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 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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Explain Pain Section 2: The Alarm System

This is a summary of section 2 of “Explain Pain” by David Butler and Lorimer Moseley. Alarm Signals Our body’s alarm system alerts us to danger or potential danger. This alarm system is composed of sensors throughout the body, the eyes, nose, and ears. It is these sensors that are our first line of defense against harm. If one sensor fails the others take over. Most of these sensors are located in the brain and respond to various stimuli. Some to mechanical movement, some to temperature change; the sensors in the brain particularly respond to chemical activity. What is important to know with sensors is that they have a very short life expectancy of a few days. This cycling means our body’s sensitivity is constantly changing. It is with these life cycles that there is hope for those with chronic pain. Moreover, the rate at which sensors are made is normally stable but can change very quickly in regards to a particular stimulus. So if we take for example one with persistent pain, the rate at which pain sensitivity occurs can be changed. Nociception We lack pain receptors in our bodies. Instead, the various tissues have special neurons that respond to different stimuli. These receptors are called nociceptors, which translates into “danger receptors.” Nociception is occurring all the time, but only sometimes will it end in pain. Nociception is neither necessary nor sufficient for pain. The sensors correspond to particular neurons. In order for these neurons to become excited and

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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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