Why does hernia mesh hurt?

Why should it not hurt? It is a foreign material that does not belong in our body. It is recognized as foreign by our innate immune system and by our nervous system. It stimulates inflammation which triggers pain. It stimulates nociceptors which triggers pain. However only about 20% of patients with hernia mesh develop chronic pain.

Hernia mesh explant

Pain is a cognitive experience produced by the brain, not simply an input from the body. Pain is a warning to the body that there is danger. It starts with a stimulus, thermal, mechanical or chemical which is picked up by a receptor, exceeds a threshold, triggers a nerve fiber signal, is received by a neuron, is relayed to a spinal neuron, is amplified or muted, is relayed to the amygdala, triggers emotional processing and then is relayed to the cerebral cortex where is enters consciousness. It is a delicately balanced process with modulation and processing at multiple levels. The complexity of pain processing makes pain disorders difficult to treat.

Our nervous and immune systems modulate the sense of pain so that not every stimulation produces pain. Pain perception has a threshold below which no pain is perceived. Pain is different from touch. It is not just a matter of degree. Pain of any degree triggers protective behavior and emotional conditioning. Imagine the chaos in our lives if every touch caused pain to some degree.

Allodynia is pain detection below the normal stimulation threshold. That is, pain caused by a light stimulation which does not normally cause pain is called allodynia. Patients with chronic pain frequently experience allodynia. Experimentally this can be reproduced in human test subjects by applying pressure to a limb with a pressure cuff until the subject experiences pain. When the pressure cuff is then applied to the opposite limb the pain is reported by the subject at a lower pressure. This is also known as central sensitization.

Hyperalgesia is pain whose amplitude is amplified. Central sensitization causes Hyperalgesia. The test subject with the pressure cuff on one limb will report a more intense pain in the opposite limb at the same pressure.

Chronic pain states are disorders of central sensitization and failure of desensitization mechanisms.

Chronic inflammation causes the production of nerve growth factor (NGF). NGF causes central and peripheral sensitization. This is shown experimentally by administering NGF intravenously in human test subjects. Hernia mesh causes chronic inflammation and may be causing central and peripheral sensitization by this mechanism.

Tanezumab is a monoclonal anti-NGF antibody which has just successfully passed Phase III clinical trials (7/1/2018 and should be availeble soon for clinical application) for the treatment of low back pain and pain of osteoarthritis of hips and knees. It is of particular interest to me as an adjuvant for the treatment of hernia mesh pain. Hernia mesh pain patients have allodynia and hyperalgesia which is mediated by nerve NGF and neuroplastic changes in the central nervous system. A significant number of mesh explant patients still have pain one year after explant, which is undoubtedly caused by central sensitization. Patients with persistent pain at one year do continue to get better at 2 years. I have a patient who attributes his recovery going into his second year to Pilates and another to bicycling. I have seen the same recovery with no specific therapy and it is my opinion delayed recovery is due to slow reversal of central sensitization. Tanezumab could be the key to treating these difficult cases. Blocking NGF may mitigate the central sensitization and accelerate the normalization of pain sensitivity, that is, correcting allodynia and Hyperalgesia.

Nerve growth factor: an update on the science and therapy. Seidel MF, Wise BL, Lane NE. Osteoarthritis and cartilage / OARS, Osteoarthritis Research Society. 2013/09/01 00:00; 21(9): 1223-1228