Preoperative Significance of Ipsilateral Manual Neck Compression in Patients With Pulsatile Tinnitus Secondary to Sigmoid Sinus Dehiscences and Diverticula

Abstract

Venous pulsatile tinnitus (PT) is characterized by an auditory perception of pulse-synchronous sound, suppressed by compression of the ipsilateral internal jugular vein. We sought to determine the preoperative prognostic significance of the effect of ipsilateral neck manual compression on the PT loudness and audiometric changes in patients with sigmoid sinus dehiscences (SS-Deh) and diverticula (SS-Div) by comparing postoperative improvements in ipsilateral low-frequency hearing loss (LFHL) in pure-tone audiogram (PTA) and PT symptoms. Twenty-two subjects with PT originating from SS-Deh/Div were recruited. Air-conduction hearing thresholds were measured using PTA at three time points: twice preoperatively (with neutral neck position and with ipsilateral manual compression of internal jugular vein) and once at 3-months postoperatively with neutral neck position. We defined a positive neck compression effect as a threshold improvement of ≥ 10 dB HL at 250 or 500 Hz after manual neck compression. All but two subjects presented with ipsilateral LFHL in the neutral position. The average hearing threshold in the neutral position markedly improved after manual neck compression, indicating that LFHL originated from the masking effect of venous PT. All subjects had subjective improvements in PT and LFHL after sigmoid sinus surgeries, confirming that LFHL resulted from the masking effect of PT. Additionally, improvement of LFHL after neck compression could be regarded as a positive prognostic indicator after surgery. Collectively, elimination of PT loudness and improvement of LFHL with manual compression over the ipsilateral neck may suggest the venous origin of the PT and predict a favorable outcome following repair of SS-Deh/SS-Div.

Noninvasive Treatment of Venous Pulsatile Tinnitus with an Internal Jugular Vein Compression Collar

“…In the second mechanism, blood flow vibrating against the walls of abnormal venous structures is transduced through the temporal bone as audible sound 21,42,43 . Indeed, with respect to the latter mechanism, recent studies on sigmoid sinus dehiscence and diverticulum specifically have shown that variations in the sigmoid sinus geometry accelerate the disruption of local laminar flow and that the intensity of vascular bruit is correlated with venous flow velocity 42,44,45 . Computational flow study has identified reduction in high‐speed blow flow as the therapeutic mechanism of symptom relief from stenting in jugular diverticulum stenosis 26 .…”

“…21,42,43 Indeed, with respect to the latter mechanism, recent studies on sigmoid sinus dehiscence and diverticulum specifically have shown that variations in the sigmoid sinus geometry accelerate the disruption of local laminar flow and that the intensity of vascular bruit is correlated with venous flow velocity. 42,44,45 Computational flow study has identified reduction in high-speed blow flow as the therapeutic mechanism of symptom relief from stenting in jugular diverticulum stenosis. 26 Therefore, interventions that reduce velocity of blood flow through the anomalous venous or bony region should reduce the turbulence or vibration that creates the perception of symptoms in objective VPT.…”

Recent Updates on Tinnitus Management

“…Patients with venous pulsatile tinnitus experience tinnitus synchronized with their heartbeat, and ipsilateral neck compression directly alleviates tinnitus and improves low-frequency hearing loss. The elimination of pulsatile tinnitus after compression has been reported as an excellent prognostic factor following repair of the sigmoid sinus [56]. The results of the water occlusion test may also predict the surgical outcome after resurfacing surgery [57].…”

Causes and outcomes of revision surgery in subjects with pulsatile tinnitus

“…The three major mechanisms by which vascular abnormalities may cause PT are alterations in vascular hemodynamics (causing turbulent blood flow leading to sound transmission), vibration of a dehiscent vascular wall in the absence of turbulent flow, and abnormal sound perception of a normal internal stimulus, such as in third-window lesions in the inner ear ( 2 , 3 ). Therefore, identification of the causative vascular pathology and etiology-specific management are crucial for optimal treatment of PT, as adequate management targeting structural anomalies can result in complete resolution of PT ( 4 , 5 ).…”