Yep, that is a concern I would have for patients susceptible to or a family hostory of transient ischemic attacks (TIAs), or those at risk for similar thromboembolic events. CGRP sensory neurotransmission is complex, but I wonder how much peptide is sopped up by an antibody if there is synaptic release and direct post-synaptic receptor activation?
To understand the issue pharmacologically, we really need data in humans, as the animal models for both are neither good or have been shown to be predictive in my opinion.