Central Sensitivity Syndrome
Central Sensitivity Syndrome (CSS)
In 1984, Dr. Muhammad B. Yunus included a number of difference processes with shared characteristics in CSS, all of them with unknown causes but similar physiopathology.
The main symptoms of this pathology include:
Patients with these symptoms are frequently diagnosed, by different specialists, with Fibromyalgia, Chronic Fatigue Syndrome, Irritable Bowel Syndrome, Migraine or Tension Headache, Restless Legs Syndrome, Multiple Chemical Syndrome, among others. Central Sensitivity Syndrome (CSS) currently encompasses all of these pathologies, which, instead of being independent entities have shared production mechanisms. This means that the patient does not have several diseases but a single disorder that can cause all of the symptoms described.
Further study of the SSC revealed a hyperexcitability of the neurons, which causes a central sensitisation to different peripheral stimuli: pain, smell, noise, food, chemicals, electromagnetic fields, weather changes, stress, infections, use of drugs, etc., and also presents an immune hypersensitivity to different food antigens, chemical antigens (drugs, detergents, soaps, creams, make up, etc.), physical antigens (light, noise, heat, cold weather change, etc.). Together, the deregulation to these two systems, the immune and central systems, produces an imbalance in the endocrine system.
Central and immunological sensitisation are responsible for lowering the thresholds to the various stimuli and, therefore, for increasing sensitivity, causing the wind-up phenomenon and persistent pain in spite of having removed the stimulus.
This wind-up phenomenon can also be responsible for an excessive response to different stimuli. When this sensitisation is sustained over time, changes in neuroplasticity occur that can be shown in imaging tests such as functional MRIs. Characteristic findings can also be shown in SPECT (single photon emission computed tomography) or magnetoencephalography, among others.
The malfunctioning of the CNS and the immune system ends up affecting the endocrine system.
In CSS, therefore, there is a neurosensorial deregulation that produces neuroendocrine and immune system alterations, creating a vicious circle that is the origin of the multiple symptoms and syndromes that appear in this process.
The chronification of the process leads to an increase in oxidative stress and free radicals, triggers the release of pro-inflammatory and immunological substances, causes dysfunction in the mitochondria, etc. As a result of the deregulation of all of these closely related systems, a complex and varied symptomatology appears as no organ is free from the action of these systems.
- Genuis, S. J. (2010). Sensitivity-related illness: the escalating pandemic of allergy, food intolerance and chemical sensitivity. Science of the Total Environment, 408(24), 6047-6061.
- Barnes, J. G. (2001). ‘Sensitivity syndromes’ related to radiation exposures. Medical hypotheses, 57(4), 453-458.
- De Luca, C., Scordo, M. G., Cesareo, E., Pastore, S., Mariani, S., Maiani, G.,& Raskovic, D. (2010). Biological definition of multiple chemical sensitivity from redox state and cytokine profiling and not from polymorphisms of xenobiotic-metabolizing enzymes. Toxicology and applied pharmacology,248(3), 285-292.
- Staud, R. (2015). Cytokine and immune system abnormalities in fibromyalgia and other central sensitivity syndromes. Current rheumatology reviews, 11(2), 109-115.
- S Boomershine, C. (2015). Fibromyalgia: the prototypical central sensitivity syndrome. Current rheumatology reviews, 11(2), 131-145.
- Latremoliere, A., & Woolf, C. J. (2009). Central sensitization: a generator of pain hypersensitivity by central neural plasticity. The Journal of Pain, 10(9), 895-926.
- Woolf, C. J. (1983). Evidence for a central component of post-injury pain hypersensitivity. Nature.
- Woolf, C. J., & Ma, Q. (2007). Nociceptors—noxious stimulus detectors. Neuron, 55(3), 353-364.
- Chen, X., Tanner, K., & Levine, J. D. (1999). Mechanical sensitization of cutaneous C-fiber nociceptors by prostaglandin E 2 in the rat. Neuroscience letters, 267(2), 105-108.
- Guenther, S., Reeh, P. W., & Kress, M. (1999). Rises in [Ca2+] i mediate capsaicin‐and proton‐induced heat sensitization of rat primary nociceptive neurons. European Journal of Neuroscience, 11(9), 3143-3150.
- Hucho, T., & Levine, J. D. (2007). Signaling pathways in sensitization: toward a nociceptor cell biology. Neuron, 55(3), 365-376.
- Pethö, G., Derow, A., & Reeh, P. W. (2001). Bradykinin‐induced nociceptor sensitization to heat is mediated by cyclooxygenase products in isolated rat skin. European Journal of Neuroscience, 14(2), 210-218.
- Pezet, S., Marchand, F., D’Mello, R., Grist, J., Clark, A. K., Malcangio, M. & McMahon, S. B. (2008). Phosphatidylinositol 3-kinase is a key mediator of central sensitization in painful inflammatory conditions. The Journal of Neuroscience, 28(16), 4261-4270.
- Tao, Y. X., Huang, Y. Z., Mei, L., & Johns, R. A. (2000). Expression of PSD-95/SAP90 is critical for N-methyl-D-aspartate receptor-mediated thermal hyperalgesia in the spinal cord. Neuroscience, 98(2), 201-206.
- Liu, X. J., Gingrich, J. R., Vargas-Caballero, M., Dong, Y. N., Sengar, A., Beggs, S. & Salter, M. W. (2008). Treatment of inflammatory and neuropathic pain by uncoupling Src from the NMDA receptor complex. Nature medicine, 14(12), 1325-1332.
- Lin Q, Palecek J, Paleckova V, Peng YB, Wu J, Cui M, Willis WD. Nitric oxide mediates the central sensitization of primate spinothalamic tract neurons. J Neurophysiol 1999;81:1075–108
- Lin, Q. I. N. G., Peng, Y. B., & Willis, W. D. (1996). Inhibition of primate spinothalamic tract neurons by spinal glycine and GABA is reduced during central sensitization. Journal of neurophysiology, 76(2), 1005-1014.
- Governo, R. J. M., Morris, P. G., Prior, M. J. W., Marsden, C. A., & Chapman, V. (2006). Capsaicin-evoked brain activation and central sensitization in anaesthetised rats: a functional magnetic resonance imaging study. Pain,126(1), 35-45.
- Sun RQ, Tu YJ, Lawand NB, Yan JY, Lin Q, Willis WD. Calcitonin gene-related peptide receptor activation produces PKA- and PKC-dependent mechanical hyperalgesia and central sensitization. J Neurophysiol 2004;92:2859–2866
- Yunus, M. B. (2007). Role of central sensitization in symptoms beyond muscle pain, and the evaluation of a patient with widespread pain. Best Practice & Research Clinical Rheumatology, 21(3), 481-497.
- Ren, K., & Torres, R. (2009). Role of interleukin-1β during pain and inflammation. Brain research reviews, 60(1), 57-64.
- Desmeules, J. A., Cedraschi, C., Rapiti, E., Baumgartner, E., Finckh, A., Cohen, P. & Vischer, T. L. (2003). Neurophysiologic evidence for a central sensitization in patients with fibromyalgia. Arthritis & Rheumatism, 48(5), 1420-1429.
- Katano, T., Furue, H., Okuda‐Ashitaka, E., Tagaya, M., Watanabe, M., Yoshimura, M., & Ito, S. (2008). N‐ethylmaleimide‐sensitive fusion protein (NSF) is involved in central sensitization in the spinal cord through GluR2 subunit composition switch after inflammation. European Journal of Neuroscience, 27(12), 3161-3170.
- Yunus, M. B. (2008, June). Central sensitivity syndromes: a new paradigm and group nosology for fibromyalgia and overlapping conditions, and the related issue of disease versus illness. In Seminars in arthritis and rheumatism (Vol. 37, No. 6, pp. 339-352). WB Saunders.
- Kindler, L. L., Bennett, R. M., & Jones, K. D. (2011). Central sensitivity syndromes: mounting pathophysiologic evidence to link fibromyalgia with other common chronic pain disorders. Pain Management Nursing, 12(1), 15-24.
- Lorduy, K. M., Liegey‐Dougall, A., Haggard, R., Sanders, C. N., & Gatchel, R. J. (2013). The prevalence of comorbid symptoms of central sensitization syndrome among three different groups of temporomandibular disorder patients. Pain Practice, 13(8), 604-613.