Our current understanding of the nature of chronic pain requires an understanding the phenomenon of Central Pain Sensitization. This is under acknowledged in the General medical community. New graduates of anesthesia are trained about this. Other specialists and doctors in practice more than 15 years don't deal with it unless they are self taught, Central Pain Sensitization explains why hernia mesh pain is so difficult to treat, why most treatments fail utterly and why some patients never get better. Central Pain Sensitization is a component of all chronic pain conditions such as osteoarthritis, chronic back pain and fibromyalgia.
Central Pain Sensitization also explains why the clinical picture of hernia mesh pain is so confusing to patients and doctors. The three classic symptom features of Central Pain Sensitization are 1) Allodynia, 2) Hyperesthesia and 3) Widening of the pain field. Patients who come to me have typically had very extensive work ups including multiple forms of medical imaging, colonoscopies, upper endoscopies nerve conduction studies, local anesthetic peripheral nerve blocks, blood tests and more with no diagnosis or rational treatment plan. Allodynia literally means "other pain". It is when a light touch stimulus is perceived as pain. This happens because in Central Pain Sensitization the pain pathways become cross connected with the touch pathways in the central nervous system. Hyperesthesia means a mild pain stimulus results in severe pain. This happens because in Central Pain Sensitization nerve connections in the pain pathways are enhanced resulting in amplification of pain. But the most confusing feature of Central Pain Sanitization is Widening of The Pain Field. Your brain has a lot of trouble figuring out where the pain is really coming from anatomically. Patients will say the pain is coming from the groin where the mesh is. But they will also say is is coming from the other side, from the genitalia, from the rectum, from the lower abdomen, from the upper abdomen and down one or both legs. Some patients have all of these. Another very confusing feature of chronic hernia mesh pain is A.S.I.A. Syndrome.
The medical literature on hernia mesh pain for the most part barely acknowledges this phenomenon. The literature talks about nociceptive and peripheral neuropathic pain, both of which are easily treated. The real story however is much more complicated. The Central Pain Sensitization component of all chronic pain conditions is not curable in 25% of patients in spite of what should be curative surgical treatment. 30% of patients with chronic knee osteoarthritic pain are not cured of their pain even after total knee replacement. 30% of patients with chronic back pain have significant persistent back pain after definitive anatomical surgical correction. In our experience only 75% of patients with hernia mesh pain are cured by surgical mesh explant.
Central Pain Sensitization can fade away over time after removal of the primary pain generator. Persistence of pain stimulus from the peripheral nervous system absolutely causes persistence of Central Pain Sensitization. So, for example, completely removal of hernia mesh without replacement is required for the best possible results.
Peripheral neurectomy does not give good long term results because it is not possible nor is it even desirable to completely denervate the groin. It does not address the sympathetic pain pathways or Central Pain Sensitization. Peripheral nerves repopulate denervated areas slowly over time. Also, as part of chronic inflammation, new nerve sprouts grow into the mesh.
New drugs are being released to market by the FDA which offer some hope in the treatment of Central Pain Sensitization. Tanezumab® is a monoclonal antibody drug against nerve growth factor. Nerve growth factor is a mediator of Central Pain Sensitization. This medication is indicated for the treatment of chronic osteoarthritic pain. We anticipate that this medication will be of value in the treatment of Central Pain Sensitization of other chronic pain conditions. Medications modulating Calcitonin Gene Related Peptide receptors are effective in treating chronic migraine pain and its gastrointestinal symptoms. It may be of use in treating other forms of chronic pain.
The anatomical pathophysiology of Central Pain Sensitization has been worked out in animal models. A lab animal is given chronic pain by placing a clip on the sciatic nerve of the animal which is later sacrificed, dissected and neurological structures examined under the microscope. There are clear anatomical changes in the dorsal horn of the spinal cord and pain pathways through the limbic system all the way up to the somatosensory cortex. In the dorsal horn of the spinal cord new cross connections between the different lamina. Cross connections develop and between touch sensory pathways and pain pathways. This accounts for the phenomenon of allodynia, a symptom of central pain sensitization where light touch causes perception of pain.
Below are some excellent articles which will give you a solid foundation for understanding Central Pain Sensitization and the role it plays in chronic hernia mesh pain and all chronic pain conditions. Free full text article PDFs are available for all of these articles.