Page 18 - JCBP-3-1

Journal of Clinical and
Basic Psychosomatics Somatic symptom disorder etiology

National Institute of Health’s open database, Genbank’s even harmful treatments for the disorders. Pointedly, many
B.L.A.S.T., which is a protein sequence matching tool (http:// treatment methods have been unsuccessful and PD/FSD
blast.ncbi.nlm.nih.gov/Blast.cgi). It is hypothesized that patients are sometimes blamed for their lack of progress.
113
119
acetylcholinesterase or butyrylcholinesterase, or both, are Dr. Jeffrey Staab of Minnesota’s Mayo Clinic was a researcher
endogenous versions of atropine because atropine binds involved in the field trials for the diagnostic criteria for SSD,
with high affinity to acetylcholinesterase enzymes. and he acknowledged:
114
Further, the research presented above indicates that they “Most psychiatrists assume that some sort of trauma,
differentially affect memory systems in the way atropine tragedy or conflict in the past is driving health-anxious
does. 20,115 Parasympatholytics, or PNS inhibitors, such as
atropine (https://pubchem.ncbi.nlm.nih.gov/compound/ fears and behaviors. Moreover, if we can’t find it, and
Atropine), are a concern because PNS inhibition is a the patient can’t find it, it can become a speculative wild
116
core problem for FSD sufferers. If acetylcholinesterase is goose chase for trauma. Trauma is more likely in these
endogenous atropine, then its profusion is likely causing or patients, but if we don’t find a history of trauma, we can
exacerbating FSD. look at stress, and if we don’t find that, we can still talk
about exaggerated preoccupations with health and help
7.2. PAMP patients reset and reframe that without digging around in

The role PAMP has in the HPA axis as an antagonist of the past.” 122
nAChRs and mAChRs should be considered, such as T-A-P theory posits not a completely new idea – the
acetylcholinesterase, as also antagonizing the PNS. This body keeps the score – but it is the first to delineate a
paper argues that PAMP reinforces cortisol in the T-A-P neuroendocrinological sequelae between dissociative
pathway. High levels of PAMP (discussed above as amnesia and SSD. In 2021, when looking at future directions,
associated with elevated catecholamines and hypercortisol Mueller et al. called for an answer to the question “does the
82
in the controllable stress paradigm) could interfere with hippocampus provide the anatomical substrate for the link
SIA and the beginning of tonic immobility in two ways. between disorders of central inflammation, dysautonomia,
First, PAMP could prevent analgesia at the level of MrgX and a dysregulated HPA axis?” T-A-P theory answers their
2
receptors in the spinal dorsal horn, 67,117 because PAMP question with a thorough map of the defense cascade that
blocks MrgX receptors with stronger affinity than six initiates and maintains SSD, locking trauma into the body
2
of that receptor’s ligands, preventing analgesis that is for many patients. Importantly, the theory argues that
normally associated with activation of MrgX by endorphin somatic and emotional memory is what is persistently
2
or enkephalin. 85,117 Second, after hypercortisol activates the re-experienced in SSD, a parallel process to PTSD patients’
SNS by way of NMDA receptors, the PNS’ attempts to persistent remembering of their trauma. The hippocampus’
70
return the system to allostasis could be blocked by PAMP. autobiographical memory is shut down by hypercortisol
If low ACh is circulating early in the controllable stress during traumatic amnesia, but amygdala-based memory,
paradigm due to high catecholamines, since PAMP is an motor memory, and somatosensory memory systems are
ACh receptor antagonist, it could prevent the little ACh enhanced or unaffected by hypercortisol, encoding the
that is circulating from activating the stabilizing effort of trauma. When internal and external reminders or cues of
the PNS. If PAMP and cortisol bind with mAChRs in the the trauma occur, in the same way they frequently do with
PNS, then tonic immobility and analgesia are turned “off.” PTSD patients, SSD patients’ neurochemistry is triggered

8. Conclusions into SNS activation without PNS deactivation, leading
to unexplained pain and other neurological or somatic
8.1. Chronic pain and somatic symptom sufferers symptoms. Somatic symptoms could be considered
PD, FSD, and SSD patients experience a great deal of flashbacks and treated as such in many patients. The
suffering and sometimes face huge costs for treatments and defense cascade travels familiar neurological pathways to
medications. They stand to lose functional ability at work, old injury sites or previously diagnosed medical problems
in relationships, and socially. 2,118-120 They are often told their (also known as “priors”), and sends signals there, or
symptoms have no clear explanation or origin, which is interprets signals from there, saying, “something is wrong.
frightening or frustrating. Many patients feel their needs are I still hurt!” The true message from the body may be,
not being served well by either medical doctors or mental “something bad happened; you don’t remember it; pain
health clinicians. In fact, only about 25% of patients with is our only voice to say the world is not safe; you may be
SSD ever seek psychotherapy, in part due to stigma. Worse, under attack at any moment!” Relatedly, catastrophizing
121
123
without clear knowledge of underlying pathogenesis, their and alexithymia are primary traits associated with SSD.
health providers may suggest inappropriate, ineffective, or Patients cannot voice how they feel, or it is greatly reduced

Volume 3 Issue 1 (2025) 12 doi: 10.36922/jcbp.4254