Understanding Pain, A Ten+ Week Ecourse: Part 9
By Jonathan Blood Smyth
Week 9. Integration of Pain in the Nervous System
Welcome to the ninth instalment of my Ten+ Week Ecourse, I hope you are still with me and finding it interesting and stimulating.
Part Nine covers the way pain inputs are modulated (changed) as they make their way up to the sensory cortex.
You are welcome to publish this course in your newsletters or on your web site, on condition you do not alter it and that you keep the resource box at the bottom of each instalment.
Last time we talked about the effect pain has on the control of movement, and how it can both interfere with normal movement patterns and set up abnormal ones.
The Integration of Pain Inputs
The interpretation and understanding of pain which goes on in the nervous system must take place in the higher centres of the brain. This is because pain can have such profound effects on the motor, sensory, autonomic and emotional aspects of a person.
Pain status can also be greatly influenced by descending inputs from many areas in the brain. Most of the time the pain system is being actively inhibited in all of us.
Descending Inhibition of Pain
Experimental studies have electrically stimulated areas of animal brains, causing significant levels of pain relief. Stimulation in some cases resulted in the animal immobilizing itself and trying to recuperate, in others it stimulated fighting behaviour and avoidance. This depended where the stimulation was applied.
These areas of nerve cells which cause this inhibition are located in the brainstem. Similar systems occur in us, causing pain relief and stimulating behaviour which suits the situation for recovery.
Descending Facilitation of Pain
There are also systems coming down from the brain which increase the likelihood of pain transmission and cause hyperalgesia. The same areas which can inhibit pain transmission turn out to be able to increase it too. Low levels of input from these systems may increase pain, with higher levels inhibiting it.
These “lower” areas of brain, the forebrain, can control spinal cord processing of pain inputs via their descending connections and this allows pain to be altered. Alteration can come from a person’s emotional state, their understanding and attitudes and their attention/concentration at the time.
If these systems do not function normally this could be a strong factor leading to the development of some pain conditions. One example is fibromyalgia, a condition in which there appears to be no tissue abnormality but a high degree of pain perception.
Glutamate receptors other than NMDA
NMDA receptors may not be that important in the development of all types of central sensitization. They are thought to be more important in thermal sensitization and less in mechanical.
Other glutamate receptors exist and may drive the acute mechanical sensitization we see in injury and other pain syndromes.
This is an important and interesting concept. It may be important in contributing to up-regulation, and help explain some changes which occur especially in nerve injury.
After nerve injury, incoming myelinated axons which normally make connections in lamina 3 and 4 of the spinal cord can sprout into lamina 2 and make connections there. In this way incoming nerves which conduct touch and pressure could connect directly with the pain conducting nerves in the spinal cord.
This may be an explanation for allodynia, where an input which is not normally painful is felt as pain. I think of it as a form of short-circuit or mis-wiring, leading to the wrong information being received by the brain. In this case the wrong information is pain.
Responses of the cell groups in the spinal cord
The wide dynamic range cells are common in the deeper laminae of the spinal cord. They take inputs from pain and non-pain nerves and respond in proportion to the intensity of the input. If they become sensitized they may fire off a much higher rates, even following mild touch or heat stimulation.
This may help explain secondary hyperalgesia, where pain is felt on stimulation of normal, non-injured tissues.
Cells which are specific to pain transmission are common in the more superficial spinal cord laminae. They get their inputs from unmyelinated C fibres, and do not usually respond to non-harmful inputs.
However, the responses of these cells can change in response to sensitizing inputs from pain nerves. They start to respond to inputs from myelinated nerves which would not normally cause a response.
The results are felt at higher levels in the nervous system and may be a factor contributing to increased perception of pain from inputs from both injured and un-injured tissues.
Summary of central sensitization
I know it’s a bit mind boggling, at least it is for me, but an understanding of this is vital to assessing and managing pain syndromes. If you or your patient has a highly sensitized nervous system this both explains some of the odd features and makes you think about how you might treat or manage the problem.
There are five major ways which tissue injury causes up-regulation of the pain producing system, leading to increased pain perception:
This ability of the nervous system to be so plastic, and to bring in extra pain nerves and nerves which don’t normally contribute to our pain experience, explains why an injury can cause such a strong up-regulation of the pain system.
Now it’s time to move out of the technical domain, to leave all the neurons, the synapses, the neurotransmitters. Next we’ll move on to the effects pain has on the whole person, to psychological aspects of the pain experience.
Understanding Pain, A Ten+ Week Ecourse by Jonathan Blood Smyth.
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