Commentary on “Calcitonin-gene related peptide and neurologic injury: An emerging target for headache management”

Abstract

Mehkri et al. have presented a thorough review of calcitonin-gene related peptide (CGRP) and its relationship with headaches, both primary (e.g., migraine headaches) and secondary headaches (e.g., headaches secondary to subarachnoid hemorrhage (SAH) and traumatic brain injury (TBI)) [1]. They have provided an accurate depiction of the literature and the current knowledge regarding CGRP’s association with neurologic injury, as well as some of the physiologic mechanisms and therapeutic targets. This commentary aims to further discuss the veracity of this article and to add an alternative viewpoint in terms of neuromodulators influencing post-traumatic headaches (PTH). Regarding PTH, the authors accurately depict a current understanding that is grounded in literature – CGRP’s association with neurologic injury is incompletely understood. Whether it be intracellular signaling leading to a pseudo-inflammatory response or hyperstimulation of the brain, CGRP is known to exacerbate headache symptoms. However, CGRP’s interactions in the setting of secondary headaches, such as those induced by subarachnoid hemorrhage (SAH) or traumatic brain injury (TBI), are variable depending on the timeframe. CGRP is thought to be neuroprotective in the acute setting time, CGRP levels normalize despite low-to-normal levels, patients with hypersensitized thorough