We are learning more and more about the origins of pain. And the more we learn, the more we can help understand and treat it. But we do know this, pain is personal. Each of us feels it differently. Why? Because it not only depends on what’s happening in the body but how the brain responds to it through the pain matrix. The pain matrix monitors our entire body. Pain is the alarm it uses when a perceived threat occurs. Chronic, persistent pain happens when the matrix is turned on and doesn’t turn off.
This can happen from trauma or a combination of long term triggers that keep the pain matrix active:
- Severe or long term stress
- Childhood trauma
- Tissue injury
- Persistent sleep issues
- Chronic inflammation
- Deficiencies in nutritional intake
- Persistent elevations of blood sugars
- Long term high blood pressures
- Excessive organ fat
- Isolation and loneliness
- Chronic anxiety
- Chronic muscle tension/ pain
The pain matrix involves different areas of the brain that control emotions, behavior, movement, perception and thought. Which means each of these factors can change how we perceive that pain. The brain processes information coming from the peripheral and central nervous system that tell us where a danger or injury has occurred then responds by increasing or decreasing our sensitivity to those signals. This defines the intensity of the pain we feel. It does this two ways. By inducing anti-nociception, a reduction in sensitivity to pain or pro-nociception, an increase in pain sensitivity. Both are integral to the body’s effectiveness at dealing with an attack.
- Anti-nociception uses our natural resources like endorphins, dopamine, oxytocin to block or reduce incoming signals. This is often needed to allow us time to fight or flee an adverse situation.
- Pro-nocioception is due to swelling and chemical changes e.g. inflammation and the immune response that occurs in the nerve endings after an injury. That’s why even a paper cut can seem so much more painful than it should.
Functional MRIs have identified six common regions in the brain are activated when we feel pain.
Primary somatosensory cortex. This is responsible for sensory discrimination, determining where exactly the pain is coming from. In chronic pain a more widespread contra lateral activation was observed. But in acute pain only the ipsilateral activation was seen. One study found those with chronic pain had a small primary somatosensory cortical representation. Implying there was a dissociation between its activation and the actual cause of the inciting pain. This may explain why chronic pain sufferers feel a more diffuse pain and often can’t even specify the location of the pain at all. Or why it travels from the initial injury e.g. the knee to the entire leg as greater areas of this part of the brain are activated.
Secondary somatosensory cortex. This is associated with discriminating the intensity of pain. In chronic pain patients there’s a bilateral activation pattern as compared to a contralateral activation in acute pain patients. Again, giving evidence why chronicity leads to a more widespread, vague description.
Anterior cingulated cortex. This is where the emotional and cognitive aspects of pain are processed. In chronic pain, there’s again more bilateral and widespread activation. This may indicate a more heightened sensation of pain and a shift towards a more emotional aspect that might contribute to ongoing and higher levels.
Insular cortex. This includes both sensory and affective perceptions of pain- the suffering aspect. It’s often activated along with the anterior cingulated cortex in chronic pain suffers and has a more widespread activation. Here is where we try to process all the data coming in from the periphery which might be why we see allodynia- pain from something that doesn’t normally cause pain e.g. a feather, and hyperalgesia-extreme sensitivity to pain- in chronic pain syndromes.
Prefrontal cortex. This is where we cognitively evaluate pain. In one study patients with chronic back pain showed a significantly hyperactive state in this area, which may reduce activity in other areas which might then affect the brain’s ability to perform other tasks. This change in the prefrontal cortex represents a shift towards increased emotional processing in chronic pain patients.
Thalamus. This is where all the multiple ascending pain pathways converge. It’s not just a relay station. It’s an important factor in how nociceptive data is processed before it’s transmitted to various parts of the cortex.
All this proves that not only are different parts of the brain activated with chronic pain but there can also be a “smudging” of the sensory and motor areas. These are changes in the brain that make it more difficult to process exactly where the pain is coming from and allows the sensitization of other areas as well.
The pain matrix helps us to understand how acute pain, from any source, can morph into a chronic, debilitating one. Next week I’ll discuss how understanding this process can help us learn ways to modify the signals that get through and ultimately lessen what we feel.