Trigeminal neuralgia: An overview from pathophysiology to pharmacological treatments

Abstract

The trigeminal nerve (V) is the fifth and largest of all cranial nerves, and it is responsible for detecting sensory stimuli that arise from the craniofacial area. The nerve is divided into three branches: ophthalmic (V1), maxillary (V2), and mandibular (V3); their cell bodies are located in the trigeminal ganglia and they make connections with second-order neurons in the trigeminal brainstem sensory nuclear complex. Ascending projections via the trigeminothalamic tract transmit information to the thalamus and other brain regions responsible for interpreting sensory information. One of the most common forms of craniofacial pain is trigeminal neuralgia. Trigeminal neuralgia is characterized by sudden, brief, and excruciating facial pain attacks in one or more of the V branches, leading to a severe reduction in the quality of life of affected patients. Trigeminal neuralgia etiology can be classified into idiopathic, classic, and secondary. Classic trigeminal neuralgia is associated with neurovascular compression in the trigeminal root entry zone, which can lead to demyelination and a dysregulation of voltage-gated sodium channel expression in the membrane. These alterations may be responsible for pain attacks in trigeminal neuralgia patients. The antiepileptic drugs carbamazepine and oxcarbazepine are the first-line pharmacological treatment for trigeminal neuralgia. Their mechanism of action is a modulation of voltage-gated sodium channels, leading to a decrease in neuronal activity. Although carbamazepine and oxcarbazepine are the first-line treatment, other drugs may be useful for pain control in trigeminal neuralgia. Among them, the anticonvulsants gabapentin, pregabalin, lamotrigine and phenytoin, baclofen, and botulinum toxin type A can be coadministered with carbamazepine or oxcarbazepine for a synergistic approach. New pharmacological alternatives are being explored such as the active metabolite of oxcarbazepine, eslicarbazepine, and the new Nav1.7 blocker vixotrigine. The pharmacological profiles of these drugs are addressed in this review.

Chronic Facial Pain: Trigeminal Neuralgia, Persistent Idiopathic Facial Pain, and Myofascial Pain Syndrome—An Evidence-Based Narrative Review and Etiological Hypothesis

“…Additional therapeutic approaches include interventions such as percutaneous rhizotomy, radiofrequency thermocoagulation, balloon compression, botulinum toxin, gamma knife radiosurgery, and microvascular decompression. Today, there is a rather large number of potential pharmacologic and interventional therapies for TN [ 40 ]. Even so, initial treatment of TN is usually pharmacologic, even for secondary TN, utilizing anticonvulsant medications.…”

“…There is low quality evidence for the use of other anticonvulsant drugs such as lamotrigine and gabapentin [ 38 ]. Newer pharmaceuticals such as eslicarbazepine, an active metabolite of oxcarbazepine, and an Nav1.7 channel blocker vixotrigine, are being evaluated as treatments [ 40 ].…”

Trigeminal Neuralgia Induced Headache: A Case Report and Literature Review

“…Inflammation is usually caused by an infection, and compression of trigeminal results from the blood vessel or tumor. Trigeminal neuralgia also has an association with multiple sclerosis and inflammatory or autoimmune conditions [8]. Any trigger such as a light stimulus to the region supplied by the trigeminal nerve may lead to the onset of symptoms.…”

Schwann cells and trigeminal neuralgia

“…Myelin removal can reduce compression injury during nerve regeneration and eliminates potential myelin regeneration inhibitors 15 . However, demyelination inevitably causes TN 36 .…”