Trigeminal neuralgia: assessment and management by oral and maxillofacial surgeons in the United Kingdom

Functional and sensory evaluation of patients with idiopathic trigeminal neuralgia: Comparison with controls

“…The etiology is still unclear, and the neurovascular conflict is often associated [4]. Abnormal expression of voltage-dependent sodium channels (Nav1.7 and Nav1.3) has been described [4], and immune-glial pathophysiological mechanisms may be involved [5,6].…”

Cervicofacial pain associated with Eagle’s syndrome misdiagnosed as trigeminal neuralgia

“…Most other anti-epileptic drugs used in trigeminal neuralgia are less effective and are best considered either in addition to carbamazepine or as an option when it cannot be used because of side effects or allergy. The drug combinations that are most effective have not been established, and there is little evidence to recommend one over another [11]. Analgesics such as aspirin and ibuprofen are generally not effective against trigeminal neuralgia and anticonvulsants are commonly used in the treatment, with good results, different form elongation of styloid process [12].…”

Florid cemento-osseous dysplasia as a possible aggravating factor in a case of trigeminal neuralgia.

“…Trigeminal neuralgia is a neuropathic condition characterized by unilateral short-lasting, lancinating, electric-shock-type pain that arises from one or more branches of the trigeminal nerve (2,3). The precise mechanism underlying this pain disorder remains unclear (4).…”

“…Among the numerous theories put forth (1)(2)(3)(4), the microvascular compression aetiological concept is the most widely accepted. Accordingly, vascular compression of nerve roots by tortuous vessels causes segmental demyelination of the affected nerve which in turn leads to nonsynaptic or ephaptic transmission of nerve impulses (2)(3)(4)(5). Clinically, trigger points and innocuous triggering stimuli such as touch, chewing, talking may be identified.…”

“…Clinically, trigger points and innocuous triggering stimuli such as touch, chewing, talking may be identified. Current diagnostic criteria recognized two distinct subsets of trigeminal neuralgia: classical/ idiopathic/primary form which accounts for vast majority of trigeminal neuralgia and symptomatic/ secondary variant which occurs secondary to microvascular compression, intracranial tumours or multiple sclerosis (2)(3)(4). A third form unrecognized by current classification is atypical trigeminal neuralgia which accounts for up to a third of these cases.…”