會議議程

Executive Summary：
Yen-Feng Wang obtained his MD degree from National Yang-Ming University School of Medicine, Taiwan, and completed his neurology residency training in the Department of Neurology, Taipei Veterans General Hospital. He did his fellowship training in headache medicine with Professors Shuu-Jiun Wang and Jong-Ling Fuh, and earned his PhD degree from the Institute of Clinical Medicine, National Yang-Ming University. He is currently an attending physician and the Section Chief of the Division of General Neurology of the Department of Neurology, Taipei Veterans General Hospital, and also a professor of neurology of College of Medicine, National Yang Ming Chiao Tung University. His major research interests focus on the clinical and neuroimaging aspects of headache and pain disorders.

Lecture Abstract：
OnabotulinumtoxinA (onabotA) is indicated for preventive treatment of chronic migraine (CM) across different guidelines, treatment recommendations, and reimbursement regulations. efficacy is anchored in pooled PREEMPT 1/2 data showing clinically meaningful reductions in headache outcomes and responder rates over time, with attention to temporal response across repeated cycles and the standardized injection paradigm: fixed-site, fixed-dose 155 U, with optional “follow-the-pain” add-ons up to a total of 195 U. Treatment-emergent adverse events are typically local and transient, with low serious-event signals. For episodic migraine (EM), in the PRELCUDE randomized study (6–14 monthly migraine days), all arms improved from baseline, but active onabotA doses did not significantly outperform placebo, likely influenced by a high placebo (injectable) response, CM-specific sensitization, etc. Therefore, onabotA injection remains a proven first-line therapy for CM rather than EM. Long-term effectiveness in CM was proven through 1-, 5-, and 11-year studies, showing sustained reductions in monthly headache days, improved quality-of-life/disability metrics, and durable reductions in acute medication overuse with continued treatment. Comparative real-world studies suggest CGRP mAbs may result in larger short-term improvements and better retention, while onabotA remains effective and may still benefit a subset after CGRP mAb failure, consistent with distinct biological targets (C-fiber vs trigeminal ganglion signaling). Studies focusing on pregnancy outcomes did not show higher risk for those who were treated with onabotA, although relapse could ensue after discontinuation. Therefore, the clinical decisions should be based on weighing the benefits over potential risks.

Executive Summary：
Dr. Fu-Chi Yang is Professor and Chair of Neurology at Tri-Service General Hospital, National Defense Medical University (Taipei, Taiwan). He serves on the Board of the Taiwan Headache Society and is an International Headache Society–certified Headache Master. Dr. Yang received his M.D. from the National Defense Medical University and completed neurology training at Tri-Service General Hospital. He earned his Ph.D. in Brain Science from National Yang Ming University and furthered his academic training as a Visiting Professor at the University of California, Los Angeles.
With leadership experience in national professional societies—including Deputy Secretary General of the Taiwan Neurological Society—and institutional appointments spanning clinical neurology and precision medicine, Dr. Yang integrates patient-centered care with translational research. His research focuses on neuroimaging, genetics, and biomarker discovery, with particular emphasis on headache and cognitive disorders. His scholarly contributions include numerous publications in peer-reviewed international journals and book chapters. Clinically, Dr. Yang specializes in advanced migraine therapeutics, including CGRP-targeted treatments and botulinum toxin injections, as well as cognitive and cerebrovascular disorders. Board-certified in neurology and critical care medicine, Dr. Yang is committed to advancing mechanism-based understanding and evidence-driven care in headache and cognitive disorders.

Lecture Abstract：
Migraine is a highly prevalent and disabling neurological disorder with a pronounced female predominance, reflecting complex interactions among genetic susceptibility, brain network excitability, and neurovascular–neuroimmune mechanisms. This presentation reviews contemporary migraine biology, emphasizing the calcitonin gene-related peptide (CGRP) pathway—a key mediator within the trigeminovascular system and a validated therapeutic target. We summarize the evolution of acute management from triptans, analgesics, and nonsteroidal anti-inflammatory drugs to modern preventive strategies, including onabotulinumtoxinA and CGRP-targeted therapies.
We provide a focused update on CGRP-pathway treatments, encompassing monoclonal antibodies and small-molecule CGRP receptor antagonists (gepants), which offer clinically meaningful reductions in attack frequency and disability, particularly for patients with inadequate response or intolerance to conventional options. Sex-related considerations are highlighted: hormonal instability—especially estrogen withdrawal—contributes to heightened susceptibility in many women, and emerging translational evidence implicates sex-dependent signaling in migraine-relevant pathways, including prolactin-related mechanisms. Because men remain underrepresented in many CGRP trials, definitive sex-stratified conclusions are limited. Taken together, a personalized approach—integrating sex-specific risk factors, comorbidities, and patient preferences—is essential when selecting CGRP-based therapy.

Executive Summary：
Dr. Chen is a physician-scientist who graduated from the School of Medicine and Institute of Clinical Medicine at National Yang-Ming University in Taiwan. His career path led him through a comprehensive neurology resident training program at the Department of Neurology, Taipei Veterans General Hospital, followed by post-doctoral fellowship training at the Neurovascular Research Lab, Massachusetts General Hospital, Harvard Medical School. He currently serves as an attending physician at Department of Medical Research and an adjunct attending neurologist at the Neurological Institute of Taipei Veterans General Hospital. He is dedicated to unraveling the intricate pathophysiology of headache and neurovascular disorders using directional translational approach encompassing clinical, neuroimaging, genetics, and preclinical animal studies. He has authored over 160 research articles, including those from esteemed journals such as JAMA Neurology, Brain, Annals of Neurology, and Neurology, etc. He currently also serves as an Associate Editor of The Journal of Headache and Pain and is a board member of the Science and Research Committee in the International Headache Society.

Lecture Abstract：
Migraine aura is a transient neurological syndrome that occurs in approximately one-third of individuals with migraine. While classically defined by visual disturbances such as scintillating scotoma or fortification spectra, aura encompasses a broader range of cortical symptoms, including sensory, language, and, less commonly, motor manifestations. These symptoms typically evolve over minutes and resolve within an hour, reflecting a dynamic process within the cerebral cortex.
Clinically, migraine aura is highly heterogeneous. Variations include atypical aura, prolonged aura, and aura without headache, all of which may pose diagnostic challenges and overlap with other neurological conditions. Additionally, it has been associated with an increased risk of ischemic stroke, particularly in younger individuals and women with additional vascular risk factors. Cortical spreading depression (or depolarization) (CSD) is considered the neurobiological substrate of aura, based on evidence from electrophysiology, neuroimaging, and human experimental models. This phenomenon accounts for the gradual progression and topographic nature of aura symptoms. Advances in neuroimaging and electrophysiology have provided strong support for CSD as the biological substrate of aura, linking clinical phenomenology with underlying cortical dynamics. CSD may also cause trigeminovascular activation, which clinically manifest as migraine headache, via a cascade of cortico-meningeal inflammatory processes.
By demystifying migraine aura, this talk aims to bridge fundamental mechanisms with clinical practice, offering an in-depth understanding of this intriguing neurological phenomenon.