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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Explain Pain Section 3: The Damaged and Deconditioned Body

This is a summary of section 2 of “Explain Pain” by David Butler and Lorimer Moseley. Tissue Injury 101 When a body is damaged, pain is often the best guide to promote optimal healing. Sometimes it is good for us to rest, other times it is better to move. A similar healing process occurs for all tissue injuries. First, inflammation floods the injured area with immune and rebuilding cells. This reason is why inflammation is a good thing in early injury stages. A scar forms once the inflammatory process is over. The tissue then remodels to attempt to become as good as the original. Blood supply and tissue requirements determine how fast the healing process occurs. For example, ligaments heal much slower than skin because the former has a lower blood supply than the latter. This may also be a reason why aerobic exercise may speed up the healing process. If present, pain usually diminishes as the tissues heal. However, pain may persist if the nervous system still feels under threat. Acid and Inflammation The alarm sensors described here constantly work and often get us to move. Movement keeps our system flushed. When we don’t move or a physical obstruction is present (e.g. sitting), acid and by-products build up in the body tissues. Oftentimes we will start to feel aches and pains when we stay in a prolonged position, which is our body’s way of saying “get up and move.” Much like the alarm system, inflammation is a primitive way for our

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Course Notes: Graded Motor Imagery

I recently attended another great course through the NOI Group called “Graded Motor Imagery” (GMI) taught by Bob Johnson. These guys are the industry leaders in all things pain so please check them out. It was great connecting with Bob and learning what I think will be an excellent adjunct to what I am currently doing. So here is the run down on GMI. Overview GMI is a three-pronged sequential process of establishing early, nonpainful motor programming. Johnson calls this synaptic exercise to limit negative peripheral pain expression. GMI is a 3 step process: 1)      Laterality reconstruction (Implicit Motor Imagery). 2)      Motor imagery (Explicit Motor Imagery). 3)      Mirror Therapy. The Neuromatrix Paradigm & Pain States Before delving into the neuromatrix, we first must define pain. Pain is a multiple system output or expression by an individual-specific pain neuromatrix that activates when the brain concludes that body tissues are in danger and action is required. The neuromatrix, like I talk about in this post here, is the nervous system’s coding space and network. It is first and foremost affected by genetics, sculpted by experience, and constantly evolving. It is the entity that makes us who we are—the self. The neurosignature, or neurotag, is an output’s representation in the brain. For example, regions in the brain will activate in response to produce the pain output. This sequence is the neurosignature. Some common activated areas when pain is expressed include both primary and secondary somatosensory cortices, insula cortex, anterior cingulgate cortex, thalamus, basal

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The Sensitive Nervous System Chapter XI: Neurodynamic Testing for the Spine and Lower Limb

This is a summary of Chapter XI of “The Sensitive Nervous System” by David Butler. Intro For today’s chapter, I have decided that the best way to learn these tests is to show you. I will write in any pertinent details you need for a good test performance. The Straight Leg Raise (SLR) SLR hacks. Add sensitizers (dorsiflexion, plantarflexion, etc) to determine nervous system involvement. Add cervical flexion or visual input to enhance responses. Be mindful of symptoms before and after pain responses. If this test is positive post-operation, it will likely be inflammatory in nature. You can preload the system further with cervical flexion or sidebending the trunk away from the test side. Here are some other ways to perform the SLR with sensitizers first. (I apologize for the way the camera shot in advance). For tibial nerve-bias. For fibular nerve bias. For sural nerve bias. Passive Neck Flexion (PNF) Here is how to perform the test. PNF Hacks. Add SLR to further bias the test. Be mindful of Lhermitte’s sign, which is an electric shock down the arms or spine. This is a must-refer sign as there is potential spinal cord damage. Slump Test Here is how to perform the slump. Slump Knee Bend In the book itself, Butler uses the prone knee bend as his base test. However, NOI does not teach this motion as much and now favors the slump knee bend. This movement allows for much more differentiation to be had. And the saphenous nerve

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The Sensitive Nervous System Chapter VIII: Palpation and Orientation of Peripheral Nervous System

This is a summary of Chapter VIII of  “The Sensitive Nervous System” by David Butler. Intro Palpation is a major component to therapeutic touch, and gives us a way to build rapport and interact with our patients. When palpating the nervous system, it is important to palpate in sensitive positions so the nervous system is placed on load. Here are some general nerve anatomical rules. Where a nerve has fewer fascicles and less connective tissue, palpation will be more sensitive (ulnar nerve). Where there is a lot of connective tissue, there will be a more localized and less “nervy” response. Where there is increased sensitivity does not mean there is damage locally. Damage could have occurred more proximally (that whole nerves fire in both directions thing). You must also be mindful that anatomical variations are common, especially if symptoms seem anatomically weird. Here are some of the more common ones: Martin-Gruber anastomosis: Median and ulnar communicate distally. Rieche-Cannieu anastomosis: Deep branch of ulnar and recurrent branch of median nerve. Absent musculocutaneous nerve. Palpation 101 Here are some basic nervous system palpation guidelines. Nerves feel hard and slippery. Palpate with your finger tip or thumb, and follow it proximally or distally. Use sustained pressure up to 30 seconds. Twang if easily accessible. If using a Tinel’s, tap the nerve 4-6 times. Spinal Nerve Palpation Here are the craniocervical nerves. The Trunk Upper Extremity Nerve Palpation Brachial plexus The median nerve The Ulnar nerve The Radial Nerve The Musculocutaneous Nerve Lower Extremity

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The Sensitive Nervous System Chapter VII: Assessment with a Place for the Nervous System

This is a summary of Chapter VII of “The Sensitive Nervous System” by David Butler. Education When it comes to patient education, there are four things that every patient wants to know: 1)      What is wrong with me? 2)      How long will it take to get better? 3)      What can I do for it? 4)      What can you (the clinician) do for it? When we do educate, we must not forget that pain is a biopsychosocial phenomenon and multifactorial. The onion skin model below provides a good relationship analogy for this. The first goal addressed in education is making the patient understand pain.  Patients must realize that pain is the defender, not the offender. It is our body’s way to perceive a threat. Therefore, we must quell this fear before focusing on function. Here are some suggested ways to describe pain in non-threatening ways. Back trouble. Neck discomfort. Twinges. Feelings. When obtaining pain information from our patients, this is something that we do not have to measure. Instead, it is important to look at variables associated with pain, namely. 1)      Geography & nature, aggravating/relieving factors, links. 2)      Mechanism of injury. 3)      Explore how patient’s classify their symptoms (e.g. my joints are worn out), and ask why they think the symptoms still persist. 4)      Consequences of the pain. 5)      Coping types. 6)      How the patient relates to pain (do they get angry or play the blame game). When determining treatment course, instead of focusing on the structure at fault, look at

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The Sensitive Nervous System Chapter VI: Clinicians and Their Decisions

This is a summary of Chapter VI of “The Sensitive Nervous System” by David Butler. Intro All approaches (Maitland, Mckenzie, Mulligan) have myths. The common bond between them all is pain. Today we will look at building a clinical framework with pain as the cornerstone. Evidence-Based Medicine (EBM) EBM is defined as a conscientious, explicit, and judicious use of current best evidence in making patient care decisions. This concept is not merely reading researches articles, but it combines scientific evidence and clinical expertise. You have to know when to apply what. For manual therapists everywhere, this creates issues and unease. 1)      Decision making moves toward an external body. 2)      Evidence suggests manual therapy improvements are more psychosocial than physical. 3)      A disconnect between researcher and clinician. The researcher thinks: “What does this work contribute to the literature?” The clinician thinks: “What does this work do for my patient?” The movement towards outcome-based therapy per EBM is also problematic for several reasons. 1)      Clinicians begin to think statistical analysis becomes greater than any other form of knowledge rather than complimentary. 2)      Research doesn’t take into account the inherent uncertainty and subjectivity in a clinical encounter. 3)      Good evidence can lead to bad practice if applied in uncaring and unappealing environments. 4)      Outcomes may be coming out too quickly, leading to research development stopping in certain areas. Butler’s thoughts are summed up very nicely when he states it would be a sad day if meta-analyses have the final say instead of exposing

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The Sensitive Nervous System Chapter V: Neurodynamics

This is a summary of Chapter V of “The Sensitive Nervous System” by David Butler. Intro Neurodynamics is the study and relationship of nervous system mechanics and physiology. The testing protocols for neurodynamics assess the nervous system’s ability to lengthen, glide, and change amongst interfacing structures. When discussing neurodynamics, it is important to think of the nervous system as a continuum. Mechanical, electrical, and chemical changes in one part of the nervous system affect other related parts. Gross Movements and Dynamics When having a nervous system, the following qualities, movements, and buffering capabilities are necessary: Slide, glide, strain. Elongate (think gymnasts) and return from elongated position. Compress (ulnar nerve during elbow flexion). Stength (kicking a field goal). Jolting (whiplash). Repetitive forces Bending Fluid/chemical selectivity. Neural Connective Tissue These include the meninges, nerve root complex, and peripheral nerve structures. Broken down as follows: Meninges Dura mater (outer, tougher) Arachnoid mater Pia mater (inner, thinner) Nerve root complex Root Sleeve Dorsal and ventral roots DRG Spinal nerve. Peripheral nerves Epineurium Perineurium Endoneurium Mesoneurium – Sheath that surrounds a nerve. Contracts like an accordion to glide along adjacent tissues. Can become fibrotic with injury. Important Attachments Meningovertebral ligaments – anchor down to spinal canal, which could become symptomatic. Rectus capitus posterior is connected to the dura mater between the occiput and atlas; helping the dura fold. Makes you wonder what you are truly doing when you release this structure. The sympathetic trunk’s proximity to the spinal column makes it susceptible to increased loads

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The Sensitive Nervous System Chapter IV: Central Sensitivity, Response, and Homeostatic Systems

This is a summary of Chapter IV of David Butler’s “The Sensitive Nervous System.” Intro Central sensitization is a phenomenon that occurs in the dorsal horn, which can be best described via 4 different states: 1)      Normal: Inputs = outputs; innocuous sensations are perceived as such. 2)      Suppressed: Inputs that would hurt do not; think an athlete who injures himself but finishes the game. 3)      Increased sensitivity: Pain system has lower activation threshold, leading to pain spreading and pain with light touch and gentle movement. This change occurs because A beta fibers begin taking over C fiber locations in the dorsal horn. 4)      Maintained afferent barrage, CNS influences, and morphological changes: Long lasting changes in the dorsal horn from a persistent driver, such as… A fiber phenotype changes. Persistent DRG discharge. Persistent inflammation. Supraspinal influences Gene transcription change in dorsal horn neurons. Inflamed dorsal horn or DRG Maladaptive beliefs, fears, and attitudes. Dorsal horn sprouting; A Beta fibers take over C fiber space. Persistent glutamate activity. Descending Control The CNS has an endogenous pain control system which activates during injury threat, noxious cutaneous input, or expectations and learning. Such an example of this is when you go to a healthcare practitioner’s office and no longer hurt. Another example of when this system is activated is during aggressive manual therapy. Think about how good your body may feel after sustained pressure or even a needle to a trigger point. Central Sensitization Patterns Areas/descriptors Symptoms not in neat anatomical/dermatomal boundaries. Original pain

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The Sensitive Nervous System Chapter III: Pain Mechanisms and Peripheral Sensitivity

This is a summary of Chapter III of “The Sensitive Nervous System” by David Butler. Intro When we discuss peripheral issues, we are not only talking about the pathoanatomical source, but pathobiological processes dominating the clinical picture. There are several instances in which the pathoanatomical model falls short: Phantom limb pain. Why pain persists post-healing. Why similar injuries heal faster in certain people. Why 10-14% of the world’s population have an ongoing pain state. Tissues do get injured, but we must not forget the nervous system’s intricate link to injury. When tissues are hurt, they repair but are unlikely to ever be the same again. To protect against further threat, the CNS has the ability to increase nerve sensitivity. This change happens only if the person decides consciously or subconsciously that there is a need for it, and does not occur in everyone. There are two ways in which this sensitivity develops; Primary sensitivity: Increased sensitivity to input at the injury site. Secondary sensitivity: Increased sensitivity to uninjured tissues around the injury. All pain is neurogenic, operates in a continuum, and has many components. Nociception (NOC) NOC is tissue pain that occurs at a neuron’s end that is excited by mechanical, thermal, or chemical stimuli. It does not always match up with tissue health status. A normal nerve ending has a very high firing threshold, and nearly 1/3 will never fire. These are called silent nociceptors. Looking at a chemical process such as inflammation shows us how these nerves fire. 

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The Sensitive Nervous System Chapter II: A Bird’s Eye View of the Nervous System

This is Chapter II summary of “The Sensitive Nervous System.” Intro Here we develop a framework for understanding the nervous system with pain as the centerpiece. The nervous system is very much misunderstood as an input/output system: Myth: Input/output system. Reality: The nervous system is an active activity constructor. It evolves and learns rather than computes. It is    also widely distributed without a master neuron pool for a particular sensation. The nervous system is made up of two components, hardware and wetware. The Hardware Neurons make up the hardware. These components respond and keep a chemical history of many different inputs and outputs. This is true for each individual neuron, which allows each one to be ready to go when called upon. This hardware is one time when the part actual does equal the whole, as one neuron’s activity resembles the entire Central Nervous System’s (CNS) behavior. The nervous system’s size is near-astronomical. There are approximately 100 billion neurons with 1014 synapses. This figure only factors in the functionally known nervous system components. If we throw in 103 nodes/centers (connected by 105 pathways) and the 10:1 glial cell:neuron ratio, and we have an incredibly dense system in place. A pinhead speck of brain tissue has 350 million connections. This hardware is also very redundant, as very few neurons go straight from sensory organ to cortex.  There are several feedback loops in place which allows for constant checking and rechecking. The Wetware Wetware includes the different neurotransmitters and neuromodulators. Examples

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The Sensitive Nervous System Chapter I: Painting a Bigger Canvas

This is a summary of Chapter I of The Sensitive Nervous System. This book is an all-encompassing manual regarding neurodynamics. This concept is defined as the physical and related physiological abilities of the nervous system. Before delving into neurodynamic nitty-gritty, a brief history of physical therapy is laid out via a very cool brachial plexus design (you have to get the book to see it). There are three different progressions in physical therapy history: manual therapy, exercise, and neurological manual therapy. The first time PTs learned manipulation was in 1916 at St. Thomas Hospital in London. The thought process of the time, as well as most early manual therapy, was predominantly biomechanically joint-centric. Eventually, muscle and other tissues were targeted. These approaches were championed by Geoffrey Maitland’s signs and symptoms approach and Graves’ pathological model. Concomitant with manual therapy has been exercise, which had moved from nonspecific (aerobics, tai chi) to specific movements a la Vladimir Janda and Shirley Sahrmann. On the other side of orthopedic manual therapy were manual techniques from the likes of Bobath’s NDT and PNF. What is sad about these techniques is that they have not interacted much during manual therapy’s development. Butler makes arguably one of the most important statements in the book by saying our patients are ultimately all neurological. We will all meet at the brain. Aside from various manual approaches, recent techniques have been developed including psychology, counseling, exercise physiology, and acupuncture. Butler feels these are nice adjuncts to the plan of

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