In the current article, we, therefore, focus on the TZ.Įxact anatomic knowledge of the position and morphology of the TZ is of fundamental importance for the interpretation of neuroimaging findings in suspected NVCS ( Fig 1). For example, in the vestibulocochlear nerve (CN VIII), the TZ is clearly distal to the REZ. 8 The TZ appears to be the more relevant and vulnerable anatomic structure, and it is not always located in the same position as the REZ. 10 In some publications, the term “REZ” is used as a synonym for TZ, whereas in other publications, the term “REZ” is used to define the portion of the nerve that includes the TZ, the central myelin root portion, and the adjacent brain stem surface 11 the 2 terms should, therefore, not be used interchangeably. The term “root entry/exit zone” (REZ) is often used in the context of NVCS. 8 Skinner 9 already demonstrated in 1931 that the length and location of the TZ varies between cranial nerves, with CN VIII having a long and distal TZ in comparison with CNs V, VII, and IX. The transition zone (TZ) between central and peripheral myelin 7 is an anatomic area with increased mechanical vulnerability, which is of particular interest in the context of symptomatic NVCS. Oligodendrocytes form the myelin in the central nervous system, whereas Schwann cells form the myelin in the peripheral nervous system. 5, 6 Second, the anatomic location of the neurovascular contact can also be a relevant factor.Ĭranial nerves are surrounded by a myelin sheath, which provides insulating and metabolic support for the axon. First, arteries are more likely to cause symptomatic NVCS than veins, presumably due to the higher pressure and pulsatility. Because neurovascular contacts are frequent imaging findings in asymptomatic patients, several factors will determine whether a neurovascular contact may become symptomatic. 1 ⇓ ⇓ ⇓– 5 The most common neurovascular compression syndromes are trigeminal neuralgia (TN compression of CN V), hemifacial spasm (HFS CN VII), vestibulocochlear neuralgia (CN VIII), and glossopharyngeal neuralgia (GN CN IX). Neurovascular compression syndrome (NVCS) is defined as a direct contact with mechanical irritation of cranial nerves (CNs) by blood vessels. 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.ĪBBREVIATIONS: AICA anterior inferior cerebellar artery CN cranial nerve GN glossopharyngeal neuralgia HFS hemifacial spasm NVC neurovascular compression NVCS neurovascular compression syndrome REZ root entry/exit zone TN trigeminal neuralgia TZ transition zone 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. 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. 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. 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. 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. The transition zone between the central and peripheral myelin is the most vulnerable region for symptomatic neurovascular compression syndromes. Not all cases of neurovascular contact are clinically symptomatic. SUMMARY: Neurovascular compression syndromes are usually caused by arteries that directly contact the cisternal portion of a cranial nerve.
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