Clinical Definition of Fibromyalgia Tender (Pressure) Points
Fibromyalgia is a chronic, centralized pain disorder characterized by widespread musculoskeletal pain, fatigue, sleep disturbance, and sensory hypersensitivity. One historical diagnostic feature of fibromyalgia is the presence of tender points (often called “pressure points”), which are discrete, anatomically predictable areas of localized soft-tissue hypersensitivity that produce disproportionate pain in response to mild digital pressure.
Definition
Tender points are specific sites within muscles, tendons, or periarticular soft tissues that demonstrate:
Pathophysiology
Tender points are believed to reflect central sensitization rather than local tissue injury. Individuals with fibromyalgia exhibit:
Definition
Tender points are specific sites within muscles, tendons, or periarticular soft tissues that demonstrate:
- heightened pain sensitivity to palpation
- lower mechanical pain thresholds
- pain disproportionate to applied force
- absence of visible inflammation or structural pathology
Pathophysiology
Tender points are believed to reflect central sensitization rather than local tissue injury. Individuals with fibromyalgia exhibit:
- amplified nociceptive signaling
- reduced descending pain inhibition
- increased CNS excitability
- altered neurotransmitter activity (e.g., substance P elevation, serotonin/norepinephrine dysregulation)
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Historical Diagnostic Role
The 1990 American College of Rheumatology fibromyalgia diagnostic criteria required:
Modern criteria (2010/2016 ACR revisions) no longer require formal tender point examination, recognizing that fibromyalgia reflects systemic pain processing dysregulation, not isolated peripheral tenderness. However, pressure point sensitivity remains clinically useful for:
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Clinical Summary
Tender (pressure) points in fibromyalgia represent neurophysiologic hypersensitivity to mechanical stimulation, secondary to central pain amplification, rather than localized injury or inflammation.
Tender (pressure) points in fibromyalgia represent neurophysiologic hypersensitivity to mechanical stimulation, secondary to central pain amplification, rather than localized injury or inflammation.
References (APA 7th Edition)
Brosschot, J. F., Verkuil, B., & Thayer, J. F. (2017). Generalized unsafety theory of stress: Prolonged autonomic stress activation and health consequences. Neuroscience & Biobehavioral Reviews, 74, 287–296. https://doi.org/10.1016/j.neubiorev.2016.11.001
Cleare, A. J. (2004). The HPA axis and the genesis of chronic fatigue syndrome. Trends in Endocrinology & Metabolism, 15(2), 55–59. https://doi.org/10.1016/j.tem.2003.12.002
Institute of Medicine. (2015). Beyond myalgic encephalomyelitis/chronic fatigue syndrome: Redefining an illness. National Academies Press. https://doi.org/10.17226/19012
Jason, L. A., Sunnquist, M., & Brown, A. (2015). Chronic fatigue syndrome: Diagnostic criteria reconsidered. Journal of Clinical Psychology, 71(5), 466–479. https://doi.org/10.1002/jclp.22174
McEwen, B. S., & Akil, H. (2020). Revisiting the stress concept: Implications for affective disorders. Journal of Neuroscience, 40(1), 12–21. https://doi.org/10.1523/JNEUROSCI.0733-19.2019
Pace, T. W. W., & Heim, C. M. (2011). A short review on the psychoneuroimmunology of chronic fatigue syndrome. Brain, Behavior, and Immunity, 25(1), 7–13. https://doi.org/10.1016/j.bbi.2010.06.003
VanElzakker, M. B., Brumfield, S. A., & Lara Mejia, P. S. (2019). Neuroinflammation and cytokines in chronic fatigue syndrome. Frontiers in Psychiatry, 10, 102. https://doi.org/10.3389/fpsyt.2019.00102
Yehuda, R., & LeDoux, J. (2007). Response variation following trauma: A translational neuroscience approach to PTSD. Neuron, 56(1), 19–32. https://doi.org/10.1016/j.neuron.2007.09.006
Walker, M. P. (2017). Why we sleep: Unlocking the power of sleep and dreams. Scribner.
Brosschot, J. F., Verkuil, B., & Thayer, J. F. (2017). Generalized unsafety theory of stress: Prolonged autonomic stress activation and health consequences. Neuroscience & Biobehavioral Reviews, 74, 287–296. https://doi.org/10.1016/j.neubiorev.2016.11.001
Cleare, A. J. (2004). The HPA axis and the genesis of chronic fatigue syndrome. Trends in Endocrinology & Metabolism, 15(2), 55–59. https://doi.org/10.1016/j.tem.2003.12.002
Institute of Medicine. (2015). Beyond myalgic encephalomyelitis/chronic fatigue syndrome: Redefining an illness. National Academies Press. https://doi.org/10.17226/19012
Jason, L. A., Sunnquist, M., & Brown, A. (2015). Chronic fatigue syndrome: Diagnostic criteria reconsidered. Journal of Clinical Psychology, 71(5), 466–479. https://doi.org/10.1002/jclp.22174
McEwen, B. S., & Akil, H. (2020). Revisiting the stress concept: Implications for affective disorders. Journal of Neuroscience, 40(1), 12–21. https://doi.org/10.1523/JNEUROSCI.0733-19.2019
Pace, T. W. W., & Heim, C. M. (2011). A short review on the psychoneuroimmunology of chronic fatigue syndrome. Brain, Behavior, and Immunity, 25(1), 7–13. https://doi.org/10.1016/j.bbi.2010.06.003
VanElzakker, M. B., Brumfield, S. A., & Lara Mejia, P. S. (2019). Neuroinflammation and cytokines in chronic fatigue syndrome. Frontiers in Psychiatry, 10, 102. https://doi.org/10.3389/fpsyt.2019.00102
Yehuda, R., & LeDoux, J. (2007). Response variation following trauma: A translational neuroscience approach to PTSD. Neuron, 56(1), 19–32. https://doi.org/10.1016/j.neuron.2007.09.006
Walker, M. P. (2017). Why we sleep: Unlocking the power of sleep and dreams. Scribner.