Neurovascular contact in trigeminal neuralgia

While selectively sectioning the pain fibers in trigeminal neuralgia (which usually lie posteriorly) of the trigeminal nerve via an occipital craniectomy Walter Edward Dandy, as quoted in Wilkins, noted that vascular compression of the trigeminal nerve at the pons was a frequent finding 1).

However some patients may present with clinically classical trigeminal neuralgiabut no vascular conflict on MRI or even at surgery. Several factors have been cited as alternative or supplementary factors that may cause neuralgia.

The vessel that most often causes TN is the superior cerebellar artery (SCA), other known offending vessels include the anterior inferior cerebellar artery(AICA) and the vertebrobasilar artery and vein.

Veins as the source of trigeminal neuralgias (TN) lead to controversies. Only a few studies have specifically dealt with venous implication in neurovascular conflicts (NVC).

A study shows the frequent implication of veins not only at TREZ but also at mid-cisternal portion and porus of Meckel cave 2).

Trigeminal neuralgia in pediatric patients is very rare. A case of typical trigeminal neuralgia in a child, demonstrating the pathogenesis of the neurovascular conflict due to subarachnoidal adhesions after meningoencephalitis was reported 3).


It is widely accepted that a neurovascular contact in the cisternal segment of the trigeminal nerve is the primary cause of classical trigeminal neuralgia 4). However, previous studies have cast doubt on this hypothesis because a neurovascular contact was reported to be prevalent on both the symptomatic and the asymptomatic side and therefore suggested that the severity of the neurovascular contact should be taken into account 5)6) 7). The previous studies were limited by small sample size, lack of blinding, MRI was done with low magnetic field strength or study populations were highly selected consisting only of patients from neurosurgical departments.

Grading the neurovascular contact in classical trigeminal neuralgia is scientifically and probably also clinically important. Findings demonstrate that neurovascular contact is highly prevalent on both the symptomatic and asymptomatic sides. Maarbjerg et al., demonstrated that severe neurovascular contact is involved in the aetiology of classical trigeminal neuralgia and that it is caused by arteries located in the root entry zone. Findings also indicate that in some patients with classical trigeminal neuralgia a neurovascular contact is not involved in the aetiology of the disease or may only be a contributing factor in combination with other unknown factors. The degree of neurovascular contact could thus be important when selecting patients for surgery 8).


Jani et al., from the University of Pittsburgh Medical Centerprospectively recruited 27 patients without facial pain who were undergoing microvascular decompression for hemifacial spasm and had undergone high-resolution preoperative MRINeurovascular contact/compression (NVC/C) by artery or vein was assessed both intraoperatively and by MRI, and was stratified into 3 types: simple contact, compression (indentation of the surface of the nerve), and deformity (deviation or distortion of the nerve).

Intraoperative evidence of NVC/C was detected in 23 patients. MRI evidence of NVC/C was detected in 18 patients, all of whom had intraoperative evidence of NVC/C. Thus, there were 5, or 28% more patients in whom NVC/C was detected intraoperatively than with MRI (Kappa = 0.52); contact was observed in 4 of these patients and compression in 1 patient. In patients where NVC/C was observed by both methods, there was agreement regarding the severity of contact/compression in 83% (15/18) of patients (Kappa = 0.47). No patients exhibited deformity of the nerve by imaging or intraoperatively.

There was moderate agreement between imaging and operative findings with respect to both the presence and severity of NVC/C 9).

References

1)

Wilkins RH: Historical perspectives, in Rovit RL, Murali R, Jannetta PJ (eds): Trigeminal Neuralgia. Baltimore: Williams & Wilkins, 1990, pp 1–25
2)

Dumot C, Sindou M. Trigeminal neuralgia due to neurovascular conflicts from venous origin: an anatomical-surgical study (consecutive series of 124 operated cases). Acta Neurochir (Wien). 2015 Jan 22. [Epub ahead of print] PubMed PMID: 25604274.
3)

Solth A, Veelken N, Gottschalk J, Goebell E, Pothmann R, Kremer P. Successful vascular decompression in an 11-year-old patient with trigeminal neuralgia. Childs Nerv Syst. 2008 Jun;24(6):763-6. doi: 10.1007/s00381-008-0581-0. Epub 2008 Feb 22. PubMed PMID: 18293001.
4)

Devor M, Amir R, Rappaport ZH. Pathophysiology of trigeminal neuralgia: the ignition hypothesis. Clin J Pain. 2002 Jan-Feb;18(1):4-13. Review. PubMed PMID: 11803297.
5)

Masur H, Papke K, Bongartz G, Vollbrecht K. The significance of three-dimensional MR-defined neurovascular compression for the pathogenesis of trigeminal neuralgia. J Neurol. 1995 Jan;242(2):93-8. PubMed PMID: 7707097.
6)

Anderson VC, Berryhill PC, Sandquist MA, Ciaverella DP, Nesbit GM, Burchiel KJ. High-resolution three-dimensional magnetic resonance angiography and three-dimensional spoiled gradient-recalled imaging in the evaluation of neurovascular compression in patients with trigeminal neuralgia: a double-blind pilot study, Neurosurgery , 2006, vol. 58 pg. 666-73
7)

Miller JP, Acar F, Hamilton BE, Burchiel KJ. Radiographic evaluation of trigeminal neurovascular compression in patients with and without trigeminal neuralgia, J Neurosurg , 2009a, vol. 110 pg. 627-632
8)

Maarbjerg S, Wolfram F, Gozalov A, Olesen J, Bendtsen L. Significance of neurovascular contact in classical trigeminal neuralgia. Brain. 2015 Feb;138(Pt 2):311-9. doi: 10.1093/brain/awu349. Epub 2014 Dec 24. PubMed PMID: 25541189.
9)

Jani RH, Hughes MA, Gold MS, Branstetter BF, Ligus ZE, Sekula RF Jr. Trigeminal Nerve Compression Without Trigeminal Neuralgia: Intraoperative vs Imaging Evidence. Neurosurgery. 2019 Jan 1;84(1):60-65. doi: 10.1093/neuros/nyx636. PubMed PMID: 29425330.

Decision Making in Neurovascular Disease

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Neurovascular medicine has emerged as an established, semi-independent subspecialty of neurology and neurosurgery. Decision Making in Neurovascular Disease focuses on the challenging process of determining the best approach for managing patients with intracranial atherosclerosis, carotid artery disease, stroke, aneurysms, arteriovenous malformations, arteriovenous fistulae, cavernous malformations, and hypervascular tumors. Leonardo Rangel-Castilla, Robert Spetzler, esteemed coauthors, and an impressive cadre of experts discuss highly divergent modalities including medical management, open cerebrovascular, endovascular, radiosurgery, and combined/multimodality alternatives.
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