Commentary: Calcitonin Gene Related Peptide and Its Clinical Utility for the Treatment of Traumatic Brain Injury, Subarachnoid Hemorrhage and Associated Migraine
{"title":"Commentary: Calcitonin Gene Related Peptide and Its Clinical Utility for the Treatment of Traumatic Brain Injury, Subarachnoid Hemorrhage and Associated Migraine","authors":"Y. Mehkri, Maxwell G. Woolridge, B. Lucke-Wold","doi":"10.33696/neurol.3.065","DOIUrl":null,"url":null,"abstract":"Commentary Calcitonin gene related peptide (CGRP) is a potent vasodilator and neurotransmitter that has been extensively studied in the context of migraine pathophysiology. Recently, studies have explored its role in the treatment of traumatic brain injury (TBI) and subarachnoid hemorrhage (SAH). Although a multitude of therapies exist for migraine, there has been little study on the management of migraine following neurologic injury. As the incidence of TBI continues to grow, especially in the United States, it is essential to explore additional therapeutic options such as CGRP inhibition (CGRPi). Given its differential effects in TBI and SAH, an important next step is to see how patients with both TBI and SAH treated with CGRPi respond differently than patients with TBI alone. There is also a need for study in patients with severe TBI who could benefit most from this novel strategy. Calcitonin gene-related peptide (CGRP) is a 37-amino acid neurotransmitter that has been shown to be involved in cranial and facial pathology. Most commonly, CGRP’s role as a potent vasodilator [1,2] has been associated with migraine [3]. It’s use in the treatment of traumatic brain injury [3–5] and subarachnoid hemorrhage (SAH) [6–9] has recently been explored in the literature. While there have been numerous studies on mice and other animal models describing exogenous CGRP’s therapeutic effects, its limited efficacy in humans due to its low half-life [10] has prevented its advancement to human trials. Migraines","PeriodicalId":73744,"journal":{"name":"Journal of experimental neurology","volume":"3 1","pages":"71 - 74"},"PeriodicalIF":0.0000,"publicationDate":"2022-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of experimental neurology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.33696/neurol.3.065","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Commentary Calcitonin gene related peptide (CGRP) is a potent vasodilator and neurotransmitter that has been extensively studied in the context of migraine pathophysiology. Recently, studies have explored its role in the treatment of traumatic brain injury (TBI) and subarachnoid hemorrhage (SAH). Although a multitude of therapies exist for migraine, there has been little study on the management of migraine following neurologic injury. As the incidence of TBI continues to grow, especially in the United States, it is essential to explore additional therapeutic options such as CGRP inhibition (CGRPi). Given its differential effects in TBI and SAH, an important next step is to see how patients with both TBI and SAH treated with CGRPi respond differently than patients with TBI alone. There is also a need for study in patients with severe TBI who could benefit most from this novel strategy. Calcitonin gene-related peptide (CGRP) is a 37-amino acid neurotransmitter that has been shown to be involved in cranial and facial pathology. Most commonly, CGRP’s role as a potent vasodilator [1,2] has been associated with migraine [3]. It’s use in the treatment of traumatic brain injury [3–5] and subarachnoid hemorrhage (SAH) [6–9] has recently been explored in the literature. While there have been numerous studies on mice and other animal models describing exogenous CGRP’s therapeutic effects, its limited efficacy in humans due to its low half-life [10] has prevented its advancement to human trials. Migraines