novel radiographic measurement algorithm demonstrating a ... · pdf filenovel radiographic...

Original Research—Sinonasal Disorders

Novel Radiographic MeasurementAlgorithm Demonstrating a Link betweenObesity and Lateral Skull BaseAttenuation

Otolaryngology–Head and Neck Surgery2015, Vol. 152(1) 172–179� American Academy ofOtolaryngology—Head and NeckSurgery Foundation 2014Reprints and permission:sagepub.com/journalsPermissions.navDOI: 10.1177/0194599814557470http://otojournal.org

Shawn M. Stevens, MD1, Paul R. Lambert, MD1, Habib Rizk, MD1,Wesley R. McIlwain, MD2, Shaun A. Nguyen, MD1, andTed A. Meyer, MD, PhD1

No sponsorships or competing interests have been disclosed for this article.

Abstract

Objectives. (1) To describe a validated algorithm for measur-ing tegmen thickness on computed tomography scans. (2)To compare the tegmen thickness in 3 groups: patients withspontaneous cerebrospinal fluid (CSF) leaks, obese controls,and nonobese controls.

Study Design. Retrospective review.

Setting. Patients with spontaneous CSF otorrhea often havehighly attenuated tegmen plates. This is associated with obe-sity and/or idiopathic intracranial hypertension (IIH). No evi-dence exists, however, that objectively links obesity and/orIIH with skull base attenuation.

Subjects and Methods. This was a retrospective review from 2004to the present. Patients with spontaneous CSF otorrhea andmatched obese (body mass index [BMI] .30 kg/m2) and nonobese(BMI \30 kg/m2) controls were selected. Tegmen thickness wasmeasured radiographically. Interrater validity was assessed.

Results. Ninety-eight patients were measured: 37 in the CSFgroup (BMI, 36.6 kg/m2), 30 in the obese group (BMI, 34.6kg/m2), and 31 in the nonobese group (BMI, 24.2 kg/m2).The CSF group had a significantly thinner tegmen comparedto both the obese control (P \ .01) and nonobese control(P = .0004) groups. Obese controls had a thinner tegmenthan nonobese controls (P \ .00001). A significant inversecorrelation was detected between skull base thickness andBMI. Signs/symptoms of IIH were most commonly found inthe CSF group. Good to very good strength of agreementwas detected for measures between raters.

Conclusion. This is the first study to (1) quantify lateral skullbase thickness and (2) significantly correlate obesity with lat-eral skull base attenuation. Patients who are obese withspontaneous CSF leaks have greater attenuation of theirskull base than matched obese controls. This finding sup-ports theories that an additional process, possibly congeni-tal, has a pathoetiological role in skull base dehiscence.

Keywords

spontaneous, CSF leak, obesity, idiopathic intracranial hyper-tension, tegmen, dehiscence

Received July 20, 2014; revised September 12, 2014; accepted October

8, 2014.

Spontaneous cerebrospinal fluid (CSF) otorrhea is a rela-

tively rare phenomenon in which CSF enters the con-

fines of the temporal bone in a manner unrelated to

other causes. Spontaneous CSF otorrhea occurs in 2 popula-

tions: young children and middle-aged adults. Children typi-

cally present after episodes of recurrent meningitis, and the

leak is often associated with congenital anomalies.1-6 In adults,

a diagnosis is often made after myringotomy for a persistent

effusion in obese, middle-aged females.7,8 Two major theories

predominate regarding the pathophysiology in adults. The first

posits that skull base attenuation occurs chronically secondary

to increased intracranial pressure, which in turn is closely

linked to obesity and idiopathic intracranial hypertension

(IIH).9-18 The second theory, suggested by Gacek et al19 and

corroborated by others, suggests that aberrant arachnoid granu-

lations may instigate skull base erosion.18-21 A congenital pre-

disposition may exist in either process.22-24

The radiographic appearance of the skull base in obese

individuals is often one of broad attenuation.18 Quantifiable

evidence correlating obesity, CSF leaks, and skull base

1Department of Otolaryngology–Head and Neck Surgery, Medical

University of South Carolina, Charleston, South Carolina, USA2Department of Otolaryngology–Head and Neck Surgery, Madigan Army

Medical Center, Tacoma, Washington, USA

This article was presented at the 2014 AAO-HNSF Annual Meeting and

OTO EXPO; September 21-24, 2014; Orlando, Florida.

Corresponding Author:

Shawn M. Stevens, MD, Department of Otolaryngology–Head and Neck

Surgery, Medical University of South Carolina, 135 Ashley Avenue, MSC

550, Charleston, SC 29425, USA.

Email: [email protected]

at SOCIEDADE BRASILEIRA DE CIRUR on January 17, 2015oto.sagepub.comDownloaded from

http://oto.sagepub.com/

attenuation is lacking, however. In the present study, we

sought to overcome this by developing a novel radiographic

measurement algorithm for the lateral skull base. Using

temporal bone computed tomography (CT) scans from

patients with spontaneous leaks, obese controls, and nonob-

ese controls, we sought to address 3 hypotheses: (1) current

CT imaging/formatting technology can now achieve precise

and reproducible measurements of lateral skull base thick-

ness, (2) obese patients will have a quantifiably thinner

skull base than nonobese patients, and (3) patients with

spontaneous CSF otorrhea will have more skull base

attenuation than obese patients without leaks. The aims of

the study were to validate the algorithm for interrater relia-

bility and to correlate radiographic findings with demo-

graphic, clinical, and body mass index (BMI) data.

MethodsStudy Approval

Approval was obtained from the Medical University of South

Carolina (MUSC) Institutional Review Board (Pro00023289).

Group Selection

This retrospective chart review from 2004 to 2013 utilized

ICD-9 codes and operative notes. Inclusion criteria for the

primary study group were the following: diagnosis of spon-

taneous CSF otorrhea, surgical intervention performed, age

.18 years, and dedicated high-resolution temporal bone CT

scans available. Demographic data recorded were age, sex,

and race. Moreover, BMI (kg/m2) was calculated based on

height and weight at the time of surgery. Clinical variables

documented included hypertension, diabetes mellitus, osteo-

penia/osteoporosis, IIH, and smoking status. Exclusion cri-

teria were the following: history of temporal bone trauma,

cholesteatoma, neoplasm, prior lateral skull base and/or

mastoid surgery, congenital ear anomaly, and age \18

years.

Control subjects were culled from adult cochlear implant

patients. The subjects were separated according to BMI into

obese (BMI .30 kg/m2) and nonobese (BMI \30 kg/m2)

groups. Inclusion criteria included age .18 years and dedi-

cated high-definition CT scans available. Demographic data,

clinical data, and exclusion criteria were identical to those

of the primary study group.

Imaging and Hardware

Dedicated temporal bone CT scans were obtained with a

standard collimation of 0.625 mm. Images were reconstructed

in axial, coronal, and sagittal planes. The majority of scans

were obtained at MUSC on either a Siemens Somatom

Sensation 16 or Siemens Definition 128 (Siemens Medical

Solutions, Malvern, Pennsylvania). Spatial resolution was

rated as accurate to 0.1 to 0.2 mm using this protocol.

All images were analyzed on standardized personal comput-

ing stations equipped with Intel Core 2 Duo CPUs (Intel

Corporation, Santa Clara, California). Processing speed was 2.3

GHz with 4 GB of available random-access memory (RAM).

Stations were all equipped with Lenovo Think Vision 19-inch,

square, backlit light-emitting diode (LED) and flat panel liquid-

crystal display (LCD) monitors (Lenovo, Raleign, North

Carolina) set to a maximum resolution of 1280 3 1024 dpi.

Software

Reformatted images were analyzed via the proprietary digi-

tal radiology imaging system AGFA Impax 6 (AGFA

Impax, Mortsel, Belgium). Temporal bone thickness was

measured via the partial volume averaging formula (measure-

ment caliper) in this software. Accuracy was rated to 0.1 mm.

CT Measurement Algorithm: Tegmen Tympani

Skull base measurements were made at predefined points.

Measurements of the tegmen tympani (TT) were conducted

within a coronal cut best depicting the malleus, the incus,

and at least 2 turns of the cochlea (Figure 1). Measurements

were made at the thickest and thinnest visible points of the

tegmen plate as well as at a fixed point directly cephalad to

the ossicles. All measures were made on both sides of the

skull base. Due to software limitations of the Impax measure-

ment calipers and the quoted CT spatial resolution, we set an

absolute minimum limit for thickness of 0.4 mm. This limit

applied to dehiscent areas with no measurable bone density.

CT Measurement Algorithm: Tegmen Mastoideum

Measurements were made of the tegmen mastoideum (TM)

in a coronal cut best demonstrating the most lateral curvature

of the posterior semicircular canal (Figure 1). Measurements

included the thickest and thinnest visible points along with a

fixed point at the center of the tegmen plate between the cor-

tical bone and posterior semicircular canal medially.

Measurements were repeated on both sides of the skull base.

The minimum thickness limit was applied.

Additional Calculations for Statistics

Using the above protocol, a total of 12 measurements were

made for each patient (6 of the TT/TM on each side). To facil-

itate statistical comparisons, mean aggregate thickness values

were calculated by averaging the data for the TT and TM on

each side of the skull base. The overall mean skull base thick-

ness was also calculated by averaging the mean aggregate TT

and TM thicknesses of both sides. This value was statistically

correlated with BMI and other demographic/clinical factors.

Validation Measures

The intraclass correlation coefficient (K) was calculated for

the purpose of assessing interrater reliability among 3 raters

at staggered levels of training in otolaryngology–head and

neck surgery. This included a medical student, a fourth-year

resident, and a second-year neurotology fellow. For the

assessment, a total of 39 scans were randomly selected from

the overall study cohort including 13 from each of the 3

study groups. The clinical diagnosis, group allocation,

demographic data, operative notes, and clinical information

were withheld from the raters. Over a period of 2 weeks,

each rater independently performed a full set of measure-

ments as described above on each of the 39 scans (468

Stevens et al 173



measurements per rater). The raters were blinded to each

other’s measurements. Results were expressed as the intra-

class correlation coefficient (K) and 95% confidence interval.

Strength of agreement relative to K can be interpreted as the

following: \0.20 = poor; 0.21-0.40 = fair; 0.41-0.60 = mod-

erate; 0.61-0.80 = good; and 0.81-1.00 = very good.25

Statistics

All analyses and graphs were performed with Sigma Plot 12.5

(Systat Software Inc, San Jose, California) and MedCalc

13.3.0.0 (MedCalc Software bvba, Ostend, Belgium). Disease

information and demographic variables were summarized by

means of summary statistics. Continuous variables were sum-

marized by the mean 6 standard deviation. Nominal variables

were summarized by the frequency and percentage. All contin-

uous variables were tested for normal distribution as deter-

mined by the Kolmogorov-Smirnov test. Comparisons of

outcomes (nominal variables) were performed using the Fisher

exact test or x2 test with Yates correction. For continuous vari-

ables, comparisons were made using an independent t test. A

correlation model was used to determine the relationship

among variables such as skull base thickness, age, and sex. A

value of P \ .05 was considered indicative of statistical

significance.

Results

A total of 42 patients were identified with a diagnosis of

spontaneous CSF otorrhea. Of these, 5 patients were

excluded for inadequate temporal bone CT scans, leaving

37 patients for the CSF group. Only 31 total patients were

identified from the control cohort who were obese. As the

number of nonobese controls was relatively large, 31 con-

secutive patients were selected to numerically match the

obese controls. Of these, only 1 obese control failed to meet

inclusion criteria, leaving 30 patients for the obese control

group and 31 patients for the nonobese control group.

The demographic and clinical information of each group

is summarized in Table 1. The mean ages of the CSF group,

obese control group, and nonobese control group were 60.9

years, 57.0 years, and 62.2 years, respectively. The mean

Table 1. Group Demographics and Clinical Data.

Spontaneous

CSF Leak

Obese Control

Group (BMI .30 kg/m2)

Nonobese

Control Group (BMI \30 kg/m2)

Statistical

Significance

Total (N = 98), n 37 30 31 N/A

Mean age, y 60.9 57.0 62.2 —

Mean BMI, kg/m2 36.6 34.6 23.7 —

Sex, n

Male 7 13 17 —

Female 30a 17 14 P = .028a

Race, n

White 21 22 24 —

Black 16 8 7 —

Hypertension, n 29a 18 12 P = .023a

Diabetes mellitus, n 12 7 7 —

Osteopenia/osteoporosis, n 4 1 1 —

Current/former smoker, n 11 8 9 —

Idiopathic intracranial hypertension, n 5 0 0 —

Abbreviations: BMI, body mass index; CSF, cerebrospinal fluid; N/A, not applicable.aAll 3 groups were similar for all measures except for the CSF group in which female sex and hypertension were significantly more common.

Figure 1. Measurements: (A) Left tegmen tympani, demonstrating the fixed (0.07 cm), thickest (0.15 cm), and thinnest/dehiscent (arrow-head) points. (B) Right tegmen mastoideum, demonstrating the thinnest (0.04 cm), fixed (0.05 cm), and thickest (0.19 cm) points.

174 Otolaryngology–Head and Neck Surgery 152(1)



BMIs of the groups were 36.6 kg/m2, 34.6 kg/m2, and 23.7

kg/m2, respectively. The CSF group and obese control group

did not significantly differ from each other in terms of BMI.

The CSF group had a significantly higher proportion of both

women and patients with hypertension. All diagnoses of IIH

were in the CSF group, but the relatively small number was

not enough to reach statistical significance. The groups did

not differ in any other clinical factor.

When reviewing temporal bone scans, the lateral skull base

of patients in both the CSF group and obese control group had

a similar, broadly attenuated appearance with a moth-eaten

quality to the bone (Figure 2). There was generally a paucity

of pneumatized bone cephalad to the otic capsule structures

and ossicles. Findings were usually bilateral and involved both

the TT and TM. Scans in nonobese controls typically demon-

strated thick and well-defined tegmen plates with a notable

amount of pneumatized bone buffering the inner ear.

Objectively, skull base thickness differed significantly

between each of the groups bilaterally (Figure 3). The non-

obese controls had the thickest skull bases, with a mean of

1.204 6 0.047 mm and 1.337 6 0.048 mm on the left and

right sides, respectively. This was significantly thicker than

skull base measurements in both the obese control group

(left: 0.981 6 0.037 mm; right: 1.008 6 0.038 mm; P \.00001) and CSF group (left: 0.862 6 0.040 mm; right:

0.811 6 0.033 mm; P \ .0004).

A comparison of skull base thickness controlling for obe-

sity was also made between the obese control group and CSF

group (Figure 4). This was accomplished by removing all

nonobese patients with CSF leaks (6 excluded; n = 31 obese

patients with CSF leaks). Between the 2 groups, patients with

CSF leaks had significantly thinner skull bases (left: 0.833 6

0.038 mm; right: 0.814 6 0.036 mm) than controls (left:

0.981 6 0.037 mm; right: 1.008 6 0.038 mm; P \ .01). The

mean BMI of this ‘‘obese only’’ CSF group was 37.7 kg/m2.

There remained no significant difference in BMI, however,

between the obese CSF and obese control groups.

When correlation modeling was performed, a significant

inverse correlation was detected between skull base thickness

and BMI (r = –0.466, P = .000001) (Figure 5). No significant

correlation was demonstrated between skull base thickness and

age (r = 0.065, P = .644) or any of the other demographic/clin-

ical parameters from Table 1 (data not shown).

Figure 2. Subjective attenuation: Coronal computed tomography scans depicting tegmen tympani from the 3 groups. The nonobese con-trol (NOC) group was normal, the obese control (OC) group was attenuated, and the cerebrospinal fluid (CSF) leak group was dehiscent.

Mean Skull Base Thickness (mm)

Skul

l Bas

e Th

ickn

ess

(mm

)

0.0

0.2

0.4

0.6

0.8

1.0

1.2

LeftRight

Obese Control Obese CSF

‡

Figure 4. Obese controls versus obese patients with cerebrosp-inal fluid leaks: mean aggregate thickness comparison. Thicknessdiffered significantly (P \.01) on both sides of the skull base (z).Black, left; gray, right. Error bars are the standard error of themean.

Mean Skull Base Thickness (mm)

Non-ObeseControl

Skul

l Bas

e Th

ickn

ess

(mm

)

0.0

0.2

0.4

0.6

0.8

1.0

1.2

1.4

1.6

LeftRight

CSF Group(All)

Obese Control

*ⱡ †

Figure 3. Mean aggregate thickness comparisons: significant differ-ences (P \.001) were detected between nonobese/obese controls(*), nonobese controls/patients with cerebrospinal fluid (CSF) leaks(z), and obese controls/patients with CSF leaks (y). Black, left;gray, right. Error bars are the standard error of the mean.

Stevens et al 175



When the intraclass correlation coefficient (K) was used

to assess interrater reliability, the results were ‘‘good’’ to

‘‘very good’’ among all 3 raters when measuring both obese

and nonobese groups. The results were ‘‘poor’’ to ‘‘good’’

among all 3 raters when measuring individual segments of

the tegmen for the CSF group. Results were ‘‘good’’ to

‘‘very good’’ when comparing mean aggregate measures for

this group (Table 2).

Discussion

In developing the measurement algorithm described above,

consideration was given to the limitations of the Impax soft-

ware package and scanner technology. As the resolution of

CT formatting and the Impax caliper is rated to 0.1 mm,

precision was felt to be adequate for detecting submillimeter

differences between groups. To this end, the absolute mini-

mum measurement convention of 0.4 mm requires addi-

tional discussion. The application of this convention was

considered necessary to overcome software limitations pre-

venting reliable measures \0.4 mm (the calipers cannot be

drawn this small). As nearly all subjects in the CSF group

and some obese controls had skull base dehiscences, use of

this convention rather than 0.0 mm likely masks a more pro-

nounced difference in thickness than that reported. In turn,

the minimum thickness value also likely prevents unneces-

sary skewing of the data toward an attenuated state by pre-

venting 0.0 mm being entered for any measurement

between 0.1 to 0.3 mm. Detection of a significant difference

between groups using our more conservative approach may

lend more support to the hypotheses than the use of a 0.0-

mm minimum value.

Table 2. Interrater Validation Measures.

Measure Intraclass Correlation Coefficient (95% Confidence Interval) Strength of Agreement

Obese control group: left side

Mean aggregate 0.8185 (0.5552 to 0.9368) Very good

Tegmen mastoideum 0.7154 (0.3020 to 0.9009) Good

Tegmen tympani 0.8505 (0.6334 to 0.9479) Very good

Obese control group: right side

Mean aggregate 0.7417 (0.3669 to 0.9101) Good


Tegmen tympani 0.6586 (0.1630 to 0.8811) Good

Nonobese control group: left side


Tegmen mastoideum 0.8585 (0.6405 to 0.9531) Very good


Nonobese control group: right side



Tegmen tympani 0.8207 (0.5445 to 0.9406) Very good

CSF group: left side

Mean aggregate 0.6775 (0.1804 to 0.8932) Good

Tegmen mastoideum 0.1441 (–1.2654 to 0.7323) Poor

Tegmen tympani 0.5584 (–0.1689 to 0.8619) Moderate

CSF group: right side


Tegmen mastoideum 0.3316 (–0.7691 to 0.7909) Fair


Abbreviation: CSF, cerebrospinal fluid.

Skull Base Thickness and BMI

BMI15 20 25 30 35 40 45 50 55

Skul

l Bas

e Th

ickn

ess

(mm

)

0.1

1

10

r = –0.466p = 0.000001

Figure 5. Correlation between skull base thickness (mm) andbody mass index: all study subjects were included. A significantnegative correlation was detected. r, correlation coefficient.




The total number of measurement samples per subject

also was intentionally kept high (6 per side/12 per subject) to

more accurately reflect aggregate thickness. The initial build

of the algorithm incorporated a solitary measurement of the

thinnest point on the tegmen. It was quickly discovered, how-

ever, that most subjects with CSF leaks and obese controls

had at least 1 ‘‘thinnest point’’ at the minimum thickness

limit. Detecting a difference between groups was therefore

impossible. Additionally, as the leading pathoetiological

theory for the development of spontaneous CSF otorrhea

entails elevated intracranial pressure and broad skull base

attenuation, a larger sampling of measurements was felt to

more accurately reflect the underlying pathophysiology.

Using these methods, our interrater validation assessment

revealed good to very good strength of agreement for aggre-

gate thickness measures between observers at all levels of

training (Table 2). The lower strength of agreement noted

for CSF group measures was likely due in part to the soft-

ware’s minimum thickness limitations and to the highly

variable presentation of the thickest point in patients with

CSF leaks. When aggregate measures were considered

though, overall agreement was much better.

Although many studies have performed radiographic assess-

ments of skull base attenuation, the vast majority of investiga-

tors have done so in a solely qualitative manner.9,11,23,26-30

Within the ear, nose, and throat literature, little quantita-

tive, measurement-driven data exist to detect differences

between groups.23,27,31,32 To our knowledge, only 1 prior

study has made quantifiable radiographic measurements

of the lateral skull base.23 The best precedent for objec-

tive radiographic investigations ultimately came from the

oral-maxillofacial literature, which heavily utilizes cepha-

lometric evaluations.33-43

Many such studies have used ‘‘smallest detectable differ-

ence’’ (SDD) calculations to further validate CT-based mea-

surement algorithms.33,35-37 The SDD is a statistical

estimate of the smallest significant amount of change that

can be detected by a given measure regardless of how reli-

ably that measure can be reproduced. When we applied

SDD calculations to our data, it was found that the differ-

ence in skull base thickness between each study group was

indeed larger than the calculated SDD. This finding strongly

suggests that the significant differences detected herein are

indeed real differences. Appendix A (available at www.oto-

journal.org) provides further detail on SDD calculations.

Although the pathophysiology underlying adult sponta-

neous CSF otorrhea is not fully understood, this condition is

associated with obesity and IIH.9-18 Our data support these

associations and are consistent with commonly cited demo-

graphic patterns. The mean BMI of our CSF group was 36.6

kg/m2, and the mean age was 60.9 years. Eighty-one percent

(30/37) of the patients were female. Five of 37 (13.5%) had

a formal diagnosis of IIH. Because CSF opening pressure

was not routinely measured, the number of individuals with

IIH was likely higher than reported.

The data also demonstrate a significant correlation between

obesity and skull base attenuation. To our knowledge, this is

the first report of a statistically significant inverse relationship

between skull base thickness and BMI. It is also the first

description of a significant difference in skull base attenuation

between obese and nonobese subjects. As BMI is an indirect

measure of obesity and not related to intracranial processes,

the reasons for the above findings cannot be entirely explained

by these data alone.

Some inferences are possible, however, when consider-

ing the physiology associated with the obese habitus. The

latter causes elevated central venous pressure, leading in

turn to elevated intracranial pressure. Also, IIH is known

to be more prevalent in obese individuals.44,45 Over time,

this steep pressure gradient across the entirety of the dura-

bone interface likely causes gradual and broad bony skull

base erosion. Subjectively, the majority of our obese sub-

jects fit such a description. Other authors have noted simi-

lar findings, and the quantitative measures here support

their prior reports.13-15,18,23,26-30 The lack of an inverse

correlation between skull base thickness and age, however,

does not fit the temporal aspect of the theory. This may be

due to the fact that changes in skull base thickness over

time may be too small to detect with currently available

technology.

In addition to supporting a theory of pressure-induced

erosion caused by obesity, our data also seem to suggest

that subjects with CSF leaks were affected by an additional

pathophysiological process. This was evidenced by that

group having significantly thinner skull bases than obese

patients without leaks. One potential explanation for this is

bias introduced by our measurement algorithm. Given the

preponderance toward skull base dehiscence in subjects

with CSF leaks, the lack of measurable bone may have

skewed the data relative to controls. As discussed previ-

ously, the inclusion of a minimum thickness measure does

render this explanation somewhat less likely. An additional

cause may be hormonal in nature, as female sex was signifi-

cantly overrepresented in the CSF group. While it is diffi-

cult to assess this directly, other indicators of the influence

of sex such as osteoporosis and osteopenia (more common

in women) did not appear to differ significantly between

groups.

One further explanation may be one of congenital predis-

position. A growing conceptual trend in the literature holds

that certain individuals may have a genetic predisposition to

accelerated bone loss or perhaps an aberration in tegmen

ossification. In 2 cadaveric studies, between 6% to 34% of

all temporal bones had at least 1 tegmen dehiscence, while a

smaller subset (1%-6%) had multiple dehiscences and poor

bone quality.46,47 Another large cadaveric study, investigating

the prevalence of superior semicircular canal dehiscence

across age groups, found tegmen thickness to be uniformly

thin in neonates/infants. Thickness gradually increased until 3

years of age and then plateaued. Interestingly, approximately

2% of adult subjects in this study had tegmen thicknesses

that differed little from the neonatal period.22 This potential

congenital predisposition to skull base attenuation has been

corroborated in other studies and case reports.23,27,48-52 Newer

Stevens et al 177



investigations linking superior semicircular canal dehis-

cence and spontaneous CSF otorrhea (rate of concomi-

tance, 15%-55%) as well as the data reported here suggest

that at least a portion of patients with spontaneous leaks

may be susceptible to more accentuated skull base thinning

than would be explained by the pathophysiology of an

obese habitus alone.26,28

Conclusion

The data gathered in this study supported the hypothesis

that our novel measurement algorithm and current imaging

technology would allow for precise and reliable quantifica-

tion of lateral skull base thickness. The data also indicated

that a significant correlation between obesity and skull base

thickness exists and that patients suffering from spontaneous

CSF otorrhea have significantly thinner skull bases than do

matched obese controls. While reasoning for the latter find-

ing is not directly clarified by our data, indirect evidence

may suggest the existence of a congenital pathoetiological

process that augments tegmen thinning already known to

occur in this cohort.

Acknowledgments

The authors acknowledge the Medical University of South

Carolina’s Department of Radiology for providing invaluable input

that helped lead to our development of the novel skull base mea-

surement algorithm.

Author Contributions

Shawn M. Stevens, conception of design, acquisition of data, analy-

sis of data, interpretation of data, drafting article, and final approval;

Paul R. Lambert, conception of design, analysis of data, interpreta-

tion of data, critical revision, and final approval; Habib Rizk, acquisi-

tion of data, analysis of data, interpretation of data, critical revision,

and final approval; Wesley R. McIlwain, acquisition of data, interpre-

tation of data, drafting article, and final approval; Shaun A. Nguyen,

analysis of data, interpretation of data, drafting article, and final

approval; Ted A. Meyer, conception of design, analysis of data, inter-

pretation of data, critical revision, and final approval.

Disclosures

Competing interests: None.

Sponsorships: None.

Funding source: None.

Supplemental Material

Additional supporting information may be found at http://otojournal

.org/supplemental.

References

1. Foyt D, Brackmann DE. Cerebrospinal fluid otorrhea through

a congenitally patent fallopian canal. Arch Otolaryngol Head

Neck Surg. 2000;126:540-542.

2. Jegoux F, Malard O, Gayet-Delacroix M, Bordure P, Legent F,

Beauvillain de Montreuil C. Hyrtl’s fissure: a case of sponta-

neous cerebrospinal fluid otorrhea. AJNR Am J Neuroradiol.

2005;26:963-966.

3. Mong S, Goldberg AN, Lustig LR. Fallopian canal meningo-

cele: report of two cases. Otol Neurotol. 2009;30:525-528.

4. Rupa V, Job A, Rajshekhar V. Adult onset spontaneous CSF

otorrhea with oval window fistula and recurrent meningitis:

MRI findings. Otolaryngol Head Neck Surg. 2001;124:344-

346.

5. Teo DT, Tan TY, Eng SP, Chan YM. Spontaneous cerebrosp-

inal fluid otorrhoea via oval window: an obscure cause of

recurrent meningitis. J Laryngol Otol. 2004;118:717-720.

6. Teufert KB, Slattery WH. Cerebrospinal fluid leak of the fallo-

pian canal. Ear Nose Throat J. 2013;92:E20-E23.

7. Sanna M, Fois P, Russo A, Falcioni M. Management of

meningoencephalic herniation of the temporal bone: personal

experience and literature review. Laryngoscope. 2009;119:

1579-1585.

8. Semaan MT, Gilpin DA, Hsu DP, Wasman JK, Megerian CA.

Transmastoid extradural-intracranial approach for repair of

transtemporal meningoencephalocele: a review of 31 consecu-

tive cases. Laryngoscope. 2011;121:1765-1772.

9. Goddard JC, Meyer T, Nguyen S, Lambert PR. New consid-

erations in the cause of spontaneous cerebrospinal fluid otor-

rhea. Otol Neurotol. 2010;31:940-945.

10. LeVay AJ, Kveton JF. Relationship between obesity, obstruc-

tive sleep apnea, and spontaneous cerebrospinal fluid otorrhea.

Laryngoscope. 2008;118:275-278.

11. Prichard CN, Isaacson B, Oghalai JS, Coker NJ, Vrabec JT.

Adult spontaneous CSF otorrhea: correlation with radiographic

empty sella. Otolaryngol Head Neck Surg. 2006;134:767-771.

12. Rosenfeld E, Dotan G, Kimchi TJ, Kesler A. Spontaneous cer-

ebrospinal fluid otorrhea and rhinorrhea in idiopathic intracra-

nial hypertension patients. J Neuroophthalmol. 2013;33:113-

116.

13. Schlosser RJ, Bolger WE. Significance of empty sella in cere-

brospinal fluid leaks. Otolaryngol Head Neck Surg. 2003;128:

32-38.

14. Schlosser RJ, Wilensky EM, Grady MS, Bolger WE. Elevated

intracranial pressures in spontaneous cerebrospinal fluid leaks.

Am J Rhinol. 2003;17:191-195.

15. Schlosser RJ, Woodworth BA, Wilensky EM, Grady MS,

Bolger WE. Spontaneous cerebrospinal fluid leaks: a variant

of benign intracranial hypertension. Ann Otol Rhinol Laryngol.

2006;115:495-500.

16. Stucken EZ, Selesnick SH, Brown KD. The role of obesity in

spontaneous temporal bone encephaloceles and CSF leak. Otol

Neurotol. 2012;33:1412-1417.

17. Vivas EX, McCall A, Raz Y, Fernandez-Miranda JC, Gardner

P, Hirsch BE. ICP, BMI, surgical repair, and CSF diversion in

patients presenting with spontaneous CSF otorrhea. Otol

Neurotol. 2014;35:344-347.

18. Wang EW, Vandergrift WA 3rd, Schlosser RJ. Spontaneous

CSF leaks. Otolaryngol Clin North Am. 2011;44:845-856, vii.

19. Gacek RR, Gacek MR, Tart R. Adult spontaneous cerebrosp-

inal fluid otorrhea: diagnosis and management. Am J Otol.

1999;20:770-776.

20. Manes RP, Ryan MW, Marple BF. A novel finding on com-

puted tomography in the diagnosis and localization of



http://otojournal.org/supplemental


cerebrospinal fluid leaks without a clear bony defect. Int

Forum Allergy Rhinol. 2012;2:402-404.

21. Yew M, Dubbs B, Tong O, et al. Arachnoid granulations of

the temporal bone: a histologic study of dural and osseous

penetration. Otol Neurotol. 2011;32:602-609.

22. Carey JP, Minor LB, Nager GT. Dehiscence or thinning of

bone overlying the superior semicircular canal in a temporal

bone survey. Arch Otolaryngol Head Neck Surg. 2000;126:

137-147.

23. Hirvonen TP, Weg N, Zinreich SJ, Minor LB. High-resolution

CT findings suggest a developmental abnormality underlying

superior canal dehiscence syndrome. Acta Otolaryngol. 2003;

123:477-481.

24. Minor LB, Solomon D, Zinreich JS, Zee DS. Sound- and/or

pressure-induced vertigo due to bone dehiscence of the super-

ior semicircular canal. Arch Otolaryngol Head Neck Surg.

1998;124:249-258.

25. Altman DG. Practical Statistics for Medical Research. 1st ed.

New York: Chapman and Hall; 1991.

26. Allen KP, Perez CL, Isaacson B, Roland PS, Duong TT, Kutz

JW. Superior semicircular canal dehiscence in patients with

spontaneous cerebrospinal fluid otorrhea. Otolaryngol Head

Neck Surg. 2012;147:1120-1124.

27. Crovetto M, Whyte J, Rodriguez OM, Lecumberri I, Martinez

C, Elexpuru J. Anatomo-radiological study of the superior

semicircular canal dehiscence radiological considerations of

superior and posterior semicircular canals. Eur J Radiol. 2010;

76:167-172.

28. El Hadi T, Sorrentino T, Calmels MN, Fraysse B, Deguine O,

Marx M. Spontaneous tegmen defect and semicircular canal

dehiscence: same etiopathogenic entity? Otol Neurotol. 2012;

33:591-595.

29. Connor SE. Imaging of skull-base cephalocoeles and cere-

brospinal fluid leaks. Clin Radiol. 2010;65:832-841.

30. Lee MH, Kim HJ, Lee IH, Kim ST, Jeon P, Kim KH.

Prevalence and appearance of the posterior wall defects of the

temporal bone caused by presumed arachnoid granulations and

their clinical significance: CT findings. Am J Neuroradiol.

2008;29:1704-1707.

31. Banu MA, Rathman A, Patel KS, et al. Corridor-based endona-

sal endoscopic surgery for pediatric skull base pathology with

detailed radioanatomic measurements. Neurosurgery. 2014;10

Suppl 2:273-293, discussion 293.

32. Psaltis AJ, Overton LJ, Thomas WW 3rd, Fox NF, Banks CA,

Schlosser RJ. Differences in skull base thickness in patients

with spontaneous cerebrospinal fluid leaks. Am J Rhinol

Allergy. 2014;28:e73-e79.

33. McNemar Q. Psychological Statistics. 4th ed.New York:

Wiley; 1969.

34. Citardi MJ, Herrmann B, Hollenbeak CS, Stack BC, Cooper M,

Bucholz RD. Comparison of scientific calipers and computer-

enabled CT review for the measurement of skull base and cra-

niomaxillofacial dimensions. Skull Base. 2001;11:5-11.

35. Damstra J, Huddleston Slater JJ, Fourie Z, Ren Y. Reliability

and the smallest detectable differences of lateral cephalometric

measurements. Am J Orthod Dentofacial Orthop. 2010;138:

546.e1-546.e8, discussion 546-547.

36. Guyatt G, Walter S, Norman G. Measuring change over time:

assessing the usefulness of evaluative instruments. J Chronic

Dis. 1987;40:171-178.

37. Kropmans TJ, Dijkstra PU, Stegenga B, Stewart R, de Bont

LG. Smallest detectable difference in outcome variables

related to painful restriction of the temporomandibular joint. J

Dent Res. 1999;78:784-789.

38. Luu NS, Nikolcheva LG, Retrouvey JM, et al. Linear measure-

ments using virtual study models. Angle Orthod. 2012;82:

1098-1106.

39. Moerenhout BA, Gelaude F, Swennen GR, Casselman JW,

Van Der Sloten J, Mommaerts MY. Accuracy and repeatability

of cone-beam computed tomography (CBCT) measurements

used in the determination of facial indices in the laboratory

setup. J Craniomaxillo Fac Surg. 2009;37:18-23.

40. Olszewski R, Zech F, Cosnard G, Nicolas V, Macq B,

Reychler H. Three-dimensional computed tomography cepha-

lometric craniofacial analysis: experimental validation in vitro.

Int J Oral Maxillofac Surg. 2007;36:828-833.

41. Suomalainen A, Vehmas T, Kortesniemi M, Robinson S,

Peltola J. Accuracy of linear measurements using dental cone

beam and conventional multislice computed tomography.

Dentomaxillofac Radiol. 2008;37:10-17.

42. Swennen GR, Schutyser F, Barth EL, De Groeve P, De Mey

A. A new method of 3-D cephalometry, part I: the anatomic

Cartesian 3-D reference system. J Craniofac Surg. 2006;17:

314-325.

43. van Vlijmen OJ, Maal T, Berge SJ, Bronkhorst EM, Katsaros

C, Kuijpers-Jagtman AM. A comparison between 2D and 3D

cephalometry on CBCT scans of human skulls. Int J Oral

Maxillofac Surg. 2010;39:156-160.

44. Friedman DI, Jacobson DM. Diagnostic criteria for idiopathic

intracranial hypertension. Neurology. 2002;59:1492-1495.

45. Hannerz J, Ericson K. The relationship between idiopathic intra-

cranial hypertension and obesity. Headache. 2009;49:178-184.

46. Kapur TR, Bangash W. Tegmental and petromastoid defects in

the temporal bone. J Laryngol Otol. 1986;100:1129-1132.

47. Lang DV. Macroscopic bony deficiency of the tegmen tympani

in adult temporal bones. J Laryngol Otol. 1983;97:685-688.

48. Branstetter BF 4th, Harrigal C, Escott EJ, Hirsch BE. Superior

semicircular canal dehiscence: oblique reformatted CT images

for diagnosis. Radiology. 2006;238:938-942.

49. Masaki Y. The prevalence of superior canal dehiscence syn-

drome as assessed by temporal bone computed tomography

imaging. Acta Otolaryngol. 2011;131:258-262.

50. Paladin AM, Phillips GS, Raske ME, Sie KC. Labyrinthine

dehiscence in a child. Pediatr Radiol. 2008;38:348-350.

51. Williamson RA, Vrabec JT, Coker NJ, Sandlin M. Coronal

computed tomography prevalence of superior semicircular canal

dehiscence. Otolaryngol Head Neck Surg. 2003;129:481-489.

52. Zhou G, Ohlms L, Liberman J, Amin M. Superior semicircular

canal dehiscence in a young child: implication of developmen-

tal defect. Int J Pediatr Otorhinolaryngol. 2007;71:1925-1928.

Stevens et al 179



novel radiographic measurement algorithm demonstrating a ... · pdf filenovel radiographic...

Documents