Title:Cerebral Inflow and Outflow Discrepancies in Severe Sudden Sensorineural Hearing Loss
Volume: 15
Issue: 3
Author(s): Andrea Ciorba*, Mirko Tessari, Manuela Mazzoli, Valentina Tavoni, Francesco Sisini, Claudia Aimoni, Francesco Stomeo, Erica Menegatti, Stefano Pelucchi and Paolo Zamboni
Affiliation:
- ENT & Audiology Department, University Hospital of Ferrara, Ferrara,Italy
Keywords:
Sudden Sensorineural Hearing Loss (SSNHL), echocolor doppler, brain hemodynamics, vascular occlusions,
CCSVI, jugular veins.
Abstract: The aim of this study is to evaluate whether cerebral inflow and outflow abnormalities,
assessed by the means of a validated ultrasound model, could be associated with Sudden Sensorineural
Hearing Loss (SSNHL).
According to Clark, a total of 42 patients affected by severe SSNHL and 19 healthy volunteers
matched by gender without any history of sudden hearing impairment have been included in this
study. Patients and controls underwent EchocolorDoppler assessment of brain hemodynamics. All
subjects affected by SSNHL were also assessed with Auditory Brainstem Responses (ABR) and
Magnetic Resonance Imaging (MRI) in order to exclude retrocochlear pathology.
The head inflow through the common carotid artery was practically equivalent between groups,
but at the level of the carotid bifurcation, the external carotid artery showed a highly significant
flow rate in SSNHL 5.4±2 vs 3.9±1.1 ml/s in controls (p=0.01). The brain inflow was similar between
patients and controls, but interestingly the flow rate of the vertebral artery was significantly
reduced in SSNHL 1.6±0.8 vs 2.8±0.9 ml/s (p=0.01). The brain outflow was found significantly
restricted at the level of the jugular outlet 6.6±6 vs 9.9±6 ml/s (p=0.002); consequently, the collateral
flow index was significantly increased in SSNHL (p=0.001).
The present study shows a discrepant distribution of the brain inflow which seems to penalize the
posterior segments of the Willis polygon in patients affected by severe SSNHL. In addition, our
study confirms the presence of chronic cerebrospinal venous insufficiency in SSNHL with significant
activation of venous collateral circulation.
