MRI Assessment of Vascular Contact of the Facial Nerve in the Asymptomatic Patient

Objective: Vascular contact of the facial nerve is widely believed to be a cause of hemifacial spasm (HFS). The prevalence of facial nerve vascular contact on MRI in patients without HFS has not been well described in the literature.

Methods: Our radiology database was queried to identify adult patients evaluated with high-resolution MRI of the posterior fossa (volumetric T2 and T1 post-contrast sequences with triplanar reconstructions). Following exclusion of patients with a history of HFS, intracranial tumor, brain radiation therapy, intracranial surgery, or trigeminal nerve vascular compression, 100 consecutive MRI’s (81 at 1.5 Tesla, 19 at 3 Tesla) were independently reviewed by two neuroradiologists for facial nerve vascular contact (200 sides). When vascular contact was identified, the facial nerve segment contacted was recorded (brainstem, root entry zone (REZ), or cisternal). When identifiable, the vessel responsible for the contact was recorded. Vascular contact was graded as mild, moderate or severe. Interobserver agreement was calculated using the kappa coefficient of agreement index.

Results: The cohort had a mean age of 56 years (range 22–89 years) and included 38 men and 62 women. The first neuroradiologist identified vascular contact in 88 of 200 facial nerves (44%). The segment contacted was brainstem in 19.3%, REZ in 31.8% and cisternal segment in 48.9%. Vascular contact was caused by the anterior inferior cerebellar artery (AICA) in 59.1%, posterior inferior cerebellar artery (PICA) in 8.0%, a vein in 15.9%, and a vessel of uncertain origin in 17.0%. Contact was mild in 84.1% and moderate in 15.9%. The second neuroradiologist identified vascular contact in 74 of 200 facial nerves (37%). The segment contacted was brainstem in 6.8%, REZ in 37.8% and cisternal segment in 55.4%. Vascular contact was caused by the AICA in 51.4%, PICA in 10.8%, a vein in 27.0%, and a vessel of uncertain origin in 10.8%. Contact was mild in 74.3% and moderate in 25.7%. No cases of severe neurovascular compression were identified by either neuroradiologist. In 94 of 200 nerves (47%), both neuroradiologists agreed that there was no vascular contact. Therefore, the presence of vascular contact in the asymptomatic patient may be as high as 53%. The kappa coefficient was 0.48 (95% CI= 0.36 to 0.61) indicating good agreement between the two observers.

Conclusion: Vascular contact of the facial nerve is frequently identified in the asymptomatic patient, typically mild to moderate in severity, most commonly involves the cisternal segment, and usually caused by the AICA. The results of this study can help a surgeon evaluating a patient preoperatively for hemifacial spasm better ascribe significance to the MRI findings, particularly in mild or equivocal cases of vascular contact. Therefore, these results should be considered in assessing the candidacy of HFS patients for microvascular decompression.