Central Sensitization: A Pathogenic Mechanism in Complex Undefined Diseases, 2019, Fernández-Solà

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Central Sensitization: A Pathogenic Mechanism in Complex Undefined Diseases
Joaquim Fernández-Solà*
Department of Internal Medicine, University of Barcelona, Spain
†Author for correspondences: Joaquim Fernández-Solà, Department of Internal Medicine. Hospital Clínic Villaroel 170, 08036. Barcelona, Spain, Tel: 34 93. 659107529

Review
Neuropsychiatry
2019p- ISSN 1758-2008e- ISSN 1758-2016
Neuropsychiatry (London) (2019) 9(6), 2485–24902485


ABSTRACT

There is a common perception that complex undefined diseases manifested with diverse combination of symptoms and a difficult clinical diagnosis have a possible common physiological mechanism of disease production.

Physical or cognitive fatigue, widespread pain without arthritis, sleep, mood and autonomic disturbances as well as multiple intolerance involving drug, food, chemical agents, electromagnetic fields or other environmental factors may be included in this category.

Along last three decades, the existence of central sensitivity as a well established common pathogenic mechanism involved in abnormal symptom development emerged in diverse areas as pain, fatigue, food and environmental intolerance, as well as in the global chronic disease epidemic.

The common fact of all of these disorders is a deregulation of the central control mechanisms at the limbic brain system.

This may relate to amplification of pain and fatigue perception and disturbance of environmental tolerance and control of circadian rhythms and mood.

This deregulation causes amplification of central somatosensory perception, but also a decrease of nociceptive inhibitory outputs.

The final result is a chronic condition with central hyperexcitability and systemic disabling symptoms highly difficult to manage.

This article comments on the current significance to evaluate central sensitization symptoms and to consider these mechanisms in the development of complex diseases, as well as in the global chronic disease epidemic.

We propose to include central sensitization to structuring a multidisciplinary concept addressed to improve scientific comprehension and clinical management of diseases, as well as future research directions on this field.

Keywords
Central sensitization, Fibromyalgia, Chronic fatigue syndrome, Multiple chemical sensitivities, Environmental Intolerance, Neuroinflammation, Limbic disorders, Complex diseases, Chronic disease Epidemic.

List of Abbreviations: CFS: Chronic Fatigue Syndrome, CS: Central Sensitization, CSS: Central Sensitivity Syndrome, EMF: Electromagnetic fields, FM: Fibromyalgia, MCS: Multiple Chemical Sensitivities, SSs: Symptom Severity scale, WPI: Widespread Pain Index.
 
Right. It could be, but where is the evidence for ME/CFS having this dysfunction of central control mechanisms at the limbic brain system?

I don't believe anything like this has been shown yet. I'm no expert on neuroimaging but it's hard to believe such a thing could be unambiguously demonstrated with current technology.

It's okay to speculate but I fear the authors are making vast conclusions while having insufficient evidence for them.
 
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It is quite odd reading this article in the same week as Naviaux hypothesis article about the rise in the same chronic illnessess that he attributes to the cell danger response, mitochondria etc.

Each sees the subject from a completely different perspective, and each is equally convinced they are right...
 
It is quite odd reading this article in the same week as Naviaux hypothesis article about the rise in the same chronic illnessess that he attributes to the cell danger response, mitochondria etc.

Each sees the subject from a completely different perspective, and each is equally convinced they are right...
One could be the cause of the other, e.g.

The cell danger response could be downstream of the affected ("sensitized") brain area. I personally am a fan of this approach, though one must be precise in all uncertain possibilties. I agree e.g. with @Michiel Tack and his thread on this that it would be bad trying to influence this sensitization by any psychobla.

A hope could be, say, that an influence on synaptical structures in the basal ganglia and thalamus - I am a huge fan of this side being affected in particular - might be in reach of available possiblitites (in some difficult manner). This hope may arise from the fact that there only seems to be triggers in these condiditons, though admittedly in MCS the thing should be more complicate, to put it a bit easy.

The other way around would be that a disturbed cell danger response would affect the limbic system or whatever. Then the questions from this perspective arise like so: a) what is the influence on the cell danger response; b) if there is none, how strong could be an influence on the "limbic" system (as the authors like to guess)?


Yeah, no...
Yes, so far no biomarkers, no monitoring, no details.

You must remember your old geometry proofs. First write down the "Given".
Completely agreed, spinoza;)
 
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