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Journal of Clinical and
Basic Psychosomatics Somatic symptom disorder etiology

examined, rather than the longer-term tonic immobility- in response to trauma in humans. Depending on the
related analgesia. 67-71 Sometimes important differences in peritraumatic response, he said that either analgesia or pain
the intensity and duration of SIA, varying in response to is differentially regulated by either opioid or non-opioid
escapability/inescapability, were not measured. For example, mechanisms. In a fight/flight response to trauma, early rapid
Pinto-Ribeiro et al. 69,70 reported long-term analgesia in rats analgesia occurs through the prevention of SNS activation
exposed to chronic inescapable stress but may have mistakenly through epinephrine’s action (non-opioid) at the trigeminal
interpreted the effect as due to hypercorticosteronism. What dorsal horn and its deactivation of ACh in the PNS.
is termed “elevated” or “high” glucocorticoid can vary Alternately, in a freeze response, slower ongoing analgesia
depending on the study. Pinto-Ribeiro et al. exogenously is maintained by ACh activation of the PNS, keeping the
administered 40 mg of corticosterone to rats in the 2009 SNS “off” through endorphins opioid. However, Janig
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study, presumably to match the levels her team noted in was incorrect when he defined the initial attentive stillness
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the plasma of rats subjected to chronic inescapable stress in phase of peritraumatic perception, which occurs in both
the 2004 study (although those levels were not reported in fight/flight and freeze responses, as the complete fight/flight
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the 2004 study). Forty milligrams would not be indicative response. Instead, early SIA caused by attentive stillness is
of hypercorticosteronism but instead indicates that low characterized by cholinergic-modulated analgesia, but
corticosterone is linked both to memory for trauma and later in the cascade, catecholamines produce hyperalgesia
analgesia. Unfortunately, Pinto-Ribeiro overlooked Uki in the fight/flight reaction, according to many. 9,66,70,73,74
et al.’s results in which plasma corticosterone levels There is agreement with Janig’s hypothesis that freeze/tonic
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indicating traumatic stress are 120 mg in rats. immobility responses to trauma involve opioid-modulated
Another critical difference is how long analgesia is analgesia.
measured. Drugan et al. monitored SIA for more than 2 h. For example, both Leite-Panissi et al. and Souza da
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They found that SIA for rats in escapable stress paradigms Silva and Menescal-de-Oliveira substantiated that SIA
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rapidly declined over 2 h until there was no analgesia, is a cholinergic-modulated analgesia. However, others

whereas rats in inescapable stress paradigms experienced found that long-term analgesia caused by inescapable
ongoing analgesia for over 24 h, indicating that a state of stress is opioid-modulated (endorphins bind with mas-
tonic immobility had also begun, although the authors did related gene [MrgX ] receptors) in the spinal horn.
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2
not assess that. They did note that rats in the inescapable Furthermore, Drugan et al. discovered that naltrexone
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stress condition had the benefit of endorphins, whereas (an opiate antagonist) completely eliminated the analgesia
the escapable stress rats did not. 73-76 By 1999, Drugan 46 in chronically inescapably shocked subjects but had no
determined that cortisol and GABA levels were significantly effect on the analgesic response of chronically escapably
elevated in the escapable stress conditions and were linked shocked subjects. In other words, in the case of inescapable
to both amnesia and interrupted SIA. stress and hypocortisol, after initial SIA in the nucleus
This research begged the question: In light of the raphe magnus, from there, projections into the spinal
results in animal models, does traumatic amnesia horn activate tonic immobility, stimulate endorphins, and
interrupt analgesia and create susceptibility to chronic thereby prevent the SNS from activating. In the case of
pain in humans as well? And, is the pain experience hypercortisol and escapable stress, after initial SIA, beta-
governed by peritraumatic perception if it is a byproduct endorphins are inhibited and excessive glutamate triggers
of traumatic amnesia, neurochemically downstream from N-methyl-D-aspartic acid (NMDA) receptor activation of
glucocorticoid (cortisol) effects? In animal models, one SNS pain while cortisol prevents ACh from calming the
study to date showed that cortisol differentiated pain SNS.
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perception along the same dose-dependent lines as it From clinical studies of human beings, we know that
differentiated memory. Cortisol is critically tied to a fight/ hypercortisol also plays an important role in the onset of
flight perception of trauma like it is tied to freeze/PTSD. many types of somatization by causing misattribution and
Souza da Silva and Menescal-de-Oliveira created chronic misperception of body signals. Furthermore, patients with
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trauma-induced pain in guinea pigs using a controllable pain disorder, fibromyalgia, and chronic back pain show
stress paradigm. Importantly, even if only exogenously reduced gray matter density in cingulate-parahippocampal
administered (no stress/trauma paradigm), high levels of or fronto-limbic areas. 11,77,78 Hypercortisol has been
corticosterone caused ongoing pain. implicated in brain matter loss in the hippocampus and
surrounding areas. We cannot assume that if chronic
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6.3. Trauma-induced analgesia SSD patients present with ongoing hypercortisolism that
In 2009, Janig came close to mapping how peritraumatic it was also the cause of SSD, but there is strong evidence
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perception dictates whether analgesia or pain is experienced indicating that hypercortisolism is key to both onset and

Volume 3 Issue 1 (2025) 8 doi: 10.36922/jcbp.4254