66 this negative expectation, the nocebo stimulus evokes increases in perceived pain, similar to the high pain intensity previously paired to the nocebo, even in the absence of high pain applications. Negative verbal suggestions can also alter pain expectations, through more explicit, instructional learning. Suggestions may induce negative expectations explicitly (i.e. explaining the potential negative effects of a treatment) and can also induce nocebo hyperalgesia for example by enhancing conditioning effects 13,14. Social observational learning can moreover induce nocebo hyperalgesia, for example when one sees someone else experiencing increased pain after a treatment 15,16. These learning processes may result in nocebo responses that may play a detrimental role in shaping pain responses following a given event, stimulus, or treatment 3,17. Over the past two decades, neuroimaging and pharmacological studies have begun to address the neurobiological underpinnings of nocebo experiences. Electrophysiological and neuroimaging methods such as electroencephalography (EEG) and magnetic resonance imaging (MRI) have provided valuable insights into the specific functional brain processes and underlying brain structures that are involved in nocebo hyperalgesia 5,18–21. Moreover, the neurochemical systems underlying nocebo hyperalgesia have been explored via pharmacological administrations, blood or salivary measurements, or via imaging techniques such as Positron Emission Tomography (PET) 18,22,23. Inconsistencies and gaps in the literature, however, render nocebo hyperalgesia a phenomenon that is still poorly understood. The nocebo literature is characterized by very diverse methods. For this reason, a comprehensive and detailed account of studies that examined neurobiological correlates of nocebo hyperalgesia may significantly aid in a better understanding of this phenomenon and can provide suggestions for improvements in the consistency of selected methodologies and reporting of results.
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