ABSTRACT
BACKGROUND: Pulsatile tinnitus (PT) may be due to a spectrum of cerebrovascular etiologies, ranging from benign venous turbulence to life threatening dural arteriovenous fistulas. A focused clinical history and physical examination provide clues to the ultimate diagnosis; however, the predictive accuracy of these features in determining PT etiology remains uncertain. METHODS: Patients with clinical PT evaluation and DSA were included. The final etiology of PT after DSA was categorized as shunting, venous, arterial, or non-vascular. Clinical variables were compared between etiologies using multivariate logistic regression, and performance at predicting PT etiology was determined by area under the receiver operating curve (AUROC). RESULTS: 164 patients were included. On multivariate analysis, patient reported high pitch PT (relative risk (RR) 33.81; 95% CI 3.81 to 882.80) compared with exclusively low pitch PT and presence of a bruit on physical examination (9.95; 2.04 to 62.08; P=0.007) were associated with shunting PT. Hearing loss was associated with a lower risk of shunting PT (0.16; 0.03 to 0.79; P=0.029). Alleviation of PT with ipsilateral lateral neck pressure was associated with a higher risk of venous PT (5.24; 1.62 to 21.01; P=0.010). An AUROC of 0.882 was achieved for predicting the presence or absence of a shunt and 0.751 for venous PT. CONCLUSION: In patients with PT, clinical history and physical examination can achieve high performance at detecting a shunting lesion. Potentially treatable venous etiologies may also be suggested by relief with neck compression.
ABSTRACT
BACKGROUND: Pulsatile tinnitus (PT) can cause significant detriment to quality of life and may herald a life-threatening condition. Endovascular evaluation is the gold standard for the definitive diagnosis of PT and facilitates treatment. However, no large study has determined the distribution of causes and treatment outcomes of PT evaluated endovascularly. METHODS: Consecutive patients evaluated at a multidisciplinary PT clinic from a single academic center were retrospectively reviewed. Patients with a suspected cerebrovascular etiology of PT based on clinical and/or non-invasive imaging, who were evaluated by endovascular techniques (arteriography, venography, manometry, and/or balloon test occlusion), were included in analysis. Baseline clinical features and treatment results by final etiology of PT were compared. RESULTS: Of 552 patients referred for PT evaluation, 164 patients (29.7%) who underwent endovascular evaluation of PT were included. Mean (±SD) age at first clinical evaluation was 54.3±14.1 years (range 25-89 years); 111 patients (67.7%) were female. PT causes were 75.6% vascular and 24.4% non-vascular. Arteriovenous shunting lesions caused 20.7% of cases, venous etiologies 48.2%, and arterial etiologies 6.7%. Of patients with a shunting lesion treated with endovascular embolization, 96.9% had lasting significant improvement or resolution in PT. Endovascular stenting for venous sinus stenosis gave 84.6% of patients lasting improvement or resolution in PT. Arterial and non-vascular PT had fewer patients treated endovascularly and less improvement in PT symptoms. CONCLUSION: PT with a suspected vascular cause is most often attributable to venous etiologies. PT caused by arteriovenous shunting or venous sinus stenosis may be effectively treated endovascularly.
