Figure 1.

Mechanisms of action of Erenumab and Topiramate. (A): Erenumab is a monoclonal antibody that blocks calcitonin gene-related peptide (CGRP) receptors, preventing CGRP from binding. By inhibiting CGRP receptor activity, Erenumab reduces neurogenic inflammation, vasodilation, and pain signal amplification, which are critical pathways involved in migraine pathophysiology. (B): Topiramate reduces neuronal excitability through multiple actions. It blocks voltage-gated sodium (Na⁺) channels, reduces calcium (Ca²⁺) influx, and inhibits glutamate release by antagonizing AMPA receptors. Additionally, it enhances GABAergic (GABA_A) activity, allowing more chloride (Cl⁻) ions into the neuron, thus increasing inhibitory signaling and dampening neuronal excitability.