Abstract

Pulsatile tinnitus (PT) occurs in many but not all patients with idiopathic intracranial hypertension (IIH). It is poorly understood why some patients with IIH develop PT, yet others do not. The purpose of this study was to determine if any clinical findings differ between those with and without PT in IIH, potentially shedding light on a pathophysiologic mechanism. Age-matched cohort analysis of patients with documented IIH and presence or absence of PT was performed, collecting data including body mass index (BMI), blood pressure, visual acuity, cerebrospinal fluid (CSF) opening pressure, sleep apnea, migraines, and transient visual obscurations, among others. Independent-sample t test and χ2 test were used to analyze continuous and binary variables, respectively, with multivariate analysis conducted including variables statistically significant on univariate analysis. Eighty subjects with IIH met the inclusion criteria (40 PT+, 40 PT-). CSF opening pressure showed no significant difference between the two groups. The PT+ cohort was found to have an average BMI of 45.1 kg/m 2 , which was significantly higher than the PT- group (37.7 kg/m 2 ; p = 0.0023). PT+ pulse pressure (60.1 mm Hg) was also significantly higher than the PT- group (51.6 mm Hg; p = 0.019). PT+ patients were also significantly more likely to have sleep apnea ( p < 0.001) and migraines ( p = 0.0036). Multiple logistic regression revealed an adjusted odds ratio of 13.9 for sleep apnea, 4.1 for migraines, and 1.01 for every increase in unit of BMI. Among patients with IIH, presence of PT is associated with higher BMI and pulse pressure, and increased incidence of sleep apnea and migraines. Given no significant difference in CSF pressures between the two groups, PT may not be a product of increased disease severity but may be related to sequelae of obesity, such as increased pulse pressure and sleep apnea.

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