Sensory characterization of somatic parietal tissues in humans with chronic fatigue syndrome

doi:10.1016/0304-3940(96)12559-3

Neuroscience Letters

Volume 208, Issue 2, 19 April 1996, Pages 117-120

https://doi.org/10.1016/0304-3940(96)12559-3 Get rights and content

Abstract

Patients with chronic fatigue syndrome (CFS) mainly complain of symptoms in the musculoskeletal domain (myalgias, fatigue). In 21 CFS patients the deep (muscle) versus superficial (skin, subcutis) sensitivity to pain was explored by measuring pain thresholds to electrical stimulation unilaterally in the deltoid, trapezius and quadriceps and overlying skin and subcutis in comparison with normal subjects. Thresholds in patients were normal in skin and subcutis but significantly lower than normal (hyperalgesia) in muscle (P < 0.001) in all sites. The selective muscle hypersensitivity corresponded also to fiber abnormalities at muscle biopsy (quadriceps) performed in nine patients which were absent in normal subjects (four cases): morphostructural alterations of the sarchomere, fatty degeneration and fibrous regeneration, inversion of the cytochrome oxidase/succinate dehydrogenase ratio, pleio/polymorphism and monstruosity of mitochondria, reduction of some mitochondrial enzymatic activities and increments of common deletion of 4977 bp of mitochondrial DNA 150–3000 times the normal values. By showing both sensory (diffuse hyperalgesia) and anatomical (degenerative picture) changes at muscle level, the results suggest a role played by peripheral mechanisms in the genesis of CFS symptoms. They would exclude the heightened perception of physiological signals from all districts hypothesized by some authors, especially as the hyperalgesia is absent in skin/subcutis.

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Chronic fatigue syndrome (CFS) and fibromyalgia (FM) are both complex conditions that are challenging to treat. This may be related to an incomplete understanding of their pathophysiology, itself obfuscated by their heterogeneity. The symptomatic overlap between them and their common comorbidity suggests a shared vulnerability, which might be explained by central sensitisation.
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CS, as defined by the presence of both enhanced TS and inefficient CPM, was present in 16 (84%) CFS cases, 18 (95%) FM cases, and none of the HC (p < 0.001). Pressure pain thresholds were lower in CFS (Median222kPaIQR 146–311; p = 0.04) and FM cases (Median 189 kPa; IQR 129–272; p = 0.003) compared to HC (Median 311 kPa; IQR 245–377). FM cases differed from HC in cold-induced (FM = 22.6 °C (15.3–27.7) vs HC = 14.2 °C (9.0–20.5); p = 0.01) and heat-induced (FM = 38.0 °C (35.2–44.0) vs HC = 45.3 °C (40.1–46.8); p = 0.03) pain thresholds, where CFS cases did not.
Central sensitisation may be a common endophenotype in chronic fatigue syndrome and fibromyalgia. Further research should address whether central sensitisation is a cause or effect of these disorders.
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Interestingly, mitochondria have their own genome, mitochondrial DNA (mtDNA), a 16,569-bp, double-strand, circular molecule that contains the genetic information necessary for the synthesis of 13 essential polypeptides of the mitochondrial respiratory chain (Verge et al., 2011). Mitochondrial dysfunction and mtDNA alterations have been hypothesized to be involved in both CFS (Myhill et al., 2013; Myhill et al., 2009; Vecchiet et al., 1996; Zhang et al., 1995) and schizophrenia (Anglin et al., 2012; Ben-Shachar, 2002; Sequeira et al., 2012; Torrell et al., 2013; Verge et al., 2011). Here, we present a three-member family consisting of a proband presenting schizophrenia and symptoms compatible with CFS and her mother and older sister who present CFS, among multiple other conditions.
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Chronic fatigue syndrome (CFS) is an often-debilitating condition of unknown origin. There is a general consensus among CFS researchers that the symptoms seem to reflect an ongoing immune response, perhaps due to viral infection. Thus, most CFS research has focused upon trying to uncover that putative immune system dysfunction or specific pathogenic agent. However, no single causative agent has been found. In this speculative article, I describe a new hypothesis for the etiology of CFS: infection of the vagus nerve. When immune cells of otherwise healthy individuals detect any peripheral infection, they release proinflammatory cytokines. Chemoreceptors of the sensory vagus nerve detect these localized proinflammatory cytokines, and send a signal to the brain to initiate sickness behavior. Sickness behavior is an involuntary response that includes fatigue, fever, myalgia, depression, and other symptoms that overlap with CFS. The vagus nerve infection hypothesis of CFS contends that CFS symptoms are a pathologically exaggerated version of normal sickness behavior that can occur when sensory vagal ganglia or paraganglia are themselves infected with any virus or bacteria. Drawing upon relevant findings from the neuropathic pain literature, I explain how pathogen-activated glial cells can bombard the sensory vagus nerve with proinflammatory cytokines and other neuroexcitatory substances, initiating an exaggerated and intractable sickness behavior signal. According to this hypothesis, any pathogenic infection of the vagus nerve can cause CFS, which resolves the ongoing controversy about finding a single pathogen. The vagus nerve infection hypothesis offers testable hypotheses for researchers, animal models, and specific treatment strategies.
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^☆: This study was supported by funds from the Italian National Research Council (CNR), C.n. 94.00671.PF41, Targeted Project ‘Prevention and Control of Disease Factors’, Subproject ‘Stress’, ‘Neurophysiological and Psychological Aspects of Fibromyalgic Syndromes’. via P.A. Valignani, 66100 Chieti, Italy. Fax: +39 871 565286/345460

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Sensory characterization of somatic parietal tissues in humans with chronic fatigue syndrome☆

Abstract

Pain

Pain

Enteroviruses and postviral fatigue syndrome

Mitochondrial abnormalities in the postviral fatigue syndrome

Acta Neuropathol.

Chornic fatigue syndrome, fibromyalgia and myofascial pain syndrome: comparative sensory evaluation of parietal tissues

A multidisciplinary approach to investigating and treating patients with chronic fatigue

Muscle histopathology and physiology in chronic fatigue syndrome

Needle biopsy of skeletal muscle in the diagnosis of myopathy and the clinical study of muscle function and repair

N. Engl. J. Med.