Chronic pain is defined as persistent or recurrent pain lasting longer than three months (1), or pain that occurs on at least half the days for six months or more. (2) Estimates suggest that chronic pain affects more than 20% of the global population. (3-10) In the US alone, over 70-100 million adults suffer from chronic pain. (120-122,126)

Chronic pain interferes with daily activities, including the ability to work, and has a profound economic impact. (11) In the US, medical expenses and lost wages due to chronic pain are estimated to exceed half a trillion dollars. (12) In Europe, chronic pain costs compromise 2-3% of the GDP. (13,14)

Chronic pain tends to affect men and women fairly equally. (15) Predisposing factors include genetics, environmental influences, social determinants, and lifestyle factors, i.e., stress, physical inactivity, smoking, poor diet, and inadequate sleep. (10,16, 129)

The International Classification of Diseases (ICD) categorizes chronic pain based upon triggers (primary, cancer, post-traumatic, post-surgical) or sites (headache, orofacial, visceral, musculoskeletal). (17) However, a more clinically useful neuroanatomical classification of chronic pain requires an understanding of pain science.

The Science of Pain

Pain is an unpleasant sensation triggered by the activation of nociceptors in response to potentially harmful stimuli. (18) Tissue irritation or damage triggers inflammation and prostaglandin release. Prostaglandins activate peripheral nociceptors, which send signals back to the spinal cord via afferent sensory nerve fibers (first-order neurons). These signals come through the spinal cord’s dorsal (sensory) root, then enter the DRG and dorsal horn of the spinal cord where the first-order neuron releases substance P to relay its signal to the second-order neuron. (19) The spinal cord’s dorsal horn is often called the “gate” because of its ability to help control pain transmission between first and second-order neurons.

After leaving the dorsal horn, the second-order neuron’s signal crosses to the opposite side and travels up to the brain via the spinothalamic tract. The second-order neuron terminates in the thalamus where it synapses with the third-order neuron, which relays this signal to the somatosensory cortex to discern the area and severity of injury.

Once a stimulus has traveled through the first, second, and third-order neurons of the ascending pathway and has been interpreted by the brain, the descending pathway sends signals back down to inhibit or control communication between the first and second-order neuron in the dorsal horn.

If noxious stimulation persists, the nervous system can learn to suppress that input via habituation, or progressively amplify the response to those stimuli via sensitization. (18,128) Habituation is a healthy neurologic response to help filter out insignificant sustained sensory input like a ticking clock or sunglasses resting on top of someone’s head. Conversely, sensitization increases responsiveness of the nervous systems to any potentially threatening stimulus. (18)

Central sensitization is an augmentation of responsiveness or “an amplification of neural signaling within the CNS that elicits pain hypersensitivity.” (21-23) Repetitive stimulation at the cortex places the brain in a state of high alert, which is clinically termed temporal summation and commonly recognized as the wind-up or central sensitization. (10,23-25) Via a neuroplastic response, the brain adapts both anatomically and physiologically to detect ongoing stimuli via an increased number of excitatory synapses operating with greater efficiency, along with concurrent suppression of descending nociceptive inhibition. (24,25).

Repetitive cortical stimulation not only sensitizes the synaptic chain between the brain and primary site of pain (primary hyperalgesia), but may also potentiate synapses in areas adjacent to the primary site of pain (secondary hyperalgesia). (18)

Augmented responsiveness to noxious or threatening stimuli may involve one, two, or all three of the following neuroanatomical sites.

Nociceptive pain involves the peripheral nociceptors sensing tissue damage or potentially threatening stimuli, i.e., lumbar disc lesion, myofascial pain syndrome.
Neuropathic pain involves augmented responsiveness in the first, second, and third-order neurons somewhere between the periphery, spinothalamic tract, and brain, i.e., complex regional pain syndrome, sciatica.
Centralized pain or central sensitization involves a “wind up” or augmented responsiveness within the brain, i.e., fibromyalgia.

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What we do in our office to help this condition:

1. Perform a detailed exam, assessing the alignment of the spine. Pain is a last effort response signal from the brain that occurs right before permanent damage. Pain is typically accompanied by inflammation and muscle tension spasm. Our goal is find the areas of the spine where this is occurring.

2. As indicated, adjust areas of spinal subluxations (misalignments), to restore proper nerve system function, which facilitates healing. Once the brain starts to receive better information from the spine, it can move out of protection mode and into healing mode. It is very common for pain to subside when this happens.

3. Apply electrical stimulation and heat to the muscles surrounding the areas of pain. Applying an electrical current helps strengthen muscles, block pain signals, and improve blood circulation.

4. Perform laser therapy which penetrates to the cellular level of the soft tissues surrounding the areas of pain. This promotes better oxygen and nutrients to these tissues, which can relieve pain and facilitate the healing process.

5. Prescribe stretches and exercises in conjunction with chiropractic care to strengthen the soft tissue in the areas of pain.