It seems like I took this course forever ago, but reviewing this post reminded me why I love the NOI group so much. I feel as though their message is one you cannot get enough of.
As for GMI itself, I find that it is great for people who most every movement hurts, as well as an educational piece. From a PRI perspective, it is also useful. I have had patients imagine contracting their glute max and go neutral. Crazy stuff.
Such a great class. Here we see updates to the science behind “The Sensitive Nervous System”, as well as some neat tweaks to our neurodynamic testing. My favorite pieces were on the immune system and genetics.
Piriformis syndrome often involves the fibular tract of the sciatic nerve. It has the capacity to create symptoms from the buttock down to the anterolateral leg. Testing the neurodynamics with a fibular nerve bias is essential.
To attempt to isolate this problem, we must best differentiate interface from neurodynamic components. Using Cyriax principles –palpation, contraction, and lengthening –can be beneficial in this regard. Keep in mind that below 70 degrees hip flexion the piriformis produces external rotation, and above 70 degrees it is an internal rotator.
When treating this problem, the goal is to change pressure between the piriformis muscle and the sciatic nerve.
Level 1a – Static opener
VID – KF, ER
Level 1b – Dynamic opener
VID – Passive ER
Level 2a – Closer mobilization using passive IR.
VID – Passive IR
Level 2b – We finish with a passive piriformis stretch
VID – Tailor stretch
If there is a neurodynamic component to things, slightly modify things by using sliders. We start things off with the same opener as the interface above. As the patient progresses, you can add proximal or distal components eventually finishing with a fibular nerve-based slump.
VID – Building the slump
To combine interface and neural treatments, contract-relax can be utilized.
Sciatic Nerve in the Thigh
Oftentimes with hamstring strains, sciatic nerve sensitivity can increase. The slump and straight leg raise tests can be utilized to help differentiate a pure hamstring issue from neural problems.
To treat this issue, sliders can be utilized, eventually working to a slump tensioner:
VID – PF at top for proximal dysfunction, DF at bottom for distal sliding…progress with spinal lateral flexion (done in slump
Knee and Thigh Pain
Implicating neurodynamic problems in this population is challenging, as these tests often show covert abnormal responses. These can be treated with simple sliders and tensioners. These are not in the Shacklock book, but are what I have been currently using.
VID of FS slider and tensioner
Here is an example of a slider and tensioner for fibular nerve impairments.
Both neck flexion and knee extension increase symptoms – Tension dysfunction.
The straight leg raise is another important test that can help determine the nervous system’s state.
The treatment parallels similar tactics as previous body areas. For reduced closing dysfunctions We start level 1 with static openers, progress to dynamic openers, then work to close.
For opening dysfunctions, we progress toward further opening/contralateral lateral flexion.
We treat these mechanisms based on which dysfunction is present. For cephalid sliding dysfunctions, we approach with distal to proximal progressions; and for caudad sliding dysfunction, we work proximal to distal
Tension dysfunctions are started with off-loading mvoements towards tensioners
Sometimes you can have interface dysfunctions that simultaneously have contradictory neurodynamic dysfunction. There are several instances of the case.
Reduced closing with distal sliding dysfunction – Treat by combining closing maneuvers while perform active knee extension.
Reduced closing with proximal sliding dysfunction – Address by closing maneuver with neck flexion.
Reduced closing with tension dysfunction – This is treated with adding closing components to tensioners
Reduced opening with distal sliding dysfunction – Here we add a dynamic opener along with leg movements.
Reduced opening with proximal sliding dysfunction – Same as above, only we add neck flexion instead of leg movements
Reduced opening with tension dysfunction – Basically a combination of the last two treatments.
The same techniques can be applied to mid-lumbar dysfunctions, this time utilizing the femoral slump:
And if all else fails, just watch this video (NSFW due to language).
When discussing TOS pathoneurodynamics, you must talk about breathing. The brachial plexus passes inferolaterally between the first rib and clavicle. When inhalation occurs, the plexus bowstrings over the first rib cephalidly. So breathing dysfunctions can contribute to one’s symptoms. Excessive scapular depression can also contribute because the clavicle approximates the plexus from above.
Clinically, TOS often presents as anteroinferior shoulder pain, with some cases passing distally along the course of the ulnar nerve. A resultant upper trapezius/levator scapula hyper or hypoactivity can occur that may affect the neural elements.
Treating the Interface
Level 1 – Static Opener with breathing
Level 2 – Static opener with rib mob during exhalation; progressing with scapular depression.
Level 3 – Rib depression with sliders and tensioners.
Pronator Tunnel Syndrome
This syndrome consists of pain in the anteromedial forearm region with or without pins and needles. Symptoms are usually provoked by repetitive activities such as squeezing, pulling through the elbow, and pronation movements.
From an interface perspective, pronator syndrome deals with excessive closing. So we will use openers to treat.
Level 1 – Static opener combining 60-90 degrees of elbow flexion with forearm pronation
Level 2 – Dynamic opener
Treating neural components depends on the present dysfunction. There are the following possible dysfunctions:
Distal sliding dysfunction – symptoms decrease with contralateral cervical flexion.
Proximal sliding dysfunction – Symptoms increase with contralateral cervical sidebend and finger flexion.
Tension dysfunction – Symptoms increase with contralateral cervical sidebend and finger extension.
We treat the distal sliding dysfunction by progression sliders from large to small distal movements, with the reverse occurring for proximal sliding dysfunctions:
Tension dysfunctions are going from anti-tension to tension mechanisms
You can also combine interfaces and neurodynamic treatment utilizing acupressure during a nerve mobilization:
Supinator Tunnel Syndrome
This syndrome involves anterolateral elbow and forearm pain with possibly pins and needles. There also can be isolated wrist dorsum pain. Symptoms are provoked by activities such as squeezing and pulling through elbow flexion and supination movements.
Interface treatment is very similar to that of pronator tunnel syndrome.
You can also have distal (improve with contralateral cervical sidebend) and proximal (worsen with contralateral cervical sidebend and wrist extension) sliding dysfunctions, which are treated in a similar fashion as the pronator tunnel syndrome. So too with tension dysfunction; the goal is to build up the test.
You can also perform neurodynamic massage over the supinator.
Carpal Tunnel Syndrome (CTS)
Treating CTS is an often underutilized area that can be of much benefit. We can mobilize the transverse ligament as an interface technique.
You can also treat the neural structures with different methods depending on the dysfunction.
Proximal sliding dysfunction – use a median nerve slider starting with distal components then adding proximal components
Distal sliding dysfunction – Use Median nerve test 1 and slowly add distal components.
The best slider for the median nerve is in fact the tensioner. This is because when you extend the wrist, the tendons and the nerve move in the same direction. Adding contralateral cervical sidebend slides the median nerve in the opposite direction of the tendons.
Tensioning dysfunction is just utilizing your basic tensioner.
You can tier your testing based on one’s dysfunctions, such as opening or closing, as well as using sensitizers for less severe problems.
Reduced Closing Dysfunction
Level 1a – Static opener to increase space and decrease pressure in the intervertebral foramen. In the picture below, we would open the right side by combining flexion, contralateral sidebend, and contralateral rotation.
Level 1b to 2b
Reduced Opening Dysfunctions
For these impairments, they are treated just the same as closing dysfunctions. The major difference is rationale. In closing dysfunction, the goal is to reduce stress on the nervous system. With opening dysfunctions, however, we are trying to improve the opening pattern.
Static openers will generally not be used because these treatments could potentially provoke symptoms.
The gentlest technique is the two-ended slider, in which an ipsilateral lateral glide and elbow extension are performed.
For tension dysfunctions, we go through the following progression:
The two main ways to treat interfaces involve opening and closing techniques. These treatments involve either sustained or dynamic components. We will discuss which techniques work best in terms of dysfunction classification.
– Reduced Closing Dysfunction – Given static openers early in this progression, continuing to increase frequency and duration. Eventually you move to more aggressive opening techniques, while finishing with closing maneuvers.
– Reduced Opening Dysfunction – Start with gentle opening techniques working to further increasing the range.
– Excessive Closing and Opening Dysfunctions – Work on improving motor control and stability.
How About Neural Dysfunctions
The main treatments are sliders and tensioners; each can be performed as one or two-ended. Sliders ought to be applied when pain is the key symptom. Sliding may milk the nerves of inflammation and increase blood flow. These techniques could also be used to treat a specific sliding dysfunction.
Sliders can be performed for 5 to 30 reps with 10 seconds to several minute breaks between sets. Increased symptoms such as heaviness, stretching, and tightness is okay, but pain should not occur afterwards. Typically sliders are performed in early stages, and in acute situations should occur away from the offending site.
Tensioners are reserved for higher level tension dysfunctions. The goal is to improve nerve viscoelasticity. Some symptoms are likely to be evoked, but this occurrence is okay as long as symptoms do not last. Tensioners are used in later-stage dysfunction.
With this test, the upper cervical tissues slide caudad, and the lower cephalid. The thoracic spine moves in a cephalid direction as well.
Normal responses ought to be upper thoracic pulling at end-range. Abnormal symptoms would include low back pain, headache, or lower limb symptoms.
Median Neurodynamic Test 1 (MNT1)
This test, also known as the base test, moves almost all nerves between the neck and hand.
Normal responses include symptoms distributed along the median nerve; to include anterior elbow pulling that extends to the first three digits. These symptoms change with contralateral lateral flexion and less often ipsilateral lateral flexion. Anterior shoulder stretching can also occur.
Ulnar Neurodynamic Test (UNT)
This test biases the ulnar nerve, brachial plexus, and potentially the lower cervical nerve roots.
Normal responses include stretching sensations along the entire limb, but most often in the ulnar nerve’s field.
Median Neurodynamic Test 2 (MNT2)
This version biases the lower cervical nerve roots, spinal nerves, brachial plexus, and median nerve.
Normal responses would be similar to MNT1.
Radial Neurodynamic Test (RNT)
This test looks predominately at radial nerve, as well as the nerve roots. It is uncertain if this test biases any particular nerve root.
Normal responses include lateral elbow/forearm pulling, stretch in the dorsal wrist.
Axillary Neurodynamic Test (ANT)
This test tenses the axillary nerve, though may not be specific.
Normal responses include posterolateral shoulder pulling with about 45-90 degrees of abducton.
Radial Sensory Neurodynamic Test (RSNT)
This test is used to rule out de Quervain’s disease as a neurodynamic problem.
Normal responses include intense pulling at the distal radial forearm.
Straight Leg Raise (SLR)
This test is performed with any posterior symptoms from the heel to the thoracic spine.
Active cervical flexion should not be used in this test because false results can occur from abdominal muscle contraction. This error may lead to posterior pelvic tilt, which reduces the hip flexion angle.
Normal response is pulling and stretching in the posterior thigh.
Tibial Neurodynamic Test (TNT)
This test is done for symptoms in the tibial nerve distribution.
Normal responses include stretching in the calf region that can go all the way to the plantar aspect of the foot.
Fibular Neurodynamic Test (FNT)
This test biases both the common and superficial fibular nerves.
Normal responses include stretching and pulling in the anterolateral leg and ankle and the foot dorsum.
Sural Neurodynamic Test (SNT)
This test biases the sural nerve, which can often be involved in a sprained ankle.
Normal responses include pulling in the posterolateral ankle region.
This test checks the peripheral and central nervous system, and can encompass symptoms from the head to the foot.
Normal responses vary depending on the sequence. Usually the movement performed earliest is where symptoms will occur.
Saphenous Neurodynamic Test (SAPHNT)
This test looks at medial knee, shin, and ankle.
Normal response is anterior thigh stretching.
Femoral Slump Test (FST) with Lateral Femoral Cutaneous Nerve and Obturator biases.
These movements bias the anterior-based nerve of the leg.
Shacklock normally performs the exam with the bottom leg in order to maximize gravity’s effects. The obturator can also be biased as such.
Normal responses includes pulling in the adductor region, anterior thigh, or lateral thigh depending on the bias.
When assessing the patient, you must look at the following information:
Symptom location, extent, quality, and behavior.
Range of motion.
Tone of voice.
Protective muscle tone.
When planning the exam, you can tier to what extent you ought to assess someone.
Level 0: neurodynamics are contraindicated for physical or psychosocial reasons.
Level 1: Limited exam where symptoms are minimally provoked. Full neurodynamic tests are not performed, and are tested separately from musculoskeletal structures. The neurodynamic tests are performed with relieving-based structural differentiation.
Level 1 is indicated when…
Symptoms are easily provoked and take a long time to settle after movement.
Severe or latent pain is present.
Progressive worsening prior to exam.
Level 2: Standard examination in which neurodynamics, interfaces, and innervated tissue are tested separately. Standard neurodynamic sequences are used and symptoms can more readily be brought on.
Level 2 is indicated when…
Less severe, latent, or easily provoked symptoms.
Absent/minor neurological symptoms.
Stable problem that is not rapidly deteriorating.
Level 3: It’s gettin’ real. Here we see greater force localization and sequences that start at the problem. Sensitizers are often used as well.
Level 3 is indicated when…
Level 2 exam is normal or provides insufficient information.
Symptoms are not severe or easily provoked.
Problem is stable.
No evidence of pathology.
There are four examination types here:
3a) sensitizers are added.
3b) Begin neurodynamic tests with a motion near the problem area.
3c) Combine neurodynamic tests with interface tests such as muscular contraction or stretching.
3d) Add neurodynamic testing to movements that bother the patient.
Do Sweat the Technique
Technique is everything with neurodynamic tests, as making small changes can lead to profound differences in findings. Realize that the literature suggests that there is not a best sequence to perform the tests, as this order will be patient-specific.
When communicating with the patient, a simple introduction to the test ought to be performed, but do not go into detail on its purpose. The explanation can affect the test outcome. It is also important that the patient not move during the test, as this error can bias results. Ask the patient to verbally describe what is felt.
The most important aspect of test performance is maintaining applied movements. If the position of body parts are not maintained, the test changes. Small variation can lead to completely different results.
In neurodynamic tests, there are two movement types:
1) Sensitizing: Increase force on neural structures.
2) Differentiating: Emphasizing nervous system by moving the neural structure as opposed to musculoskeletal tissue.
The reason why sensitizers are not considered differentiating structures is because they also move musculoskeletal structures. Examples of sensitizing movements include:
Cervical or lumbar spine contralateral lateral flexion.
Humeroglenoid (HG) horizontal extension
HG external rotation
Hip internal rotation
The ability to interpret neurodynamic findings is crucial when determining the nervous system’s involvement. Findings such as asymmetry, symptoms, and increased sensitivity are all important. But to implicate neurodynamics, structural differentiation ought to be performed.
Just because there is a positive test does not mean that it is relevant to the patient’s complaints. There are several ways to classify findings:
Neurodynamic responses can have different interpretations:
Normal: Fits normal responses per literature.
Abnormal: Differ from normal responses. Can be broken down further into…
Overt abnormal responses: Symptoms reproduction.
Covert abnormal response: No symptoms, but may have other subtle findings such as asymmetry, abnormal location, and/or different resistance.
From here, one must determine if the findings are relevant or irrelevant to the condition in question. You may also come across subclinical findings, in which the neurodynamic test is related to a minor problem that may become major at some point.
It seems the more and more that I read the more and more and read the more and more addicted I become to appreciating the nervous system and all its glory. To satisfy this addiction, I took Mobilisation of the Nervous System with my good friend Bob Johnson of the NOI Group.
This was the second time I have taken this course in a year’s span and got so much more value this time around. I think the reason for this enrichment has been the fact that I have taken many of their courses prior and that I prepared by reading all the NOI Group’s books. A course is meant to clarify and expand on what you have already read. So if you are not reading the coursework prior, you are not maximizing your learning experience.
What made this course so much more meaningful was being surrounded by a group of like-minded and intelligent individuals. As many of you know, I learned much of my training through Bill Hartman. Myself, Bill, the brilliant Eric Oetter and Matt Nickerson, my good friend Scott, and my current intern Stephanie, all attended. When you surround yourself with folks smarter than you, the course understanding becomes much greater. This course was so much more with the above individuals, so thank you. Try to attend courses with like-minded folks. Here are the highlights of what I learned. If you would like a more in-depth explanation of these concepts, check out my blogs on “The Sensitive Nervous System.”
Neurodynamics, Clinical Reasoning, and Neuroscience
When discussing clinical reasoning and neuroscience, we have to discuss processing. The pain processes are what we end up treating in rehabilitation, so we have to know where our patient’s problem occurs along the process:
Input – Issues in the tissues; typical therapeutic approaches.
Processessing – How the brain interprets inputs.
Output – The experiences and emotions we feel.
Processes, as opposed to structures, are what we really treat. We can define processes as changes in the physiology. These changes can include degeneration, ischemia, stiffness, inflammation, etc.
In terms of inputs, the two types of input processes that may lead to a pain mechanism include nociception (the firing of A delta and C fibers from tissues) and peripheral neuropathic (involving the neural tissues outside the dorsal horn). The above mechanisms have predictable stimulation responses.
Understand that all injuries to structures are the same, but the context and environment affect processing and output. We have all experienced this phenomenon. A paper cut can hurt like hell, but a cut from a branch while hiking in the forest may not even be noticed. Context makes all the difference.
The pain mechanism related to processing occurs in the central nervous system. With processing problems, the stimulation-response relationship is unpredictable. Thoughts, feelings, past experiences, knowledge, and other states can affect responses here. These components are designed to help us survive our environment.
Lastly, there are several outputs related to pain mechanisms. These outputs involve all our body systems, with the central nervous system acting as the driver.
All these pain mechanisms–input, processing, and output—are involved in some way during a pain state or sensory alteration. One can be more dominant than the others, but all areas are active. It is similar to energy systems. The aerobic, lactic, and alactic energy systems are always active with one often as the primary driver. So too are the involved pain mechanisms.
Often, genetics is the biggest contributing factor to chronic pain development. It is strongly hereditary, like having blue eyes. Here were some values given in the course as to what percentage of pain is genetic:
50% of migraines.
55% of menstrual pain.
35-68% of lower back or neck pain.
50% of shoulder and elbow pain.
40% of pain with carpal tunnel syndrome.
The Nervous System is a Continuum
The nervous system is one of three continuous systems, the other being vascular and fascial. If you move the nervous system at any one place, the entire system moves. It is like moving a tree branch and creating motion throughout the whole tree. Continuum concepts cannot be enhanced by tissue dominant approaches.
There are four ways in which the nervous system is continuous:
Discussing nerves often puts people at unease. However, this feeling should not be the case. Nerves are like any other tissue. Therefore, they live under the same rules as all other tissues. They can bend, twist, and slide transversely. Nerves can also take on increased pressure by loading.
This interconnected quality often confounds traditional segmental-based testing such as myotomes and dermatomes. The nervous system ought to be thought of instead as a continuous piece with multiple reference points.
Moreover, everyone has a different nervous system. Therefore, each person may require a different sequence when performing neurodynamic tests.
Ion channels are the molecular targets for manual therapy. These channels go where no myelin is present:
Dorsal root ganglion
Nodes of Ranvier
There are six points to describe these ion channels:
1) They are proteins with holes in the middle.
2) They have holes that open or close.
3) Some stay open for longer.
4) There are different kinds of channels.
5) They have a half-life of 2-7 days.
6) They represent needs and perceived needs.
I will not go over all the neurodynamic tests in this post, but there were some different variations that I liked in this course compared to what I was doing. The biggest thing when performing these tests is to have a consistent starting position every time. And if you are doing a straight leg raise, pay attention to potential responses on the contralateral leg.
Here is a radial neurodynamic test…proximal to distal style.
The biggest thing that I got out of the nociception section involved inflammation. First off there are two types of inflammation:
1) Non-neurogenic – occurs with tissue damage; creating bleeding and fluid buildup. NSAIDs work well on non-neurogenic inflammation.
2) Neurogenic – Created via C-fibers, which is driven by changes in peripheral tissues and threat perception. It can occur even if the nervous system was not fully involved in the injury. Pregabalin,Gabapentin, Cymbalta, and other similar drugs work well with these.
Peripheral Neuropathic Highlights
Injury to peripheral nerves involves blood flow, axoplasmic flow, and development of abnormal impulse generating sites (AIGS) along the nerve. There are also three different issues that can occur in the nervous system:
Physiologic conduction blocks – local circulatory changes
Neuropraxia – Local conduction block where axon is okay and conduction returns in weeks to months.
Axonotmesis – Axon continuity loss with intact endoneurial tubes; Wallerian degeneration occurs.
Central Sensitivity Highlights
It is important to understand with central sensitization is that it occurs with all injuries. The difference between those with and without chronic pain is that the sensitivity stays turned on.
The CNS utilizes opiate components to combat nociception. There are three major endogenous opioids produced in the central nervous system to create an anti-nociceptive response:
Endorphins – produced in the periaqueductal gray matter
Enkephalins – Produced in the Nucleus raphe magnus
Dynorphins – produced in the spinal cord.
There are also exogenous opioids, which include epidurals, TENS units, and counter-irritants. However, if the endogenous piece is not present first, these opioids will not work.
Arguably the most important part of the entire course was Bob’s talk on the immune system and glia. Research is starting to show that glia runs the central nervous system. They are the gate and clean up synapses. Inflammation can activate glial activity via the vagus nerve, and when glia activates are opioid systems become much less effective. Nitric oxide is also released, which can sensitize receptive fields in the periphery.
A Side Note
One area that I struggle with in pain education is patients who either dislike pain or have huge functional changes but still have some pain. Bob suggested with these folks that this problem deals with the patient’s beliefs. The best thing to do is to talk around the beliefs or find methods to get them to detach from the pain. This could involve meditation or other similar outlets.
Great Bob Johnson Quotes
“Pain is your brain loving you too much!”
“Spreading pain is connecting the dots in the nervous system.”
“We are good at gathering data, but we are not good at determining what is relevant. Gather the data and make it tell a story.”
“Ask the patient what they think the issue is.”
“Showing the patient how they are better is a central component.”
“All we do is move people.”
“We want pain freedom, not pain control.”
“If I save a patient a day, I did something good.”
“When you treat the container, you treat the nervous system.”
“Sensitivity is plastic.”
“A 30-35 degree SLR is needed for normal gait.”
“We rarely see true nerve root compression.”
“Sliders are like grade I & II mobilizations.”
“Nerves love space, movement, and bloodflow.”
“Cardiovascular health has everything to do with nervous system health.”
“The better cardiovascular fitness, the less pain people with chronic pain have.”
“Most patients have a spinal component to a peripheral piece.”
“Beliefs are a big deal.”
“A biochemical memory is left in the tissues…An immune marker.”
“Movement is Wolff’s law for the nervous system.”
“The pattern of central sensitivity is no pattern.”