The pain no exam can explain
"Today it's in my shoulder, yesterday it was in my lower back, the day before it was in my knee." Those who report pain that moves around, migrates through the body, and has no identifiable local cause frequently receive frustrating answers: "your tests are normal", "it must be anxiety", or "learn to live with it". When inflammatory, autoimmune, and infectious causes have been adequately excluded by medical assessment, part of these presentations corresponds to central sensitization — a real condition, with documented neurophysiologic substrate, that modern medicine understands better and better.
Central sensitization occurs when the central nervous system — spinal cord and brain — develops generalized hyperexcitability. The pain threshold drops drastically, and stimuli that would not normally cause pain are interpreted as painful. The pain "wanders" through the body because the problem is not in peripheral tissues, but in the central processing system — which amplifies and generalizes any nociceptive signal that arrives.
How the central nervous system becomes hypersensitive
Untreated peripheral pain
Uncontrolled acute pain — whether from injury, surgery, or inflammatory condition — generates continuous nociceptive bombardment to the spinal cord. If maintained for weeks, this bombardment induces plastic changes in the neurons of the dorsal horn: the wind-up phenomenon and spinal LTP (long-term potentiation).
Reduction of descending inhibitory systems
The brain normally "brakes" pain via descending inhibitory pathways that release serotonin and norepinephrine. In central sensitization, these inhibitory systems become less effective — whether from neurotransmitter depletion or loss of volume of the periaqueductal gray matter (documented on functional MRI).
Generalization and allodynia
With established spinal sensitization, adjacent neurons are recruited — expanding the receptive field of pain. This explains allodynia (pain on light touch) and hyperalgesia (excessive pain to moderate stimuli). Pain "migrates" because the central system amplifies signals from any region.
Neuroimaging of central sensitization
fMRI studies show hyperactivity in pain-processing regions (anterior insula, anterior cingulate córtex, thalamus) and hypoactivity of inhibition regions (dorsolateral prefrontal córtex) in patients with central sensitization — objective evidence that the alteration is real and measurable.
Acupuncture as a possible central neuromodulator
There are mechanistic hypotheses suggesting that medical acupuncture modulates the descending inhibitory pathway involving the periaqueductal gray (PAG) and favors release of serotonin, norepinephrine, and endogenous opioids, with reduction of hyperactivity in pain-amplification regions. Findings on neuroimaging and experimental models point in this direction, but exact mechanisms remain under investigation.
Data on central sensitization and fibromyalgia
Recognizing central sensitization
Central sensitization — typical pattern
- 01
Pain that changes location over days or weeks
- 02
Pain disproportionate to the stimulus — "it hurts too much for what happened"
- 03
Multiple sites of pain simultaneously or sequentially
- 04
Allodynia: pain on light touch, clothing pressure, mild temperature
- 05
Normal laboratory and imaging tests or no correlation with the pain
- 06
Worsening with emotional stress, poor sleep, and anxiety
- 07
Fatigue disproportionate to associated pain
- 08
Difficulty concentrating ("brain fog")
Myths and facts about pain that moves around
Myth vs. Fact
If the tests are normal, the pain is invented or psychosomatic
Central sensitization is a real alteration of the nervous system — documented on functional neuroimaging, electromyography, and neuroinflammation markers. Saying that the pain is "psychological" because structural tests are normal confuses two things: absence of tissue damage and absence of cause. The cause exists — it is in the central nervous system, not in peripheral tissue.
Pain that moves around has no treatment
Central sensitization has approaches that can reduce symptoms and improve function, although there is no definitive cure in many cases. The current strategy combines neuromodulation (medical acupuncture, with evidence of benefit in some patients), pharmacotherapy (duloxetine, pregabalin, tricyclics in low dose — per medical prescription), and psychosocial approaches (pain-focused cognitive behavioral therapy). Systemic medical acupuncture appears to act on descending inhibitory pathways related to the sensitization phenomenon.
Anti-inflammatories and common analgesics resolve generalized pain
Anti-inflammatories treat peripheral inflammation — which is not the mechanism of central sensitization. Chronic use of opioid analgesics and NSAIDs in central sensitization can paradoxically worsen hyperalgesia (opioid-induced hyperalgesia) and generate dependence without lasting benefit. Effective treatment is neuromodulatory, not anti-inflammatory.
The periaqueductal gray matter: the analgesia center
Systemic treatment protocol
Diagnosis and pain education
1st–2nd visitApplication of the Central Sensitization Inventory (CSI). Exclusion of inflammatory and neoplastic causes. Explanation of the mechanism of central sensitization — pain neuroscience education reduces catastrophizing and improves treatment outcomes. Assessment of sleep, anxiety, and mood.
Systemic acupuncture — intensive phase
Sessions 1–8 (2x/week)Central neuromodulation points: GV-20, GV-24, PC-6, HT-7 (anxiolytic action and limbic system modulation). Systemic analgesia points: ST-36, SP-6, LI-4, LR-3 (activation of the descending inhibitory pathway). 2 Hz electroacupuncture to maximize beta-endorphin release.
Consolidation and multimodal approach
Sessions 9–16 (1x/week)Frequency reduction with maintenance of effect. Integration with pharmacologic approach if indicated by the physician. Sleep hygiene — fundamental for sensitization reduction (sleep deprivation increases hyperalgesia). Progressive introduction of low-intensity aerobic exercise.
Maintenance and relapse prevention
Biweekly or monthlyMaintenance sessions to prevent resensitization. Monitoring of pain profile and sleep quality. Approach to perpetuating factors: chronic stress, TMJ dysfunction, peripheral trigger points that feed central sensitization.
Clinical pearl: the central sensitization inventory
Frequently asked questions
Frequently Asked Questions
Fibromyalgia is a chronic syndrome that rarely enters complete permanent remission. The realistic goal is reduction of pain, improvement of sleep and quality of life, with periods of lower disease activity. Medical acupuncture, in combination with supervised exercise and psychosocial approach, can contribute to these goals in some patients treated consistently — the magnitude of benefit varies and should be assessed individually by the physician.
In the intensive treatment phase of central sensitization, 2 sessions per week in the first 4 weeks maximizes the cumulative neuromodulatory effect. After this phase, 1 weekly session for another 4–8 weeks, followed by biweekly or monthly maintenance. The medical acupuncturist adjusts frequency according to individual response.
Yes. Medical acupuncture is safe in combination with duloxetine, pregabalin, amitriptyline, and other medications used for fibromyalgia and chronic pain. In many cases, the physician can progressively reduce the medication dose according to the response to acupuncture — always with close medical follow-up. Never discontinue medications without guidance from your physician.