based on magnifying laryngoscopy,
there were 2 patterns of nerve injury, which were (1) iso-
lated vagal trunk injury and (2) combined injury to the
vagus nerve, glossopharyngeal nerve, and accessory
nerve. The site of vagus damage was the same for both
isolated and combined injury. Amano et al22 reported a
case of Vernet’s syndrome caused by a large mycotic
aneurysm of the extracranial internal carotid artery (ICA).
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They concluded that enlargement of the extracranial ICA
directly compressed these 3 nerves. In addition, several
authors have reported that ICA dissection can cause
paralysis of the lower cranial nerves, including Vernet’s
syndrome.23-26 The ICA and these 3 nerves run close
together in the parapharyngeal space, which is at the
upper border of the operating field for CEA (Figure 3).
Accordingly, manipulation of the ICA may indirectly
damage the 3 nerves, but the cause of Vernet’s syndrome
after CEA is still unknown. We excluded patients with
moderate/severe wound hematoma and postoperative
cerebrovascular accidents in this study. Postoperative
wound hematoma may induce nerve damage via a mass
effect, with symptoms being slightly delayed after CEA
and paresis being “incomplete.” Examination revealed
that the sense of taste was normal in our patients, so glos-
sopharyngeal paresis was incomplete in all of them. If
any nerve suffered complete injury, symptoms would
probably be severe and would be detected immediately
after CEA. Magnifying laryngoscopy revealed posterior
pharyngeal wall swelling just anteromedial to the para-
pharyngeal space, which suggested that edema or swell-
ing of the parapharyngeal space had been induced by
manipulation of the distal ICA. Detection of cranial nerve
injury after CEA may be inadequate because there have
only been a few reports about the diagnosis of cranial
nerve injury using laryngoscopy.1,3,10,13,21 It is possible
that Vernet’s syndrome may occur after CEA and not be
noticed by either the patient or the medical staff.
Conclusion
We reported on the detection of Vernet’s syndrome after
CEA using the magnifying laryngoscopy technique.
Declaration of Conflicting Interests
The author(s) declared no potential conflicts of interest with
respect to the research, authorship, and/or publication of this
article.
Funding
The author(s) received no financial support for the research,
authorship, and/or publication of this article.
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