![]() ![]() 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. If you think you may have a medical emergency, call your physician or 911 immediately.SUMMARY: Neurovascular compression syndromes are usually caused by arteries that directly contact the cisternal portion of a cranial nerve. By using this Site you agree to the following Terms and Conditions. We offer this Site AS IS and without any warranties. Never disregard the medical advice of your physician or health professional, or delay in seeking such advice, because of something you read on this Site. We disclaim all responsibility for the professional qualifications and licensing of, and services provided by, any physician or other health providers posting on or otherwise referred to on this Site and/or any Third Party Site. MedHelp is not a medical or healthcare provider and your use of this Site does not create a doctor / patient relationship. It is not intended to be and should not be interpreted as medical advice or a diagnosis of any health or fitness problem, condition or disease or a recommendation for a specific test, doctor, care provider, procedure, treatment plan, product, or course of action. The Content on this Site is presented in a summary fashion, and is intended to be used for educational and entertainment purposes only. ![]()
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