Course Notes: PRI Myokinematic Restoration

What a Class Wow. That’s all that really needs to be said.  I have had a great deal of exposure to PRI in the past, but I have only had one formal class under my belt. Needless to say, I was looking forward to learning more. James Anderson and the PRI folks did not disappoint. Myokinematic Restoration was easily the best class I have taken all year. It also helped having another like-minded group attending. You learn so much more when you are surrounded by friends. Here is the course low-down. Disclaimer for the Uninitiated I know there are a lot of misconceptions about PRI on the interwebz. Even though posture is in the name, PRI has little to do with posture in the traditional sense. We know posture does not cause pain, and PRI agrees with this notion. But it’s not like they can change the name of the organization now. What? Do you think Ron Hruska is Diddy or something? After discussions with James and his mentioning this aloud in class, the target of PRI is the autonomic nervous system. Not posture, not pain, not pathoanatomy, but the brain. Essentially, they have figured out a window into the autonomic nervous system via peripheral assessment. Moreover, PRI is not in the pain business, though many think this is the case. Hell, even in the home studies they mention pain quite a bit. But realize those were done in 2005. Would you like me to hold you to things you have

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Chapter 10: Upper Limb

This is a Chapter 10 summary of “Clinical Neurodynamics” by Michael Shacklock. Thoracic Outlet Syndrome (TOS) 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 –

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Chapter 9: Cervical Spine

This is a Chapter 9 summary of “Clinical Neurodynamics” by Michael Shacklock. Physical Exam The key tests you will want to perform include: Slump test. MNT 1. 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. Neural Dysfunction 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:

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Chapter 8: Method of Treatment: Systematic Progression

This is a Chapter 8 summary of “Clinical Neurodynamics” by Michael Shacklock. Let’s Treat the Interfaces 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

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Chapter 7: Standard Neurodynamic Testing

This is a Chapter 7 summary of “Clinical Neurodynamics” by Michael Shacklock. Passive Neck Flexion 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

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Chapter 6: Planning the Physical Examination

This is a Chapter 6 summary of “Clinical Neurodynamics” by Michael Shacklock. Observe When assessing the patient, you must look at the following information: Symptom location, extent, quality, and behavior. Movement resistance. Range of motion. Compensatory patterns. Breathing quality. Tone of voice. Facial expression Protective muscle tone. Avoidance. 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. Potential pathology. Neurological deficit. 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

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Chapter 5: Diagnosis with Neurodynamic Tests

This is a Chapter 5 summary of “Clinical Neurodynamics” by Michael Shacklock. Neurodynamic Tests 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. Scapular depression Humeroglenoid (HG) horizontal extension HG external rotation Hip internal rotation Hip adduction Interpreting 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: Negative structural differentiation: Implicates musculoskeletal response. Positive structural differentiation: Implicates neurodynamic response. 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.

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Course Notes: Mobilisation of the Nervous System

I Have an Addiction 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

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Chapter 1: General Neurodynamics

This is a Chapter 1 summary of “Clinical Neurodynamics” by Michael Shacklock.  Concepts When we first started working with the nervous system, oftentimes we called pathological processes adverse neural tension. The problem with this name was that it left out nervous system physiology; it was mere mechanical concepts. Hence, we call the movement and physiology of the nervous system neurodynamics. General neurodynamics account for whole body fundamental mechanisms, regardless of region. Specific neurodynamics, on the other hand, applies to particular body regions to account for local anatomical and biomechanical idiosyncrasies. The System There are three parts to the neurodynamic structure: 1)      The mechanical interface 2)      The neural structures 3)      The innervated tissues The mechanical interface is that which is near the nervous system. It consists of materials such as tendon, muscle, bone, intervertebral discs, ligaments, fascia, and blood vessels. The neural structures are those which make up the nervous system. These structures include the connective tissues that forms the meninges (pia, arachnoid, and dura mater) and peripheral nervous system (mesoneurium, epineurium, epineurium, and endoneurium). The nervous system has mechanical functions of tension, movement, and compression. It also has physiological functions to include intraneural blood flow, impulse conduction, axonal transport, inflammation, and mechanosensitivity. The innervated tissues are simply any tissues that are innervated by the nervous system. They provide causal mechanisms for patient complaints, and are able to create nerve motion. When we have neural problems, sometimes the best treatment is to these structures. You must treat everything affected. Mechanical Functions

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Explain Pain Section 4: Altered Central Nervous System Alarms

This is a summary of section 4 of “Explain Pain” by David Butler and Lorimer Moseley. CNS Alarms While much of talk in rehab deals with tissue injury and tissue pain, realize that the brain always makes the final decision as to whether or not you should feel pain. No brain, no pain. This sentiment does not mean that pain is not real. All pain is real. However, pain is a construct that the brain creates in order to ensure your survival. Spinal Cord Alarms When an injury occurs and the DRG receives impulses from peripheral structures or the brain, the spinal cord neurons must adapt to better uptake all these signals. In essence, the DRG becomes better at sending danger messages up to the brain. This change leads to short term increases in sensitivity to excitatory chemicals. Those stimuli that didn’t hurt before now do (allodynia) and those that used to hurt now hurt more (hyperalgesia). In persistent pain, this change continues occurring to the point where neurons that do not carry danger messages start growing into space where danger messages are taking place. Now innocuous stimuli such as grazing the skin begin hurting. The pain may be normal, but the underlying processes become abnormal. When these spinal cord alarm systems become unhealthy, the brain no longer receives an accurate message of what is going on. The alarms become magnified and distorted.  The brain is told there is more damage in the tissues than is actually present. What is good is

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