Introduction: Arachnoid cysts (AC) are intracranial, benign, and often incidentally identified
CSF-filled sacs. In the past, case reports have associated AC to cranial nerve (CN)
VII and VIII symptoms such as sensorineural hearing loss, vestibular symptoms, facial
paresis/spasm, and headaches. There are isolated reports using surgical intervention
to rectify hearing deficits or other symptoms. Despite these reports, literature demonstrating
a clear link to reported symptomatology and an understanding of their natural history
is lacking. We present a case example that inspired an investigation into the possible
association of AC in the cerebellopontine angle (CPA) with sensorineural hearing loss
(SNHL) based on distortion of the CN VIII complex via mass effect.
Methods: A single-institution, retrospective chart review was conducted between 2010 and 2024
including pediatric patients with AC and a history of audiologic evaluation. From
this cohort, nineteen patients were identified with posterior fossa AC involving the
CPA. Cyst characteristics including size/volume, cisternal and internal auditory canal
(IAC) length, IAC diameter, and cochlear aperture were collected. Cysts were categorized
as with or without contact with CN VIII complex; any nerve distortion was calculated
as the perpendicular distance from the expected path at the midcisternal segment.
Information regarding SNHL and other symptoms were tabulated. Descriptive statistics
and linear regression analysis were performed.
Results: Out of 227 total patients with AC and audiometric evaluation, 19 (8.4%) patients
were identified with posterior fossa AC in the CPA. The average age was 8.1 years.
11/19 (58%) patients had contact/displacement of CN VIII complex in the CPA, while
8/19 (42%) did not. Interestingly, there was no significant difference in maximum
linear dimension and estimated spheroid volume of the groups with and without distortion
of CN VIII complex (median dimension: 2.50 vs. 2.05 cm, p = 0.2809) and (median volume: 3.285 vs. 1.523 cm3, p = 0.0506), respectively. Of the group with AC contacting with the CN VIII complex,
4/11 (36%) patients had isolated ipsilateral asymmetric SNHL not better explained
by other pathology; however, this was not statistically significant when compared
to those without CN VIII displacement (0/8 patients, p = 0.0549). We were unable to find any association between degrees of CN VIII displacement,
involvement of the root entry zone, cyst growth, or FLAIR changes in CN VIII complex
with the presence of ipsilateral asymmetric SNHL.
Conclusion: AC in the CPA is an uncommon and often incidental abnormality. Contact/displacement
of CN VIII complex by AC may portend development of ipsilateral asymmetric SNHL, though
this was not statistically significant in our cohort. An expanded investigation is
necessary to elucidate associations or predictive factors between AC and SNHL.
