Imaging of Neurovascular Compression Syndromes: Trigeminal Neuralgia, Hemifacial Spasm, Vestibular Paroxysmia, and Glossopharyngeal Neuralgia.

S Haller,H Urbach,L Etienne,E Ko Vari,M Becker,A D Varoquaux

doi:10.3174/ajnr.a4683

Abstract

Neurovascular compression syndromes are usually caused by arteries that directly contact the cisternal portion of a cranial nerve. Not all cases of neurovascular contact are clinically symptomatic. The transition zone between the central and peripheral myelin is the most vulnerable region for symptomatic neurovascular compression syndromes. Trigeminal neuralgia (cranial nerve V) has an incidence of 4-20/100,000, a transition zone of 4 mm, with symptomatic neurovascular compression typically proximal. Hemifacial spasm (cranial nerve VII) has an incidence of 1/100,000, a transition zone of 2.5 mm, with symptomatic neurovascular compression typically proximal. Vestibular paroxysmia (cranial nerve VIII) has an unknown incidence, a transition zone of 11 mm, with symptomatic neurovascular compression typically at the internal auditory canal. Glossopharyngeal neuralgia (cranial nerve IX) has an incidence of 0.5/100,000, a transition zone of 1.5 mm, with symptomatic neurovascular compression typically proximal. The transition zone overlaps the root entry zone close to the brain stem in cranial nerves V, VII, and IX, yet it is more distal and does not overlap the root entry zone in cranial nerve VIII. Although symptomatic neurovascular compression syndromes may also occur if the neurovascular contact is outside the transition zone, symptomatic neurovascular compression syndromes are more common if the neurovascular contact occurs at the transition zone or central myelin section, in particular when associated with nerve displacement and atrophy.

Highlights

We provide illustrative cases of normal anatomy and histologic sections from postmortem specimens for the understanding of the etiology of Neurovascular compression syndrome (NVCS), as well as surgically proven cases of NVCS involving cranial nerves (CNs) V, VII, VIII, and IX
glossopharyngeal neuralgia (GN) caused by NVC occurs almost exclusively (95%) in the proximal REZ,[59] which overlaps the proximal location of the TZ of 1.51 Ϯ 0.39 mm.[11]
While the TZ is close to the brain stem and overlaps the REZ in CN V, VII, and IX, it is longer, located more distally, and does not overlap the REZ in CN VIII.[9]

Summary

Cisternal Length

8–15 mmb 13.11 Ϯ 1.12 mm (range, 11.9–15.2 mm)c Motor root, 2–20 mmd 17.93 Ϯ 2.29 mm (range, 14.8–20.9 mm)c 9.9 Ϯ 3.03 mm (range, 4.78–20.13 mm) lateral sidee 16.48 Ϯ 1.78 mm (range, 14.2–19.2 mm)f 16.36 Ϯ 2.53 mm (range, 14.2–19.9 mm)c. TZ 1.13 mm (medial)b 2.47 mm (lateral)b 4.19 Ϯ 0.81 mmc 2.86 Ϯ 1.19 mmc 1.9 Ϯ 1.14e. B Peker et al.[8] c Guclu et al.[11] d Yousry et al.[13] e Tomii et al.[46] f Guclu et al.[53] by a saccular aneurysm, a persistent trigeminal artery, an arteriovenous malformation,[27,28] or a petrous vein (Figs 4 and 5). It is certainly an oversimplification to assume that NVCS can occur only at the TZ because

Hemifacial spasm Vestibular paroxysmia Glossopharyngeal neuralgia

CN IX CN VIII CN VII CN V

Findings

CONCLUSIONS