A dual concurrent mechanism explains trigeminal neuralgia in patients with multiple sclerosis

Truini, Andrea; Prosperini, Luca; Calistri, Valentina; Fiorelli, Marco; Pozzilli, Carlo; Millefiorini, Enrico; Frontoni, Marco; Cortese, Antonio; Caramia, Francesca; Cruccu, G.

doi:10.1212/wnl.0000000000002720

Cited by 91 publications

(95 citation statements)

References 32 publications

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“…It may be that both this specific transmembrane mutation and vascular compression must be present to develop HFS/TN in this family. A similar “double crush” mechanism has been proposed for multiple sclerosis associated TN, where most cases demonstrate both a pontine lesion and vascular compression of the trigeminal nerve …”

Section: Discussionmentioning

confidence: 72%

“…A similar "double crush" mechanism has been proposed for multiple sclerosis associated TN, where most cases demonstrate both a pontine lesion and vascular compression of the trigeminal nerve. 44 Supporting this theory is the family member (VI-20) with HFS but without the G163R mutation. Her HFS was apparently due to adjacent tortuous vessels, indicating that the MPZ mutation alone is not sufficient to cause HFS/TN but is acting as a strong risk factor for the trait.…”

Section: Discussionmentioning

confidence: 90%

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A charcot‐marie‐tooth type 1B kindred associated with hemifacial spasm and trigeminal neuralgia

Caress

Lewis²,

Pinyan

et al. 2019

Muscle and Nerve

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Introduction: Charcot‐Marie‐Tooth (CMT) phenotypes can be distinguished by electrophysiology and genetic analysis but few can be identified by their clinical characteristics. Distinctive phenotypes are useful in identifying affected individuals and providing additional clues about the mechanism of the neuropathy. Cranial neuropathies are uncommon features of CMT, and few reports of familial hemifacial spasm (HFS) and trigeminal neuralgia (TN) have been published. Methods: Sixty‐three members of a large CMT 1B kindred were assessed for signs of peripheral neuropathy and cranial neuropathies then tested for the G163R mutation in the myelin protein zero (MPZ) gene. Results: Of 27 individuals with the G163R mutation in MPZ, 10 had HFS or TN. Co‐existing HFS and TN were found in 3 of these and 4 had bilateral HFS or TN. Conclusions: This kindred exhibits a distinct CMT phenotype characterized by the development of HFS or TN decades after clinical signs of hereditary neuropathy are manifest. Muscle Nerve, 2019

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Section: Discussionmentioning

confidence: 72%

Section: Discussionmentioning

confidence: 90%

A charcot‐marie‐tooth type 1B kindred associated with hemifacial spasm and trigeminal neuralgia

Caress

Lewis²,

Pinyan

et al. 2019

Muscle and Nerve

View full text Add to dashboard Cite

show abstract

“…Papers studying the diagnostic accuracy of clinical characteristics for distinguishing primary from secondary TN were sought. In addition to the papers included in the previous guideline [6][7][8][9][10][11], two new papers were identified [12,13]. Involvement of the first trigeminal division and poor response to treatment were not significantly associated with secondary TN (Table 1).…”

Section: Search Strategy and Resultsmentioning

confidence: 99%

European Academy of Neurology guideline on trigeminal neuralgia

Bendtsen

Zakrzewska

Abbott

et al. 2019

Euro J of Neurology

439

492

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Background and purpose Trigeminal neuralgia (TN) is an extremely painful condition which can be difficult to diagnose and treat. In Europe, TN patients are managed by many different specialities. Therefore, there is a great need for comprehensive European guidelines for the management of TN. The European Academy of Neurology asked an expert panel to develop recommendations for a series of questions that are essential for daily clinical management of patients with TN. Methods A systematic review of the literature was performed and recommendations was developed based on GRADE, where feasible; if not, a good practice statement was given. Results The use of the most recent classification system is recommended, which diagnoses TN as primary TN, either classical or idiopathic depending on the degree of neurovascular contact, or as secondary TN caused by pathology other than neurovascular contact. Magnetic resonance imaging (MRI), using a combination of three high‐resolution sequences, should be performed as part of the work‐up in TN patients, because no clinical characteristics can exclude secondary TN. If MRI is not possible, trigeminal reflexes can be used. Neurovascular contact plays an important role in primary TN, but demonstration of a neurovascular contact should not be used to confirm the diagnosis of TN. Rather, it may help to decide if and when a patient should be referred for microvascular decompression. In acute exacerbations of pain, intravenous infusion of fosphenytoin or lidocaine can be used. For long‐term treatment, carbamazepine or oxcarbazepine are recommended as drugs of first choice. Lamotrigine, gabapentin, botulinum toxin type A, pregabalin, baclofen and phenytoin may be used either alone or as add‐on therapy. It is recommended that patients should be offered surgery if pain is not sufficiently controlled medically or if medical treatment is poorly tolerated. Microvascular decompression is recommended as first‐line surgery in patients with classical TN. No recommendation can be given for choice between any neuroablative treatments or between them and microvascular decompression in patients with idiopathic TN. Neuroablative treatments should be the preferred choice if MRI does not demonstrate any neurovascular contact. Treatment for patients with secondary TN should in general follow the same principles as for primary TN. In addition to medical and surgical management, it is recommended that patients are offered psychological and nursing support. Conclusions Compared with previous TN guidelines, there are important changes regarding diagnosis and imaging. These allow better characterization of patients and help in decision making regarding the planning of medical and surgical management. Recommendations on pharmacological and surgical management have been updated. There is a great need for future research on all aspects of TN, including pathophysiology and management.

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“…Interestingly, a recent imaging study found an association between TN and MS lesions not only in the pontine tri- geminal afferents but also in the contralateral insular region and hippocampus [21]. Finally, in some patients with MS-related TN, a demyelinating plaque and neurovascular compression coexist [22]. The treatment of TN differs from that of other neuropathic pain syndromes.…”

Section: Neuralgiasmentioning

confidence: 99%

Facial Pain: A Comprehensive Review and Proposal for a Pragmatic Diagnostic Approach

et al. 2020

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Background: Facial pain, alone or combined with other symptoms, is a frequent complaint. Moreover, it is a symptom situated at, more than any other pain condition, a crosspoint where several disciplines meet, for example, dentists; manual therapists; ophthalmologists; psychologists; and ear-nose-throat, pain, and internal medicine physicians besides neurologists and neurosurgeons. Recently, a new version of the most widely used classification system among neurologists for headache and facial pain, the International Classification of Headache Disorders, has been published. Objective: The aims of this study were to provide an overview of the most prevalent etiologies of facial pain and to provide a generic framework for the neurologist on how to manage patients presenting with facial pain. Methods: An overview of the different etiologies of facial pain is provided from the viewpoint of the respective clinical specialties that are confronted with facial pain. Key message: Caregivers should "think outside their own box" and refer to other disciplines when indicated. If not, a correct diagnosis can be delayed and unnecessary treatments might be given. The presented framework is aimed at excluding life-or organthreatening diseases, providing several clinical clues and indications for technical investigations, and ultimately leading to the correct diagnosis and/or referral to other disciplines.

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A dual concurrent mechanism explains trigeminal neuralgia in patients with multiple sclerosis

Abstract: Our observation that in many patients with MS-related TN a pontine demyelinating plaque and neurovascular compression coexist should prompt neurologists to seek possible neurovascular compression in patients with MS-related TN.

Cited by 91 publications

References 32 publications

A charcot‐marie‐tooth type 1B kindred associated with hemifacial spasm and trigeminal neuralgia

A charcot‐marie‐tooth type 1B kindred associated with hemifacial spasm and trigeminal neuralgia

European Academy of Neurology guideline on trigeminal neuralgia

Facial Pain: A Comprehensive Review and Proposal for a Pragmatic Diagnostic Approach

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