Fibromyalgia: Difference between revisions

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Clinic

  • FM is a medical condition defined by the presence of chronic widespread
  • Core symptoms are
    • Pain, which results from "central sensitization syndrome"
    • Allodynia: Heightened pain in response to tactile pressure
    • Fatigue, Depression
    • Sleep problems: Difficulty to fall or stay asleep, Awakening frequently and waking up unrefreshed.
    • Cognitive symptoms: Brainfog, Trouble concentrating, Forgetfulness and Disorganized or slow thinking

Other symptoms are

  • Lower abdominal pain or cramps
  • General hypersensitivity, Hypervigilance, Hypersensitivity to Pain /Environmental stimuli (bright lights, loud noises, perfumes, cold)
  • Musculoskeletal stiffness
  • Sexual dysfunction
  • Visual symptoms

Related disease


Pathophysiology

Pain processing abnormalities: Chronic pain can be divided into three categories.

  1. Nociceptive pain is caused by inflammation or damage to tissues.
  2. Neuropathic pain is caused by nerve damage.
  3. Nociplastic pain (or central sensitization) is less understood and is the common explanation of the pain experienced in fibromyalgia.


Because the three forms of pain can overlap, fibromyalgia patients may experience nociceptive (e.g., rheumatic illnesses) and neuropathic (e.g., small fiber neuropathy) pain, in addition to nociplastic pain.

Autonomic nervous system

  • Some suggest that fibromyalgia is caused or maintained by a decreased vagal tone, which is indicated by low levels of heart rate variability, signaling a heightened sympathetic response. Accordingly, several studies show that clinical improvement is associated with an increase in heart rate variability. Some examples of interventions that increase the heart rate variability and vagal tone are meditation, yoga, mindfulness and exercise.

Neurotransmitters

Some neurochemical abnormalities that occur in fibromyalgia also regulate mood, sleep, and energy, thus explaining why mood, sleep, and fatigue problems are commonly co-morbid with fibromyalgia. Serotonin is the most widely studied neurotransmitter in fibromyalgia. It is hypothesized that an imbalance in the serotoninergic system may lead to the development of fibromyalgia. There is also some data that suggests altered dopaminergic and noradrenergic signaling in fibromyalgia. Supporting the monoamine related theories is the efficacy of monoaminergic antidepressants in fibromyalgia.

Neurophysiology

Neuroimaging studies have observed decreased grey matter of the default mode network in people with fibromyalgia. These deficits are associated with pain processing.

Neuroendocrine system

Studies on the neuroendocrine system and HPA axis in fibromyalgia have been inconsistent. One study found fibromyalgia patients exhibited higher plasma cortisol, more extreme peaks and troughs, and higher rates of dexamethasone non-suppression. However, other studies have only found correlations between a higher cortisol awakening response and pain, and not any other abnormalities in cortisol. Increased baseline ACTH and increase in response to stress have been observed, hypothesized to be a result of decreased negative feedback.

Immune system

Inflammation has been suggested to have a role in the pathogenesis of fibromyalgia. People with fibromyalgia tend to have higher levels of inflammatory cytokines IL-6, and IL-8. There are also increased levels of the pro-inflammatory cytokines IL-1 receptor antagonist. Increased levels of pro-inflammatory cytokines may increase sensitivity to pain, and contribute to mood problems. Anti-inflammatory interleukins such as IL-10 have also been associated with fibromyalgia.

A repeated observation shows that autoimmunity triggers such as traumas and infections are among the most frequent events preceding the onset of fibromyalgia. Neurogenic inflammation has been proposed as a contributing factor to fibromyalgia.

Digestive system

Gut microbiome

Gut bacteria may play a role in fibromyalgia. People with fibromyalgia are more likely to show dysbiosis, a decrease in microbiota diversity. There is a bidirectional interplay between the gut and the nervous system. Therefore, the gut can affect the nervous system, but the nervous system can also affect the gut. Neurological effects mediated via the autonomic nervous system as well as the hypothalamic pituitary adrenal axis are directed to intestinal functional effector cells, which in turn are under the influence of the gut microbiota.

Gut-brain axis

The gut-brain axis, which connects the gut microbiome to the brain via the enteric nervous system, is another area of research. Fibromyalgia patients have less varied gut flora and altered serum metabolome levels of glutamate and serine, implying abnormalities in neurotransmitter metabolism.

Entities


Miasm

FM belongs to 3IFMC Cluster Of Disease. Therfore its main underlying miasms are (HSV-1, HSV-2, PLV, EBV, CMV)

I think HSV-1 would be the best

HSV-1

HTLV-1 [1]

  1. Cruz BA, Catalan-Soares B, Proietti F. Higher prevalence of fibromyalgia in patients infected with human T cell lymphotropic virus type I. J Rheumatol. 2006 Nov;33(11):2300-3. PMID: 17086610.