Central Sensitization, Chronic Pain, Fibromyalgia, Nervous System, Pain Science

Central Sensitivity Syndromes

A really important concept for anyone struggling with chronic pain, fibromyalgia, or other chronic health conditions is the idea of “central sensitivity syndromes” (CSS for short).

The term refers to any kind of condition that can be caused by a change in the way the nervous system processes pain (a process known as central sensitization).

I have described central sensitization in more detail in other posts.  (Here, I will just say that sometimes, the nervous system can begin to function differently after physical injury or trauma.  Basically, the more chances our nervous system has to “practice” sending pain signals, the better it gets at it).

Central sensitization is why you can still have pain after an injury is healed.  Your tissues are no longer damaged, but your nervous system has not forgotten the “memory” of the pain.

So… how does this happen?  What kinds of injuries or traumas are necessary to cause it?  And what symptoms can it cause?

The answer to is: central sensitization can happen in many different ways, and sometimes the things that trigger it don’t have to be very “severe.”  And there can be a wide range of symptoms, in different parts of the body.   It can be different for each individual person, depending on genetic makeup, co-existing health conditions, psychology, and, of course, the event that triggered it.

This is why the term “central sensitivity syndromes” is so helpful– there are so many health conditions, which on the surface might seem very different, yet all have central sensitization as their root cause.

***

To my knowledge, the term was first coined by physician and researcher Muhummad Yunus, who, along with his colleagues, conducted an important 1981 study linking fibromyalgia to other health conditions caused by nervous system sensitization.

Since then. Dr. Yunus has contributed to a really impressive list of studies establishing central sensitization as the likely cause of a wide range of conditions, including:

  • fibromyalgia
  • irritable bowel syndrome
  • temporomandibular disorder (TMJ)
  • restless legs syndrome
  • chronic fatigue syndrome
  • complex regional pain syndrome (CRPS)
  • chronic pelvic pain
  • migraine

Central sensitization can create different types of symptoms, from one person to another, in different parts of the body.   This one common cause can have many different manifestations.

Additionally, as Dr. Yunus writes, central sensitization can occur when someone has another health condition which creates pain and stresses their nervous system.  Central sensitization can be a resulting secondary factor in conditions such as:

  • rheumatoid arthritis
  • systemic lupus
  • ankylosing spondylitis
  • osteoarthritis
  • diabetes mellitus
  • inflammatory bowel disease

Basically, anything that stresses your nervous system out and gives it a chance to practice sending those pain signals can cause it to become better at sending those pain signals.  So even if central sensitization isn’t the primary cause of your illness, over time it can become a secondary factor.

***

The good news, however, is that the effects of central sensitization don’t have to be permanent.  It can also get better.

That’s what my blog is all about– helping people find out about the ways I, personally, have managed to reduce the effect central sensitization has upon my life, as well as raising awareness about new avenues of research.

What helped me the most is an approach to physical therapy known as pain neurophysiology education.  However, there are other forms of treatment out there, including medications some people have found to be effective for the effects of central sensitization.

***

I’m going to write more on central sensitization and its treatment, as well as the work of Dr. Muhammad Yunus, in the future.

I hope this post was helpful for you, and that you stay tuned!

Central Sensitization, Chronic Pain, Favorites, Fibromyalgia, Nervous System, Pain Neurophysiology Education, Pain Science

How Clifford Woolf discovered central sensitization (and why you shouldn’t blame yourself for chronic pain)

You’ve probably noticed that my blog is all about central sensitization— the process through which the central nervous system can change over time and become more sensitive to pain.

Personally, I find learning about central sensitization to be empowering.  I spent years trying to find an answer for the pain and other symptoms I felt, only to be told by various medical professionals that my problems were in my head, the possible result of depression or anxiety.

I knew, deep down, that this just wasn’t true.  It’s not that I was unwilling to believe that mental health factors could play a role.  But it just didn’t resonate. I didn’t feel anxious or depressed.  I felt like I was in pain, and wanted it to stop.

That’s why, when I first heard the phrase central sensitization and looked up what it meant, I was so struck.  Because there was a way to explain why my nervous system was acting funny, and causing me to feel things other people didn’t feel, that wasn’t based on my mental health.

So.  How do we know about central sensitization?

A neuroscientist named Clifford Woolf discovered the process of central sensitization back in the early 1980’s.  In 1983, he published a well-known and often-cited letter to the respected scientific journal Nature outlining his theory, entitled “Evidence for a central component of post-injury pain hypersensitivity.”

Although the scientific community didn’t quite accept Woolf’s ideas right away, ultimately he ended up sparking a new wave of research, and his theory of central sensitization is generally accepted today (although much more work still needs to be done).

Basically Woolf ended up discovering central sensitization more or less by accident, in the process of researching something else.

(Now, I’m not a huge fan of animal research, so I don’t love what I’m about to describe to you.  But I am grateful for the results, so for the sake of understanding, here we go).

Woolf was studying the “withdrawal reflex” that caused the rats to jerk their paws away from a painful stimulus.  He tested them over and over again, over the course of a day, and he noticed that he started to get different results at the end of the day.

After a long day of testing, the same rats were much jumpier.  It became much easier to trigger their withdrawal reflex.  They would jerk their paws away even at things that shouldn’t have been painful, or wouldn’t have caused them to react that way at the start of the day.

Woolf realized he was seeing completely different behavior in the same rats, and under the exact same conditions.  Only one thing had changed: their nervous systems had been “practicing” the withdrawal reflex all day long, and were now responding to stimuli differently.  He hypothesized that somehow, the central nervous system had changed to become more responsive to pain, after exposure to repeated stress.

Woolf’s theory was pretty revolutionary at the time. Generally speaking, the scientific community believed the central nervous system always processed pain the exact same way, like a simple machine performing the same task over and over.  Woolf’s discovery turned all of that on its head, by suggesting that actually, the central nervous system can be changed and shaped by its experiences.

His ideas were not widely accepted right away, but his work, along with that of others such as Muhammad Yunus, has now formed the basis for a wide body of research on central sensitization and chronic pain that’s going on today.

***

We do still have a long way to go.  Much more research is needed, not to mention new treatments to be based on that research.

However, the reason I wanted to go into detail and describe the rat experiment for you guys is this:

If you have chronic pain/fibromyalgia, people are going to tell you it’s in your head.  Unfortunately, even sometimes people who have a passing understanding of central sensitization will imply tell you it’s in your head.  In my experience, people can understand the concept of the nervous system working differently in principle, yet still think it must somehow be related to mental health.

So this is what I want you to know: central sensitization happens in rats.

Your thoughts, beliefs, and fears about pain, and your mood– those can all play a role in your experience of central sensitization/chronic pain.

But those things don’t cause central sensitization, any more than they did in the rats in Clifford Woolf’s lab.

Remember that the next time you feel someone isn’t taking you seriously.  You can’t create your whole experience of pain by “overthinking” any more than a rat can overthink something.

In some ways, your nervous system is its own being.  There are aspects of your nervous system which have way more in common with a rat nervous system than with your conscious, human mind.  (I know, think about that!  That’s evolution for ya).

So if you have chronic pain, don’t blame yourself.  Don’t scold yourself for overthinking; don’t wonder if you’re crazy.  Your body is just doing what it was always going to do, in response to whatever stress/pain/injury you experienced.

There are ways to move forward– promising ways, which I talk about on this blog.

But to me, the first step is to stop blaming yourself.   You are okay.  You didn’t cause your own central sensitization, any more than the rats caused what Clifford Woolf observed in the lab.

Neil Pearson, Nervous System, Pain Neurophysiology Education, Pain Science, physical therapy

A successful experiment with acute stress

In my last post I outlined some ideas from Neil Pearson on how to stress our bodies in positive ways, in the hopes of re-shaping the way we process pain.

I continued my experiment at the gym last night, and I think I stumbled upon the beginnings of what something like that would feel like.

Normally, when I go to the gym, I’m pretty much there to use the pool.  It’s the one form of exercise I never have to “pay for” in any way afterwards, in terms of pain or stressing out my SI joints.  I usually just do my warm-up and cool-down in the pool as well.

So usually, I don’t hang around–  I’m just in and out.  I head straight for the pool and then make an immediate beeline to shower and leave because, well, I’m freezing.  It’s fun, but it’s also kind of rushed.  Some days I feel like kind of a robot.

With the lessons from Neil Pearson’s post in mind, I decided to switch things up a little bit.

***

Last night, instead of heading straight to the pool, I first stopped by one of the empty dance studios. I had it all to myself– a big room with a smooth, polished wooden floor and one wall that was all one big mirror.

I had my headphones on, listening to a playlist of music I really liked.  And I picked up one of the yoga balls, and just started dribbling it back and forth, to the beat of the music, like it was a basketball.

Now, if you think about this in terms of exercise, it’s not particularly hard.  It doesn’t require a ton of strength, and I wouldn’t technically call it cardio.

But, if you think about it in terms of the nervous system, it actually was a bit challenging.

I don’t play basketball.  I don’t think I’ve tried to dribble a ball in years.  It’s awkward to try to dribble a giant yoga ball… but it’s kind of fun.

However, it does require quite a bit of coordination, especially as some of the songs on my playlist had pretty different beats from each other.  With each new song, I had to completely switch up my rhythm.

I ended up getting really into it, dribbling and jamming out to my tunes for about 45 minutes.  And I think I managed to reach exactly the kind of state of “acute stress” Neil was describing in his post.

It was a difficult new activity for me, but it was fun.  It was challenging, but in a controlled way.  I felt as though I was pushing the limits of my nervous system, in terms of coordinating movement patterns that were unfamiliar to me, while at the same time limiting the overall stress to my system.  (In fact, I think I probably was reducing my overall stress at that point– it was the end of a good day, I had all the time in the world, and I really love my music).

I think this is the kind of activity that, when performed regularly, could have a positive impact on reshaping the way the nervous system regulates pain signals.  It’s “distracting,” in a healthy and fun way.

Obviously these would be topics for further research, but I think two additional components of what I did, which add to its helpfulness, are

  1. That I found the activity enjoyable, and
  2. That I was listening to music, which on its own can also reduce our perception of pain

This is what I find so fascinating about Neil’s approach to chronic pain treatment— an activity can be therapeutic not just because it makes us stronger, or increases our endurance, but because of its impact on the nervous system.

It’s okay to treat pain and the nervous system as your top priority, not just as a side effect or the means to an end of another exercise program.

***

I find the concept of treating nervous system directly to be so fascinating, and I hope you do too!  If you want to know more, I would definitely suggest checking out more of Neil Pearson’s work.  And, as always, let me know if you have any questions or comments!

 

 

 

 

 

Chronic Pain, Neil Pearson, Nervous System, Pain Science, Quotes

Neil Pearson on the benefits of acute stress

I recently discovered this super thought-provoking article article from Neil Pearson on the positive effects of acute stress on the body.

We normally think of stress in as the chronic, ongoing stress that continues for weeks on end, taking a toll on our body in the process.  However, there are ways in which acute stress– that is, stress that only occurs during a short period of time, and then comes to an end– can actually benefit our bodies.

Neil writes,

If you want to make a muscle stronger, use it more.  If you want to grow more tolerant of an irritating or bothersome sensation or experience, step up to it.  Face it.  In time, it will bother you less.

Try playing a string instrument for the first time, and feel the intense pain from pushing down strings with your fingertips.  Keep doing it and your body will adapt, even creating a callous as a protective response, just like woodworkers and carpenters have on their hands and dancers have on their feet.  In other words, when you stress your body, typically it responds by being better able to tolerate that stress next time.

We are built to survive.  If there’s anything I learned in my health and science classes, it’s that our bodies are built to adapt specifically in response to the stresses we experience. If we continually perform a certain movement, the muscles that perform that movement will become stronger and better suited to the task.

If we perform a new task repeatedly, we will get better at it, until it becomes second nature.  Our nervous systems will change, and our mental map of this task will become more developed.

Our bodies crave the kind of challenge that we can rise to.  As Neil says, “acute stress is adaptive. This makes sense. When we exercise – challenging our physical abilities – we are not just improving our bodies physically; we are also making changes in our nervous systems.”

So.  How can people with chronic pain and health issues use acute stress to our advantage?

Neil suggests that we harness our body’s ability to grow and change in ways that can benefit us.  By teaching our bodies to do new things, we can give our nervous systems something to process other than pain, and try to jump-start that healthy, adaptive response.

If pain has been preventing you from exercising, Neil suggests:

Create acute stress while limiting the chronic stress of a flare-up: Make a daily plan to try an activity (or part of an activity) you want to do, but do it while you do your very best to keep your breathing even, your body tension low (only use as much as you need for the activity), and your stress level as low as possible.

So basically: we stress our bodies– our nervous systems, in particular, but also our muscles– in new ways.  But we make sure we are in the right place, mentally and physiologically, while we do it, by proactively taking steps to keep our nervous systems from going into fight or flight mode.

There’s even more in Neil’s article.  He talks about some of the positive effects of stress and exercise on the brain– how chronic pain can dim these effects, but how the techniques he suggest might present a way around that.  Definitely check it out!

***

All this talk about the positive aspects of stress reminds me of health psychologist Kelly McGonigal’s excellent TED talk on “How to Make Stress Your Friend.”  I’ve posted about it on my blog before, because it’s just really so great.

In this talk, McGonigal explains more about how stress can actually be a healthy motivator, seeking us to reach out to others and form social supports, and also spurring us on to create meaning in our lives.  She also suggests that when we learn to view stress as a potentially positive factor, it can actually limit some of the negative effects we normally assume stress will have on us.

There’s so much more to say, but for now, I think I’ll let you check these two resources out!  Happy reading/Youtubing– let me know what you think!

 

Central Sensitization, Nervous System, Pain Science, Quotes, Scientific Articles

Let’s give this a whirl: explaining a scientific article in plain English

Tonight, I’m going to try out a type of post I’ve been wanting to write for a while: taking a scientific journal article on central sensitization, and translating it into plain English for my readers.

I got the idea from Paul Ingraham of PainScience.com.  He has a fantastic “jargon-to-English” article on central sensitization on his site (a translation of a paper by renowned pain researcher Clifford Woolf), which I really love.

There is no reason why you, as a patient and chronic pain sufferer, should not be able to know a little bit about the scientific research being done on your condition.  You are going to need to be able to advocate for yourself, stand up for yourself, and remember there is a legitimate explanation for your pain, even if other people don’t always see it that way.  Knowing there is research to back you up helps.

Ever since I first learned of the term “central sensitization” back in 2011, I found so much comfort in reading these articles.  Even if I didn’t understand every word, just knowing there were people out there who would believe me about my pain, if I met them, provided me with the sense that I wasn’t alone.

These changes to our nervous systems are real, even if some of the people in our lives don’t always understand.

***

So anyway.  The article that I want to take a stab at tonight is “Central Sensitization: A Generator of Pain Hypersensitivity by Central Neural Plasticity” by Alban Latremoliere and Clifford J. Woolf.  (In the interest of keeping things manageable, I am just going to outline the abstract, which is basically a summary of the article).

The article discusses central sensitization, which is the name of the process through which our nervous systems learn to become more sensitive to pain.

Let’s look at it in bits and pieces:

“Central sensitization represents an enhancement in the function of neurons and circuits in nociceptive pathways caused by increases in membrane excitability and synaptic efficacy as well as to reduced inhibition…”

This basically means that the parts of the nervous system responsible for sending pain signals become more active than they were before.

“Increases in membrane excitability” means that it will take less stimulation for nerves to send a pain signal.

An increase in “synaptic efficacy” means that the nerve is going to learn to be more efficient with the neurotransmitters that it has.  So, even though the nervous system still has the same chemicals floating around in it, it is going to learn to start sending stronger and stronger pain signals with those same chemicals.

Reduced inhibition.   Your body has many intricate systems of checks and balances within it.  It is how our bodies maintain control over our internal environment.

One way our body maintains control is by “inhibiting” some of the signals our nervous system sends.  This serves a really practical purpose– we do not need to be bombarded with reminders that our socks are a little bit itchy at all times.  Your nervous system chooses to block out certain signals when they are not useful, or in emergency situations (which is why people can feel no pain when they are in shock).

But in the case of central sensitization, our body’s ability to “block out” or “turn the volume down” on pain signals is reduced, meaning we ultimately experience more pain.

“Central sensitization is responsible for many of the temporal, spatial, and threshold changes in pain sensibility…”.

There are several ways in which these changes to our nervous systems manifest themselves.

We may find that, when something happens that we find painful, we end up experiencing it as painful in a larger part of our body than we might have otherwise.

I’ve really found this to be true with back pain.  When my back pain was at its absolute worst (before I discovered pain neurophysiology education) one tight muscle or muscle knot could make my entire back hurt.

“Because central sensitization results from changes in the properties of neurons in the central nervous system, the pain is no longer coupled, as acute nociceptive pain is, to the presence, intensity, or duration of noxious peripheral stimuli.”

This means that, in a sensitized nervous system, pain is no longer an accurate measure of the presence of an injury, or the degree to which our tissues may have been damaged by an injury.  The central nervous system is now doing its own thing, and you can’t really go by the pain to know what’s wrong.

“Instead, central sensitization produces pain hypersensitivity by changing the sensory response elicited by normal inputs, including those that usually evoke innocuous sensations.”

This means that we now start to feel pain in response to things that are not harmful, and which would have felt painful to us before.

To give you an example, I once knew someone who also suffered from chronic pain, and she said there were days she simply could not bear the feeling of clothing against her skin.  Just the feeling of a lightweight sweater against the skin of her chest made it burn and throb.

This person wasn’t crazy.  She knew her clothes weren’t “hurting” her.  But her nervous system was reacting as though those clothes were somehow damaging her skin.  There was a disconnect between her rational mind, which knew it was only clothing, and the parts of her nervous system which were contributing to her pain hypersensitivity.

(So… lest I end the post on a gloomy note, not to worry.  That’s where pain neurophysiology education comes in, to try to fix this disconnect).

***

Phew.  Okay.  That was not quite as easy as I thought it would be, all the times I thought about writing this post.  But hopefully you made it through!

Everything I write on this subject is meant to be a trial, of sorts.  I’m experimenting with what types of stories and explanations make the most sense, because I really have it in my heart of hearts to develop a set of educational materials on these nervous system changes.

So I want to see what works– what makes sense, what resonates.  (And what doesn’t).

I suffered for so long, thinking I was crazy, when the whole time there were answers out there.  And there was no good reason for it, except that most people (including many medical professionals) still do not know anything about central sensitization.

So I, and my blog, and my future potential physical therapy practice, are hopefully going to be doing something about that.

Please let me know if you have any questions, or any feedback on what sorts of things would be helpful in the future!  I do take requests!

Central Sensitization, Chronic Pain, Nervous System, Pain Science, Resources

The best TED talk ever: Elliot Krane on the Mystery of Chronic pain

Tonight I’m throwing it back to this amazing 2011 lecture on chronic pain given by Dr. Elliot Krane of Stanford University.

I found his talk around the time I was first starting this blog, back in 2012, and it really inspired me to try to tell my own story with complex pain problems.

Dr. Krane is a pediatrician and an anesthesiologist.  He specializes in treating children with chronic pain disorders at the Lucile Packard Children’s Hospital at Stanford University.

In this talk, Dr. Krane outlines the case of a young girl who developed CRPS following a wrist sprain, and was successfully treated at his hospital.

He has some really great quotes and soundbites about chronic pain– things I want to remember, and things I think will be useful in trying to explain the multi-layered nature of pain to people who don’t quite get it (yet).

So here, I’m just going to take a few notes so I (and you, if you’re interested) can come back and remember some key points really quickly:

***

Most of the time, we think of pain as a symptom of a disease– the result of an infection or a tumor, an inflammation or an operation.  But about 10% of the time, after a patient recovers from one of those events, the pain persists for months or even years.  In those cases, pain can become its own disease.

Chronic pain is “a positive feedback loop…. It’s almost as if somebody came into your home and rewired yours walls so that the next time you turned on the light switch, the toilet flushed three doors down, or your dishwasher went on, or your computer monitor turned off.  It sounds crazy, but that’s what happens with chronic pain.”

Glial cells (a particular type of cell found in the nervous system) were once thought to be unimportant.  When I learned about them in my PT prerequisite classes, we thought of them as the supportive “glue” that provides a safe environment for neurons, the more interesting cells that were actually responsible for sending messages.

But, Dr. Krane explains, it turns out that glial cells can play a vital role in the “modulation, amplification and, in the case of pain, the distortion of sensory experiences.”  Once glial cells are triggered by chronic pain, they become overactive and help initiate that the positive feedback loop he mentioned.

Some other quotes:

“The nervous system has plasticity.  It changes, and it morphs in response to stimuli.”

On treatment:

“We treat these patients in a rather crude fashion at this point in time. ”

Dr. Krane describes the treatment protocol for CRPS patients at his center:

  • symptom modifying drugs (painkillers) “which are frankly, not very effective for this type of pain”
  • “We take nerves that are noisy and active that should be quiet, and we put them to sleep with local anesthetics.”
  • “Most importantly… we use a rigorous and often uncomfortable process of physical therapy and occupational therapy to retrain the nervous system to respond normally to the activities and sensory experiences that are part of everyday life.

The future is actually even brighter:

“…the future holds the promise that new drugs will be developed that are not symptom-modifying drugs that simply mask the problem, as we have now, but that will be disease-modifying drugs, that will actually go right to the root of the problem and attack those glial cells….that spill over and cause this central nervous system wind-up…”

***

It’s really interesting for me to look back on this talk, now, and see how my perspective has changed since I first watched it in 2011.  Back then, the point about glial cells largely went over my head (probably because I wasn’t invested at all in knowing what they were).

Now that I’ve taken anatomy & physiology as well as an undergraduate neuroscience course, I can actually see how groundbreaking this really is, to identify glial cells as a potential source of the problem.

It’s as though you’re looking at a telephone pole, and you realize that the wooden pole itself was sending signals, instead of just being there to hold up the electrical wires.  (If that metaphor makes sense).

Anyway, I really hope Dr. Krane is right, that we can begin to develop drugs that will target this mechanism for chronic pain.

Hope you enjoyed this talk!

Nervous System, Pain Science, Resources

Nervous System Basics, Part 2: Excitatory vs Inhibitory

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Continued from Part One

Nervous system cells, whether they are in the brain, the spinal cord, or the peripheral nerves, communicate with each other via a group of chemical messengers called neurotransmitters.  One nerve cell releases a neurotransmitter in order to create some kind of effect on the next nerve cell in line.

There are two major types of effects a neurotransmitter can have on a nerve cell: excitatory and inhibitory.

Excitatory refers to any stimulus that either causes a nerve cell to fire, or simply makes it more likely to fire (aka more likely to send a signal).

Inhibitory refers to any stimulus that makes a nerve cell less likely to fire (aka less likely to send a signal).

You will often find the words excitatory and inhibitory in scientific articles, whether those articles are discussing how pain works or how pain medication works.

For example, excitatory can refer to something that would encourage the nervous system to send more pain signals, more frequently. One nerve cell can have an excitatory effect on another, making that second cell want to fire.

On the other hand, some nerve cells communicate with other nerve cells and tell them not to fire. This is what is referred to as an inhibitory effect.

Many pain medications work in this way, by inhibiting the activity of nerve cells that transmit messages about pain.

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But the body also has its own built-in inhibitory system when it comes to the nervous system sending pain signals.

Scientists are still discovering how many of these pathways work, and they are incredibly complex. I read about some of them for my neuroscience class last summer, and was blown away by how intricate they are; how many different neurotransmitters and hormones are involved; how many different types of nerve cells and receptors on those cells.

But the gist of the matter is that some nerves can have an inhibitory effect on the activity of other nerves, slowing the overall transmission of pain signals.

This is one way in which the body regulates your experience of pain. Sometimes your body decides it’s important for you to feel pain– like when you are home alone and get a papercut. You look down, see you’re bleeding, and realize you need to be more careful with the papers you’re handling.

Yet sometimes, the body decides it’s more important for your survival to block out those pain signals– for example, if you’re a soldier in battle who has been badly wounded, but still needs to get out of the zone of fire. In those crisis situations, people can feel no pain at all, because of the nervous system’s own inhibitory mechanisms.

Of course, these systems do not always work perfectly. Research suggests that in people with fibromyalgia/chronic pain, the inhibitory pathways might not be working properly, which is why they seem to experience more pain in response to non-harmful stimuli than do other people.

It’s not only that the nerves sending messages about pain are working overtime (which they definitely can!). But the other piece of the puzzle is that the nerve cells responsible for reducing some of those pain signals are underactive.

I’ll be discussing this more in Part 3. Stay tuned!

The beautiful photo at the top was available through a Creative Commons license thanks to Charis Tsevis/Harrison & Star

Medication picture courtesy of Steve Smith

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Central Sensitization, Chronic Pain, Nervous System, Pain Neurophysiology Education, Pain Science

Nervous System Basics

nerves-346928_1280

As I’ve said time and time again, I really feel that people living with chronic pain/fibromyalgia can benefit immensely from learning about how the body works. Even the feeling that you are just beginning to understand the complex processes making up your experience of pain can help give you a sense of control over things.

And reading about the new research that is being done on pain, even if you don’t completely understand every word, can sometimes give you a reason to remain hopeful at times when you’re feeling stuck.

With that in mind, I’m going to back way up and publish a post I’ve been meaning to write for a very long time.  Here I’ll outline a few key terms and concepts about how the nervous system works. Hopefully it will be helpful to anyone who is interested in learning more about pain.

So let’s get started.

The nervous system can be divided into two main branches.

Photo courtesy of the Anatomy & Physiology, Connexions Web site. http://cnx.org/content/col11496/1.6/, Jun 19, 2013.
Photo courtesy of the Anatomy & Physiology, Connexions Web site. http://cnx.org/content/col11496/1.6/, Jun 19, 2013.

The central nervous system consists of the brain and spinal cord, and is shown in pink in the diagram above.

The peripheral nervous system consists of all the nerves in the body, and is shown in yellow.

The brain is the command center for your body, and it is where your experience of pain is processed. It is where you think consciously, but it also controls many unconscious functions, such as breathing, your sense of balance, and the ability to orient your body in space.

The spinal cord is the relay system for messages between the brain and the peripheral nerves. (It can also play a role in affecting how strong your ultimate experience of pain is, but we’ll talk more about that later).

The peripheral nerves have two main jobs:

Sensory: Sensory nerves send signals to the central nervous system about what you are feeling physically. When you stub your toe or get a papercut, it’s sensory nerves that send that signal up your spinal cord to your brain.

Motor: This is (to me) a kind of funny scientific word. It really just means “movement.” The motor nerves of the peripheral nervous system are what tell your muscles to move, as well as tell your organs to perform specific functions.

Pain

When people talk about how pain works, they are generally talking about the relationship between the sensory nerves, the spinal cord, and the brain. The sensory nerves send signals up to the brain about any damage that may have occurred, and the brain decides how to interpret those signals.

But Pain is a Two-Way Street

Historically, people considered this pain pathway to be a very consistent, cut-and-dry system that always worked the same way every time. If a person was in a lot of pain, they had to have a lot of physical damage/injury. If they weren’t in very much pain, they must not have a very serious physical problem.

However, scientific advances in the past few decades have shown that pain is actually much more complicated than that. It turns out that the severity of a person’s pain does not always reflect accurately the amount of physical injury they have experienced.

You can have soldiers in battle who do not even realize they’ve been shot– their peripheral nerves are sending very strong messages of “damage” up to their brains, but their brains tune those signals out because they need to focus on survival.

Conversely, you can have people with chronic pain, who– due to a number of potential factors—can experience excruciating pain in response to a very minor injury, or in fact no injury at all.

Central Sensitization

At the risk of boring my long-time readers, let me define one of my most favorite terms again.  Central sensitization is the process responsible for this last phenomenon, where people can develop an increased sensitivity to pain.

The term refers to a series of changes that can take place in the central nervous system (the brain and the spinal cord) which can ultimately make a person much more sensitive to pain.  In some cases, central sensitization can become a self-perpetuating phenomenon, in which a person continues to feel pain long after their initial injury has healed.

Central sensitization is such a fascinating topic.  There is still much research to be done on it, but so far it is believed to play a role in such seemingly-diverse conditions as fibromyalgia, chronic fatigue syndrome, irritable bowel syndrome, temporomandibular disorder, and many others.

One Last Thing

When I first started trying to understand the amazing, interesting new research that’s being done in pain, I kept hitting this one term that mystified me.  The dorsal horn.  What the heck is a dorsal horn?  I was so confused by this for a long time, and it really held me back from understanding a lot of articles.

Turns out, the term dorsal horn refers to an area in the back of the spinal cord.  The back of the spinal cord is where the sensory nerves meet with the spinal cord, so their messages can continue on up to the brain.  It’s pretty simple actually– the sensory nerves connect with the back of the spinal cord, and motor nerves connect in the front.  So when people talk about the dorsal horn, they are  talking about where sensory information is entering the spinal cord and then being relayed on up to the brain.

For more info

If you want a really great overview of the divisions of the nervous system, I highly recommend this video.

Conclusion

I really hope you’ve enjoyed this post!  As you can see, it’s written in a very different tone, and for a very different target audience, than my previous post.  I’m still in the process of figuring out what type of post works best on this blog.  I really want to be able to write about advanced scientific concepts for every day people, and I’ll probably be trying to figure out the best way to do that for a while. Your thoughts/comments/suggestions are always welcome, so please let me know if you have any! Thanks!

Part Two: click here if you’d like to keep reading!

Top photo courtesy of Geralt