Hi, this is James Fricton again. Thank you for continuing with this course. This next module is about the body which is the risk and protective factors in the musculoskeletal system and I'm coming from the University of Minnesota again and this module will have six parts. First we'll talk about some of the mechanisms associated with musculoskeletal pain. Then we'll talk about both repetitive strain, as well as postural strain and how that contributes to muscle pain and joint pain. Then we'll go through some of the protective factors including exercise for range of motion, strength and conditioning, and then talk about preventing injuries, particularly sports injuries. And then, finally, we'll follow up with some experiential learning. Like you to do some of the exercises that will help and reduce jaw pain, neck pain, back pain. So, by the end of this module, you'll be able to articulate some of the mechanisms of musculoskeletal pain. Explain how posture and repetitive strain can play a role in developing chronic pain. Review how the exercises can build strength, conditioning, and range of motion to help prevent musculoskeletal pain. We'll review how injuries play a role in chronic pain and how do you know the distinction between an injury and strain and muscle building. And then, last, we'll perform five different exercises to protect you from chronic pain. So/ the first module, segment of this module is called musculoskeletal pain mechanisms. So/ the big question is really, not necessarily even whats causing the pain, but where is the pain coming from? That's the question that most people want to know at first. But it's not so simple. There are many mechanisms that underline whether you have chronic pain or not. Concepts such as hyperalgesia, sensitization, and expanding repti, receptor fields are all very important. Let's discuss a few of those. So, with regard to the nerves that come from the musculoskeletal system, there's several different types, particularly focused on muscle. Sensory nerves, there's a Type 1 muscle spindle which is involved in really bringing sensation of movement. It responds when muscle length or velocity changes when the muscle is contracted. a, if a muscle, and b, if a tendon. And then there are these stretch receptors, which really focus on postural input to the central nervous system. This responds to position sense when muscles or joints are at rest. And then the third type is a nociceptor. Now these are pain receptors. Nerve endings that signal pain. And this, of course, responds to strain or injury with a continuous pain, and you have a sensation of a dull, achy feeling when you have. And the last type is a type four nocicepter, and these are also pain receptors, but instead of a sensation of a dull ache or a pain in the area, it's more of a tenderness within the muscle. So, when you press on the muscle and joints, it responds to strain and injury. It is tender. So, with regard to these peripheral nerve endings, there's a number of mechanisms of musculoskeletal pain that is important to know about. One of the concepts is sensitization. Now, this is an increase in synaptic efficiency due to repeated firing of a synapse that occurs at the peripheral level but also at the central nervous system level. So, it's a way to ramp up the pain if there is repeated injury. Now, there's a concept of allodynia, which is this is an enhanced pain report from just simple normal stimuli like touch for instance. And then there's two types of hyperalgesia. One is primary hyperalgesia where you have a decreased threshold for pain in an injured tissue. So, the same stimulus causes more pain. And then there's a secondary hyperalgesia which is a decreased threshold for pain in the surrounding tissues. Not only is their pain locally in that area of, of injury, but it spreads out so that it tells you even more that there is an injury that is sustained over time. Now, let's go through each of these concepts in a little more detail. Now here's a graph that shows sensitization. Now, as the stimulus intensity increases, you would expect the pain intensity to increase. And here is a normal pain response right here. Now, when you have hyperalgesia and if the injury occurs here, that over time what you have is a heightened sense of pain to the same noxious stimuli. So, as the stimulus intensive goes up not only do you get this pain, but you have an increase of pain in this area. Now, if that stimulus intensity continues, the sensitization continues. Even normal stimuli, such as a light touch or a gentle pressure in the area, now will also cause pain. And that's called allodynia. So, both hyperalgesia and allodynia are characteristics of this sensitization that occurs. It's like the princess and the pea. The king wanted to make sure his prince married a woman that was a princess, and so he put a pea under the bed, and that little bit of sensitivity caused her inability to sleep. Thus he knew, knew that she was a princess. Well, hyperalgesia is this hypersensitivity to pain that occurs directly as a result of sensitization due to damaged peripheral tissues or dysregulation of the central nervous system. So again, this graph illustrates this. This is a normal pain graph. As the stimulus intensity goes up, the pain goes up. But with hyperalgesia, you have an amplified pain response to the same stimulus. So, as the stimulus goes up, you have an increase in pain response. This is a protective mechanism. Designed to help alert us to any repeated stimuli that causes injury, or potentially causes injury. So, let's go through a number of two aspects of sensitization, first one is peripheral sensitization, and the next one will be central sensitization. Now peripheral sensitization is what happens at the periphery of the nervous system, where the nerves are, where the nociceptors are. In peripheral sensitization you have a hypersensitivity of the nociceptive primary afferent neurons, or the pain nerves, in the tissues. Now, there are mediators to this peripheral sensitization, including bradykinin, prostaglandins, neuropeptides, and cytokines. It is also upregulated during any type of injury, like a burn to the finger, as an example in this picture. Or inflammation, or injury, or repetitive strain. So, the same degree of stimulus over a period of time will increase and ramp up that pain sensations that you experience, so that it begins to tell you more and more that the pain that you need to change something to avoid the injury. Now let's shift to central sensitization. So, the sensitization can occur both peripherally, but when it becomes even more amplified or more insult to the body, what you have is development of hypersensitivity of the nociceptive neurons in the central nervous system. This includes both the spinal cord and the brain. And the mediator for this sensitization is, includes glutamate through NMDA receptors and biochemical substance P or calcitonin gene-related peptide or CGRP. There are many other mediators too, but this is to simplify it as an example. Now, these are upregulated also during sustained pain or injury or any type of threat to the body. So, you have this mechanism, both peripheral and central sensitization, that ramps up your reaction to any type of repeated insult to the situation, sit, to, to yourself, and particularly to the muscles and joints. Now let me go through another concept called wind up. Now, wind up is interesting, it's just like a pitcher throwing a ball. They have to really get ready to go and as they start to, to wind up and throw the ball, all those movements cause a highly accelerated baseball to be thrown. The same thing occurs with wind-up in the central and peripheral nervous system. So, an increase in pain over time occurs when a stimulus is delivered repeatedly, so repeatedly is the key, above a critical rate. So this diagram illustrates that. So, again, here's the stimulus intensity. Here's the pain sensitivity. And here's a stimulus that comes up, right here. So then it starts, the stimulus stops, and it starts getting better. But then, if you have another stimulus that occurs. It ramps up, and this time the reaction, the pain is even higher. And then, as that tapers off, if you have another stimulus, it will again even go higher. So this wind up, it keeps going higher and higher and higher as the insults repeat over time. And again, this is a protective mechanism to minimize insult. And to make sure a person knows that there's a threat. Now, another mechanism that occurs with increasing insult to the central and peripheral nervous system is what's called an expanding pain pattern or a pain receptor field. So in this case, stimulation of the pain receptors occur from when the strain occurs and continues. The tissues let you know it by expanding the pain pat, pattern through convergence facilitation. So, it's like a rock hitting you over the head. Now, a perfect example of this is with myofacial pain. You have a trigger point in the temporalis muscle right here, and initially, the pain is right around here. Well, first of all, there's tenderness. And then, after tenderness, a certain period of time continues if the strain that continues, say, from clenching the teeth as an example, and the pain then will become localized and you get a temple headache. But if that pain continues and the clenching continues, the repetitive strain on that muscle continues. Then it spreads to other areas. It might got to the forehead, behind the eye, or even down to the teeth, so you first have tenderness in the X, then you have localized pain, and then you finally have referred pain or a broader pain pattern. So, the next segments that we're going to talk about are the risk factors and protective factors in the physical or the body realm. Protective factors, as I mentioned, balanced posture and exercises and even some genetics factors that predispose you. And then there's risk factors, such as posture, repetitive strain, loss of flexibility, weakness or poor conditioning. Injuries and co-morbid conditions are important also. Thank you. [NOISE] [BLANK_AUDIO]
