OMM: Neurologic Model of Osteopathic Treatment

by Sheldon C. Yao, DO

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    00:00 Neurologic Model of Osteopathic Treatment. So with osteopathic medicine, we have 5 models of treatment. These approaches include the psychobehavioral model, the bioenergetic model, the biomechanical model, the neurologic model and the respiratory/circulatory model. So we're going to take a closer look at the neurologic model in today’s lecture. So, if we look at the nervous system it could be broken down to the nervous system innervating somatic muscle and the autonomic innervations to all the tissue. The autonomic innervation could be divided to the sympathetic system and the parasympathetic system. These all combine to help regulate and balance homeostasis in the body. So taking a historical perspective, A.T. Still in the late 1800s recognized that functioning of the entire body including the nervous system was paramount to health and healing. He felt that osteopathic lesions arise from visceral disturbances and also vice versa. This was further studied by Louisa Burns, DO in the 1900s. She was able to show that strains in the spinal cord actually affected visceral function and then Denslow & Korr further performed further studies looking at EMG studies and documented facilitation in the muscles from organ stimulation. So taking a look at the nervous system, our nervous system consists of a system where afferent input goes into the spinal cord causing an output action in the muscle or organ. So we have spinal reflexes in place for survival and preservation. These spinal reflexes are automatic. It does not need any intervention from conscious thought to take effect. So let's take for instance when your hand touches a really hot pot. If the signal from your hand that you're touching a hot pot had to go to the spinal cord, go up to the brain for you to interpret that if you don't move your hand you're going to burn your hand and then send a signal back down to your muscles to withdraw that would take too much time and your hand would really scalding it hurt. So, the spinal reflexes here are automatic. As soon as you touch that hot pot, the signal goes to the spinal cord and automatically your muscles are triggered to withdraw from pain. So, we have a lot of different spinal reflexes in place to try to preserve and prevent us from injury. So viscero-somatic reflexes are an example of a spinal reflex. It's not something that we could control. So, inflammation is a very powerful stimulator of nociceptors and so we have nociceptors in our organs that detect inflammation and pain. This signal converges onto the spinal cord and because of the strength of the signal sometimes it will interact with other interneurons which then trigger a signal causing referred pain and sometimes it will cause segmental facilitation at the spinal cord level. So, here is a diagram where you could see how everything converges on to the spinal cord so you could receive visceral signals, signals from the skin, signals from your musculoskeletal system and when that converges on to the spinal cord that could send signals away again back to the viscera and back to our tissue and muscles and so you could see how there could be different types of reflexes that occur that if I have a reflex occurring from muscle, from my fascia going to the spinal cord and then going back out to a different region of my musculoskeletal system then that is a somato-somato reflex. If I have something going from my muscle to the spinal cord and then reflexing and causing a change to the viscera then that's a somato-visceral reflex. If I have an input from the viscera going to the spinal cord causing a somatic change to the muscles, then that's viscerosomatic and then you could also have a signal from the viscera stimulating additional visceral changes and that will be a viscero-visceral reflex. So this diagram demonstrates how we could have input into the spinal cord and then a resultant change outside of the spinal cord and these are all neurologic reflexes that could occur. So these reflexes are usually stimulated by PANS or primary afferent nociceptors. These nociceptors could be activated by stretch or chemicals in the surrounding area. There are different factors that potentially could activate these nociceptors including bradykinins, histamines, prostaglandins, serotonins, protons, cytokines, ATP and neuropeptides.

    04:45 So all these different substances could stimulate those nociceptors triggering a spinal response.

    04:52 So these PANS will then release dilatory peptides such as substance P, calcitonin gene-related polypeptide and somatostatin. Normally when you release these peptides, they target the resistance arterial. So they act a counterbalance sympathetic nervous system. The release of these peptides could cause a neurogenic inflammatory response especially if they release that very high level.

    05:18 So the results of PAN activation lead to lowering thresholds and clinically increase sensitivity to light touch as pain. So, TART findings will occur. TART stands for tenderness, asymmetry, restriction of motion, tissue texture changes. These are somatic changes that help define somatic dysfunction. So you may find muscle spasms and sensitivity to touch and then the result of PAN activation to the spinal cord leads to increase afferent drive. This is due to the sensitization of the primary afferent fibers. So taking a look at the spinal cord, we have somatosensory afferents to the spinal cord. These include proprioception, touch and pressure, nociception and temperature.

    06:08 All the somatosensory afferents enter the spinal cord along the dorsolateral fasciculus. So when we look at the spinal cord and facilitation, there is reduced threshold for firing of the interneurons receiving that nociceptive input. So there are interneurons which are neurons between a primary sensory neuron and a final motor neuron or any neuron whose processes are entirely confined within a specific area. There are also internuncial neurons. These help transmit impulses between 2 different parts. The change for spinal facilitation occurs at the level of the genes along those interneurons and internuncial neurons. So with spinal cord facilitation, we have exaggerated segmental autonomic and alpha motor response. These produces boggy spasm, increased temperature and increased sweat. These are all the changes that we find with acute changes and acute input.

    07:10 The input of the exaggerated ascending tract then goes to the higher centers which produce hyperesthesia and referred pain. There is also altered autonomic outflow to the viscera itself.

    07:22 So there has been research done further investigating the concept of spinal facilitation. So what they did here in animal models, they performed a cut after the dorsal root ganglion and what they found was even though they cut the sensory input, 85% of facilitation still remained. So the muscle spindle alone did not have to sustain somatic dysfunction. So, there's a small caliper system necessary to initiate spinal facilitation but once initiated you no longer need that afferent drive, you don't need that input from outside to sustain the spinal facilitation. So this is a slide demonstrating the level of visceral sympathetics. We utilize this chart to get a sense of possible facilitation where viscerosomatic reflexes may occur in the soma and so we need to really memorize these different levels and what correlates with each organ. One of the ways to help remember the general region is that you could break this into 3 general areas; above the diaphragm, below the diaphragm in the abdomen but above the pelvis region and then in the pelvic region. So, most structures like the esophagus, heart, lungs, the thyroid that is above the diaphragm, the head and neck will be innervated by sympathetic nerve roots from T1 to T6, below the diaphragm; the stomach, the liver, gallbladder, spleen, your intestines, your colon, you are looking at innervation from the sympathetic nerve roots usually generally from T6 down to T12 and then in the pelvis most of the structures in the pelvis including the distal GI tract, the bladder, the distal uterus that will be from T12 to L2. The main exception here is that your ovary and testis which are in the pelvis actually originate in the abdomen in development and descend down into the pelvis.

    09:28 So the ovary and testis are innervated by the levels of T10 to T11. So, again this is an important chart to commit to memory to really memorize the different possible sympathetic reflexes that could occur when an organ is inflamed. So, there are other spinal reflexes that we should be aware of. There are somato-somatic reflexes. So, the knee jerk reflex is a somato-somatic reflex. So what we're doing is we're putting an input on the soma, which is the patellar tendon with a quick impact and because of that quick impact you get a muscle contraction. So that's a somato-somatic reflex. A somato-visceral reflex would be an example of if I had a change to my musculoskeletal system and it affected the viscera. So an example of this would be if I stimulated muscles in the neck it could affect my heart rate. And a viscero-visceral reflex, an example is when you change and have an input from the viscera and it causes another visceral change. So distention of the intestines will result in contraction of the intestinal muscle. So that's an example of a viscero-visceral reflex.

    About the Lecture

    The lecture OMM: Neurologic Model of Osteopathic Treatment by Sheldon C. Yao, DO is from the course Osteopathic Treatment and Clinical Application by System.

    Author of lecture OMM: Neurologic Model of Osteopathic Treatment

     Sheldon C. Yao, DO

    Sheldon C. Yao, DO

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