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

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.

© 2016 by American Journal of Neuroradiology.

Figures

Fig 1.

Histologic images of the transition zone of the trigeminal (CN V, A), facial (CN VII, B), vestibulocochlear (CN VIII, C), and glossopharyngeal (CN IX, D) nerves. Note the very distal TZ of CN VIII, which is beyond the field that can be analyzed with the current methodology compared with CNs V, VII, and IX (hematoxylin-eosin, scale bar on D = 0.5 mm).

Fig 2.

Normal anatomy of the cisternal segment of CN V obtained at 3T. Axial 0.6-mm thin-section (A), coronal (B), and sagittal (C) 2D reconstructions (same thickness) from a 3D T2-weighted balanced steady-state free precession sequence. Note that multiple individual nerve fibers can be identified in both cisternal CN Vs. The short arrow in C points to the motor root of the left CN V, while the long arrow points to the sensory root.

Fig 3.

NVCS in a 55-year-old woman with right TN. Fusion of CISS (0.6-mm sections) and TOF angiography sequences (A, axial; C, coronal; E, sagittal) show contact between the duplicated superior cerebellar artery and the superior portion of the cisternal CN V (arrows). Tractography reconstruction from DTI (B, superior view; D, right CN V; F, left CN V) shows a slightly diminished number of fibers on the right, as opposed to the left. Fiber color-coding is the following: anteroposterior = green; left-right = red; craniocaudal = blue. Fractional anisotropy measurements show diminished values on the right.

Fig 4.

Right TN in a 45-year-old man caused by venous compression. Axial (A) and coronal (C) 2D reconstruction from CISS (0.7-mm thin sections). Contrast-enhanced 3D T1-weighted reconstructed images (0.9 mm) in the axial (B) and coronal (D) planes. Intraoperative views before (E) and after (F) the operation. MR imaging shows bifocal CN V (white arrows) compression by the Dandy vein (white short arrows) and by a transverse pontine vein (black arrows), respectively. Teflon (Dupont, Wilmington, Delaware) (asterisk, F) was interposed between CN V (white arrow, F) and the Dandy vein (white arrowhead, F). The transverse pontine vein was coagulated (black arrow, F). Intraoperative images are courtesy of Dr Arnaud Deveze, MD, Department of Ear, Nose and Throat Surgery, University Hospital, Hôpital Nord, Marseille, France.

Fig 5.

NVCS in a 70-year-old man with left TN. Axial T2-weighted image (A, 0.5 mm). Contrast-enhanced T1-weighted image (B, 0.5 mm). Fusion of 3D T2 and TOF angiography sequences (C and D, sagittal; E and F, coronal sections). Note contact between the tortuous vertebral arteries (white arrowheads), the left AICA (black arrows), the superior cerebellar artery (white arrows), and the cisternal left CN V (black arrowheads). Note that the TZ of CN V is thinned, while the more distal portion of CN V close to the Meckel cave has a normal rounded shape. Gray arrowhead points to the right CN V.

Fig 6.

TN in an 81-year-old man treated with stereotactic radiosurgery. Axial images (0.5 mm) obtained by fusion of CISS and TOF angiography sequences (A and B) and contrast-enhanced 3D T1-weighted volumetric interpolated brain examination (C and D, 0.6 mm) show NVCS caused by the superior cerebellar artery (arrowheads). There is contrast enhancement of the right CN V at the stereotactic radiosurgery site (arrow, D). Contrast enhancement on follow-up examinations disappeared gradually.

Fig 7.

HFS caused by a posterior inferior cerebellar artery (PICA) loop in a 54-year-old man. Axial oblique (A) and coronal oblique (B) reformatted images obtained by fusion of CISS (0.6 mm) and TOF angiography sequences show NVC of CN VII (arrows, A and B) by the PICA at the presumed TZ (arrowhead). 3D MIP reconstruction of the TOF sequence (C) shows a PICA loop on the right, responsible for HFS. Findings were confirmed surgically.

Fig 8.

Right HFS caused by an AICA loop in a 60-year-old man. Fusion of 3D T2 and TOF angiography sequences (0.6-mm thin sections; A, axial; B and C, coronal sections). Axial oblique reformatted T2-weighted image along the cisternal CN VII (D). Coronal oblique reformatted contrast-enhanced T1-weighted image (E). Note contact between an AICA loop and the presumed TZ of CN VII (white arrows), which is slightly indented. There is a second contact between the AICA and the more distal CN VII (arrowheads). Black arrows point to CN VII. NVCS due to the AICA loop impinging on the TZ was confirmed surgically. After the operation, symptoms disappeared.

Fig 9.

NVC in a 70-year-old man with tinnitus and vertigo. A, Axial oblique reformatted T2-weighted image (0.5 mm). Coronal oblique T2-weighted images (0.5 mm; B, anterior section; C, posterior section). Note the tortuous AICA (arrows) displacing and indenting the cochlear nerve (B) and the vestibular nerve (C). Brain and temporal bone MR imaging and high-resolution temporal bone CT findings were otherwise normal.

Fig 10.

GN caused by a tortuous vertebral artery in a 64-year-old man. Axial T2-weighted (A), fused T2-weighted and TOF (B) images, and contrast-enhanced 3D T1 gradient recalled-echo image (C) show displacement and contact between CN IX (long arrows) and a tortuous vertebral artery (short arrows). Note that in B, 2 contact points are seen, 1 proximal and 1 more distal. Black arrows point to the contralateral IX–X nerve complex. Findings were confirmed surgically.

Fig 11.

Left invalidating GN caused by a posterior inferior cerebellar artery (PICA) loop in an 80-year-old otherwise healthy female patient. Fusion of 3D T2 and TOF angiography sequences (A, axial; B, coronal oblique) reveals displacement of CN IX (white arrows) and contact between the TZ of CN IX and the left PICA (arrowheads). Right CN IX is indicated by a black arrowhead.

Fig 12.

Schematic illustration of the cisternal length and location of the transition zone for CN V, VII, VIII, and IX.