Chronic Pain Recovery

Chronic Pain Recovery

People suffering with chronic pain not only feel it physically, but also suffer a wide array of other symptoms. Chronic pain often leads to discouragement, lethargy, depression, and trouble sleeping.

What causes chronic pain?

The brain connects to and controls every part of the body. Research clearly demonstrates that chronic pain is often associated with overactivity in the frontal cortex, the part of the brain most responsible for processing emotions. If this part of the brain just never stops firing pain signals, this can result in neuropathic pain. More often chronic pain is often the result of nerve damage, or damage to the central nervous system which is a system of pain receptors throughout the body. Without treatment, much of this damage lasts lifelong.

The solution

Supported by medical evidence, the Brain reBuilder program works with the body’s natural plasticity, the ability to form and reorganize connections, to allow our body's pain receptors and neurons to heal and adapt. The program focuses on the NMDA receptor, which is associated with learning, memory, pain, and reward. This has the effect of not only allowing patients to recover from chronic pain, but also assists in reducing overall perception of and sensitivity to pain.


Keri S. Taylor, K.S., Anastakis, D.J., Davis, K.D. 2009. Cutting your nerve changes your brain. Brain 2009: 132; 3122–3133. doi:10.1093/brain/awp231 

Peripheral nerve damage decreases that nerve’s function for 1.5 years after the nerve heals, and also causes associated decreased function in the sensory portions of the brain connected to that nerve.

Cooke, S.F., Bliss, T.V.P. 2006. Plasticity in the human central nervous system. Brain (2006), 129, 1659–1673. doi:10.1093/brain/awl082.

This describes the mechanism for plasticity, which is more substantial than long-term potentiation, and also has a different mechanism which involves the NMDA receptor. I’m thankful for this article, because it describes the science behind what I do, and little research is published regarding the NMDA receptor. Instead, usually the AMPA receptor is studied, because there is little pharmaceutical interest in NMDA. “These techniques have potential therapeutic application in manipulating neural plasticity to treat a variety of conditions, including depression, Parkinson’s disease, epilepsy and neuropathic pain.”

Inhibitor kappa B kinase beta dependent ccytokine upregulation in nociceptive neurons contributes to nociceptive hypersensitivity after sciatic nerve injury.

Kanngiesser, M., Haussler, A., Myrczek, T., et al. 2012. The Journal of Pain, Vol 13, No 5 (May), 2012: pp 485-497. doi:10.1016/j.jpain.2012.02.010.

Explains the mechanism by which injury to the sciatic nerve regulates processes that increase sensitivity to pain, and potentially the perception of pain that is brain based and not related to a sickness or injury of a body part.

Bliss, T.V.P., Cooke, S.F. 2011. Long-term potentiation and long-term depression: A clinical perspective. Clinics. 2011;66(S1):3-17.

Neuroplasticity can be used to treat conditions such as neuropathic pain, epilepsy, depression, amblyopia, tinnitus and stroke. Specific mechanisms are discussed, used to create plasticity by activating the brain. The importance of calcium is discussed. The various signaling events and neurotransmitters needed for long-term potentiation (LTP) are described. Specific methods for activation and plasticity are discussed: LTP involves protein synthesis and transport to specific receptors. Repetitive Transcranial Magnetic Stimulation, Transcutaneous electrical nerve stimulation (TENS), Event related potential, Interventional Paired Associative Stimulation, Direct Current Stimulation, Pharmaceutical Modulation, Photic and auditory tetanization, and Vagal nerve stimulation.

The specific brain presentations and plasticities are described for these conditions: depression, Parkinson’s disease, schizophrenia, epilepsy, stroke, chronic pain, amblyopia, and tinnitus.

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