RT Journal Article
SR Electronic
T1 Correlation between Histopathology and Signal Loss on Spin-Echo T2-Weighted MR Images of the Inner Ear: Distinguishing Artifacts from Anatomy
JF American Journal of Neuroradiology
JO Am. J. Neuroradiol.
FD American Society of Neuroradiology
SP 1464
OP 1469
DO 10.3174/ajnr.A7625
VO 43
IS 10
A1 B.K. Ward
A1 A. Mair
A1 N. Nagururu
A1 M. Bauer
A1 B. Büki
YR 2022
UL http://www.ajnr.org/content/43/10/1464.abstract
AB BACKGROUND AND PURPOSE: MR imaging of the inner ear on heavily T2-weighted sequences frequently has areas of signal loss in the vestibule. The aim of the present study was to correlate the anatomic structures of the vestibule with areas of low signal intensity.MATERIALS AND METHODS: We reviewed T2-weighted spin-echo MR imaging studies of the internal auditory canal from 27 cases and cataloged signal intensity variations in the vestibulum of inner ears. Using a histologic preparation of a fully mounted human ear, we prepared 3D reconstructions showing the regions of sensory epithelia (semicircular canal cristae, utricular, and saccular maculae). Regions of low signal intensity were reconstructed in 3D, categorized by appearance, and compared with the 3D histologic preparation.RESULTS: The region corresponding to the lateral semicircular canal crista showed signal loss in most studies (94%). In the utricle, a focus of signal loss occurred in the anterior-cranial portion of the utricle and corresponded to the location of the utricular macula and associated nerve on histopathologic specimens (63% of studies). Additional areas of low signal were observed in the vestibule, corresponding to the fluid-filled endolymphatic space and not to a solid anatomic structure.CONCLUSIONS: Small foci of signal loss within the inner ear vestibule on T2-weighted spin-echo images correlate with anatomic structures, including the lateral semicircular canal crista and the utricular macula. More posterior intensity variations in the endolymphatic space are likely artifacts, potentially representing fluid flow within the endolymph caused by magneto-hydrodynamic Lorentz forces.