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Journal of Clinical and
Basic Psychosomatics Somatic symptom disorder etiology

This novel conceptualization of the etiology of traumatic may assist clinicians in helping patients manage or prevent
amnesia and SSD also explains why SSD is comorbid ongoing pain. 29,32,33,102,125 This type of experience has been
with dissociative amnesia. The findings are based on a termed a “body-loop feedback” for pain, or “top-down”
large body of neurological, physiological, and clinical pain signals by some authors, 1,11,47 and may be likened
research, which converges to conclude that hypercortisol to a type of repetitive re-experiencing of the trauma, as
and peritraumatic perception of control are key factors in in PTSD, but through the procedural memory systems.
both disorders. The shared etiology of PD, somatization For the T-A-P theory to be fully substantiated, not only
disorder, and FSD also legitimizes the DSM-5-TR move to replication of some of the animal studies is needed, but
unify the disorders under one umbrella, SSD. Considered human studies that control for peritraumatic perception
as a whole for the 1 time, this comprehensive review are also required. The inclusion of amnestic trauma victims
st
provides definitive evidence that how trauma is perceived in clinical samples is a must.
is the linchpin that explains the dose-dependent effects of Future studies should validate the T-A-P pathway
cortisol (and its co-contributors, acetylcholinesterase, and using consistent glucocorticoid (cortisol) measurement,
PAMP) on both memory and somatic symptoms. It appears especially reporting and standardization of “high” versus
that traumatic amnesia affords individuals protection from “low” glucocorticoid amounts. Future research should
excessive fear, anxiety, and intrusive explicit memories. also focus on determining how much predictive influence
However, the by-product of this escape route is either pain, acetylcholinesterase and PAMP have relative to cortisol
extra sensitivity to pain, or unpleasant somatic symptoms. in the T-A-P pathway in both animal and human trials.
3
Sufferers of dissociative amnesia and patients with SSD Furthermore, future studies need to address the other
deserve a better understanding of their symptoms and two primary causes of SSD, reinforcement learning of
challenges. T-A-P theory predicted what Vinkers’ research the sick role due to social acceptability, and biological
found with the NESDA cohort: Remembered childhood sensitivity to pain. Both of these conceivably strengthen
trauma does not lead directly to dysregulations of the T-A-P connections, but how so remains to be discovered.
HPA axis and autonomic nervous system. The people Furthermore, prevention and intervention with these
124
not captured in Vinkers’ study were those who do not factors were beyond the scope of this paper.
remember childhood trauma, yet are much more likely
to experience HPA and PNS dysregulation. By taking Treatment should explore the use of new
into account the perception of trauma and its underlying pharmacotherapy options in SSD intervention, in light
neuroendocrinological processes, we will drive more of research presented here regarding the neurochemicals
effective clinical treatment methods and appropriate and receptors involved in SSD. The effectiveness of
pharmacological interventions. nAChR agonists in the treatment of both neuropathic
and psychogenic pain is emerging. In the same way that
9. Recommendations ACh—nAChR agonist – is the mind’s natural way to

When screening for SSD, clinicians need to also screen for enhance memory and provide analgesia, other nAChR
dissociative amnesia. If a history of cumulative traumatic agonists have shown initial effectiveness in treating pain.
effects, especially emotional abuse or sexual abuse can The effectiveness and lack of side effects of nAChR and
be informed by family or other sources, clinicians must mAChR agonists, such as acetyl-L-carnitine (ALCAR) and
treat underlying trauma alongside somatic symptoms. ABT-594, an epibatidine analog, has been established in the
126,127
Cognitive-behavioral treatment strategies have shown treatment of pain in animal models. Future research
some effectiveness with PD, SSD, and FSDs, such as with humans is needed and will contribute to further
fibromyalgia, chronic back pain, and irritable bowel validation of the T-A-P connection. nAChR antagonists
syndrome. As an adjunct to the core cognitive-behavioral such as MK-801, atropine – and its isomers scopolamine
1,11
strategies, clinicians can monitor whether patient pain and hyoscyamine – have also been used as pain relievers
experience is maintained by regular internal “procedural under the suspicion that an endogenous nAChR antagonist
memory” triggers and intervene with each trigger either (like PAMP) was the primary culprit in displacing ACh
128
through avoidance, system-calming techniques, or and triggering pain. Interestingly, the newest nAChR
experience validation and normalization. 1,125 We know α9/10-specific antagonists RgIA and Vc1.1, are showing
102,129,130
memory is retrieved and influenced by pre-existing beliefs, potential as analgesics, and PAMP shares an exact
expectations, and knowledge, but it is also influenced by protein match with nACh α9/10 receptor subtypes.
the context of retrieval. 49,52 Recognition that SSD patients Acetylcholinesterase inhibitors like neostigmine
may have procedural memory fragments (well-preserved have also been tested as possible analgesics (assuming
in the amygdala) that trigger elevated HPA axis responses, acetylcholinesterase is the primary culprit in degrading

Volume 3 Issue 1 (2025) 14 doi: 10.36922/jcbp.4254