Low back pain 6- Central Sensitization

The mechanisms I described in the previous post  involve a process termed "central sensitization."  Let me explain.  The brain has a certain threshold at which it perceives pain.  This threshold is variable, not absolute.  In other words, there are moments when you have a lowered pain threshold and other moments when it is raised.  For example, if you are in the middle of an athletic event, your pain threshold is elevated because of a change in your neuroendocrine milieu.  A cut on your hand may not even be perceived until the game is over.  You don't actually feel "pain" even though the pain signals are being actively generated at the tissue.  While there are numerous places where this pain modulation occurs (spinal cord, brain stem, thalamus are a few...), it ultimately leads to a decrease in pain related activity in the brain.

"Central sensitization" is just the opposite.  When a pain loop has been running for some time, your brain gets really good at perceiving and running that loop. This can happen after an injury where a vicious cycle emerges to perpetuate the pain.

These authors describe one model where a painful stimulus may...

"...induce multiple inflammatory and neuropathic processes in the spinal cord dorsal horn, and trigger modification and plasticity of local neural circuits. As a result, ongoing noxious signals to the brain are amplified and prolonged, a phenomenon known as central sensitization."  Curr Pain Headache Rep. 2010 Jun;14(3):213-20.

Scientists are in agreement that this phenomenon occurs regularly.  The question that remains unanswered (although we can make educated guesses), is whether or not central sensitization is more likely to occur when there is pre-existing inflammation in the brain or the periphery.

Does an unhealthy physiology have a greater probability of allowing central sensitization to occur?  Does a person who eats well, has no inflammation, sleeps well, exercises regularly and manage his stress have a better environment that will resist the induction of these noxious pathways?

To be fair, we don't have a clear answer for this yet.  The science pretty much says, "maybe- but we can't preach that particular message with full confidence."  But when you consider the many health related "shades of gray" that brain can live in, when you consider our current understanding of pain physiology, when you appreciate the influence of food and nutrition on brain health and inflammation levels, it is not a giant leap of faith to believe that food is related to central sensitization.

If you know someone with chronic low back pain, I hope you are beginning to appreciate the absurdity of throwing multiple pain management modalities (ice, steroids, anti-inflammatory medications, exercises, physical therapy) at the individual without making fundamental changes to his diet.

Low back pain 5- Chemistry

Common mechanical causes of low back pain include disc herniations. Most clinicians acknowledge that if a tissue is damaged, there is a reasonable probability that it will produce pain.  In the 'old days', we used to believe that a disc herniation would pinch a nerve and lead to pain.  But as we realized that true nerve impingement (although it does occur) was less common than previously believed, the low back community began to look outward.

When there is tissue damage, lots of noxious chemicals are released. These chemicals are generally used to communicate with different components of your body that are responsible for healing and repair.  But it is becoming clear that these chemicals (broadly termed 'cytokines'), can be problematic if they persist.

This paper describes the production of inflammatory cytokines by damaged tissues. As they activate immune cells and the brain, the brain responds by promoting further release of these inflammatory triggers.  These authors describe the way that these signals cross the blood brain barrier and influence our perception of pain through a "cascade of altered neural activity."  This can promote the efficiency of the "pain pathways" to the brain and lead to persistent pain.

So far, so good.  But another question remains; is there anything else that leads to the production of these inflammatory cytokines?  In other words, can another event, apart from tissue damage at the low back, produce these nasty chemicals.  If so, then this would have the potential to make relatively minor tissue damage... a REALLY BIG DEAL.  The answer is a resounding yes.  Before we detail some of these components, picture this.

Have you ever caught a friend at just the wrong moment? Perhaps you made an innocent comment, "I like your other shoes more than the ones you're wearing."  And all of a sudden, your friend explodes!  It may have been a minor statement, but if she just got fired from her job, broke up with her boyfriend, had her credit cards stolen and her car is making funny noises, then your minor statement was the "straw that broke the camel's back" in an already traumatic day. 

If your brain is already compromised by a poor diet and lifestyle, then even a minor stimulus will lead to a major symptomatic eruption.  Remember, the brain not only maintains normal body mechanics, but also perceives pain.  Alteration in its function can heighten sensitivity and generate vicious cycles of pain.

Low back pain 4- Brain

We have further evidence that there are central neurological changes in individuals with chronic low back pain.  In this study, researchers found that in people with chronic low back pain, there was a decrease in gray matter in both the thalamus and prefrontal cortex.  The authors go on and state, 

"We hypothesize that atrophy of the brain circuitry involved in pain perception may dictate the properties of the pain state, such that as atrophy of elements of the circuitry progresses, the pain condition becomes more irreversible and less responsive to therapy."

In other words, the longer you have pain, the more that pain will establish itself as a regular part of your life by "rewiring" your brain.  At the very least, research like this suggests that in order to ameliorate low back pain, we must not only correct your peripheral structures (muscles, joints), but also address the brain.

Other experts agree with this idea.

"There is increasing evidence that chronic pain problems are characterised by alterations in brain structure and function. Chronic back pain is no exception. There is a growing sentiment, with accompanying theory, that these brain changes contribute to chronic back pain..." Man Ther. 2010 Jul 23. [Epub ahead of print]

Where does this leave us?  It suggests that everything we know about maintaining the health of your brain applies (to varying degrees) to chronic low back pain.  Brain research has exploded in the past 2 decades and we now recognize a variety of mechanisms to compromise the brain; inadequate nutrition, oxidative stress, stress hormones, lack of sleep, environmental triggers, gluten (to those who are sensitive), lack of exercise and so much more!  

There is truth to the thought that low back exercises will aid in brain function.  However, if those exercises are performed and the brain is then swamped with a Happy Meal (and the saturated fat, blood sugar surge, oxidative components, noxious chemicals, trans fats etc.) as you drive home from your physical therapy session, you are working against yourself.   Your are trying to re-wire the brain with the exercises, and then proceeding to assault it with your diet.  Food and low back pain are related.

In the next post, we will address other metabolic perspectives on low back pain.