82 / 264
A summary of vertigo control and hearing preservation
in the long-term (
9
24 months) is provided in Tables 3 and 4,
respectively.
Current ESS Procedures From Studies With Both
Short-term and Long-term Follow-ups. Vertigo:
Six
articles provided continual data for the same patient co-
hort, allowing both short-term and long-term follow-ups.
These articles, totaling 448 patients, were analyzed to
determine the efficacy of current ESS techniques (sac
decompression and mastoid shunting
with
or
without
si-
lastic) in controlling vertigo. With a mean short-term
follow-up of 16.0 months (range, 12
Y
24 mo), complete
or substantial (Category A/B) vertigo control occurred in
72.6% (95% CI, 68.3%
Y
76.7%) of patients (Fig. 18).
With mean long-term follow-up in the same patient co-
hort of 79.0 months (range, 48
Y
120 mo), complete or
substantial (Category A/B) control was present in 63.4%
(95% CI, 51.3%
Y
74.7%) of patients (Fig. 19). A sum-
mary of short-term and long-term vertigo control from
these articles is provided in Table 5.
Hearing:
We did not find any continual articles that
provided both short-term and long-term follow-ups.
Complete meta-analysis data are provided in the Supple-
mental Results Section,
http://links.lww.com/MAO/A221.
DISCUSSION
The endolymphatic sac is thought to provide immu-
nologic responses and maintain hydrostatic pressure and
endolymph homeostasis for the inner ear (57). Loss of these
functions may contribute to the etiopathophysiology of
MD (57). Initial studies on the endolymphatic sac of mice
demonstrated an inner ear immunologic response to key-
hole limpet hemocyanin (58). More recent studies have
shown an inner ear proimflammatory expression of cyto-
kine tumor necrosis factor
>
in response to keyhole limpet
hemocyanin in the human endolymphatic sac (59). These
studies suggest that the endolymphatic sac performs innate
immunologic response (initial antigen presentation) for the
inner ear, similar to the mucosa associated lymphatic tissue
in the gastrointestinal tract (58
Y
60).
A possible contributor to the etiopathophysiology of MD
is the repetitive presentation of viral and bacterial antigens
to the endolymphatic sac, generating a proinflammatory
response through numerous fenestrated subepithelial blood
vessels within the inner ear. Single or multiple inflamma-
tory responses eventually may cause destruction of the
endolymphatic sac, obliterating its role in inner ear func-
tion (60
Y
62). In addition to innate immunity, others have
speculated that endolymphatic sac dysfunction results
from a humoral-mediated immunologic response. In this
hypothesis, antibodies to the endolymphatic sac and/or
immune complex deposition contribute to endolymphatic
sac dysfunction (60,63,64). Loss of endolymphatic sac
function impairs the ability to maintain hydrostatic pres-
sure and endolymph homeostasis, eventually causing
rupture in Reissner membrane triggering episodic vertigo
attacks (61).
Recent studies have suggested that stress-related events
may impair the endolymphatic sac’s ability to maintain
homeostasis (65
Y
67). These studies have demonstrated
elevated levels of the plasma stress hormone vasopres-
sin along with an elevated level of vasopressin receptor
(V2R) mRNA expression in the endolymphatic sac of
patients with MD in comparison to their respective con-
trol group counterparts (65
Y
67). Others have suggested
that dysfunction of Na
+
/K
+
/2Cl
j
cotransporters and
aquaporins, similar to those in renal tubules, on the endo-
lymphatic sac membrane may contribute to the inability to
maintain hydrostatic pressure and endolymph homeostasis
(65,67,68). Regardless of dysfunction mechanism, the
TABLE 4.
Summary of endolymphatic sac surgery procedures of hearing preservation in the long term (
9
24 mo)
Procedure
Mean weighted follow-up (mo)
Hearing stable/improved (%)
$
PTA (dB; hearing worsened)
Sac decompression
34.0
71.6%
a
,
b
1.4
Mastoid shunt (
with
and
without
silastic)
41.5
69.3%
a
6.0
Mastoid shunt
with
silastic
38.8
64.4%
c
6.2
Mastoid shunt
without
silastic
49.8
79.8%
b
,
c
n/a
a
Sac decompression versus mastoid shunt (with and without silastic) hearing stable/improved;
p
= 0.59.
b
Sac decompression versus mastoid shunt
without
silastic hearing stable/improved;
p
= 0.05.
c
Mastoid shunt
with
silastic versus mastoid shunt
without
silastic hearing stable/improved;
p
= 0.0001.
n/a indicates not available; PTA, pure-tone audiometry.
TABLE 3.
Summary of endolymphatic sac surgery procedures with Category A/B vertigo control in the long term (
9
24 mo)
Procedure
Mean weighted follow-up (mo)
Category A/B vertigo control
Sac decompression
34.8
81.6%
a
,
b
Mastoid shunt (
with
and
without
silastic)
40.7
75.7%
a
Mastoid shunt
with
silastic
40.7
75.3%
c
Mastoid shunt
without
silastic
40.8
79.0%
b,c
a
Sac decompression versus mastoid shunt Category A/B vertigo control;
p
= 0.09.
b
Sac decompression versus mastoid shunt
without
silastic Category A/B vertigo control;
p
= 0.54.
c
Mastoid shunt
with
silastic versus mastoid shunt
without
silastic Category A/B vertigo control;
p
= 0.22.
A. J. SOOD ET AL.
Otology & Neurotology, Vol. 35, No. 6, 2014
61