Chapter 3 – Comprehensive review 79 found in the nocebo group relative to the control group. Cortisol increase was found only in the nocebo group. Aspirin relieved the headache and blocked PG and TXA2 increases in headache sufferers of the nocebo and control groups, while placebo administration had these effects only in the nocebo group. At 1500 meters there were no significant nocebo effects or increases in PG and TXA2. The authors concluded that socially induced nocebo effects affected the biochemical pathway related to PG synthesis; however, negative expectations were insufficient in initiating pain and PG synthesis in the absence of hypoxia. This study indicates that nocebo hyperalgesia can affect peripheral biochemical pain mechanisms. In a PET study, Scott and colleagues (2008) examined the contribution of the endogenous opioid and dopaminergic (DA) systems in the induction of placebo hypoalgesia. Participants underwent intramuscular pain inductions and four PET scans were obtained, two with and two without placebo administration. While this study aimed to induce placebo effects, five participants showed significant increases in pain reports during placebo administration who can be considered nocebo responders. The researchers found significant changes in μ-opioid and DA (D2/D3 receptor) neurotransmission between high placebo and nocebo responders. Compared to placebo responders, nocebo responders demonstrated a deactivation of μ-opioid and DA neurotransmission in specific brain regions: the right nucleus accumbens and left ventral putamen. For μ-opioids these regions additionally included the nucleus accumbens, subgenual ACC, orbitofrontal cortex (OFC), anterior insula, periaqueductal gray (PAG), and amygdala. Notably, the regions and neurotransmitter systems involved in placebo and nocebo effects overlapped. Collectively, these studies have contributed to an early understanding of biochemical variables that may be implicated in nocebo hyperalgesia.
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