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.

EANS Basic Spine Course

January 10, 2019 — January 11, 2019

LyonFrance

Message from Course Chairmen Prof. Torstein R. Meling and Prof. Cédric Barrey:

It is our pleasure to welcome you to the inaugural EANS Spinal Step II Hands-On Course in Lyon. The event will be held from January 10th – 11th 2019 and is organized in the Laboratoire d’Anatomie de la Faculté de Médecine de Lyon.

This dissection course is most suitable for neurosurgical residents in their last years of training as it will focus on the essential neurosurgical anatomy, the planning of surgical procedures, the handling of neurosurgical equipment, and the advanced neurosurgical spinal approaches.

This course will be limited to 24 participants.

Course dates: 10-11 January 2019

For more information please contact petra.koubova@eans.org.

Venue: Département Universitaire d’Anatomie, Faculté de Médecine Lyon Est, 8 avenue Rockefeller, 69373 Lyon Cedex 08

Curriculum: Participants will learn essential neurosurgical anatomy, planning of surgical procedures, handling of neurosurgical equipment, and advanced neurosurgical spinal approaches.

Preliminary programme available HERE.

Registration fees:
EANS Individual Member: €700
Non-Member: €800

The registration fee includes all tuition costs, subsitence during the course, two night accommodation and one networking event.

Accommodation:
Lagrange City Apparthotel
Lyon Lumiere
81-85, cours Albert Thomas
69003 LYON
France

View: The hotel website

NB: This is course is not part of the EUROSPINE equivalence programme. 

Neurologic Injury after Lateral Lumbar Interbody Fusion

Since the first description of LLIF in 2006, the indications for LLIF have expanded and the rate of LLIF procedures performed in the USA has increased. LLIF has several theoretical advantages compared to other approaches including the preservation of the anterior and posterior annular/ligamentous structures, insertion of wide cages resting on the dense apophyseal ring bilaterally, and augmentation of disc height with indirect decompression of neural elements. Favorable long-term outcomes and a reduced risk of visceral/vascular injuries, incidental dural tears, and perioperative infections have been reported. However, approach-related complications such as motor and sensory deficits remain a concern. In well-indicated patients, LLIF can be a safe procedure used for a variety of indications 1).

Hijji et al. published a systematic review analyzing the complication profile of LLIF. Their study included a total of 63 articles and 6819 patients. The most commonly reported complications were transient neurologic injury (36.07%). The clinical significance of those transient findings, however, is unclear since the rate of persistent neurologic complications was much lower (3.98%) 2)

The risk of lumbar plexus injury is particularly concerning at the L4-5 disc space. Although LLIF is associated with an increased prevalence of anterior thigh/groin pain as well as motor and sensory deficits immediately after surgery, our results support that pain and neurologic deficits decrease over time. The level treated appears to be a risk factor for lumbosacral plexus injury 3).

Interestingly, the use of rhBMP-2 was associated with higher rates of persistent motor deficits, which might be explained by a direct deleterious effect of this agent on the lumbosacral plexus 4).

In a retrospective chart review of 118 patients, Cahill et al. determined the incidence of femoral nerve injury, which is considered one of the worst neurological complications after LLIF. The authors reported an approximate 5% femoral nerve injury rate of all the LLIF procedures performed at L4-5. There were no femoral nerve injuries at any other levels 5).

During a 6-year time period of performing LLIF Aichmair et al., noted a learning curve with a decreasing proportional trend for anterior thigh pain, sensory as well as motor deficits 6)

Le et al. also observed a learning curve with a significant reduction in the incidence of postoperative thigh numbness during a 3-year period (from 26.1 to 10.7%) 7).

Levi AD from the University of Miami Hospital, adopted an exclusive mini-open muscle-splitting approach in LLIF with first-look inspection of the lumbosacral plexus nerve elements taht may improve motor and sensory outcomes in general and the incidence of postoperative groin/thighsensory dysfunction and psoas-pattern weakness in particular 8).

References

1)

Salzmann SN, Shue J, Hughes AP. Lateral Lumbar Interbody Fusion-Outcomes and Complications. Curr Rev Musculoskelet Med. 2017 Dec;10(4):539-546. doi: 10.1007/s12178-017-9444-1. Review. PubMed PMID: 29038952; PubMed Central PMCID: PMC5685966.
2)

Hijji FY, Narain AS, Bohl DD, Ahn J, Long WW, DiBattista JV, Kudaravalli KT, Singh K. Lateral lumbar interbody fusion: a systematic review of complication rates. Spine J. 2017 Oct;17(10):1412-1419. doi: 10.1016/j.spinee.2017.04.022. Epub 2017 Apr 26. Review. PubMed PMID: 28456671.
3)

Lykissas MG, Aichmair A, Hughes AP, Sama AA, Lebl DR, Taher F, Du JY, Cammisa FP, Girardi FP. Nerve injury after lateral lumbar interbody fusion: a review of 919 treated levels with identification of risk factors. Spine J. 2014 May 1;14(5):749-58. doi: 10.1016/j.spinee.2013.06.066. Epub 2013 Sep 5. PubMed PMID: 24012428.
4)

Lykissas MG, Aichmair A, Hughes AP, Sama AA, Lebl DR, Taher F, Du JY, Cammisa FP, Girardi FP. Nerve injury after lateral lumbar interbody fusion: a review of 919 treated levels with identification of risk factors. Spine J. 2014 May 1;14(5):749-58. doi: 10.1016/j.spinee.2013.06.066. Epub 2013 Sep 5. PubMed PMID: 24012428.
5)

Cahill KS, Martinez JL, Wang MY, Vanni S, Levi AD. Motor nerve injuries following the minimally invasive lateral transpsoas approach. J Neurosurg Spine. 2012 Sep;17(3):227-31. doi: 10.3171/2012.5.SPINE1288. Epub 2012 Jun 29. PubMed PMID: 22746272.
6)

Aichmair A, Lykissas MG, Girardi FP, Sama AA, Lebl DR, Taher F, Cammisa FP, Hughes AP. An institutional six-year trend analysis of the neurological outcome after lateral lumbar interbody fusion: a 6-year trend analysis of a single institution. Spine (Phila Pa 1976). 2013 Nov 1;38(23):E1483-90. doi: 10.1097/BRS.0b013e3182a3d1b4. PubMed PMID: 23873231.
7)

Le TV, Burkett CJ, Deukmedjian AR, Uribe JS. Postoperative lumbar plexus injury after lumbar retroperitoneal transpsoas minimally invasive lateral interbody fusion. Spine (Phila Pa 1976). 2013 Jan 1;38(1):E13-20. doi: 10.1097/BRS.0b013e318278417c. PubMed PMID: 23073358.
8)

Sellin JN, Brusko GD, Levi AD. Lateral Lumbar Interbody Fusion Revisited: Complication Avoidance and Outcomes with the Mini-Open Approach. World Neurosurg. 2019 Jan;121:e647-e653. doi: 10.1016/j.wneu.2018.09.180. Epub 2018 Oct 3. PubMed PMID: 30292030.
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