Not all cases of neurovascular contact are clinically symptomatic. Presentation can be extremely variable depending on which structure is compressed. It can range from trigeminal neuralgia or glossopharyngeal neuralgia (somatic sensory), hemifacial spasm (somatic motor), tinnitus and vertigo (special sensory) and some cases of essential hypertension.
They are typically caused by arteries that directly contact the cisternal portion of a cranial nerve. The transition zone between the central and peripheral myelin is considered the most vulnerable region for symptomatic neurovascular compression syndromes.
- 1. Wilkins RH. Neurovascular compression syndromes. (1985) Neurologic clinics. 3 (2): 359-72. Pubmed
- 2. Castiglione M, Broggi M, Cordella R, Acerbi F, Ferroli P. Immediate disappearance of hemifacial spasm after partial removal of ponto-medullary junction anaplastic astrocytoma: case report. (2015) Neurosurgical review. 38 (2): 385-90; discussion 390. doi:10.1007/s10143-014-0586-y - Pubmed
- 3. Ryu H, Yamamoto S, Sugiyama K, Uemura K, Miyamoto T. Hemifacial spasm caused by vascular compression of the distal portion of the facial nerve. Report of seven cases. (1998) Journal of neurosurgery. 88 (3): 605-9. doi:10.3171/jns.1998.88.3.0605 - Pubmed
- 4. Haller S, Etienne L, Kövari E, Varoquaux AD, Urbach H, Becker M. Imaging of Neurovascular Compression Syndromes: Trigeminal Neuralgia, Hemifacial Spasm, Vestibular Paroxysmia, and Glossopharyngeal Neuralgia. (2016) AJNR. American journal of neuroradiology. 37 (8): 1384-92. doi:10.3174/ajnr.A4683 - Pubmed
- 5. Jannetta PJ. Neurovascular compression in cranial nerve and systemic disease. (1980) Annals of surgery. 192 (4): 518-25. Pubmed