Trigeminal autonomic cephalalgias: current insights into pathophysiology, diagnosis and therapeutic strategies
Marina Alejandra Olivier1,2, Margareth Alexandra Contreras Martínez3, Carlos Andrés Díaz Garza4, Javier Andrés Galnares Olalde4, Adolfo Leyva Rendon4, Paula Alexandra Martínez Corredor5, Verónica Lourdes Molina6, María Celeste Rada Fernández7, María Soledad Smechow8, Osvaldo Carlos Jesús Bruera9
1Headache unit, La Fe University and Polytechnic Hospital, Valencia, Spain
2La Fe Health Research Institute, Valencia, Spain
3Neurologist, Duitama Regional Hospital, Boyaca, Colombia
4Headache Clinic, Manuel Velasco Suárez National Institute of Neurology and Neurosurgery, México
5Favaloro Foundation University Hospital, Buenos Aires (CABA), Argentina
6José de San Martín Clinical Hospital, Buenos Aires (CABA), Argentina
7Señor del Milagro Hospital, Salta, Argentina
8CEINSA Comprehensive Neurological Center and Julio de Vedia Hospital, 9 de Julio, Buenos Aires Province, Argentina
9Head of the Headache and Pain Department at the Buenos Aires Institute of Neurosciences “INEBA”, Buenos Aires, Argentina
Introduction
Trigeminal autonomic cephalalgias (TAC) are primary headache disorders
characterized by unilateral craniofacial pain, usually periorbital or temporal,
accompanied by ipsilateral autonomic symptoms such as tearing, nasal congestion,
conjunctival injection, miosis, and ptosis. They include cluster headache, paroxysmal
hemicrania, hemicrania continua, and short-lasting unilateral neuralgiform
headache attacks (SUNCT and SUNA). Diagnosis depends on attack duration,
frequency, and intensity, though clinical overlap may occur. Accurate identification is
crucial, as treatment differs among subtypes. Understanding TAC pathophysiology,
particularly trigeminal autonomic activation, is essential for improving diagnosis,
distinguishing them from similar disorders like migraine, and optimizing therapeutic
management.
Results
Trigeminal autonomic cephalalgias represent a group of rare but disabling
primary headache disorders characterized by overlapping pathophysiological
pathways involving the hypothalamus and trigemino-autonomic reflex. Advances in
neuroimaging and neuromodulation have refined understanding of their mechanisms
and expanded therapeutic options beyond traditional pharmacotherapy. Early
recognition and tailored, mechanism-based interventions remain essential to
improving outcomes.
Conclusions
We believe it is very important and necessary to offer a comprehensive and up-todate
review of trigeminal autonomic headaches, emphasizing their common and
distinctive clinical features, the underlying neurobiological mechanisms, and current
evidence-based approaches for timely diagnosis and treatment.