Theory of Mesh Pain

Mesh is recognized by our immune system and nervous system as foreign to our bodies. This process is very complex and very efficient. The primary consequence is chronic inflammation which leads to pain, scar formation and contraction, nerves sprouting into the mesh and many other phenomenon which in turn leads to chronic pain and other mesh complications.

Mesh pain lasting more than 3 months is chronic pain and rarely if ever gets better without treatment. Unfortunately most conventional treatments just mask the symptoms and do not treat the underlying cause of the pain.

Chronic pain is a combination of acute pain and central sensitization. In most cases of severe chronic mesh pain central sensitization is the largest component of the pain.

Central sensitization is the neurological phenomenon responsible for phantom pain, allodynia, hyperalgesia, pain ramping and widening of the pain field. In a nutshell Central Sensitization is a sensitization of the neural pathways handling the processing of pain from the spinal cord to the brain stem to the amygdala to the somatosensory cortex. The central nervous system modulates our threshold for pain, our sensitivity to pain, the threat meaning of pain and our conscious and subconscious response to pain. See the article on Central Sensitization for a more in depth explanation.

Long term exposure to acute pain causes central sensitization which means that the way our central nervous system handles pain changes. This can be a permanent chronic state when it is continuously or intermittently reinforced by acute pain.

Sensitization is how our central nervous system  tells us to knock it off. There is also a process of desensitization which is how our central nervous system tells us we are okay, at least for now, and we should keep doing the things we need to do now for our survival. An athlete will not be bothered by a broken toe until the play is completed, unless his brain also tells him his career is ended. A parent experiences no pain while their child is in danger. A soldier does not experience pain until he is out of the battle. The experience of pain is not a simple perception of thermal, mechanical or chemical stimuli. Our central nervous system modulates the signal generated by the stimuli and then finally qualifies the signal. They detect a specific stimuli at levels lower than we would normally experience pain. Our central nervous system makes the distinction of whether a signal received from a nociceptor represents pain.

Mesh causes chronic inflammation which is known to generate chemical mediators which stimulate nociceptors which are the receptors that sense noxious stimuli and generate the signal which then enters the neural pathways that handle the processing of pain. Nociceptors do not distinguish pain.

The intensity of the chronic inflammation correlates with the intensity of pain. However mesh produces chronic inflammation in every case but does not produce chronic pain in every case. Pain is not a reliable indicator of tissue injury because of central sensitization. Hernia mesh does not cause pain in 80% of patients but they all have chronic inflammation stimulated by the mesh. I believe central desensitization is why 80% of patients are comfortable.

Successful treatment of chronic mesh pain starts with eliminating the nociceptive signals generated in the peripheral nervous system which reinforce central sensitization. If this is done effectively the central sensitization will fade in time. Neurectomy and permanent peripheral nerve blocks have been the traditional approach to this. The problem with this approach is that it is not possible to completely and permanently denervate a small region of the body. Nerves grow back or are recruited from nearby nerves and the region is reinnervated in time with return of the pain.

If mesh is removed the noxious stimuli of the nociceptors is eliminated. But no matter how the nociceptive signal is interrupted the patient is left with central sensitization which may cause phantom pain, allodynia and hyperalgesia. Even a spinal cord patient may experience pain below the level of his permanent and complete injury.