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\begin{document}

\title{Morphometric evaluation of facial and vestibulocochlear nerves using
magnetic resonance imaging in patients with Meni\selectlanguage{ngerman}ère's disease - a
retrospective study\selectlanguage{english}}



\author[1]{Wilhelm Flatz}%
\author[2]{Annika Henneberger}%
\author[3]{Robert Guerkov}%
\author[4]{Regina Schinner}%
\author[1]{Ullrich Müller-Lisse}%
\author[1]{Maximilian Reiser}%
\author[5]{Birgit Ertl-Wagner}%
\affil[1]{University of Munich}%
\affil[2]{LMU}%
\affil[3]{Ludwig-Maximilians-University Munich}%
\affil[4]{Ludwig-Maximilians-Universität München Medizinische Fakultät}%
\affil[5]{The Hospital for Sick Children}%


\vspace{-1em}



  
  \date{June 13, 2024}


\begingroup
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\selectlanguage{english}
\begin{abstract}
Objectives: Several studies proposed a loss of neural structures in
Meni\selectlanguage{ngerman}ère's disease (MD). It has also been shown that VIIth and VIIIth
cranial nerves are enlarged within MD patients compared to normal
controls. We aimed to investigate potential differences in these two
nerves in patients with MD. Setting: 71 patients with MD were included,
53 showed clinically unilateral affection.
Constructive-interference-in-steady-state(CISS) and
3D-FLAIR-inversion-recovery(IR) sequences with two different slice
thicknesses were acquired on a clinical 3T magnetic resonance imaging
scanner. We evaluated morphometric properties of the VIIth and VIIIth
cranial nerves passing from the cerebellopontine angle to the inner ear
modiolus. In patients with clinically unilateral MD, we compared the
unaffected to the clinically affected side. In addition, we evaluated
the morphology of the nerves in correlation to symptom duration.
Results: The clinically unilateral MD-patients showed no significant
differences after Bonferroni correction when comparing the affected side
to the non-affected side of VIIth and VIIIth cranial nerves. There was
no significant difference between patients with different symptom
durations. Conclusions: Our data showed no differences in nerve
morphometry between the clinically non-affected and the clinically
affected side in patients with clinically unilateral MD. There was also
no correlation to duration of symptoms, in contrast to previously
demonstrated correlations between clinical features and the extent of
endolymphatic hydrops. A disease process starting before onset of
clinical symptoms could be a potential explanation.%
\end{abstract}\selectlanguage{ngerman}%



\sloppy


\selectlanguage{ngerman}\textbf{Morphometric evaluation of facial and vestibulocochlear nerves
using magnetic resonance imaging in patients with Menière's disease -- a
retrospective study}

\textbf{Abstract:}

\emph{Objectives:} Several studies proposed a loss of neural structures
in Menière's disease (MD). It has also been shown that
VII\textsuperscript{th} and VIII\textsuperscript{th} cranial nerves are
enlarged within MD patients compared to normal controls. We aimed to
investigate potential differences in these two nerves in patients with
MD.

\emph{Setting:} 71 patients with MD were included, 53 showed clinically
unilateral affection. Constructive-interference-in-steady-state(CISS)
and 3D-FLAIR-inversion-recovery(IR) sequences with two different slice
thicknesses were acquired on a clinical 3T magnetic resonance imaging
scanner. We evaluated morphometric properties of the
VII\textsuperscript{th} and VIII\textsuperscript{th} cranial nerves
passing from the cerebellopontine angle to the inner ear modiolus. In
patients with clinically unilateral MD, we compared the unaffected to
the clinically affected side. In addition, we evaluated the morphology
of the nerves in correlation to symptom duration.

\emph{Results:} The clinically unilateral MD-patients showed no
significant differences after Bonferroni correction when comparing the
affected side to the non-affected side of VII\textsuperscript{th} and
VIII\textsuperscript{th} cranial nerves. There was no significant
difference between patients with different symptom durations.

\emph{Conclusions:} Our data showed no differences in nerve morphometry
between the clinically non-affected and the clinically affected side in
patients with clinically unilateral MD. There was also no correlation to
duration of symptoms, in contrast to previously demonstrated
correlations between clinical features and the extent of endolymphatic
hydrops. A disease process starting before onset of clinical symptoms
could be a potential explanation.

\textbf{Keywords:}

Menière's disease, MRI, vestibulocochlear nerve, facial nerve, cranial
nerve size

\textbf{Key points:}

Menière's disease is characterized by episodic vertigo associated with
fluctuating hearing loss, tinnitus, aural fullness and endolymphatic
hydrops.

\begin{itemize}
\tightlist
\item
  A loss of neural structures was proposed in Menière's disease, but
  also a swelling of VII\textsuperscript{th} and
  VIII\textsuperscript{th} cranial nerves compared to normal controls
  was shown.
\item
  The aim of this observational study was to investigate potential
  differences in these two nerves in patients with Menière´s disease,
  also considering the duration of the disease.
\item
  The VII\textsuperscript{th} and VIII\textsuperscript{th} cranial
  nerves were measured within the cerebellopontine angle and the
  branches in their course through the internal auditory canal.
\item
  Furthermore different MRI sequences (two CISS- and two IR-sequences)
  with different spatial resolution and slice thickness were used for
  morphometric analysis.
\end{itemize}

\textbf{1. Introduction}

Menière's disease (MD) is characterized by episodic vertigo associated
with tinnitus, fluctuating hearing loss, aural fullness and
endolymphatic hydrops (ELH) (1, 2). Several studies proposed a loss of
neural structures (such as hair cells or neurons within the spiral
ganglion) in Menière's disease (MD) (3). In recent years several studies
have evaluated and quantified ELH in patients with MD (4). Only few
studies, however, have analyzed morphometric parameters of cranial
nerves VII and VIII on MRI (5-8).

The course of cranial nerves VII and VIII from the pons through the
cerebellopontine angle and the internal auditory canal (9) make these
nerves amenable to morphometric evaluation in anatomical and MRI
studies. The VIII\textsuperscript{th} cranial nerve divides within the
IAC into its three branches: cochlear nerve (CN), superior vestibular
nerve (SVN) and inferior vestibular nerve (IVN). In the anterosuperior
portion of the IAC the facial nerve is found, and inferior to it the
cochlear nerve (10). To our knowledge, no morphometric analyses of these
nerves have been performed using different MRI sequences with different
spatial resolution in patients with clinically unilateral MD in
correlation to symptom duration.

We previously demonstrated a swelling of VII\textsuperscript{th} and
VIII\textsuperscript{th} cranial nerves on MR imaging in patients with
MD (8). The aim of this study was to investigate morphometric
differences of the VII\textsuperscript{th} and VIII\textsuperscript{th}
cranial nerve within MD patients using different MR imaging techniques.

\textbf{2. Methods}

Ethical review board approval was provided by the institutional review
board for this observational study. All examinations were performed in
concordance with the Helsinki Declaration revised 2013.

2.1. Participants

Patients with certain MD according to the AAO-HNS classification
(1995)(11) and with MR morphologic confirmation of endolymphatic hydrops
(ELH) as an equivalent to the required histopathological findings were
included in the study (4, 12-14). All of these patients underwent MRI on
a clinical 3 Tesla scanner investigation with a sequence protocol
comprising several different MR sequences described below. All patients
gave their informed consent for the locally enhanced inner ear MRI
(LEIM). Morphometric analysis of the VII\textsuperscript{th} and
VIII\textsuperscript{th} cranial nerves was performed retrospectively.
24 hours prior to the MRI scan a gadolinium-based contrast agent diluted
8-fold in saline solution, was intratympanically injected (15). After
administration, the patient remained in a supine position for another 30
minutes with the head turned approximately 45 degrees toward the
contralateral side.

Patient data consisting of CISS-0.6-sequence measurements was compared
in our previous study to clinical healthy controls (8). In the current
study we compared the affected side with the non-affected side of
unilaterally affected MD patients as well as the bilaterally affected MD
patients vs. unilateral affected MD patients using the mentioned
different MRI sequences.

2.2. Setting with MR Imaging

All MR imaging examinations were performed on a 3T MR unit (Magnetom
Verio, Siemens Healthcare, Erlangen, Germany) using a commercially
available 4-channel flexible surface coil combined with an 8-channel
head coil.

The following MR-sequences were acquired of the temporal bone:

\emph{CISS-0.6} : A strongly T2-weighted constructive interference in
steady state sequence (CISS) with the following parameters was used: TR
7.2 ms, TE 3.16 ms, flip angle of 70°, field of view of 192 x 192 mm²,
matrix size of 320 x 320, averages 1 and slice thickness of 0.6 mm.

\emph{CISS-0.4} : The second CISS had the following parameters: TR 6.24
ms, TE 2.87 ms, flip angle of 70°, field of view of 160 x 160 mm²,
matrix size of 320 x 320, averages 1 and slice thickness of 0.4 mm.

\emph{IR-0.5} : The inversion recovery sequence was acquired using the
following parameters: TR 6000 ms, TE 155 ms, flip angle of 180°, field
of view of 160 x 160 mm², matrix size of 320 x 320, averages 1 and slice
thickness of 0.5 mm.

\emph{IR-0.3} : The second inversion recovery sequence had the following
parameters: TR 6000 ms, TE 155 ms, flip angle of 180°, field of view of
160 x 160 mm², matrix size of 256 x 256, averages 1 and slice thickness
of 0.3 mm.

2.3. Design and analysis

We used a commercially available DICOM-Viewer (OsiriX v.4.0, 64-bit
version, Pixmeo, Switzerland) for measuring the diameters of the
VII\textsuperscript{th} and VIII\textsuperscript{th} cranial nerves.
Consistent windowing levels and thin slice thickness were used
performing transverse reformats at different locations throughout the
course of the nerves from the cerebellopontine angle (CPA) to the
internal auditory canal (9) fundus. Locations of the transverse sections
were defined as follows:

\begin{itemize}
\tightlist
\item
  VIII -- CPA,
\item
  CN, SVN and IVN - meatus of the IAC;
\item
  VII -- CPA, meatus of the IAC, fundus of the IAC.
\end{itemize}

On each transverse section the long diameter (LD), short diameter (SD)
perpendicular to LD and cross-sectional area (CSA) were measured.
Several dot-markers were positioned on the outline of the examined
nerves. These markers were linked and the CSA was calculated. All
measurements were performed by the same two readers based on consensus
readings. Both readers were blinded for the diagnosis of the patients.
All these measurements were made for the CISS-0.4, the CISS-0.6, the
IR-0.3 and the IR-0.5 sequences to investigate different nerve sizes
depending on the used MRI sequence.

All patients received locally enhanced inner ear MRI (LEIM). The study
group was subdivided into two cohorts: The first cohort consisted of
unilaterally affected MD patients; the second consisted of bilaterally
affected MD patients.

For comparing the affected and the clinically non-affected side a paired
samples (dependent) t-test was employed using MedCalc v.12.7.2 (MedCalc
Software bvba, Belgium) and SAS v. 9.4 for Windows (Copyright SAS
Institute Inc., Cary, NC, USA). After Bonferroni correction P
\textless{} 0.05 was reduced to P \textless{} 0.000595 for statistical
significance. For comparing the subgroups of different symptom duration
a two-sided independent samples t-test was used. Furthermore we used
Scatterplots, Pearson Correlation Coefficients and Bland-Altman plots
for visualization of the degree of correlation as well as measurement
differences between the employed MRI sequences.

\textbf{3. Results}

Both ears of the 71 MD patients (27 females, 44 males, mean age 54.4
years, age range 23 - 77 years) were measured and analysed. 53 of these
patients were classified as unilaterally affected (20 females, 33 males,
mean age 50.5 years, age range 23 - 77 years). Further clinical patient
data were also collected, such as symptom duration (range 4 - 252
months, mean 76 months) and four-tone average calculated from hearing at
0.5, 1, 2 and 3 kHz (range unaffected side 2.5 -- 31.75 dB, mean 13.87
dB, range affected side 2.5 - 83.5 dB, mean 42.02 dB).

No significant differences were observed when comparing the affected
side to the non-affected side of the VII\textsuperscript{th} and
VIII\textsuperscript{th} cranial nerves in the cohort of clinically
unilaterally affected MD patients (table 1) when adjusting for multiple
testing. Without adjustment for multiple testing, in order for catering
for an explorative approach, significant differences were found
following no certain pattern, e.g. p\textless{}0.05 could be found for
SD at the level of CPA in the VIII\textsuperscript{th} nerve and LD at
level of CPA and fundus of the VII\textsuperscript{th} nerve. These
results were found to be independent of the used MRI sequence (CISS-0.4,
CISS-0.6, IR-0.5 or IR-0.3) when adjusting for multiple testing (tables
2 and 3) at the level of the CPA. Without Bonferroni correction
significant differences were found in the VIII\textsuperscript{th} nerve
at this level only for SD in CISS-0.4 (table 1) and CSA in IR-0.3 at the
level of CPA (table 3), obviously also not following a specific pattern.

Also, no significant differences between the morphometric measurements
of the VII\textsuperscript{th} and VIII\textsuperscript{th} cranial
nerves of the different sides were observed after Bonferroni correction
in the cohort of clinically bilaterally affected patients.

When comparing the affected side of the unilaterally affected cohort
with the LEIM-assessed side of the bilaterally affected cohort, no
significant difference was shown along our measuring points of
VII\textsuperscript{th} and VIII\textsuperscript{th} cranial nerves
(Table 4, cross sectional areas within CISS-0.4, CISS-0.6, IR-0.3 and
IR-0.5). Similar results were found investigating the clinically
non-affected side of the first cohort and the contralateral ear of the
bilaterally affected cohort. These results were again independent of the
used MRI sequence.

An overview of the significant p-values without adjustment for multiple
testing is summarized in table 5, no specific pattern is recognizable.

We furthermore evaluated the morphometric properties of the
VII\textsuperscript{th} and VIII\textsuperscript{th} cranial nerves of
the first cohort in dependence of symptom duration. We initially divided
the cohort of unilaterally affected patients in a subgroup with a
symptom duration of a maximum of 12 months (n = 9) and compared these to
the rest of the group (n = 26); we observed no significant differences
between the groups neither when comparing the affected sides nor when
comparing the non-affected sides. Subsequently, we compared patients
with a symptom duration of at least 120 months (n = 14) to the patients
with a symptom duration of a maximum of 12 months (n = 9). Again, there
were no significant differences for the morphometric parameters (table
6).

\textbf{4. Discussion}

In our patient cohorts we observed no significant differences between
the clinically non-affected side and the clinically affected side of
unilaterally affected patients with MD independently of the used MRI
sequence when using the Bonferroni correction for multiple testing.

4.1. Different models of ethiopathogenesis

The pathogenesis of MD is still incompletely understood and the disease
can be difficult to diagnose in early stages (2, 13, 16). Autoimmune
processes (17) and viral infections, such as latent herpes simplex virus
type-1 that may cause vestibular neuritis (18), may play a role in the
induction of MD. The involved immunological mechanisms are still not
clear, but approximately one-third of the MD cases may have an
autoimmune origin (19-21). Further pathophysiological aspects have been
discussed, such as genetic predisposition (22), excitotoxicity, chronic
otitis media (20), cellular apoptosis and oxidative stress. Reactive
oxygen species, specifically nitric oxide generated by nitric oxide
synthase, regulate the cochlear blood flow and lead to the release of
mitochondrial cytochrome c, which is an important mediator of the
intrinsic pathway of apoptosis (23, 24). The presence of hydrops may
thus cause neuronal damage in the inner ear via a process of
excitotoxicity (1, 25). This neuronal damage could possibly affect the
VIII\textsuperscript{th} and potentially also the
VII\textsuperscript{th} cranial nerve.

Our data, however, demonstrated no differences in nerve diameters when
comparing the clinically non-affected to the clinically affected side of
unilaterally affected MD patients, possibly pointing toward a more
systemic process that leads to subclinical reaction of the contralateral
ear in clinically unilaterally affected MD patients. Kariya et al found
equal results when comparing the mean number of spiral ganglion cells,
the mean loss of inner and outer hair cells in patients and the damage
of the stria vascularis with unilateral MD (3). This may support
autoimmune processes or genetic predispositions, whereas local processes
such as excitotoxicity and reactive oxygen species seem less likely.
Moreover, our data did not show a correlation to clinical symptom
duration, which again may point toward a very longstanding underlying
process prior to the onset of clinical symptoms. On the other hand, it
could also indicate that there is no change in the 7th and 8th cranial
nerves in MD. However, this contradicts our previous study, which showed
thicker nerves in patients with MD compared to a healthy control group
(8).

4.2. MRI difficulties

Moreover our data showed different means for the same patients at the
same measuring levels in dependence of the employed MRI sequence. These
differences occur due to different variable sequence parameters such as
slice thickness, different partial volume effects and the relatively
small sample size. Where measurements varied largely between
VII\textsuperscript{th} and VIII\textsuperscript{th} cranial nerve,
differences between the 4 employed sequences were small. However, due to
the limited sample size, a significant positive correlation could only
be shown for the IR-0.3 and IR-0.5 for VII\textsuperscript{th} and
VIII\textsuperscript{th} cranial nerve. This reflects the difficulty of
comparing absolute morphometric parameters in different MRI-studies
performed with different sequences on different scanners.

In an explorative approach, without catering for multiple testing,
scattered single parameters were found to be significant, these findings
showed no specific pattern. Therefore Bonferroni correction was applied.

4.3. Study Limitations

Our study has several limitations that need to be taken into account
when interpreting the data. First, our sample size was limited,
especially when performing the subgroup analyses. Larger studies are
warranted to confirm our results. Second, we did not compare our
measurements to an age- and sex-matched healthy control cohort to
analyze differences to a clinically unaffected control population. As
shown in our previous study (8) only few surveys (5-7, 10) with
measurements of the VII\textsuperscript{th} and VIII\textsuperscript{th}
cranial nerves had been published, mostly in normal hearing patients.
The comparison of these published data also showed differences of nerve
diameters according to the measuring point and the used MRI sequence.

\textbf{5. Conclusion}

Our data showed no significant differences in diameters and
cross-sectional areas of the VII\textsuperscript{th} and
VIII\textsuperscript{th} cranial nerves between the affected and the
clinically non-affected side of unilaterally affected patients with MD
after Bonferroni correction for multiple testing. There was also no
correlation to duration of clinical symptoms. This may potentially point
toward a systemic process starting long before the onset of first
clinical symptoms. On the other hand, it could also indicate that there
is no change in the 7th and 8th cranial nerves in MD. However, this
contradicts our previous study, which showed thicker nerves in patients
with MD compared to a healthy control group (8).

Normative nerve diameters should only be used if comparable MRI sequence
parameters are used as our data showed different means for the same
patients at the same measuring points depending on the MRI sequences
used.

\textbf{References}

1. Semaan MT, Alagramam KN, Megerian CA. The basic science of Meniere's
disease and endolymphatic hydrops. Current opinion in otolaryngology \&
head and neck surgery. 2005;13(5):301-7.

2. Plontke SK, Gürkov R. {[}Menière's Disease{]}. Laryngo- rhino-
otologie. 2015;94(8):530-54.

3. Kariya S, Cureoglu S, Fukushima H, Kusunoki T, Schachern PA,
Nishizaki K, et al. Histopathologic changes of contralateral human
temporal bone in unilateral Meniere's disease. Otology \& neurotology :
official publication of the American Otological Society, American
Neurotology Society {[}and{]} European Academy of Otology and
Neurotology. 2007;28(8):1063-8.

4. Gurkov R, Flatz W, Ertl-Wagner B, Krause E. Endolymphatic hydrops in
the horizontal semicircular canal: a morphologic correlate for canal
paresis in Meniere's disease. The Laryngoscope. 2013;123(2):503-6.

5. Jaryszak EM, Patel NA, Camp M, Mancuso AA, Antonelli PJ. Cochlear
nerve diameter in normal hearing ears using high-resolution magnetic
resonance imaging. The Laryngoscope. 2009;119(10):2042-5.

6. Nakamichi R, Yamazaki M, Ikeda M, Isoda H, Kawai H, Sone M, et al.
Establishing Normal Diameter Range of the Cochlear and Facial Nerves
with 3D-CISS at 3T. Magnetic resonance in medical sciences : MRMS : an
official journal of Japan Society of Magnetic Resonance in Medicine.
2013.

7. Kang WS, Hyun SM, Lim HK, Shim BS, Cho JH, Lee KS. Normative
diameters and effects of aging on the cochlear and facial nerves in
normal-hearing Korean ears using 3.0-tesla magnetic resonance imaging.
The Laryngoscope. 2012;122(5):1109-14.

8. Henneberger A, Ertl-Wagner B, Reiser M, Gurkov R, Flatz W.
Morphometric evaluation of facial and vestibulocochlear nerves using
magnetic resonance imaging: comparison of Meniere's disease ears with
normal hearing ears. European archives of oto-rhino-laryngology :
official journal of the European Federation of Oto-Rhino-Laryngological
Societies (EUFOS) : affiliated with the German Society for
Oto-Rhino-Laryngology - Head and Neck Surgery. 2017;274(8):3029-39.

9. Savastano M, Giacomelli L, Marioni G. Non-specific immunological
determinations in Meniere's disease: any role in clinical practice?
European archives of oto-rhino-laryngology : official journal of the
European Federation of Oto-Rhino-Laryngological Societies (EUFOS) :
affiliated with the German Society for Oto-Rhino-Laryngology - Head and
Neck Surgery. 2007;264(1):15-9.

10. Giesemann AM, Raab P, Lyutenski S, Dettmer S, Bultmann E, Fromke C,
et al. Improved imaging of cochlear nerve hypoplasia using a 3-Tesla
variable flip-angle turbo spin-echo sequence and a 7-cm surface coil.
The Laryngoscope. 2014;124(3):751-4.

11. Committee on Hearing and Equilibrium guidelines for the diagnosis
and evaluation of therapy in Meniere's disease. American Academy of
Otolaryngology-Head and Neck Foundation, Inc. Otolaryngology--head and
neck surgery : official journal of American Academy of
Otolaryngology-Head and Neck Surgery. 1995;113(3):181-5.

12. Gurkov R, Pyyko I, Zou J, Kentala E. What is Meniere's disease? A
contemporary re-evaluation of endolymphatic hydrops. Journal of
neurology. 2016;263 Suppl 1:S71-81.

13. Nakashima T, Pyykko I, Arroll MA, Casselbrant ML, Foster CA, Manzoor
NF, et al. Meniere's disease. Nature reviews Disease primers.
2016;2:16028.

14. Li X, Wu Q, Sha Y, Dai C, Zhang R. Gadolinium-enhanced MRI reveals
dynamic development of endolymphatic hydrops in Ménière's disease.
Brazilian journal of otorhinolaryngology. 2020;86(2):165-73.

15. Liu Y, Jia H, Shi J, Zheng H, Li Y, Yang J, et al. Endolymphatic
hydrops detected by 3-dimensional fluid-attenuated inversion recovery
MRI following intratympanic injection of gadolinium in the asymptomatic
contralateral ears of patients with unilateral Ménière's disease.
Medical science monitor : international medical journal of experimental
and clinical research. 2015;21:701-7.

16. Paparella MM, Djalilian HR. Etiology, pathophysiology of symptoms,
and pathogenesis of Meniere's disease. Otolaryngologic clinics of North
America. 2002;35(3):529-45, vi.

17. Liu Y, Yang J, Duan M. Current status on researches of Meniere's
disease: a review. Acta oto-laryngologica. 2020;140(10):808-12.

18. Arbusow V, Derfuss T, Held K, Himmelein S, Strupp M, Gurkov R, et
al. Latency of herpes simplex virus type-1 in human geniculate and
vestibular ganglia is associated with infiltration of CD8+ T cells.
Journal of medical virology. 2010;82(11):1917-20.

19. Greco A, Gallo A, Fusconi M, Marinelli C, Macri GF, de Vincentiis M.
Meniere's disease might be an autoimmune condition? Autoimmunity
reviews. 2012;11(10):731-8.

20. Paparella MM, de Sousa LC, Mancini F. Meniere's syndrome and otitis
media. The Laryngoscope. 1983;93(11 Pt 1):1408-15.

21. Derebery MJ, Berliner KI. Prevalence of allergy in Meniere's
disease. Otolaryngology--head and neck surgery : official journal of
American Academy of Otolaryngology-Head and Neck Surgery. 2000;123(1 Pt
1):69-75.

22. Klockars T, Kentala E. Inheritance of Meniere's disease in the
Finnish population. Archives of otolaryngology--head \& neck surgery.
2007;133(1):73-7.

23. Hess A, Bloch W, Huverstuhl J, Su J, Stennert E, Addicks K, et al.
Expression of inducible nitric oxide synthase (iNOS/NOS II) in the
cochlea of guinea pigs after intratympanical endotoxin-treatment. Brain
research. 1999;830(1):113-22.

24. Kong WJ, Ren T, Nuttall AL. Electrophysiological and morphological
evaluation of the acute ototoxicity of sodium nitroprusside. Hearing
research. 1996;99(1-2):22-30.

25. Ishiyama G, Lopez IA, Sepahdari AR, Ishiyama A. Meniere's disease:
histopathology, cytochemistry, and imaging. Annals of the New York
Academy of Sciences. 2015;1343:49-57.

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\verb`Morph. eval. - Clin. Otol. - Table 2.docx`  available at \url{https://authorea.com/users/472805/articles/563359-morphometric-evaluation-of-facial-and-vestibulocochlear-nerves-using-magnetic-resonance-imaging-in-patients-with-meni%C3%A8re-s-disease-a-retrospective-study}

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\verb`Morph. eval.  - Clin. Otol. - Table 3.docx`  available at \url{https://authorea.com/users/472805/articles/563359-morphometric-evaluation-of-facial-and-vestibulocochlear-nerves-using-magnetic-resonance-imaging-in-patients-with-meni%C3%A8re-s-disease-a-retrospective-study}

\textbf{Hosted file}

\verb`Morph. eval. - Clin. Otol. - Table 4.docx`  available at \url{https://authorea.com/users/472805/articles/563359-morphometric-evaluation-of-facial-and-vestibulocochlear-nerves-using-magnetic-resonance-imaging-in-patients-with-meni%C3%A8re-s-disease-a-retrospective-study}

\textbf{Hosted file}

\verb`Morph. eval. - Clin. Otol. - Table 5.docx`  available at \url{https://authorea.com/users/472805/articles/563359-morphometric-evaluation-of-facial-and-vestibulocochlear-nerves-using-magnetic-resonance-imaging-in-patients-with-meni%C3%A8re-s-disease-a-retrospective-study}

\textbf{Hosted file}

\verb`Morph. eval. - Clin. Otol. - Table 6.docx`  available at \url{https://authorea.com/users/472805/articles/563359-morphometric-evaluation-of-facial-and-vestibulocochlear-nerves-using-magnetic-resonance-imaging-in-patients-with-meni%C3%A8re-s-disease-a-retrospective-study}

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