Headache and Pain Research

Review Article

Trigeminal Neuralgia: Pathophysiology, Clinical Features, and Therapeutic Management: Ekene Nnagha, Chidubem Adi, Daniel Akpan; Received January 27, 2026 Accepted March 17, 2026 Published online June 4, 2026; DOI: https://doi.org/10.62087/hpr.2026.0005 [Epub ahead of print]

Abstract PDF: Trigeminal neuralgia (TN) is a severe, disabling neuropathic facial pain disorder classified among cranial neuralgias within headache medicine. Despite well-established diagnostic criteria, TN remains frequently misdiagnosed, particularly in dental and primary care settings. This review provides a clinically focused overview of the epidemiology, pathophysiology, classification, diagnostic approach, and contemporary management of TN, with relevance to headache and pain research and clinical practice. Neurovascular compression with focal demyelination at the trigeminal nerve root entry zone is considered the predominant mechanism in classical TN. Diagnosis is primarily clinical and guided by International Classification of Headache Disorders, 3rd edition criteria, with magnetic resonance imaging essential for excluding secondary and idiopathic causes. Carbamazepine and oxcarbazepine remain first-line therapies, whereas microvascular decompression and minimally invasive neurosurgical procedures provide effective options for medically refractory disease. TN requires accurate diagnosis and individualized management. Advances in pharmacological and interventional treatments have improved outcomes and underscore the importance of multidisciplinary care within headache and pain medicine.

Case Report

Isolated Dental and Lower-Facial Pain Mimicking Trigeminal Neuropathy: An Indirect Carotid-Cavernous Fistula: Byoungchul Choi, Chulho Kim, Sung-Hwan Kim, Jong-Hee Sohn; Headache Pain Res. 2025;26(3):226-231. Published online October 22, 2025; DOI: https://doi.org/10.62087/hpr.2025.0020

Abstract PDF: Carotid-cavernous fistula (CCF) is a pathological arteriovenous communication in which carotid arterial flow is diverted into the cavernous sinus. Clinical manifestations typically include ocular signs, cranial neuropathies, and headache. Neurologic deficits most commonly reflect involvement of cranial nerves III, IV, V1/V2, and VI within or along the cavernous sinus; in contrast, isolated trigeminal presentations are rare, and V3 involvement is particularly uncommon. A 69-year-old woman presented with isolated V2/V3-territory pain, perceived as molar, gingival, and lower facial discomfort. Her symptoms were initially misattributed to trigeminal neuropathy or dental pathology. Subsequently, she developed horizontal diplopia, and bedside testing localized a right abducens palsy. Brain magnetic resonance imaging revealed findings suspicious for a CCF, which was angiographically confirmed as an indirect CCF. Following embolization, the patient’s pain markedly improved, implicating the CCF as the source of the V2/V3 symptoms. This case highlights that an atypical, trigeminal-predominant onset—even with pain limited to the V2/V3 distribution—may indicate an indirect CCF. When atypical trigeminal neuropathy is suspected and dental or other peripheral causes are excluded, clinicians should consider the possibility of a CCF.

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