Vascular compression in hemifacial spasm [Neurosurgery Wiki]

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====== Vascular compression in hemifacial spasm ======

[[Hemifacial spasm]] (HFS) is usually caused by compression of the [[facial nerve]] at the [[root exit zone]] (REZ) by a vessel, which is most often an artery (most commonly [[AICA]] (either pre- or postmeatal), but other vascular possibilities include an elongated [[PICA]], [[SCA]], a tortuous [[VA]], the [[cochlear artery]], a dolichoectatic [[basilar artery]], AICA branches…), aneurysm, a vascular malformation, and rarely, veins have been implicated.

In typical HFS (onset in the orbicularis oculi, and progressing downward over the face), the vessel impinges on the antero-caudal aspect of the VII/VIII nerve complex; in atypical HFS (beginning in the buccal muscles and progressing upward over the face), the compression is rostral or posterior to VII.

Vessels contacting the REZ of the vestibular nerve may cause vertigo, whereas tinnitus or hearing
loss may result from cochlear nerve REZ compression.

Infrequently, benign tumors or a cyst in the cerebellopontine angle, multiple sclerosis, adhesions,
or osseous skull deformities will be the cause of HFS.

Evidence indicates that there is not cross (ephaptic) conduction at the compressed REZ, but that
the facial motonucleus is involved secondarily as a result of the REZ compression, via a phenomenon
similar to kindling. In addition to the spasm, a 2nd electrophysiological phenomenon associated with HFS is synkinesis, where stimulation of one branch of the facial nerve results in delayed discharges
through another branch (average latency: 11 mSec160).
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[[Hemifacial spasm]] is usually caused by arterial compression at the [[root exit zone]] of the [[facial nerve]]. However, other etiologies have been reported. 

Purely venous compression is rarely encountered. 
El Refaee et al. reported for the very first time arachnoid bands strangulating the nerve as a cause for hemifacial spasm without involvement of any vessel
((El Refaee E, Marx S, Rosenstengel C, Baldauf J, Schroeder HWS. Arachnoid bands
and venous compression as rare causes of hemifacial spasm: analysis of etiology
in 353 patients. Acta Neurochir (Wien). 2019 Nov 21. doi:
10.1007/s00701-019-04119-5. [Epub ahead of print] PubMed PMID: 31754846.
)).
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Imaging data of 341 patients with a HFS who underwent [[microvascular decompression]] were reviewed retrospectively and compared with 360 controls. The [[hemodynamic]]s of typical anatomical variations of the [[vertebral artery]] (VA) were analyzed using [[computational fluid dynamics]] (CFD) software.

Asymmetry of the left and right VAs was prevalent, and the left VA was the most dominant VA. A dominant VA was more prevalent in the HFS group than in the control group (p=0.026). A Left HFS had a significantly higher proportion of a left dominant VA, and a right HFS had a significantly higher proportion of right dominant VA (p<0.001). CFD models showed that angulation and tortuosity of vessels caused remarkable pressure difference between vascular walls of opposite sides. Dynamic clinical observations showed the mode of vessel transposition coincided with biomechanical characteristics.

Anatomical variations and hemodynamics of the vertebrobasilar arterial system are likely to contribute to vascular compression formation in a HFS
((Wang QP, Yuan Y, Xiong NX, Fu P, Huang T, Yang B, Liu J, Chu X, Zhao HY.
Anatomical variation and hemodynamic evolution of vertebrobasilar arterial system
may contribute to the development of vascular compression in hemifacial spasm.
World Neurosurg. 2018 Dec 26. pii: S1878-8750(18)32897-3. doi:
10.1016/j.wneu.2018.12.074. [Epub ahead of print] PubMed PMID: 30593967.
)).