Trigeminal Neuralgia
- PMID: 28375911
- DOI: 10.1212/CON.0000000000000451
Trigeminal Neuralgia
Abstract
Purpose of review: Although trigeminal neuralgia is well known to neurologists, recent developments in classification and clinical diagnosis, new MRI methods, and a debate about surgical options necessitate an update on the topic.
Recent findings: Currently, a worldwide controversy exists regarding the classification, diagnostic process, and surgical treatment of trigeminal neuralgia. This controversy has been caused on one side by the recognition that some 50% of patients with trigeminal neuralgia, apart from characteristic paroxysmal attacks, also have continuous pain in the same territory, which results in greater diagnostic difficulties and is associated with a lower response to medical and surgical treatments. In contrast, recent developments in MRI methods allow differentiation between a mere neurovascular contact and an effective compression of the trigeminal root by an anomalous vessel, which implies more difficulties in the choice of surgical treatment, with the indication for microvascular decompression becoming more restricted.
Summary: This article proposes that the diagnosis of trigeminal neuralgia, with or without concomitant continuous pain, must rely on clinical grounds only. Diagnostic tests are necessary to distinguish three etiologic categories: idiopathic trigeminal neuralgia (nothing is found), classic trigeminal neuralgia (an anomalous vessel produces morphologic changes of the trigeminal root near its entry into the pons), and secondary trigeminal neuralgia (due to major neurologic disease, such as multiple sclerosis or tumors at the cerebellopontine angle). Carbamazepine and oxcarbazepine (ie, voltage-gated, frequency-dependent sodium channel blockers) are still the first-choice medical treatment, although many patients experience significant side effects, and those with concomitant continuous pain respond less well to treatment. The development of sodium channel blockers that are selective for the sodium channel 1.7 (Nav1.7) receptor will hopefully help. Although all the surgical interventions (percutaneous ganglion lesions, gamma knife radiosurgery, and microvascular decompression) are very efficacious, precise MRI criteria for differentiating a real neurovascular compression from an irrelevant contact will be of benefit in better selecting patients for microvascular decompression.
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