Page 13 - JCBP-3-1

Journal of Clinical and
Basic Psychosomatics Somatic symptom disorder etiology

6 months after trauma, compared to the accident victims Although there is only one study directly controlling
who felt no control over the accident (because someone cortisol’s role in the T-A-P pathway, Zohar et al. successfully
61
else was to blame). Delahanty’s team realized they should prevented PTSD in hospitalized trauma victims by
follow up with victims of motor vehicle accidents who had administering a high dose of hydrocortisone immediately
amnesia for an accident (21 of 99) but had been initially post-trauma. In their double-blind randomized controlled
excluded from the research. Those victims’ urinary trial, they were able to facilitate a return to HPA axis
catecholamines (epinephrine, norepinephrine, dopamine) homeostasis in both human and animal models and
and cortisol levels were tested immediately after arrival increase or facilitate normal hippocampal dendritic growth
to the hospital and 15 h later. Their cortisol levels were in animals. Their groundbreaking finding was that a 1-time,
extremely high. Cortisol was the only neurochemical that 100 – 140 mg weight-dependent dose of hydrocortisone
significantly differentiated between motor vehicle accident administered within 6 h of trauma prevented PTSD
victims who reported intrusive memory, and 1 month symptoms and indelible, intrusive memory.
later, PTSD symptoms, and motor vehicle accident victims The inverted U-shaped relationship cortisol has
who had no intrusive memory or PTSD. 51 with memory has been widely reported. 15,18,62-64 At very
We can now pinpoint exactly how long-term memories low and very high levels, cortisol is problematic in the
are consolidated or interrupted in humans. High levels hippocampus. At moderate levels, cortisol does not overly
of cortisol are associated with declarative memory impede or facilitate memory. Yet, many studies have not
impairment. 10,15,18,52 When there have been conflicting measured cortisol in a systematic way or accounted for
results about levels of cortisol and PTSD versus traumatic its nonlinear relationship. This may explain why some
amnesia, it was due to comparison across studies that authors’ findings conflict. Future studies of human models
measured cortisol at the onset of the disorder versus cortisol should report milligrams per volume unit of urine for
levels over the duration of the disorder. T-A-P theory is cross-comparison. Furthermore, precise measurement of
concerned with cortisol levels at initiation, as opposed to urinary cortisol levels of amnestic trauma victims needs
maintenance during the course of traumatic amnesia or to be included in future studies, so that exact dose ranges
PTSD. Conflicting results are also born of measurement within which cortisol alters memory, such as the suggested
inconsistencies. A number of researchers have commented guidelines above, can be confirmed.
that salivary levels in one study have been compared to
plasma or urinary levels in another study, or basal levels 6.2. Pain
at different times of day have been compared, yet failed to The initiation and maintenance of pain in the body is
take into account circadian rhythm effects. 51,53-56 a complex process that involves an interplay of both the
Below is a summary of the specific amounts of cortisol SNS and PNS, simply put, tends to involve activation of the
that affect memory. The lowest levels, between 9 and SNS first (which turns “on” the pain response), and then an
120 mg, induce intrusive memory and PTSD; moderate activation of the PNS (which turns “off” the pain response),
levels, between 140 and 450 mg, stabilize the HPA axis returning the system to allostasis. In actuality, the process
and lead to normal memory and functioning; high levels involves many different neurotransmitters and the
of cortisol, between 450 and 650mg, create amnesia. The potentiation or depotentiation of both neuronal brain cells
47,65
effects of cortisol can be reversed or increased within a few and afferent and efferent neurons in the spine and body.
hours if a patient receives agonist or antagonist therapy. Many of the neurotransmitters, receptors, and anatomical
For example, in three human studies, administration of areas of the brain involved in pain perception are also
25 mg of hydrocortisone (exogenous cortisol) immediately involved in the body’s response to trauma, particularly
post-trauma decreased memory for trauma and prevented regarding the actions of the HPA axis and catecholamines.
66,67
PTSD, but was not sufficient to induce traumatic Catecholamines trigger cortisol production and release.
amnesia. 56-58 In rats, plasma corticosterone levels are 400% Early PTSD researchers proposed that the freeze or
higher after inescapable stress compared to controls (637.5 tonic immobility response associated with PTSD involved
± 99.8 ng/mL vs. 176.6 ± 50.6 ng/mL). Furthermore, in sustained analgesia, an analgesia more potent and longer-
59
accident victims with PTSD symptoms, 15 h after trauma, lasting than stress-induced analgesia (SIA) usually seen in
the average of their urinary cortisol level was 131 mg. The animals. SIA involves attentive stillness/immobility early
urinary cortisol level in accident victims without PTSD in the defense cascade. Animal research overwhelmingly
symptoms averaged 443 mg at 15 h after trauma. Wahbeh supported both a hypocortisol-analgesia connection
51
and Oken also found long-term lower cortisol in veterans and a hypercortisol-pain connection. In the only studies
60
with PTSD than in veterans without PTSD. that refuted the hypercortisol-pain connection, SIA was

Volume 3 Issue 1 (2025) 7 doi: 10.36922/jcbp.4254