In our last post we talked about the foundations of pain. In a snapshot, pain is not an input, pain is an output. This means that the brain actually creates pain in response to the information it gets from sensors in the body, previous experiences already stored in the brain and your general emotional state. We also covered some of the structures involved and how nerves relay messages from the sensors to the spinal cord and to the brain. Today we're going to cover what happens when an injury occurs and how the brain modulates these messages and signals.
We left off talking about how the brain creates pain in response to you touching a hot burner with your finger. Remember, nerve endings have receptors that are sensitive to things like temperature, pressure and chemicals. If you have enough of that stimulus (temperature, pressure, chemical) it opens up that particular receptor and "ping!" an alert gets sent along the length of the nerve. Think of the nerves as highways and the alerts as cars on the road. We have highway 1 – the nerve running from your fingertip to the spinal cord, and highway 2 – the nerve running up the spinal cord to the brain, with an intersection in between (nerve synapse).
What happens when you damage to your finger?
On the surface your finger hurts, and now a touch that wouldn't normally hurt (like slight pressure) makes you cringe. This is your brain's protective response – a pain sensation causes you to protect the area while it heals.
In the nerves:
If we go a little deeper we'll find that the swelling and inflammation at the injury site sets off a cascade of chemicals that begin the repair process. However, this 'inflammatory soup' as it's called, also sets off its own additional set of danger signals. As long as that inflammation persists, the nerve (highway 1) will adapt to become more sensitive by requiring even less stimulus to open up the receptors. In other words there's a lower threshold required to create future danger alerts – this is called peripheral sensitization. More danger alerts = more traffic on highway 1.
In the spinal cord:
All this traffic (danger signals) floods the intersection, so the nervous system undergoes some construction to help all this traffic get through. 1) The sensors stay open longer to let more alerts through. In other words the light stays green longer to allow more cars through to highway 2, on route to the brain. 2) Some sensors stay in a sleeping state until they need to be activated. This is like roadblocks being lifted to open up more lanes on highway 2. More danger signals arriving at the intersection means a more sensitive nerve in the spinal cord too (central sensitization), and that can cause a couple of things to happen:a)It can cause previously non-painful sensations to feel painful
b)It can cause mildly painful sensations to feel very painful
In the brain:
Lets keep moving up to the brain and discuss what's happening there. Just like pressure, chemical and temperature sensors can send pain signals, so can your attitudes, thoughts and beliefs. In our fingertip example, if you earn a living playing the guitar a fingertip injury could be very serious. You might experience a whole set of stressors that a non-guitarist might not. You might think "I can't pay my rent if I can't play guitar", or "I can't play at the concert I've been looking forward to all year." Because your brain creates a pain response based on the inputs (including the ones from the fear centers of your brain), these types of inputs may cause your brain to interpret your injury as more threatening and heighten your pain response. It's also why no two people will ever have the same response to the same painful experience.
How does pain become chronic?
Now this is all okay if the sensitivity of the neuron returns to normal once 1) the painful stimulus is removed 2) inflammation resolves and 3) the tissue heals. But sometimes the nerves stay sensitized anyway – that's what chronic pain (more accurately, persistent pain) is. The brain is somehow misguided to think that the body is still under threat, even though the dangerous stimulus has been removed and the tissues have healed (this is called central sensitization)
It is very common in cases of chronic pain for patients to end up with labels like fibromyalgia, repetitive strain injury, non-specific low back pain because the reported sensation of pain (which is very real) doesn't really match up with the physical evidence found in the body. Often for these people the pain keeps spreading, get worse or occurs with more and more movements.
How all the signals come together to create the pain experience:
Interestingly, there is no one distinct pain center in the brain. When creating a pain response the brain draws on all kinds of areas in the brain – areas that control sensation, emotion, memory etc. Pain scientists call these ignition nodes. A pain experience is created when all these ignition nodes connect to each other in a unique pattern. This creates a custom map of connections for that particular pain experience – and it's called a neurotag. When a neurotag is produced, it hurts!
At the end of the day the sensory inputs from peripheral body parts are not enough to create the sensation of pain. The brain has to be involved. So technically pain IS all in your head! That is to say that pain is generated by the brain - though still a very valid and real sensation.
So remember pain is not an input – it's an output based on sensory and emotional experiences associated with potential tissue damage in the body.
That is the tip of the iceberg when it comes to understanding pain. If you want to learn more I highly recommend checking out this Ted Talk by Lorimer Moseley https://www.youtube.com/watch?v=gwd-wLdIHjs as well as his book (co-authored with David Butler). He is a physical therapist at the forefront of pain research, and he's hilarious!
If you want to hear more about chronic pain management from us, let us know and if we get enough interest we'll post a part 3 of this series!
Butler, David and Lorimer Moseley. "Explain Pain."Adelaide: Noigroup publications, 2003. Print.
Latremoliere, Alban and Clifford J. Woolf"Central Sensitization: A Generator of Pain Hypersensitivity by Central Neural Plasticity." The Journal of Pain 10 (2009):895-926. The Journal of Pain Online.
Souvlis, Tina. "Introduction to the neurobiology of pain." University of Queensland, Australia. July 5 2012. Lecture.