Correlation between Anterior Inferior Cerebellar Artery Loop and Otologic Symptoms

Jeon, Eun ju; Park, Yong Soo; Lee, Jung Whee; Lee, Seung Kyun; Chang, Ki Hong; Lee, Jung Hak; Jun, Beom Cho

Abstract

BACKGROUND AND OBJECTIVES: The correlation of anterior inferior cerebellar artery (AICA) vascular loop around cerebellopontine angle (CPA) and otologic symptoms remains controversial. The objective of this study was to evaluate the relationship of the anatomical type of AICA loop and otologic symptoms according to the findings of 3-dimensional Fourier transformation constructive interference in steady state (3DFT-CISS) MRI.
SUBJECTS AND METHOD
316 ears from 165 patients were included in this study. Otologic symptoms and the results of pure tone audiometry, auditory evoked potential, and electronystagmography were checked by retrospective chart review. AICA loops were classified by its configuration on 3DFT-CISS MRI. According to their extension depth in internal auditory canal (IAC), the loops were classified as type I (lying within CPA), type II (from porus acusticus to 50% of the length of IAC), and type III (extending beyond 50% of IAC). In addition, the loops were classified as S (small) and L (large) by comparing the thickness of the loop with adjacent facial nerve.
RESULTS
The predominant type of AICA loop was type I (62.0%) and type S (72.8%). Ears with type III loop presented significantly higher rate of hearing impairment than those with type I or II. There were no significant differences in pure tone threshold, hearing loss in 3 consecutive frequencies, canal paresis, and AEP latencies among 3 AICA types classified with the depth of the loop. Ears with type S AICA loop showed significantly higher rate of hearing impairment, elevated threshold, hearing loss in 3 consecutive frequencies, and canal paresis than those with type L loop.
CONCLUSION
The small diameter of AICA loop had significant association with hearing impairment and otologic test abnormalities. Impaired blood flow through the vascular loop and resultant hypoperfusion of inner ear may be the pathophysiologic mechanism of vestibulocochlear nerve compression syndrome.