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HEAD AND NECK
CT evaluation of sigmoid plate dehiscence causing pulsatile
tinnitus
Pengfei Zhao
1
&Han Lv
1
&Cheng Dong
1
&Yantao Niu
2
&
Junfang Xian
2
&Zhenchang Wang
1
Received: 23 December 2014 / Revised: 11 April 2015 /Accepted: 24 April 2015 / Published online: 20 May 2015
#European Society of Radiology 2015
Abstract
Objectives To evaluate the characteristics of sigmoid plate
dehiscence (SPD) causing pulsatile tinnitus (PT) on CT arte-
riography and venography (CTA + V).
Methods Thirty PT patients treated successfully with SPD
reconstruction were enrolled. Sixty asymptomatic patients
were matched. The location, extent, number of SPD cases
and concomitant signs, including venous outflow dominance,
transverse sinus stenosis, high jugular bulb, temporal bone
pneumatization, height of pituitary gland and pituitary fossa,
abnormal mastoid emissary vein, were detected and compared
using CTA + V.
Results More than one SPD was found on the symptomatic
side in 13/30 PT patients (43.3 %). The upper segment of the
sigmoid plate was involved in 29/44 SPDs in the vertical
direction (65.9 %); the lateral wall was involved in 38/44
SPDs in the horizontal direction (86.4 %). Singular SPD was
detected in 3/60 asymptomatic patients (1.67± 0.35 mm
2
), less
so in PT patients (7.97± 5.17 mm
2
). Compared with the con-
trol group, ipsilateral venous outflow dominance, high jugular
bulb and bilateral transverse sinus stenosis were more com-
mon in the PT group, together with deeper pituitary fossa and
flatter pituitary glands.
Conclusion SPD causing PT has characteristic CT findings. It
may be generated by vascular or intracranial pressure
abnormalities and act as a common key to triggering PT’s
perception.
Key Points
•Pulsatile tinnitus (PT) caused by sigmoid plate dehiscence
(SPD) may be cured.
•SPD causing PT has some characteristic findings on CT.
•SPD may be a common key to triggering PT’s perception.
•Thin-slice high resolution CT venography is recommended
for SPD assessment.
•The relationship between intracranial pressure and SPD
causing PT should be studied.
Keywords Pulsatile tinnitus .Sigmoid sinus .Dehiscence .
Intracranial pressure .Computed tomography
Abbreviations
SPD Sigmoid plate dehiscence
SSD Sigmoid sinus diverticulum
TBP Temporal bone pneumatization
IH Intracranial hypertension
HRCTV High resolution CT venography
Introduction
Pulsatile tinnitus (PT) is predominantly a pulse-synchronous
acoustic perception, which accounts for approximately 4 % of
all tinnitus. Unlike non-PT, PT can usually be found with
potential causes [1]. CT arteriography/venography (CTA/V)
is mostly recommended for PT patients with normal otoscopic
findings, which allows assessment of arterial, venous and neo-
plastic causes with a single examination [2–6].
Venous variants and anomalies as causes of PT have been
given more and more attention in recent years [7]. Sigmoid
*Zhenchang Wang
cjr.wzhch@vip.163.com
1
Department of Radiology, Beijing Friendship Hospital, Capital
Medical University, No.95, Yongan Road, Xicheng District,
Beijing 100050, China
2
Department of Radiology, Beijing Tongren Hospital, Capital Medical
University, No.1, Dongjiaominxiang, Dongcheng District,
Beijing 100730, China
Eur Radiol (2016) 26:9–14
DOI 10.1007/s00330-015-3827-8
plate dehiscence (SPD) with or without sigmoid sinus diver-
ticulum (SSD), accounting for approximately 1 % of asymp-
tomatic individuals [8,9], has been reported as a treatable
cause of PT [10–14]. SPD with SSD (also known as sigmoid
aneurysm) was found in about 20 % of PT patients [10,15].
The sound is widely considered to be due to turbulent flow in
the pouch. After surgical reconstruction, it can be totally elim-
inated. SPD without SSD is currently reported as the most
common cause of PT on CTA/V, with an incidence of 23 %
(7/30) to 40 % (12/30) [6,8]. However, SPD without SSD had
not been reported as a cause of PT until 2011, when Eisenman
DJ first stated that PT with SPD could be treated successfully
after simply covering the SPD with substitutes [10]. Since
then, consistent results have been obtained in three other stud-
ies, two of which are case reports. They had the same opinion
that SPD causing PT was usually located on the dominant side
of venous outflow in young ormiddle-aged women. However,
comprehensive characteristics of SPD without SSD causing
PT remain unknown. In this study, CT images of 30 PT pa-
tients treated successfully with surgical reconstruction of SPD
and 60 matched asymptomatic patients were assessed. The
characteristics of SPD causing PT were evaluated. The roles
of SPD and its concomitant signs in PT’s perception are
discussed.
Methods
Patients
The ethics committee in our institution approved this study.
Informed consent was obtained from all patients. Over 1500
PT patients have received a CTA + V examination during the
last five years at our hospital. Patients who met the following
criteria were enrolled: 1. unilateral and pulse-synchronous tin-
nitus, which could be eliminated by ipsilateral jugular com-
pression; 2. normal laboratory, otoscopic, audiometric,
tympanometric and digital subtraction angiography (DSA) re-
sults; 3. SPD was identified as PT’s main causative finding
and some other potential causes were excluded (Table 1); 4.
PT disappeared after surgical reconstruction and remained
negative at follow-up. Finally, 30 patients (27 females, 3
males) were enrolled, of whom 11 had left-sided PT and 19
had right-sided PT. The mean age was 37.93 ± 10.85 years
old (age range, 20–56 years). The mean clinical duration
of PT was 3.08±2.82 years (time range, 0.5–19 years).
The mean follow-up time was 2.24± 0.83 years (time
range, 0.5–4years).
Sixty patients with CTA+V examination were enrolled
as a control group with a 1:2 matching. The inclusion
criteria were as follows: age and gender matched; with-
out PT or established intracranial hypertension (IH). The
most common patient complaints in the control group
were trauma and headache. The mean age was 38.70±
9.68 years old (age range, 18–57 years).
Imaging technique
All images were obtained by a Brilliance 64-section CT sys-
tem (Philips Healthcare, Cleveland, Ohio) using a bolus track-
ing program (Trigger Bolus software; region of interest area,
200 mm
2
; trigger point, the ascending aorta; trigger threshold,
120 HU). Patients were placed in a supine position. The im-
aging parameters were as follows: 3.04 mSv: 100 kV, 250mAs
for arterial phase and 300 mAs for venous phase; collimation,
64× 0.625 mm; matrix, 512× 512; rotation time, 0.75 seconds.
Arterial phase images were scanned in the cranio-caudal di-
rection; venous phase images were scanned in the opposite
direction after 8 seconds. Contrast (Iopamidol, 370 mg iodine
per millilitre; BRACCO, Shanghai, China) was intravenously
administered at 1.5 ml/kg using a power injector at a rate of
5ml/s.
A standard algorithm was applied to both arterial and
venous images (width 600 HU, level 100 HU). Addition-
ally, a high-spatial-resolution bone algorithm with edge
enhancement was only applied to the venous images
(width 4000 HU, level 700 HU). All original images were
delivered into a post-processing workstation(Extended
Brilliance Workspace, Philips Healthcare). Axial images
were reformatted parallel to the horizontal semicircular
canal, while sagittal images were reformatted perpendicu-
lar to the dorsum sellae, both with a 1-mm thickness and a
1-mm increment.
Imaging interpretation
All images were analyzed by two experienced radiologists,
who were blind to the clinical and operative situation. The
final findings were made in consensus. The number, location
and extent of SPDs on the symptomatic side were carefully
observed on axial sections of high resolution CT venography
(HRCTV) (Fig. 1). In the vertical direction, the sigmoid plate
was divided into upper, middle and lower segments, with the
reference structure of the common crus and cochlear fenestra.
It was also divided into anterior, lateral and posterior walls,
with the borders of the anterior and posterior points of the
maximal curvature of the sigmoid sulcus estimated in the hor-
izontal direction (Fig 2). The diameter of each section was
measured on the reconstructed axial images. The whole SPD
area was numerically equal to the sum of the SPD’sdiameter
on each section.
A high jugular bulb (HJB) was defined as being above the
level of the internal auditory canal floor [16]. Brain venous
systems were considered as co-dominant if there was a differ-
ence of 3 mm or less between the diameters of the bilateral
mid-transverse sinuses. If not, the side with the larger diameter
10 Eur Radiol (2016) 26:9–14
was regarded as dominant [2]. A transverse sinus with focal
reduction of the luminal diameter by 50 % or more on the axial
images was considered stenosed. A mastoid emissary vein
diameter more than 4.0 millimetres was seen as abnormal
[6]. HJBs and mastoid emissary veins were detected on axial
HRCTV section. Transverse sinus stenosis and outflow dom-
inance were detected on axial CTV sections. The heights of
the pituitary gland and pituitary fossa were separately mea-
sured on sagittal CTVand HRCTV sections with the pituitary
stalk shown.
The volume of temporal bone pneumatization (TBP), in-
cluding the spaces of the middle ear cavity and temporal air
cells, was automatically calculated using three-dimensional
reconstruction on the post-processing workstation. The maxi-
mal threshold was set as -225 HU [4]. The incision function
was the only tool used to process the images. The key was to
cut the whole external auditory canal, which was separated
from the middle ear by a tympanic annulus detected on recon-
structed images (Fig. 3).
Statistical analysis
Statistical analyses were performed using SPSS 13.0 for Win-
dows. Independent-sample T tests were used to compare the
height of the pituitary fossa, height of pituitary gland and
volume of TBP between the two groups. Chi-square tests were
used to compare the occurrence of venous outflow domi-
nance, transverse sinus stenosis, and an HJB between the
two groups. A Pvalue less than 0.05 denotes a statistically
significant difference.
Results
Forty-four SPDs were detected on the symptomatic side in the
PT group. The upper segment was most frequently involved
(65.9 %) in the vertical direction (Table 2), and the lateral wall
was most frequently involved (86.4 %) in the horizontal di-
rection (Table 3). The mean maximal transverse diameter of
all SPDs was (2.83±1.29) mm (range, 1.5–7.0 mm), and the
mean area was (7.97± 5.17) mm
2
(range, 2.0–23.7 mm
2
).
Tabl e 1 Excluded causes of
pulsatile tinnitus Type Causes
Arterial Aberrant or lateralized internal carotid artery, internal carotid artery stenosis
(>75 %) or aneurysm, persistent stapedial artery, vascular malformations or fistula
Neoplastic Paragangliomaa, endolymphatic sac tumour, meningioma, vascular metastases,
hemangiopericytoma, haemangioma
Venous Jugular bulb dehiscence with or without diverticulum, sigmoid plate dehiscence with
diverticulum
Systemic Migraine, anemia, hyperthyreosis, pregnancy, hypertension with longer course than PT,
drug induced high output
Others Chronic middle-ear disease, semicircular canal dehiscence, otospongiosis, Paget’s disease,
established or clinically suspected intracranial hypertension
Fig. 1 Axial high resolution CT venography through the right temporal
bone showing a focal defect of the sigmoid plate (white arrow), with the
lateral wall of the upper segment involved
Fig. 2 Estimated points of the sigmoid sulcus’s maximal curvature
(black arrows) divide the wall into anterior, lateral and posterior ones
Eur Radiol (2016) 26:9–14 11
Three singular SPDs were detected on the matched sides
in the control group, all of which were located at the non-
dominant side of venous outflow. The number of SPDs in
the control group was much lower than in the PT group
(P=0.000). In the vertical direction, there were two SPDs
in the upper segment and one in the lower segment. In the
horizontal direction, there were tow SPDs in the lateral
wall and one in the anterior wall. The mean maximal trans-
verse diameter was (1.03± 0.31) mm (range, 0.7–1.3 mm),
and the mean area was (1.67± 0.35) mm
2
(range, 1.3–
2.0 mm2), which were both smaller than in the PT group
(P=0.021, P’=0.000).
Compared with the control group, the presence of an
HJB, transverse sinus stenosis and ipsilateral venous out-
flow dominance was more common in the PT group, which
also showed a deeper pituitary fossa and a flatter pituitary
gland. There was no significant difference in the degree of
TBP and abnormal mastoid emissary vein between the two
groups (Table 4).
Discussion
Various imaging algorithms including CT, magnetic reso-
nance (MR) and conventional angiography have been applied
in the evaluation of PT. SPD is increasingly detected now due
to the advent of multi-detector CT and high resolution CT
techniques. CTA/V was recently recommended for PT pa-
tients with normal otoscopic findings, as most causes of PT
may be evaluated in this singular examination. Those images
were obtained in a single scan to reduce the radiation dose,
with both arterial and venous structures obviously opacified
[2]. In this study, dual-phase images were performed to pres-
ent the details of each anatomic structure. Arterial phase im-
ages were obtained with dural sinuses mildly opacified to
detect arterial causes of PT, especially for a dural arteriove-
nous fistula, which was mainly suggested by the presence of
the venous structures’advanced opacification because of an
arterial-venous connection. Venous phase images were recon-
structed with a standard algorithm to show venous structures.
Meanwhile, HRCTV images were reconstructed with a bone
algorithm to detect osseous dehiscence, other associated tem-
poral bone variations/anomalies and neoplastic lesions. Axial
images reformatted with thin slice thickness were applied to
show the presence of SPD, which was very small in this study.
Previously, venous causes of PT were mainly treated with
ligation of the jugular vein. This measure increased the risk of
serious neurologic injury, as intracranial venous hypertension
would occur if the ligatured blood flow could not be compen-
sated. Recently, four studies indicated that PT with SPD but
without diverticulum could be totally eliminated by surgical
reconstruction [10–13], two of which were case reports and
the remaining two did not mention the sample size. As far as
we know, our study may be the largest one with PT patients
successfully treated with SPD reconstruction. During the sur-
gery, the dehiscence was covered with substitutes while the
hemodynamic state was not changed, which proved that the
intact sigmoid plate acted as a conduction barrier wall on the
PT’s auditory pathway, whereas the SPD acts as an open win-
dow to transmit the sound from the sigmoid sinus to the co-
chlea. This hypothesis may also apply to dehiscence around
other vessels in temporal bone. If so, dehiscence may act as a
Fig. 3 Three-dimensional air volume reconstruction shows the air
density of left temporal bone pneumatization, but the air of the external
auditory canal is excluded. The volume is automatically calculated, which
is 4.8639 cm3 in this patient
Table 2 Characteristics of 44 SPDs in the vertical direction in 30
patients with PT caused by SPD
Type/Location A P L A + L P + L A + L + P Total
Single 2 0 6 8 0 1 17
Two 3 0 16 5 0 0 2 4
Three 1 0 0 1 1 0 3
Tot a l 6 0 2 2 14 1 1 44
SPD-sigmoid plate dehiscence, PT-pulsatile tinnitus, A-anterior wall, P-
posterior wall, L-lateral wall
Tabl e 3 Characteristics of 44 SPDs in the horizontal direction in 30
patients with PT caused by SPD
Type/ Location U M L U + M M + L U + M + L Total
Single 12 2 1 1 0 1 17
Two 11 9 1 2 1 0 24
Three 2100 0 0 3
Total 251223 1 1 44
SPD-sigmoid plate dehiscence, PT-pulsatile tinnitus, U-upper segment,
M-middle segment, lower segment
12 Eur Radiol (2016) 26:9–14
common and necessary key point of vascular causes to make
the sound consciously perceived.
The key point of the surgery was to find the SPD, which
was usually shielded by air cell partitions. For the purpose of
positioning the SPD to reduce unnecessary excision of mas-
toid air cells, the sigmoid plate was divided into three parts in
the vertical and horizontal directions. The results showed that
the upper segment and lateral wall were most frequently in-
volved. With the angle formed by the transverse-sigmoid si-
nus, this area seems to suffer a stronger shear force of blood
flow from the ipsilateral transverse sinus, which indicates that
the hemodynamic state may play an important role in the
occurrence of SPD causing PT. SPDs were larger in the PT
group than that in the control group, which suggested that a
relatively large SPD is more likely to make the sound transmit.
43.3 % of the PT patients were found to have more than one
SPD. For those patients, special attention should be paid pre-
and intra-operatively as the sound may persist if not all SPDs
were completely recovered.
The mechanism of PT is still unknown. Some studies re-
ported that PT is associated with abnormal hemodynamics
[2–4,17–19]. Consistent with previous studies, our results
showed that SPD causing PT usually occurred on the domi-
nant side of the venous outflow, which suggested PT’sgener-
ation might require large blood flow. HJBs were more com-
monly found in the PT group, which may play a role in chang-
ing the blood flow pattern of ipsilateral sigmoid sinus, as
turbulent flow may be generated in an HJB. Whether an
HJB was the cause of PT was controversial. We think an
HJB may cause turbulent flow to generate PT but jugular bulb
dehiscence is necessary to make PT transmit to the cochlea.
The presence of bilateral transverse sinus stenosis was also
more common in the PT group, which may play a role in
increasing the blood flow rate of the adjacent sigmoid sinus.
Recently, bilateral transverse sinus stenosis has been reported
to have a close relationship with intracranial hypertension
[20]. Therefore, the heights of the pituitary and its fossa were
measured to further reflect intracranial pressure. The results
showed a deeper pituitary fossa and a flatter pituitary gland in
the PT group, which further indicated that elevated intracrani-
al pressure might play a role in this disease. Intracranial hy-
pertension (IH) is known as a common cause of PT, but how
IH causes PT is still unknown. We speculate that IH may
elevate long-term intracranial pressure to erode the sigmoid
plate and lead to dehiscence around vessels. Then, the sound
generated in the vessels may be transmitted through the dehis-
cence and be perceived. Although ipsilateral venous outflow
dominance, HJB, transverse sinus stenosis and IH were
regarded as causes of PT, our study demonstrated that these
factors may not be isolated but have synergistic effects on
SPD causing PT. TBP was also a necessary pathway for
PT’s transmission from vessels to the cochlea. There was no
difference in the volume of TBP between the two groups,
which highlighted the importance of SPD in PT. An abnormal
mastoid emissary vein had also been reported as a cause of PT.
There are some limitations of this study. PT patients in this
study were exposed to higher radiation doses than in previous
studies, since dual phase images were performed. The purpose
was mainly to detect dural arteriovenous fistula, which was a
common cause of PTrequiring surgical intervention. HRCTV
accuracy on SPD quantitative evaluation was not verified with
intraoperative findings because the extent of SPD was estimat-
ed by visual inspection during surgery. The roles of ipsilateral
venous outflow dominance, an HJB and bilateral transverse
sinus stenosis in SPD causing PT, which were speculated
based on CT findings in this study, are being studied using
MR and an in vitro model of PT caused by SPD. Since our
study was retrospective and all PT patients had no clear IH or
typical symptoms, intracranial pressure was not mea-
sured. The relationship between intracranial pressure
and SPD causing PT should be further studied. Until
now, only five patients with poor prognoses have been
rechecked using CT, four of whom were found with sub-
stitutes shifting. The remaining patient had two SPDs
while the larger SPD was not recovered with substitutes.
We will continue to enlarge the sample size of SPD
causing PT patients with a poor prognosis to show more
reliable results in further study.
Tabl e 4 Concomitant signs of
SPD in two groups Concomitant signs PT group Control group P
High jugular bulb 15/30 9/60 0.000
Bilateral transverse sinus stenosis 25/30 11/60 0.000
Ipsilateral transverse sinus stenosis 25/30 13/60 0.000
Contralateral transverse sinus stenosis 30/30 18/60 0.000
Ipsilateral venous outflow dominance 22/30 16/60 0.000
Height of pituitary fossa (10.04±2.70) mm (8.61±2.70) mm 0.015
Height of pituitary (3.04± 2.06) mm (4.88±2.06) mm 0.001
Temporal bone pneumatization (3.70±1.81) ml (4.10±1.81) ml 0.491
Abnormal mastoid emissary vein 1/30 3/60 1.0
Eur Radiol (2016) 26:9–14 13
In summary, SPD causing PT is characterized by one or
more bony defects of the sigmoid plate at the dominant side of
venous outflow, with the lateral wall and upper segment most
frequently involved. SPD causing PT acts as a key point to
make the sound transmit to the cochlea, which may be gener-
ated by vascular or intracranial pressure abnormalities.
Acknowledgements The scientific guarantor of this publication is
Zhenchang Wang. The authors of this manuscript declare no relationships
with any companies whose products or services may be related to the
subject matter of the article. This study has received funding by Grant
2012BA112B05 from the National Science & Technology Pillar Program
during the Twelfth Five-year Plan Period of China, Grant 81171311 from
the National Natural Science Foundation of China, Grant
KZ20110025029 from the Beijing Municipal Commission of Education.
No complex statistical methods were necessary for this paper. Institution-
al Review Board approval was obtained. Written informed consent was
obtained from all subjects (patients) in this study. Methodology: retro-
spective, case-control study, performed at one institution.
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