About this Research Topic
Migraine is among the most disabling forms of primary headache, endowed with a serious social impact and ranking as one of the top causes of years lived with disability worldwide, particularly in people under fifty.
It is characterized by recurrent attacks of moderate to severe throbbing and pulsating pain on one side of the head and untreated attacks last from four to 72 hours. Pain is caused by the activation of nerve fibers within the wall of brain blood vessels traveling inside the meninges. Other common symptoms include increased sensitivity to light, noise, odors, nausea, and vomiting.
Clustered populations suffering from the disease leave open the role of endogenous as well as exogenous triggers helping the definition of diverse pathophysiological paradigms for the exercise of research. Indeed, in the past, this clinical field has been characterized by poor knowledge of the pathophysiology of the disease leading to preventive approaches borrowed from drugs originally developed for other therapeutic indications, with consequent limited efficacy and endowed with unacceptable levels of side effects causing scarce adherence.
At variance with this situation, more than 35 years of pharmacological research effort have established a strong rational basis upon which the actually available disease-modifying drugs have been developed. In fact, systematic investigations on calcitonin gene-related peptide (CGRP) have established its fundamental role in the pathophysiology of migraine through nociceptive mechanisms in the trigeminovascular system.
The role of CGRP in migraine can now be considered demonstrated also at the level of clinical trials of small-molecule CGRP-receptor antagonists in acute migraine and it is further supported in trials of biotech drugs including onabotulinum toxin A and monoclonal antibodies targeting the CGRP pathway in episodic and chronic migraine. Whilst all this will have a great impact on the frequency and management of acute manifestations as well as the whole history of chronic migraine, new and old questions remain to be answered.
In this new scenario, several pathophysiological as well as therapeutic and regulatory questions remain open.
The organizers of this collection intended to contribute by calling basic and clinical scientists, among the most knowledgeable at the national and international level, as well as national and regional regulators to provide postgraduate students, young researchers, and clinicians with their most up-to-date view on these matters.
It is characterized by recurrent attacks of moderate to severe throbbing and pulsating pain on one side of the head and untreated attacks last from four to 72 hours. Pain is caused by the activation of nerve fibers within the wall of brain blood vessels traveling inside the meninges. Other common symptoms include increased sensitivity to light, noise, odors, nausea, and vomiting.
Clustered populations suffering from the disease leave open the role of endogenous as well as exogenous triggers helping the definition of diverse pathophysiological paradigms for the exercise of research. Indeed, in the past, this clinical field has been characterized by poor knowledge of the pathophysiology of the disease leading to preventive approaches borrowed from drugs originally developed for other therapeutic indications, with consequent limited efficacy and endowed with unacceptable levels of side effects causing scarce adherence.
At variance with this situation, more than 35 years of pharmacological research effort have established a strong rational basis upon which the actually available disease-modifying drugs have been developed. In fact, systematic investigations on calcitonin gene-related peptide (CGRP) have established its fundamental role in the pathophysiology of migraine through nociceptive mechanisms in the trigeminovascular system.
The role of CGRP in migraine can now be considered demonstrated also at the level of clinical trials of small-molecule CGRP-receptor antagonists in acute migraine and it is further supported in trials of biotech drugs including onabotulinum toxin A and monoclonal antibodies targeting the CGRP pathway in episodic and chronic migraine. Whilst all this will have a great impact on the frequency and management of acute manifestations as well as the whole history of chronic migraine, new and old questions remain to be answered.
In this new scenario, several pathophysiological as well as therapeutic and regulatory questions remain open.
The organizers of this collection intended to contribute by calling basic and clinical scientists, among the most knowledgeable at the national and international level, as well as national and regional regulators to provide postgraduate students, young researchers, and clinicians with their most up-to-date view on these matters.
Keywords: Chronic migraine, CGRP, monoclonal antibodies, ditans, onabotulinumtoxin A, regulatory aspects
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
