Pathology of the Trigeminal Nerve

Becker, Minerva; Köhler, R; Vargas, Maria Isabel; Viallon, Magalie; Delavelle, J.

doi:10.1016/j.nic.2007.11.002

Cited by 57 publications

(61 citation statements)

References 44 publications

(77 reference statements)

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“…[12][13][14][15][16] This combination can successfully guide neurosurgical treatment and may predict treatment response. [17][18][19] A variety of high-resolution 3D heavily T2-weighted sequences is currently available, including CISS; FIESTA; balanced steady-state free precession; driven equilibrium and radiofrequency reset pulse; and sampling perfection with application-optimized contrasts by using different flip angle evolution (SPACE sequence; Siemens, Erlangen, Germany), providing accurate visualization of the cisternal portion of the involved CN.…”

Section: Imaging Recommendationsmentioning

confidence: 99%

“…More recently, diffusion tensor imaging with tractography has been increasingly used, mainly in trigeminal neuralgia. 15,20,21 Trigeminal Nerve (CN V) Anatomic Considerations. CN V is a mixed nerve responsible for the sensory innervation of the face and motor functions of the masticatory muscles and tensor veli palatine muscle.…”

Section: Imaging Recommendationsmentioning

confidence: 99%

“…5 Both the superior cerebellar artery and AICA usually compress the nerve in its superomedial portion (60%) (Fig 3). 5 Less often, CN V is compressed by the basilar and vertebral arteries, 15,16 by a saccular aneurysm, a persistent trigeminal artery, an arteriovenous malformation, 27,28 or a petrous vein (Figs 4 and 5). A small cerebellopontine angle cistern appears to predispose to NVCS.…”

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confidence: 99%

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Imaging of Neurovascular Compression Syndromes: Trigeminal Neuralgia, Hemifacial Spasm, Vestibular Paroxysmia, and Glossopharyngeal Neuralgia

Haller

Etienne

Kovari

et al. 2016

American Journal of Neuroradiology

181

104

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SUMMARY: Neurovascular compression syndromes are usually caused by arteries that directly contact the cisternal portion of a cranial nerve. Not all cases of neurovascular contact are clinically symptomatic. The transition zone between the central and peripheral myelin is the most vulnerable region for symptomatic neurovascular compression syndromes. 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. 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. 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. 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. 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. 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. ABBREVIATIONS:AICA ϭ anterior inferior cerebellar artery; CN ϭ cranial nerve; GN ϭ glossopharyngeal neuralgia; HFS ϭ hemifacial spasm; NVC ϭ neurovascular

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Section: Imaging Recommendationsmentioning

confidence: 99%

Section: Imaging Recommendationsmentioning

confidence: 99%

mentioning

confidence: 99%

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Imaging of Neurovascular Compression Syndromes: Trigeminal Neuralgia, Hemifacial Spasm, Vestibular Paroxysmia, and Glossopharyngeal Neuralgia

Haller

Etienne

Kovari

et al. 2016

American Journal of Neuroradiology

181

104

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“…More recently, among the MR sequences, the diffusion-tensor imaging with tractography can allow the analysis of white matter integrity from the V nerve by measuring in vivo the molecular diffusivity (9,22,28,33). This sequence practically assesses the damage and degeneration of white matter tracts appearing as a consequence of the loss of myelin and axonal membranes at the level of the neurons composing the V nerve (7,38).…”

Section: Imagingmentioning

confidence: 99%

To be or not to be a neurovascular conflict: importance of the preoperative identification of the neurovascular conflict in the trigeminal neuralgia

Turliuc¹,

Dobrovăț²,

Cucu³

et al. 2016

Romanian Neurosurgery

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“…ZMC-fractured patients may have various presentations, such as soft tissue swelling, edema, ecchymosis, cheek numbness, trismus, diplopia, and epistaxis, depending on the associated injuries. In addition to these, ear-associated problems such as sudden hearing loss [5][6][7], tinnitus [8,9], trigeminal neuralgia [10,11], and vertigo [12,13] have also been reported.…”

Section: Introductionmentioning

confidence: 99%

Risk of Ear-Associated Diseases After Zygomaticomaxillary Complex Fracture

Yang

Tai

Chien

et al. 2015

J. Maxillofac. Oral Surg.

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Purpose Investigate the risk of ear-associated diseases after zygomaticomaxillary complex (ZMC) fracture in a population-based retrospective cohort study. Materials and Methods This is a retrospective cohort study using Taiwan's National Health Insurance Research Database of reimbursement claims. A total of 1,330 ZMC fracture patients and 5,320 non-ZMC fracture participants were included and newly developed ear-associated disease data were collected. A Poisson regression and multivariate Cox proportion hazard regression were used for data analysis. Results The ZMC fracture cohort had a higher incidence of tinnitus than non-ZMC fracture cohort (IRR 1.64, 95 % CI 1.37-1.96), particularly in younger patients (B34 years of age; IRR 4.05, 95 % CI 3.18-5.15) and male patients (IRR 2.08, 95 % CI 1.12-3.73). ZMC fracture patients also showed a significantly increased risk of having trigeminal neuralgia [IRR 4.06, 95 % CI 3.34-4.94, adjusted HR 4.07 (1.02-16.3)]. For sudden hearing loss and peripheral vertigo, the incidence densities were higher in the ZMC fracture cohort, but these relationships were not significant in the multivariate Cox proportional hazard regression analyses (HR 2.69, 95 % CI 0.76-9.53 for risk of sudden hearing loss; HR 1.36, 95 % CI 0.77-2.40 for risk of peripheral vertigo). Conclusions The findings of the study suggest an increased risk of ear-associated diseases among individuals with ZMC fractures, particularly within 2-years follow-ups after injury. We suggest performing detailed examinations for ear-associated diseases in patients with ZMC fractures for early diagnosis and adequate treatment.Chao-Chih Yang and Chih-Jaan Tai have contributed equally to this work.

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Pathology of the Trigeminal Nerve

Cited by 57 publications

References 44 publications

Imaging of Neurovascular Compression Syndromes: Trigeminal Neuralgia, Hemifacial Spasm, Vestibular Paroxysmia, and Glossopharyngeal Neuralgia

Imaging of Neurovascular Compression Syndromes: Trigeminal Neuralgia, Hemifacial Spasm, Vestibular Paroxysmia, and Glossopharyngeal Neuralgia

To be or not to be a neurovascular conflict: importance of the preoperative identification of the neurovascular conflict in the trigeminal neuralgia

Risk of Ear-Associated Diseases After Zygomaticomaxillary Complex Fracture

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