SHORT REPORT

Full list of author information is available at the end of the articleSickle cell disease (SCD) is due to a point mutation in the beta chain of hemoglobin that causes polymerization of deoxyhemoglobin that distorts the shape of erythro-cytes, contributing to vascular obstruction and ischemia of tissues and organs [1]. A hallmark feature of the dis-ease is severe pain that arises during acute sickling events, as well as the recently recognized and less well many of these individuals. Patients report heightened sensitivity to touch and spontaneous pain, suggesting complex physiological underpinnings that may include both inflammatory and neuropathic etiologies [2]. The array of pain descriptors and triggers for acute and chronic pain suggest contribution from both central and peripheral mechanisms, involving changes in neural signaling, gene expression and plasticity [3]. Primary af-ferent sensitization, in particular, is a correlate of psy- * Correspondence