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Central sensitization is a state of the nervous system that’s related to the development and maintenance of chronic pain. When central sensitization occurs, the nervous system goes through a procedure known as wind-up and gets regulated in a constant condition of increased reactivity. This persistent, or regulated, state of reactivity decreases the threshold for what causes pain and subsequently learns to keep pain after the initial injury has healed. Central sensitization has two major characteristics. Both have an increased sensitivity to pain and to the feeling of touch. These are referred to as allodynia and hyperalgesia.
Allodynia occurs when an individual experiences pain with circumstances that are normally not supposed to be painful. For instance, chronic pain patients often experience pain even with things as simple as touch or a massage. In these situations, nerves in the region which has been touched sends signals through the nervous system into the brain. Because the nervous system is in a constant condition of heightened reactivity, the brain doesn’t generate a mild feeling of touch as it should, given that the stimulus that initiated it was an easy touch or massage. Instead, the brain produces a feeling of pain and discomfort.
Hyperalgesia occurs when a stimulus that’s usually considered to be somewhat painful is perceived as a much more debilitating pain than it ought to be. For instance, chronic pain patients that experience a simple bump, which generally would be mildly painful, will often feel intense pain. Again, once the nervous system is in a constant condition of high reactivity, it amplifies pain.
Chronic pain patients sometimes believe they might be suffering from a mental health issue because they understand from common sense that touch or simple bumps produce tremendous amounts of pain or discomfort. Other times, it’s not the patients themselves who feel this way, but their friends and family members. Individuals who don’t suffer with chronic pain may witness others who have central sensitization experience pain at the slightest touch or cry out at the simplest bump. However, because they don’t have the condition, it may be difficult for them to understand what someone who does is going through.
In addition to allodynia and hyperalgesia, central sensitization has other well-known features, though they may occur less commonly. Central sensitization may lead to heightened sensitivities throughout all senses, not only the feeling of touch. Chronic pain patients can sometimes report sensitivities to light, smell and sound. As such, regular levels of light may seem overly bright or even the perfume aisle in the department shop can produce a headache. Central sensitization can also be associated with cognitive deficits, such as poor concentration and poor short-term memory. Central sensitization also interferes with increased levels of psychological distress, particularly fear and axiety. After all, the nervous system is responsible for not merely senses, like pain, but also emotions. If the nervous system is trapped in a constant condition of reactivity, patients are going to be nervous or anxious. Lastly, central sensitization is also correlated with sick role behaviors, such as resting and malaise, and pain behavior.
Central sensitization has long been known as a potential consequence of stroke and spinal cord injury. However, it is increasingly believed that it plays a part in several different chronic pain disorders. It may happen with chronic low back pain, chronic neck pain, whiplash injuries, chronic tension headaches, migraine headaches, rheumatoid arthritis, osteoarthritis of the knee, endometriosis, injuries sustained in an automobile accident, and even following surgeries. Fibromyalgia, irritable bowel syndrome, and chronic fatigue syndrome, all appear to occur due to central sensitization as well.
What Causes Central Sensitization?
Central sensitization involves specific changes to the nervous system. Changes in the dorsal horn of the spinal cord and in the brain occur, particularly at the cellular level, such as at the receptor sites. As mentioned previously, it has long been proven that fractures and spinal cord injuries can cause central sensitization. It stands to reason. Strokes and spinal cord injuries cause harm to the central nervous system, including the brain, in the event of strokes, and the spinal cord, in the case of spinal cord injuries. These injuries change the sections of the nervous system which are involved in central sensitization.
However, what about the other, more prevalent, types of chronic pain disorders, recorded above, such as headaches, chronic back pain, or pain in the extremities? The accidents or conditions which lead to these kinds of chronic pain are not direct injuries to the brain or spinal cord. Rather, they include injuries or condition which affect the peripheral nervous system, particularly in that are of the nervous system which lies outside the spinal cord and brain. How can health issues associated with the peripheral nervous system contribute to modifications in the central nervous system and cause chronic pain in the isolated area of the initial injury? In summary, how can isolated migraine headaches eventually become chronic daily headaches? How can an acute low back lifting injury become chronic low back pain? How does an injury to the hand or foot turn into a complex regional pain syndrome?
There are probably multiple factors that cause the development of central sensitization in these ‘peripheral’ chronic pain disorders. These variables may be divided into two classes:
- Factors that are associated with the state of the central nervous system before onset of the initial pain or injury condition
- Factors that are associated with the central nervous system following onset of the initial pain or injury condition
The first group involves those factors that might predispose individuals to developing central sensitization once an accident occurs and the next group involves antecedent factors that boost central sensitization once pain begins.
Dr. Alex Jimenez’s Insight
Chronic pain can often modify the way the central nervous system itself functions, so much so that a patient may become more sensitive to pain with less provocation. This is what’s referred to as central sensitization and it generally involves changes in the central nervous system, or CNS, more specifically, in the brain and the spinal cord. Central sensitization has been associated with several common diseases and it’s even been reported to develop with something as simple as a muscle ache. Central sensitization has also been documented to persist and worsen even in the absence of obvious provocation. Several factors have also been attributed with the development of central sensitization, although the true cause is still unknown.
Predisposing Factors for Central Sensitization
There are probably biological, emotional, and environmental predisposing factors for central sensitization. Low and higher sensitivity to pain, or pain thresholds, are perhaps in part due to numerous genetic factors. While there’s absolutely no research as of yet to support a causal link between pre-existing pain thresholds and following development of central sensitization after an incident, it’s largely assumed that it will be eventually found.
Psychophysiological factors, like the stress-response, are also apt to play a part in the development of central sensitization. Direct experimental evidence on animals and humans, as well as prospective studies on humans, have demonstrated a connection between stress and the decrease of pain thresholds. Similarly, different kinds of pre-existing anxiety about pain is consistently related to higher pain sensitivities. All these psychophysiological aspects suggest that the preexisting state of the nervous system is also an important determinant of creating central sensitization after the onset of pain. If the stress response has made the nervous system responsive prior to injury, then the nervous system might be more prone to become sensitized once onset of pain happens.
There is considerable indirect evidence for this theory as well. A prior history of anxiety, physical and psychological trauma, and depression are predictive of onset of chronic pain later in life. The most common denominator between chronic pain, anxiety, nervousness, injury, and depression, is the nervous system. They’re all states of the nervous system, especially a persistently changed, or dysregulated, nervous system.
It’s not that such pre-existing health issues make individuals more vulnerable to injury or the onset of illness, as injury or illness is apt to happen on a somewhat random basis across the populace. Instead, these pre-existing health issues are more inclined to make people prone to the development of chronic pain once an injury or disease occurs. The dysregulated nervous system, at the time of injury, for instance, may interfere with the normal trajectory of healing and thereby stop pain from subsiding once tissue damage is healed.
Factors Resulting in Central Sensitization After Onset of Pain
Predisposing factors may also be part of the development of central sensitization. The onset of pain is frequently associated with subsequent development of conditions, such as depression, fear-avoidance, nervousness or anxiety and other phobias. The stress of those responses can, in turn, further exacerbate the reactivity of the nervous system, leading to central sensitization. Inadequate sleep is also a frequent effect of living with chronic pain. It’s associated with increased sensitivity to pain as well. In what’s technically known as operant learning, interpersonal and environmental reinforcements have long been proven to lead to pain behaviors, however, it is also evident that such reinforcements may lead to the development of central sensitization.
Treatments of Central Sensitization
Treatments for chronic pain syndromes that involve fundamental sensitization typically target the central nervous system or the inflammation which corresponds with central sensitization. All these often generally include antidepressants and anticonvulsant medications, and cognitive behavioral treatment. While usually not considered to target the central nervous system, regular mild aerobic exercise changes structures in the central nervous system and contributes to reductions in the pain of many ailments which are mediated by central sensitization. As such, moderate aerobic exercise is used to treat chronic pain syndromes marked by central sensitization. Non-steroidal anti-inflammatories are utilized for the inflammation associated with central sensitization.
Finally, chronic pain rehabilitation programs are a standard, interdisciplinary treatment that employs each of the above-noted therapy strategies in a coordinated manner. They also make the most of the research on the role of operant learning from central sensitization and also have developed behavioral interventions to reduce the pain and discomfort associated with the health issue. Such applications are typically considered the most effective treatment option for chronic pain syndromes. The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .
Curated by Dr. Alex Jimenez
Additional Topics: Sciatica
Sciatica is medically referred to as a collection of symptoms, rather than a single injury and/or condition. Symptoms of sciatic nerve pain, or sciatica, can vary in frequency and intensity, however, it is most commonly described as a sudden, sharp (knife-like) or electrical pain that radiates from the low back down the buttocks, hips, thighs and legs into the foot. Other symptoms of sciatica may include, tingling or burning sensations, numbness and weakness along the length of the sciatic nerve. Sciatica most frequently affects individuals between the ages of 30 and 50 years. It may often develop as a result of the degeneration of the spine due to age, however, the compression and irritation of the sciatic nerve caused by a bulging or herniated disc, among other spinal health issues, may also cause sciatic nerve pain.
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1. Phillips, K. & Clauw, D. J. (2011). Central pain mechanisms in chronic pain states – maybe it is all in their head. Best Practice Research in Clinical Rheumatology, 25, 141-154.
2. Yunus, M. B. (2007). The role of central sensitization in symptoms beyond muscle pain, and the evaluation of a patient with widespread pain. Best Practice Research in Clinical Rheumatology, 21, 481-497.
3. Curatolo, M., Arendt-Nielsen, L., & Petersen-Felix, S. (2006). Central hypersensitivity in chronic pain: Mechanisms and clinical implications. Physical Medicine and Rehabilitation Clinics of North America, 17, 287-302.
4. Wieseler-Frank, J., Maier, S. F., & Watkins, L. R. (2005). Immune-to-brain communication dynamically modulates pain: Physiological and pathological consequences. Brain, Behavior, & Immunity, 19, 104-111.
5. Meeus M., & Nijs, J. (2007). Central sensitization: A biopsychosocial explanation for chronic widespread pain in patients with fibromyalgia and chronic fatigue syndrome. Clinical Journal of Rheumatology, 26, 465-473.
6. Melzack, R., Coderre, T. J., Kat, J., & Vaccarino, A. L. (2001). Central neuroplasticity and pathological pain. Annals of the New York Academy of Sciences, 933, 157-174.
7. Flor, H., Braun, C., Elbert, T., & Birbaumer, N. (1997). Extensive reorganization of primary somatosensory cortex in chronic back pain patients. Neuroscience Letters, 224, 5-8.
8. O’Neill, S., Manniche, C., Graven-Nielsen, T., Arendt-Nielsen, L. (2007). Generalized deep-tissue hyperalgesia in patients with chronic low-back pain. European Journal of Pain, 11, 415-420.
9. Chua, N. H., Van Suijlekom, H. A., Vissers, K. C., Arendt-Nielsen, L., & Wilder-Smith, O. H. (2011). Differences in sensory processing between chronic cervical zygapophysial joint pain patients with and without cervicogenic headache. Cephalalgia, 31, 953-963.
10. Banic, B, Petersen-Felix, S., Andersen O. K., Radanov, B. P., Villiger, P. M., Arendt-Nielsen, L., & Curatolo, M. (2004). Evidence for spinal cord hypersensitivity in chronic pain after whiplash injury and fibromyalgia. Pain, 107, 7-15.
11. Bendtsen, L. (2000). Central sensitization in tension-type headaches – possible pathophysiological mechanisms. Cephalalgia, 20, 486-508.
12. Coppola, G., DiLorenzo, C., Schoenen, J. & Peirelli, F. (2013). Habituation and sensitization in primary headaches. Journal of Headache and Pain, 14, 65.
13. Stankewitz, A., & May, A. (2009). The phenomenon of changes in cortical excitability in migraine is not migraine-specific – A unifying thesis. Pain, 145, 14-17.
14. Meeus M., Vervisch, S., De Clerck, L. S., Moorkens, G., Hans, G., & Nijs, J. (2012). Central sensitization in patients with rheumatoid arthritis: A systematic literature review. Seminars in Arthritis & Rheumatism, 41, 556-567.
15. Arendt-Nielsen, L., Nie, H., Laursen M. B., Laursen, B. S., Madeleine P., Simonson O. H., & Graven-Nielsen, T. (2010). Sensitization in patients with painful knee osteoarthritis. Pain, 149, 573-581.
16. Bajaj, P., Bajaj, P., Madsen, H., & Arendt-Nielsen, L. (2003). Endometriosis is associated with central sensitization: A psychophysical controlled study. The Journal of Pain, 4, 372-380.
17. McLean, S., Clauw, D. J., Abelson, J. L., & Liberzon, I. (2005). The development of persistent pain and psychological morbidity after motor vehicle collision: Integrating the potential role of stress response systems into a biopsychosocial model. Psychosomatic Medicine, 67, 783-790.
18. Fernandez-Lao, Cantarero-Villanueva, I., Fernandez-de-Las-Penas, C, Del-Moral-Avila, R., Arendt-Nielsen, L., Arroyo-Morales, M. (2010). Myofascial trigger points in neck and shoulder muscles and widespread pressure pain hypersensitivity in patients with post-mastectomy pain: Evidence of peripheral and central sensitization. Clinical Journal of Pain, 26, 798-806.
19. Staud, R. (2006). Biology and therapy of fibromyalgia: Pain in fibromyalgia syndrome. Arthritis Research and Therapy, 8, 208.
20. Verne, V. N., & Price, D. D. (2002). Irritable bowel syndrome as a common precipitant of central sensitization. Current Rheumatology Reports, 4, 322-328.
21. Meeus M., & Nijs, J. (2007). Central sensitization: A biopsychosocial explanation for chronic widespread pain in patients with fibromyalgia and chronic fatigue syndrome. Clinical Journal of Rheumatology, 26, 465-473.
22. Schwartzman, R. J., Grothusen, R. J., Kiefer, T. R., & Rohr, P. (2001). Neuropathic central pain: Epidemiology, etiology, and treatment options. Archives of Neurology, 58, 1547-1550.
23. Alexander, J., DeVries, A., Kigerl, K., Dahlman, J., & Popovich, P. (2009). Stress exacerbates neuropathic pain via glucocorticoid and NMDA receptor activation. Brain, Behavior and Immunity, 23, 851-860.
24. Imbe, H., Iwai-Liao, Y., & Senba, E. (2006). Stress-induced hyperalgesia: Animal models and putative mechanisms. Frontiers in Bioscience, 11, 2179-2192.
25. Kuehl, L. K., Michaux, G. P., Richter, S., Schachinger, H., & Anton F. (2010). Increased basal mechanical sensitivity but decreased perceptual wind-up in a human model of relative hypocortisolism. Pain, 194, 539-546.
26. Rivat, C., Becker, C., Blugeot, A., Zeau, B., Mauborgne, A., Pohl, M., & Benoliel, J. (2010). Chronic stress induces transient spinal neuroinflammation, triggering sensory hypersensitivity and long-lasting anxiety-induced hyperalgesia. Pain, 150, 358-368.
27. Slade, G. D., Diatchenko, L., Bhalang, K., Sigurdsson, A., Fillingim, R. B., Belfer, I., Max, M. B., Goldman, D., & Maixner, W. (2007). Influence of psychological factors on risk of temporomandibular disorders. Journal of Dental Research, 86, 1120-1125.
28. Hirsh, A. T., George, S. Z., Bialosky, J. E., & Robinson, M. E. (2008). Fear of pain, pain catastrophizing, and acute pain perception: Relative prediction and timing of assessment. Journal of Pain, 9, 806-812.
29. Sullivan, M. J. Thorn, B., Rodgers, W., & Ward, L. C. (2004). Path model of psychological antecedents to pain experience: Experimental and clinical findings. Clinical Journal of Pain, 20, 164-173.
30. Nahit, E. S., Hunt, I. M., Lunt, M., Dunn, G., Silman, A. J., & Macfarlane, G. J. (2003). Effects of psychosocial and individual psychological factors on the onset of musculoskeletal pain: Common and site-specific effects. Annals of Rheumatic Disease, 62, 755-760.
31. Talbot, N. L., Chapman, B., Conwell, Y., McCollumn, K., Franus, N., Cotescu, S., & Duberstein, P. R. (2009). Childhood sexual abuse is associated with physical illness burden and functioning in psychiatric patients 50 years of age or older. Psychosomatic Medicine, 71, 417-422.
32. McLean, S. A., Clauw, D. J., Abelson, J. L., & Liberzon, I. (2005). The development of persistent pain and psychological morbidity after motor vehicle collision: Integrating the potential role of stress response systems into a biopsychosocial model. Psychosomatic Medicine, 67, 783-790.
33. Hauser, W., Galek, A., Erbsloh-Moller, B., Kollner, V., Kuhn-Becker, H., Langhorst, J… & Glaesmer, H. (2013). Posttraumatic stress disorder in fibromyalgia syndrome: Prevalence, temporal relationship between posttraumatic stress and fibromyalgia symptoms and impact on clinical outcome. Pain, 154, 1216-1223.
34. Diatchenko, L., Nackley, A. G., Slade, G. D., Fillingim, R. B., & Maixner, W. (2006). Idiopathic pain disorders – Pathways of vulnerability. Pain, 123, 226-230.
35. Azevedo, E., Manzano, G. M., Silva, A., Martins, R., Andersen, M. L., & Tufik, S. (2011). The effects of total and REM sleep deprivation on laser-invoked potential threshold and pain perception. Pain, 152, 2052-2058.
36. Chiu, Y. H., Silman, A. J., Macfarlane, G. J., Ray, D., Gupta, A., Dickens, C., Morris, R., & McBeth, J. (2005). Poor sleep and depression are independently associated with a reduced pain threshold: Results of a population based study. Pain, 115, 316-321.
37. Holzl, R., Kleinbohl, D. & Huse, E. (2005). Implicit operant learning of pain sensitization. Pain, 115, 12-20.
38. Baumbauer, K. M., Young, E. E., & Joynes, R. L. (2009). Pain and learning in spinal system: Contradictory outcomes from common origins. Brain Research Reviews, 61, 124-143.
39. Becker, S., Kleinbohl, D., Baus, D., & Holzl, R. (2011). Operant learning of perceptual sensitization and habituation is impaired in fibromyalgia patients with and without irritable bowel syndrome. Pain, 152, 1408-1417.
40. Hauser, W., Wolfe, F., Tolle, T., Uceyler, N. & Sommer, C. (2012). The role of antidepressants in the management of fibromyalgia: A systematic review and meta-analysis. CNS Drugs, 26, 297-307.
41. Hauser, W., Bernardy, K., Uceyler, N., & Sommer, C. (2009). Treatment of fibromyalgia syndrome with gabapentin and pregabalin – A meta-analysis of randomized controlled trials. Pain, 145, 169-181.
42. Straube, S., Derry, S., Moore, R. A., & McQuay, H. J. (2010). Pregabalin in fibromyalgia: Meta-analysis of efficacy and safety from company clinical trial reports. Rheumatology, 49, 706-715.
43. Tzellos, T. G., Toulis, K. A., Goulis, D. G., Papazisis, G., Zampellis, Z. A., Vakfari, A., & Kouvelas, D. (2010). Gabapentin and pregabalin in the treatment of fibromyalgia: A systematic review and meta-analysis. Journal of Clinical Pharmacy and Therapeutics, 35, 639-656.
44. Thieme, K. Flor, H., & Turk, D. C. (2006). Psychological pain treatment in fibromyalgia syndrome: Efficacy of operant behavioral and cognitive behavioral treatments. Arthritis Research & Therapy, 8, R121.
45. Lackner, J. M., Mesmer, C., Morley, S., Dowzer, C., & Hamilton, S. (2004). Psychological treatments for irritable bowel syndrome: A systematic review and meta-analysis. Journal of Clinical and Consulting Psychology, 72, 1100-1113.
46. Salomons, T. V., Moayedi, M. Erpelding, N., & Davis, K. D. (2014). A brief cognitive-behavioral intervention for pain reduces secondary hyperalgesia. Pain, 155, 1446-1452. doi: 10.1016/j.pain.2014,02.012
47. Erickson, K. I., Voss., M. W., Prakesh, R. S., et al. (2011). Exercise training increases size of hippocampus and improves memory. Proceedings of the National Academy of Sciences, 108, 3017-3022.
48. Hilman, C. H., Erickson, K. I., & Kramer, A. F. (2008). Be smart, exercise your heart: Exercise effects on brain and cognition. Nature Reviews Neuroscience, 9, 58-65.
49. Busch, A. J., Barber, K. A., Overend, T. J., Peloso, P. M., & Schachter, C. L. (Updated August 17, 2007). Exercise for treating fibromyalgia. In Cochrane Database Reviews, 2007, (4). Retrieved May 16, 2011, from The Cochrane Library, Wiley Interscience.
50. Fordyce, W. E., Fowler, R. S., Lehmann, J. F., Delateur, B. J., Sand, P. L., & Trieschmann, R. B. (1973). Operant conditioning in the treatment of chronic pain. Archives of Physical Medicine and Rehabilitation, 54, 399-408.
51. Gatzounis, R., Schrooten, M. G., Crombez, G., & Vlaeyen, J. W. (2012). Operant learning theory in pain and chronic pain rehabilitation. Current Pain and Headache Reports, 16, 117-126.
52. Hauser, W., Bernardy, K., Arnold, B., Offenbacher, M., & Schiltenwolf, M. (2009). Efficacy of multicomponent treatment in fibromyalgia syndrome: A meta-analysis of randomized controlled clinical trials. Arthritis & Rheumatism, 61, 216-224.
53. Flor, H., Fydrich, T. & Turk, D. C. (1992). Efficacy of multidisciplinary pain treatment centers: A meta-analytic review. Pain, 49, 221-230.
54. Gatchel, R., J., & Okifuji, A. (2006). Evidence-based scientific data documenting the treatment and cost-effectiveness of comprehensive pain programs for chronic non-malignant pain. Journal of Pain, 7, 779-793.
55. Turk, D. C. (2002). Clinical effectiveness and cost-effectiveness of treatments for patients with chronic pain. The Clinical Journal of Pain, 18, 355-365.
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