Chronic pain is at epidemic levels and has become the highest-cost condition in health care. This course uses evidence-based science with creative and experiential learning to better understand chronic pain conditions and how they can be prevented through self-management in our cognitive, behavioral, physical, emotional, spiritual, social, and environmental realms. The goal of this course is to blend creative, experiential, and evidence-based teaching strategies to help participants understand chronic pain conditions and how a human systems approach can be applied to self-management strategies to reduce risk factors, enhance protective factors, and prevent chronic pain. There are four major objectives to the course; 1. Describe the prevalence, personal impact, and health care dilemma associated with chronic pain. 2. Recognize the clinical characteristics and underlying etiology of several common pain conditions and the peripheral, central, and genetic mechanisms of chronic pain 3. Based on the literature associated with risk and protective factors in the seven realms of our lives, learn specific strategies in each realm that can be employed daily to prevent chronic pain and enhance wellness. 4. Appreciate the value of a human systems approach to health care and how it can provide a basis for integrative, interdisciplinary, and individualized care to preventing pain and enhancing wellness. CONTINUING EDUCATION CREDIT OPTION Accreditation Statement: University of Minnesota, Interprofessional Continuing Education is accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team. American Medical Association (AMA) The University of Minnesota, Interprofessional Continuing Education designates this enduring material for a maximum of 24.0 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity. American Nurses Credentialing Center (ANCC) This activity is awarded up to 24.0 ANCC contact hours. Other Health Care Professionals Other health care professionals who participate in this CE activity may submit this certificate statement of participation to their appropriate accrediting organizations or state boards for consideration of credit. The participant is responsible for determining whether this activity meets the requirements for acceptable continuing education. Registration and disclosure information is available here at http://z.umn.edu/chronicpain and pay the additional fee. Then, email your Coursera certificate statement of completion to cme@umn.edu.
2 Myofascial Pain: Causes
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Do curso por University of Minnesota
Preventing Chronic Pain: A Human Systems Approach
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Common Pain Conditions and their Mechanisms (Week 3)
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Dr. James Fricton, DDS, MSProfessor and Pain Specialist
University of Minnesota, HealthPartners Institute, and Minnesota Head and Neck Pain Clinic
Myofascial trigger points often develop after acute trauma.
Typically in muscles that are strained during the trauma or in
muscles that are recruited for protect the muscle splinting of injured body parts.
Examples of acute trauma are falls that result in a back injury, a knee injury,
hand or shoulder injury, or even a whiplash injury from a car accident.
The muscles around the injured body part Were injured along with the traumatized
areas, contract to immobilized the region and allow healing to occur.
If the muscles are shortened and immobile long enough, trigger points develop.
So here we have somebody that has a back injury, they have protective muscle
splinting, and then they develop quadratus lumborum trigger points and
get the referred pain from that.
So after the acute injury has healed,
persistent pain is often due to these trigger points, and
the pain is typically referred back into the same injured body part.
Unfortunately, unless recognized as myofascilian origin, this persistent pain.
Results in a futile search for non existent continued pathology.
Oftentimes resulting in unnecessary testing, imaging and
sometimes even unnecessary surgical procedures.
Myofascial trigger points may also develop acutely after excessive or
unusual exercise.
Such as packing or handling boxes when moving, or
even prolonged jaw opening at the dental appointment.
This may include activation of pre-existing,
latent trigger points that developed from prior injuries or.
From chronic long-term muscle overload.
Chronic muscle overload is also a huge problem in
terms of the development of trigger points.
These are overuse syndromes from microtrauma, more insidious factors
such as poor posture and body mechanics or repetitive motion activities.
Poor posture is by far and away the biggest contributing factor to
myofascial trigger point development, and to it's perpetuation.
In the head and neck region,
poor posture can cause a cascade of events that leads to overload of the shoulder and
neck muscles, as well as the muscles of mastication, the chewing muscles.
As we see here in this diagram,
the head is not perfectly balanced on the cervical spine.
It is slightly weighted forward.
Because of this, the posterior cervical muscles are much larger and
stronger than those on the front of the neck.
The muscles at the back of the neck are designed to hold your head up so
that your eyes are level and you can see where you're going.
And this requires about ten pounds of work,
that's what these muscles are designed for.
So that they can-,
you can walk around and see where you're going.
When we collapse into poor posture, these muscles have to work
overtime to rotate your head back up so that your eyes can still see forward, so
for example, if you're standing in good posture, you drop down.
You really can't see where you're going so your head rotates up.
And what happens is all these muscles back here.
And the sternocleidomastoid muscle have to work overtime in order to
keep your head in that position.
So for every inch that your head comes forward of its normal position,
in ears align with the shoulders.
Comes forward.
For every inch it's forward of where it should be,
it's an extra ten pounds of work that this, these muscles have to do.
So we have the erect head carrying about ten pounds of weight.
And for every inch it comes forward it, it needs to do more work.
So when your head is rotated up so that your eyes are still level with.
With the ground, something else happens.
Because these muscles that are attached to your
hyoid process are only about this long when you're standing in good posture.
When you round your shoulders forward, and
then extend your head, they're now on the stretch.
And with this movement.
There's a gentle pulling down on the mandible, and
if unopposed, your jaw would open up.
But since nobody walks around with their mouth open, there's a reflex
contraction of the chewing muscles, and that closes the mouth again.
So, just by falling into poor posture, we activate not only the,
these posterior cervical muscles that we see here.
But we also activate the sternocleidomastoid muscle, and these
muscles start pulling down on the jaw, and that activates the reflex contraction of
the mastaticory muscles, the chewing muscles, to keep the mouth, mouth closed.
Another consequence of having this increased clenching for
poor posture is that the intrarticular pressure in
the temporal mandibular joint is also increased.
And if a person has a slightly mis-shapened disc in
the temporomandibular joint this increased intra-articular pressure can cause that
disc to slip out of place and cause a very early click.
So, oftentimes, postural cor, correction can correct early clicks and
pops in the temporomandibular joint as well,
because it reduces the intra-articular pressure again.
Here is an example of poor posture with computer use,
an all too common problem these days.
In this picture we can see that the computer screen is too high,
requiring the head to go into extension to look up.
This overloads the neck and shoulder muscles.
The chair is too high and so we see under thigh compression here.
And the, because of the angle here, we lose the normal curve in the low back.
We've lost the lumbar lordosis.
In addition, the keyboard is way too high.
So we get an unnatural curve in the wrist.
And the arms get hiked up in order to type on the keyboard.
So we get activation of the upper trapezius, the levator scapulae muscles,
and an awkward wrist angulation.
Here we see a woman carrying a very heavy shoulder bag.
This results in activation of the upper trapezius and
the levator scapulae muscles.
She ends up tilting her torso and overloads various back muscles.
And when this type of activity occurs on a regular basis.
Trigger points develop over time.
Now, there are also trigger points that
develop secondary to other painful conditions.
So any kind of painful condition or underlying disease or
inflammation will be a source of pain that can cause trigger points to develop.
This includes things like inflammatory disorders of the tempromadicular joint in
the head and neck regions, chronic ear infections, persistent toothaches,
migraine, cancer, post-repetic neuralgia, any other chronic painful condition.
So, for
example if we have the primary noxious stimulus of a third molar infection.
This causes protective muscle splinting and we call that myospasm or trismus.
But if it lasts long enough, it becomes independent of the primary pain cause.
So, for example, if this is the infected tooth.
It sends signals to the spinal cord.
We get here the secondary protective muscle activity, splinting the area,
keeping it quiet until the infection heals.
If this painful input lasts long enough.
Then there's painful impulses that go back into the spinal cord, and
this loop becomes self, self perpetuating.
And so even once we remove the offending infection and
the tooth is gone, and the inflammation and infection has resolved.
This now stands by itself and continues to cause pain.
It turns out that even when the primary cause of a particular pain is not
muscular, central excitatory effects tend to be expressed in the muscles.
Making myofascial trigger points like frequent complication accompanying other
causes of pain.
It is really important to identify the secondary myofascial pain.
This reduces pain and ref,
and improves response to other therapies especially if the initiating
source is also a chronic pain problem such as migraine or post-herpetic neuralgia.
Now, we discussed this in our earlier, in an earlier presentation, when the pain
from one trigger point is referred into another muscle, that muscle tightens up.
Over time, the referred motor activity results in
the development of satellite myofascial trigger points in the secondary muscle.
And this often creates additional referred pain patterns and
confuses the clinical picture.
So, again, we have here the upper trapezius muscle
that is referring pain into the temple, into the jaw, over the masseter muscle.
The secondary trigger point, the satellite trigger point, develops in
the masseter muscle and refers pain forward into the jaw and up into the ears.
Now, this is often what we see happening in whiplash injury, where the primary
problem is really the cervical muscles, we get pain referred into the face.
Patients think they have TMJ problems, jaw problems, or they have now toothache.
Which is all due to satellite trigger points developing in
response to the acute muscle splinting, the development of trigger points, or
activation of trigger points from the cervical whiplash injury.
If you want to eliminate these pains here then we also need to take care of
the primary trigger point here this, the key trigger point.
Further complicating this sort of this concept is the,
is the fact that upper trapezius trigger points for
example may be perpetuated by lower trapezius trigger points.
And these are the ones that will then need treatment before this will resolve,
before the facial pain will resolve.
Once trigger points have been established, they will tend to wax and
wane between active and latent states and
what are the factors that will typically activate a trigger point?
Well, one of the biggest factors is stress or nervous tension.
There are at least three different studies that have documented the increased in ear,
in trigger point activity in response to stressful situations.
The first and, study was done by McNulty et al.
they, originally, looked at and
found that trigger points have a very distinct spontaneous electrical activity.
And this is illustrated in this slide, here.
If a special monopolar EMG electrode is inserted directly into the trigger point,
there is electrical activity that is unique.
To that tr, to the trigger point.
And if the same electrode is moved just very slightly, just needs to be
a millimeter or two outside of the trigger point, the muscle is electrically silent.
And if you place a needle electrode in the normal muscle adjacent to
the trigger point, it's also silent.
So you can see the electrical activity that's characteristic of trigger point
here, and here's a, an electrode that's placed just a centimeter away and
there's basically electrical silence.
Now, what they did was they put these needles into a group of patients and
they had a control situation and the active situation.
So what they did was, they put the needle into the trigger point site, this is
the pink line here, and they put another electrode into the, the normal muscle,
not in the trigger point, that's this yellow dotted line here.
The x-axis represents time and depicts various task conditions along here,
so we have baseline, forward counting, interval, backward counting and recovery.
The y-axis here represents the microvoltage,
the microvolt amperage found in the, these two different muscle sites.
Now, the normal muscle
fibers had very low electrical activity throughout the experiment.
So what they did was they, first just recorded from the muscles.
Then they had the patients count forward: one, two, three, four, five.
Then they gave them a brief rest.
Then they had them subtract serial seven's from a hundred.
193, 86, that kind of thing.
Considered stressful.
And what we see is that during the entire experiment the normal
muscle really doesn't change in terms of how much electrical activity is going on.
It's the same.
But the trigger point site, as soon as the stressful activity starts,
the, the amplitude of the spontaneous electrical activity got bigger and
bigger and bigger.
And it wasn't until the backward counting was stopped and
they were allowed to go into recovery mode that the electrical activity the amplitude
of the spontaneous electrical activity started to calm down again.
So this very clearly shows that there is a correlation between the electrical
adds stress and this correlates very nicely with what we see clinically.
When people are very stressed they tend to have more pain.
So, in summary myofascial trigger points tend to
develop after acute trauma, with chronic muscle overload.
Poor, this includes poor posture, body mechanics, repetitive activities.
They tend to occur secondary to other chronically painful conditions.
Migraine, post-herpetic neuralgia, toothache, arthritis.
They also develop secondary to referred pain from other trigger points.
What activates trigger points?
They can be activated by additional acute muscle overload but
also through psychological stress.
It is obvious that myofascial trigger points are extremely common and everyone
will likely experience pain or at the very least some stiffness and restricted motion
perhaps without pain from this disorder at some point in their lives.
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