As mentioned, the majority of somatic FSS symptoms can be directly deduced from the physiological responses triggered by disinhibited aversive memories. Therefore, I would like to continue here directly with a brief description of how some unusual FSS develop on the basis of the mechanism described.
The symptom formation of these FSS cannot be directly inferred from the presented model. To keep the text short, I would like to give just a brief explanation, with links to scientific articles that allow readers with neuroscientific knowledge to more accurately understand the respective mechanisms.
The symptoms of premenstrual syndrome arise via the mechanism of temporary symptom formation described above. The mechanism is triggered by the premenstrual low estrogen level, which impairs the function of extinction memories via reduced activation of estrogen receptors in extinction neurons. See reference 45 in PMID 25796471 (3).
The (normally not noticeable) physiological reactions provoked in this way shift various physiological parameters beyond the symptomatic threshold. When the estrogen level rises again, the activity of extinction neurons increases to a normal level and the symptoms disappear.
In short, the overactivity of these memories reinstantiates the brain-internal cytokine profile of the original infection. This cytokine profile induces through respective neuronal receptors the original feeling of illness that prevailed during the infection. Even though this is a brain-internal process, it has a paralyzing effect on the body.
This mechanism sounds quite far-fetched, but a detailed explanation, supported by many scientific studies, can be found here (4) in chapter 3.4. The term “e/x balance” used there refers to the collection of aversive memories and extinction memories present in an individual. I’ll write a dedicated article on this subject.
The symptoms of electrosensitivity arise when the currents induced by EMFs (electromagnetic fields) in the brain, or other physiological EMF effects, lead to dysfunction or demise of particularly vulnerable extinction neurons, and as a result, temporary symptoms arise via the mechanism of temporary symptom formation described above.
A study by the renowned researcher Nora D. Volkow (11) is here of special interest. The study undoubtedly proves a dose-dependent influence of EMFs on neuronal activities in humans. See PMID 21343580 (16). Quote:
“These results provide evidence that the human brain is sensitive to the effects of RF-EMFs [radiofrequency electromagnetic fields] from acute cell phone exposures. The findings of increased metabolism in regions closest to the antenna during acute cell phone exposure suggest that brain absorption of RF-EMFs may enhance the excitability of brain tissue.”, p. 811
On the basis of the presented mechanism, the observed increase in metabolism could be interpreted as temporary overactivity of aversive memories triggered by EMF-induced dysfunction of extinction neurons.
The symptoms of multiple chemical sensitivity arise analogously when inhaled chemicals cross the blood-brain barrier and disturb or damage vulnerabilised extinction neurons or induce their demise.
Both stressors, chemicals and EMF, may induce in the brain of the affected persons a transiently escalating inflammatory process. As mentioned above, this process affects vulnerabilised extinction neurons and therefore may play an important role in the symptom formation of these disorders.
The amplifying effect of this process could play a role in the high sensitivity to extremely low concentrations of stressors in these syndromes.
A clinical picture similar to the FSS, somatic symptom disorder, may also develop via the mechanism described.
The mechanism could also play a role in many other diseases with inflammatory or allergy-like components as an amplifying factor, or even as a trigger by shifting an asymptomatic predisposition to a disease into the symptomatic range.
The mechanism also explains further, so far poorly understood properties of the FSS. In particular the frequent psychological comorbidity and the frequent occurrence in traumatized persons. You can find these explanations in the last chapter of the original article on my homepage.
What the heck are extinction memories?
What’s missing now is an explanation of extinction memories. Here it is:
Extinction learning, or extinction for short, is the process of learning to forget an old reaction pattern by learning a new, more favorable reaction pattern.
It is crucial that the old reaction pattern is completely retained during this learning process.
In order to avoid reactivation of the old reaction pattern, a so-called extinction memory is formed in the course of extinction learning. This extinction memory permanently blocks or extinguishes the old reaction pattern.
Extinction is evolutionarily advantageous over real forgetting since extinction is reversible and the old reaction pattern is therefore available again when needed.
Importantly, extinction learning often takes place in order to deal better with more or less aversive (i.e., negative) everyday inconveniences and adversities.
Therefore, in the course of life, a quite high number of extinction memories develop. And the memories extinguished by them often have aversive components.
Due to the high number of extinction memories formed in the course of life, the described disease mechanism can cause severe symptoms in anyone who has been exposed to a strong stressor that vulnerabilised extinction neurons.
More introductory information on extinction learning can be found at (1), in the chapter „Erasing Classical Learning“ of (10), and in the free part of (13). I strongly recommend reading them, because they demonstrate the frequent occurrence of extinction learning in daily life. For deeper understanding see also the abstracts of Maren (8) and Sohal (15).