Chapter 3 – Comprehensive review 77 component and alpha connectivity and with source regions for these diverse results identified in the anterior insula, cingulate gyrus, and middle temporal gyrus 5,15,31,32. Moreover, learning has been implicated at an electrophysiological level, as shown by alterations in gamma band activity under nocebo hyperalgesic conditions as well as the involvement of long-range temporal correlations (Thomaidou et al., 2021a). Neurochemical and biochemical correlates of nocebo hyperalgesia Neurochemicals play a key role in nociception and in the cognitive and affective processes that modulate pain perception 38. In nocebo hyperalgesia, where cognitive and emotional factors such as learning and anxiety have been shown to play a role 39–41, related neurochemicals may be involved. Next to neurochemicals, other biochemicals such as enzymes have been shown to modulate pain transmission 42 and may also be relevant in nocebo hyperalgesia. Three studies examined chemical processes involved in nocebo hyperalgesia, using negative suggestions 18,22,23. Benedetti and colleagues (2006) studied cortisol and the hypothalamicpituitary-adrenal (HPA) axis by using a neuropharmacological approach to examine neurochemical correlates of anxiety, a state that is related to fear and may thus, similarly to fear 43, also be linked to nocebo hyperalgesia 39. Participants were subdivided into 4 groups and underwent ischemic pain inductions. One group received a sham hyperalgesic pill and intravenous proglumide, a non-selective antagonist of cholecystokinin (CCK) type-A/B receptors 44. A second group received a sham hyperalgesic pill and intravenous diazepam, a benzodiazepine and potent anxiolytic agent that increases the effect of the inhibitory neurotransmitter gamma-aminobutyric acid 45. A nocebo control group received a sham hyperalgesic pill and an inert saline solution, while the other control group was only administered a saline
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