HSC Section 8_April 2017

A. J. SOOD ET AL.

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

81.6% a , b 75.7% a 75.3% c 79.0% b,c

Sac decompression

34.8 40.7 40.7 40.8

Mastoid shunt ( with and without silastic)

Mastoid shunt with silastic Mastoid shunt without silastic

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.

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

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. 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- DISCUSSION

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)

71.6% a , b 69.3% a 64.4% c 79.8% b , c

Sac decompression

34.0 41.5 38.8 49.8

1.4 6.0 6.2 n/a

Mastoid shunt ( with and without silastic)

Mastoid shunt with silastic Mastoid shunt without silastic

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.

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