Axofascial Therapy

Chronic widespread pain is experienced by one-third of US adults (Johannes, 2010). Large parts of the general population (34.5% to 53.7%) have been found to report pain of more than three months duration (Gerdle, 2004, Bergman, 2001). The prevalence of chronic pain is higher for women than men and is more prevalent with increasing age (Crook 1984). Chronic pain is more strongly associated with emotional symptoms such as fatigue, stress, anxiety, and depression (Bergman 2001, Croft 1993) due to a less commonly known signaling pathway called the autonomic nervous system compared with acute pain conditions.

It is thought that chronic pain is caused by impaired tissue healing or nerve damage but clinical research in this area has been limited. Fortunately, basic research is beginning to identify the mechanisms that underlie the cause of delayed healing and chronic pain syndromes.

The important molecule for tissue healing is the fuel used by all cells in the body, called glucose. Glucose is an essential molecule that keeps all cells functioning normally, and it is the preferred energy source of all cells in the body, especially the nervous system. A lesser known function of glucose is a signaling molecule to govern energy homeostasis or maintain energy use in the body (Herman 2006). This means glucose also regulates gene transcription, enzyme activity, hormone activity and glucoregulatory neurons in the form of a tissue communication network (Herman 2006).

If glucose levels drop too low, cells do not function normally, and tissue damage occurs releasing inflammatory chemicals including Substance P and CGRP (calcitonin gene-related peptide). Substance P causes in tissue edema, attracts immune cells, upregulates the body’s stress response, and impairs local muscle activation. CGRP is involved in tissue degeneration and calcification (Alfredson, 2005). This tissue damage is detected by sensory nerves called A-delta (pain and cold temperature sensitive) and c-fibers (mechanical, thermal and chemical sensitive) (MacIver, 1992). These nerves are different from the primary sensory nerves called the A-alpha and A-beta nerves which send signals to the brain after trauma, fractures, lacerations, pinched nerves and disc herniations.

Nerves sense the local internal and external tissue environments and respond accordingly by altering local tissue structures and blood flow. In the early 20th century, an American physiologist at Harvard named Walter Cannon found nerves were more irritable to local chemical agents when the neuron was injured or destroyed. This nerve irritation caused the distal neural elements and tissues to become super sensitive as well (Cannon 1949).

When the c-fibers and A-delta fibers are injured or destroyed, there is a change in the local soft tissues as well. This is called the Valleix phenomenon, which describes the development of proximal and distal limb tissue tenderness as well as nerve swelling caused by a dorsal root ganglion reflex within the spinal cord. Valleix points describe various points along the course of a nerve in which pressure causes severe pain. These points are found where the nerve emerges from a bony canal; where it pierces a muscle or fascia structure to reach the skin; where a superficial nerve is easily subject to compression; where the nerve branches off; and where the nerve terminates in the skin.

The typical common pain complaint is the result of mechanical, thermal or chemical injury and the degree of pain reflects the extent of tissue damage. These pain signals are relayed by A-beta and A-delta fibers. These signals go to the sensory cortex of the brain which allows the pain to be identified, rationalized, and localized (Raouf, 2010).

Chronic pain is different as it is caused by disturbances of glucose levels and cell homeostasis. This type of pain develops over time after an injury, fluctuates in intensity and is often difficult to localize. The nerve signals are first sent to the nerve roots within the spine and to the spinal cord where the signals sensitize adjacent nerves and can cause muscle spasm in the regional area or joint. Also the pain signal can be sent to the other side of the body, resulting in the development of a bilateral pain complaint that can spread up and down the body. The pain signals are transmitted to the insula cortex in the brain by c-fibers and A-delta fibers (Raouf, 2010). The insula cortex is associated with feelings and emotions, so this type of pain is commonly associated with fatigue, anxiety, depression and fear.

Over time chronic pain occurs via local and regional inflammation of neural tissues (Panjabi, 2006). Research has shown that the subcutaneous tissue and outer layer of the fascia has a high density of nerve fibers (Tesarz, 2011). It has also been found that the surrounding fascia is much more pain sensitive than the muscles (Gibson, 2009). These are the most important locations to treat chronic pain complaints.

Corticosteroid trigger point injections are usually used to treat these conditions. Corticosteroids temporarily block A-alpha and A-beta nerves as well as decrease blood flow in the local area but have little effect on the A-delta and C-fiber function, so they are often not useful. Corticosteroids are associated with many side effects including immunosuppression and delayed tissue healing (Ciriaco, 2013), so I rarely advocate these injections

Axofascial therapy is a process that adds glucose back into the local tissue regions to allow the nerves to return to their normal baseline function.

Check out the videos below that describe the process and the outcomes.

References

Alfredson H. The chronic painful Achilles and patellar tendon: research on basic biology and treatment. Scand J Med Sci Sports. 2005 Aug;15(4):252-9.
Bergman S, Herrstrom P, Hogstrom K, et al. Chronic musculoskeletal pain, prevalence rates, and sociodemographic associations in a Swedish population study. Journal of Rheumatology. 2001;28:1369–1377.
Ciriaco M, Ventrice P, Russo G, Scicchitano M, Mazzitello G, Scicchitano F, Russo E. Corticosteroid-related central nervous system side effects. J Pharmacol Pharmacother. 2013 Dec;4(Suppl 1):S94-8.
Croft P, Rigby AS, Boswell R, et al. The prevalence of chronic widespread pain in the general population. Journal of Rheumatology. 1993;20:710–713.
Crook J, Rideout E, Browne G. The prevalence of pain complaints in a general population. Pain.1984;18:299–314
Gerdle B, Bjork J, Henriksson C, Bengtsson A. Prevalence of current and chronic pain and their influences upon work and healthcare-seeking: A population study. Journal of Rheumatology. 2004;31:1399–1406.
Herman MA, Kahn BB. Glucose transport and sensing in the maintenance of glucose homeostasis and metabolic harmony. J Clin Invest. 2006 Jul;116(7):1767-75.
Johannes CB, Le TK, Zhou X, Johnston JA, Dworkin RH. The prevalence of chronic pain in United States adults: results of an Internet-based survey. J Pain. 2010 Nov;11(11):1230-9.
MacIver MB, Tanelian DL. Activation of C fibers by metabolic perturbations associated with tourniquet ischemia. Anesthesiology. 1992 Apr;76(4):617-23.
Panjabi MM. A hypothesis of chronic back pain: ligament subfailure injuries lead to muscle control dysfunction. Eur Spine J. 2006 May;15(5):668-76.
Raouf R, Quick K, Wood JN. Pain as a channelopathy. J Clin Invest. 2010 Nov;120(11):3745-52.
Tesarz J, Hoheisel U, Wiedenhöfer B, Mense S. Sensory innervation of the thoracolumbar fascia in rats and humans. Neuroscience. 2011 Oct 27;194:302-8.
Walter Cannon. Supersensitivity of denervated structures. New York, The Macmillan Company 1949.