Prompted by some mentee questions and blog comments, I wondered where manual therapy fits in the rehab process.
To satisfy my curiosity, I calculated how much time I spend performing manual interventions. Looking at last month’s patient numbers to acquire data, I found these numbers based on billing one patient every 45 minutes (subtracting out evals and reassessments):
Nonmanual (including exercise and education) = 80%
Manual = 20%
Modalities = 0%!!!!!!!!!!!!
Delving a bit further, here’s my time spent using PRI manual techniques versus my other manual therapy skill-set:
PRI manual = 14%
Other manual = 6%
As you can see, I use manual therapy a ridiculously low amount; skills that I used to employ liberally with decent success.
There’s a reason for the shift
I want my patients to independently improve at all cost and as quickly as possible. The learning process is the critical piece needed to create necessary neuroplastic change; and consequently a successful rehab program.
My gluttony for punishment continues. This time, I had the pleasure of learning Diane Jacobs’ manual therapy approach called Dermoneuromodulation (DNM).
My travels took me to Entropy Physiotherapy and Wellness in the Windy City. These folks were arguably the best course hosts I have ever had. We had lunch!!!! Both days!!!!! That is unheard of, so a big thanks to Sandy and Sarah for putting the course together.
I took DNM out of curiosity. I have been lurking around Somasimple on and off for the past couple years, and wanted to learn more about the methods championed there.
Believe it or not, I have yet to take a pure manual therapy course, DNM seemed like a great way to get my hands dirty. That darn PRI has lessened the hand representation in my somatosensory homunculus!
One reason I haven’t taken a manual course is due to the explanatory models many classes are presenting. It seems as though few are approaching things with a neurological mindset, but I was pleased to hear Diane’s model. It is the best explanation I have heard yet.
I know that I usually list my favorite quotes at the end of the blog, but I wanted to share the best quote of the weekend right off the bat:
“I don’t know why.”
I heard this phrase so much throughout the course and it was quite refreshing. Diane made few claims about her technique, admitted who she “stole” from, and embraced the uncertainty that goes along with how her technique works.
Diane didn’t advertise her method as the end-all-be-all, and encouraged all of us to make up techniques of our own. She is just offering a non-painful sensory input that works quickly.
I wish more courses were this way.
Let us now press onward to a fantastic explanation for manual therapy.
Manual Therapy – An Interaction Between Two Nervous Systems
Diane started off with manual therapy’s theoretical basis. Manual therapy works predominately through your nervous system. We are made up of a brain, spinal cord, and nerves that extend from the cord.
The brain can be simply broken up into two components: the human brain and critter brain. The human brain sits our higher activity centers, and the critter brain runs the processes that keep us alive.
Under threat, the critter brain is going to do everything in its power to keep us alive, and this change can involve the protective mechanisms that go along with pain.
The critter brain carries out its processes through the body’s nerves. Nerves in the body tell the brain what’s going on, and the brain then tells nerves how to respond.
In order to calm our critter brain down, the clinician can communicate with the nervous system through cutaneous nerves. Our goal with our interventions is to touch the patient without hurting them. Hurt could irritate the critter brain. Instead, we want an enjoyable context for touch.
The patient’s role…Wait, what???!!!
Yes, the patient’s role in the manual therapy process is to guide the clinician to what feels best. It is this interactive and interoceptive model that helps reduce threat perception. This context allows for the patient to be a little more in control of the manual therapy process.
It Rubs the Lotion on Its Skin
The skin is a pretty cool organ that can hold 20% of our blood supply and maintain temperature homeostasis. It has both peripheral (PNS) and central (CNS) nervous system influences. The PNS automatically activates to maintain skin temperature and the CNS can express itself through the skin. Those times in which you are embarrassed or scared reflect CNS status through your skin.
Due to the skin’s high innervation and vascularity, anytime we touch the skin we affect the neurovascular array. This change occurs through facilitating mechanoreceptors and physically altering cutaneous rami position. The nervous system then evaluates this information to determine if the touch is a threat or not.
Tissue information is received through receptors. There are tons of them, but we have a few major players:
Rapidly adapting mechanoreceptors – Turns on and shuts off by itself
Thermoreceptors – Responds to temperature change for duration of stimulus.
Nociceptors – Responds for stimulus duration. Can be set off by going perpendicular on skin.
Pacinian corpuscles – Turns on with stimulus onset and removal. Will continuously fire if stimulus fluctuates.
Meissner’s corpuscle – Turns on with stimulus onset and removal
Ruffini endings – respond to lateral skin stretch and are non-nociceptive. Slow adaptors to stimulus. Can fool the brain to alter muscle tone with skin stretch.
Merkel cells – slow adapting to stimulus.
All the above receptors respond to stimuli and communicate information to the brain along sensory nerves. It turns out sensory nerves are incredibly long. Many of these nerves go directly from the skin to the brain. One cell! Anytime you touch the skin you are touching a direct extension of the brain.
Sensory input travels via the mechanoreceptors through the dorsal columns and spinothalamic tract in the spinal cord. Interestingly enough, the spinothalamic tract does not only carry nociception, temperature, and crude touch. Pleasant touch can also travel along this pathway.
The Dorsal columns input goes to the thalamus, which sends information to the somatosensory cortex. The spinothalamic tract goes to the thalamus first as well, followed by the somatosensory cortex, anterior cingulate cortex, and the insular cortex. These three areas are what Diane noted as “threat evaluation areas.” These areas are part of your critter brain.
Once the brain receives this information, it essentially talks to itself to determine if this information is important or not. If important, an output occurs to respond to the input.
Many brain areas are a part of this conversation. The following locations contribute to the desired output in a particular way:
Anterior cingulate cortex – bridge between instinct and rational; makes us worry about pain.
Orbitofrontal cortex – defers, suppresses, differentiates touch, interprets emotions (if you are in a bad mood, this is how your patient will know it…so be happy!).
Dorsolateral prefrontal cortex – Chooses behavior. This area is where therapeutic neuroscience education targets.
Pain is one possible output in response to various inputs. If pain is the desired output, changes can occur to increase sensitivity.
One possibility is hyperalgesia, in which noxious stimuli becomes extra sensitive. Hyperalgesia can be primary or secondary.
To understand the two, we should first look at a sensory neuron.
A sensory neuron has two ends. The end that connects to the tissue is the terminal pole, and the end that travels to the spinal cord is the central pole.
Primary hyperalgesia affects the terminal pole. Substances released by injured tissue activate nociceptors at this pole, creating the information cascade sent to the brain described previously. We also know this as inflammation.
As the inflammatory process progresses, nociceptors send substances out to the tissues to promote enhanced firing. This change creates peripheral sensitivity, and is normal.
Secondary hyperalgesia (aka central sensitivity) has more fun at the central pole. TRPv1 is a receptor at the central pole that increases spinal cord and blood-brain barrier permeability, which allows for more nociceptive transmission to be received. Serotonin can descend from the brain to the spinal cord and sensitize these receptors as well.
Other changes that occur in secondary hyperalgesia include glial and satellite cells lowering the threshold at which nociceptors fire. The name of the game is to increase the nociceptive information coming in.
Both of these algesic mechanisms can simultaneously occur to protect a potentially compromised area. However, pain may not necessarily be experienced. Nociception involves threat detection, whereas pain involves threat perception. The two are not equal entities.
“The labeling of nociceptors as pain fibres was not an admirable simplification but an unfortunate trivialization.” ~Patrick Wall
Nerves n’ Stuff
The neurovascular bundle is connected via regional feeder vessels. These vessels ought to slide and glide with the nerves so blood supply is maintained. Movement is what keeps this system healthy.
These connections are vulnerable and can become sensitive to mechanical deformation. Too much or not enough movement can decrease the nerve’s oxygen and glucose supply. A nerve will let you know if it does not get fed.
Deformation could translate into neuropathic pain, which is defined as pain caused by a lesion or disease in the somatosensory system. Neuropathic pain is not a diagnosis, but a descriptor.
The way one could determine if neuropathic pain contributes to one’s complaint is done quite algorithmically. The following must be present:
Leading complaint must be pain.
Pain distribution must be neuroanatomically plausible.
History should suggest relevant lesion or disease.
Negative or positive sensory signs contained to lesioned area in question.
Diagnostic testing confirming lesion or disease explaining neuropathic pain.
The fewer of these criteria positive, the less chance there is of having neuropathic pain.
Theory into Therapy
Diane stressed that a therapeutic context must be established before implementing a manual intervention. This foundation occurs via a 4-step process
Listen – Allows the patient to map you in their story. Your listening models how they listen to themselves.
Interact – Explain pain. This part will plant seeds to regulate future stressors.
Treat – Provide non-nociceptive therapy, making sure to give the patient locus of control.
Wait – Do not correct; wait for physiology to change and the desired output to emerge.
The object is to create the largest amount of descending modulation possible. We therefore mobilize the cutaneous nerves via “yesiceptive” contact and interaction.
Though Diane does not believe in trigger points, she does believe in sore spots that often have a different feel about them. Our goal is to change these sore spots without worsening them.
Cutaneous nerves anastomose in various ways, so everyone’s anatomy is going to be slightly different. Thus, there can be no precision or specificity with treatment. We just have to somehow move nerves in a fashion that results in reduced pain.
The assessment process was my one gripe with the course. Each technique was given clinical situations that they may work with. We then assessed with active movement followed by palpating tender spots. However, these spots can be present on many people even if pain is relieved, are unreliable to assess, and do not always contribute to the patient’s complaint. How can we say that performing this intervention is the right thing to do for this patient?
Well Diane freely admitted palpation’s unreliability, she has also been practicing long enough that she has the pattern recognition to know when techniques ought to be implemented. Novice clinicians likely lack this skill. There must be some way to provide an assessment that may lead you to performing one mobilization compared to another.
I espouse Charlie Weingroff’s principle of “can your treatment beat my tests.” Since I am a PRI enthusiast, I used those objective measures to test treatment efficacy. When implemented thoughtfully, DNM can change PRI objective measures fairly quickly and in a pain-free manner.
Zac = sold on both counts.
DNM is actually fairly simple to perform. The technique is a combination of positional release with skin stretch; fine-tuning performed throughout to maximize treatment effect.
Diane gave us many techniques that seem to work over specific areas, but really you can stretch skin in any fashion. Here are some examples of the basic techniques utilized in the course.
Longitudinal distraction – Nerves move up.
Shearing distraction – Nerves are lifted and twisted.
Unloading – Nerves move up.
Contralateral unloading (the balloon) – Go to the opposite side of the sore spot.
Once these techniques are implemented and symptoms change; exercise ought be to given to reinforce the changes. Though no specifics were given, Diane suggested ideas of using positioning strategies, taping, self-DNM, etc. Her objective was to give us the manual technique, then supplement with our exercise strategies of choice.
Overall I really enjoyed Diane’s course. She has given the best manual therapy theoretical explanation I have heard, and the technique is very gentle and effective. She can beat my tests. I think that if these maneuvers are implemented into a sound assessment, you can add a very powerful sensory input to your repertoire.
Verdict: Do it. The neuroscience alone is worth the price of admission.
Nerves slide and glide like a telescope.
A rete is a dense convoluted birds nest of cutaneous nerves over a bony prominence. These are over most every bony prominence.
Dianetics (See what I did there??)
“We belong to our brain more than our brain belongs to us.”
“We’re not treating anatomy, we’re treating physiology.”
“Spinal cords have not got much smarter since fish days.”
“You can’t trust the brain pretty well. It makes up stories.”
“It’s never a good idea to treat someone who is feeling better than you are.”
“Therapeutic neuroscience education is accurate and relevant pain information.”
“Pain is physiological.”
“You are only as old as your C-fibers.”
“It probably serves us well to not believe everything our brain tells us. “
“Pain is the story built from all inputs.”
“Pain descriptors are more of a way for the patient to export their feelings.”
“Having a license to touch people is an enormous privilege.”
“I can’t think of a better thing then using human brains to help other brains.”
“The less you do the better results you are going to get.”
“I have to tell you up front. I am a trigger point atheist.”
“Evolution is weird, and it’s not that smart actually.”
“When I don’t have a monitoring hand I’ll use my head to push the skin on the butt. I call it the head butt technique.”
“There will be asymmetric positions people adopt. It’s their comfort position.”
“We’re asymmetric in our behavior.”
“We’re not going to deal with your ovary by the way.”
“Those who have IT band syndrome, I don’t even know what that means.”
“I found this on the internet so it must be true.”
“The pelvic floor holds up a bunch of stuff. And you don’t know what you’ve got ‘til its gone.”
“Heels just love to be cranked on.”
“Let your brain be creative when you treat.”
“It’s [DNM] soft and easy so you can die comfortably at your job.”
The major premise of this book is that pain is normal. It is the way that your brain judges a situation as threatening. Even if there are problems in the body, pain will not occur if your brain thinks you are not in danger.
Explaining pain can reduce the threat value and improve pain management. And the good thing about explaining pain? Research shows that it can be an easily understood concept.
Pain is Normal
Pain from bites, postures, sprains, and other everyday activities are more often than not changes in the tissues that the brain perceives as threatening. This system is very handy, as often it keeps us from making the same mistake twice. I personally akin this to patients as recognizing a certain smell and that smell reminding you of something. Pain is often the reminder of previous injuries.
Pain becomes problematic when it becomes chronic. This pain is often the result of the brain concluding that for some reason, often a subconscious one, that the person is threatened and in danger. The trick is finding out why.
Stories are some of the best ways to relate pain to patients. There are many cases when you hear soldiers sustaining major injuries yet charging further into battle. On the flipside, take a look at paper cuts. The damage is very miniscule; however, the pain levels are huge. Point being, what occurs in the tissues is only one component of the pain experience. And if pain is not perceived, then tissue changes are not deemed threatening by the brain.
Pain oftentimes can be modified by various cues that the brain experiences called ignition cues. Take prescription drugs for example. The tablet’s shape plays a huge role in how effective the drug is.
Transparent capsules with colored beads > capsules with white beads > colored tablets > square tablets with corners missing > round tablets.
Pain is dependent on the perceived cause as well. Take someone who has survived cancer. If that person attributes a painful experience to cancer returning, the pain is often worsened regardless of what is occurring in that person’s tissues.
Lacking knowledge and understanding also increases pain and fear. We are afraid of the unknown, and if we do not know why we hurt, often the pain will increase in response to fear.
Phantom in the Body
Tissue-centric pain explanations are incomplete. The biggest example of this is phantom limb pain. The reason why these phantom limbs create pain is due to the body’s virtual representation in the brain.
The virtual body, or homunculus, is what allows us to know our body’s location in space. You access the virtual body every time you perform an action with your eyes closed. In this case of phantom limb pain, the virtual leg is still present and relates to the rest of the virtual body. This experience can even occur in children born without limbs, because that virtual representation is still present.
When a phantom limb pain occurs, the virtual leg becomes smudged. This change results in an unclear representation of the limb in the brain. This phenomenon also occurs in people who have chronic pain.
Our pain perception can often be attributed to our parents. When an infant falls, they will often look to their parents to gauge the optimal response. However, the pain experience is unique to each individual.