It's been a good while since I have published anything or written anything to my web page, but it seems to be time. I have been seeing many articles and research relating to the quadratus lumborum (QL), a muscle that has held special interest to me for some time. This article is in way of explanation and exploration.
The recent writing on the QL is mostly in relation to its involvement in low back pain. This is probably due to the QL being a core or stabilizing muscle, and working core stability is the current treatment du jour. Great! I've been hypothesizing (and endeavoring to test those hypotheses) a relationship between the QL and low back pain for years. A problem I have is that most of these newer articles refer to the QL as being “tight” or “short”. While these terms may be potentially useful in explaining to the lay public, they are woefully imprecise for the audience these articles are written: physiotherapists, medical doctors, massage therapists, chiropractors, osteopaths, etc.. A “tight” muscle is one in which the tone of the muscle - defined by resistance of the muscle to stretch - is higher than when the muscle is resting. There are a couple of ways to increase muscle tone, or “tightness” if you prefer; by 1) active contraction and by 2) increasing thixotropy. (If you disagree, or wish to read more about these concepts, see Knutson G, Owens E. Active and Passive Characteristics of Muscle Tone and their Relationship to Models of Subluxation/Joint Dysfunction. Part I. J Can Chiropr Assoc 2003;47(3):168-79, Knutson G, Owens E. Active and Passive Characteristics of Muscle Tone and their Relationship to Models of Subluxation/Joint dysfunction. Part II. J Can Chiropr Assoc 2003;47(4):269-83. While I understand that it is considered poor sport to refer to your own research, these were literature review articles. If you have a problem, you'll have to take it up with the citations noted and/or my interpretation. Finally, the article I'm writing here is about how I came to my beliefs or conclusions, and so my previous work, I think, is fair game).
Let's dispense with #2 first. Most have never heard of and have no idea of what thixotropy is. Thixotropy is a property of muscles that allows them to keep the length/tension they were during a prolonged period of time. This property is useful when a muscle has to hold a length-tension for a prolonged period of time. Thixotropy allows the muscle to do this without active contraction, which can only be held for a short period of time. Ketsup has the property of thixotropy, if left to sit, it does not want to pour, and has to be shaken to allow it to pour (anticipation). Muscle (the actin-myosin filaments) tend to reform to the length-tension of the state the muscle is in. This occurs in a resting condition, as well as during contraction. For example, you've been sitting for some time, say driving the car a long distance. When you get out you are stiff, slightly bent as if still sitting. This is your muscles adapting, via thixotropy, to the long term sitting position. You stand up, stretch, and loosen up, the active stretching breaks the passive “stuckness” (for lack of a better word), actin-myosin bonds reducing the muscle tension and allowing the muscle to move through its normal range of motion. Active thixotropy can be demonstrated by doing the following: stand in a doorway with your arms at your side. Move your arms laterally away from your torso so they contact the doorway. Push on the doorway for as long as you can, then move out of the doorway and relax your arms to drop to your side. If this is done correctly, your arms will try to rise by themselves, without you trying to lift them. This is because the muscle actin-myosin bonds have locked into the short/contracted position when you were pushing out on the doorway, and those bonds tend to stay that way (thixotropy) making your arms seem to rise up by themselves. Regardless, a muscle (the actin-myosin bonds) stuck in a short, tight condition due to thixotropic changes can be broken quite easily by stretching or actively moving the muscle. As such, hypertoncity of the QL muscle would easily be broken down via stretching or moving the spine laterally.
If the QL is “tight” by means #1, then you need to explain why the muscle is *actively* contracting. This is what most theorizing about the QL, core stability and low back pain fails to do. They start with the given that the muscle is “tight” and then outline methods to “loosen” it. Fine, but tell me why it's “tight” or, more precisely, hypertonic, in the first place. What is the cause of the “tightness”? Explaining that, to me, is what we need to know. You can stretch or do massage or trigger point therapy on a hypertonic (“tight”) QL, but unless you understand why the QL is tight, you are not treating causes, but effects. A QL problem is often diagnosed as being “short”, again a nebulous concept. Yes, a muscle can be “short”, which means, as I take it, the range of motion of that muscle is restricted. These descriptive terms are often combined as “short” and “tight”. What causes a “short” muscle? Active contraction is one method, but again, as noted above, why is the muscle actively contracted? Treat the cause not the symptom. The main cause of “shortness” and reduced range of motion, in my opinion, is adaptation to ones environment. If you sit behind a desk all day, those hamstrings rest at a shortened length. Over time, this makes it more difficult to touch your toes. Most of the day those muscles are not actively contracting, but resting comfortably in a shortened state. They may be “short” (compared to younger or more athletic people), but not “tight”. A dancers hamstrings will be much “looser” - greater range of motion – as they spend their day repetitively in full range of motion. Muscles adapt to the length at which they are most often kept. They adapt by resetting tension sensors (called golgi tendon organs) and other neuro-receptors in the muscle that govern how much stretch can be applied to the muscle before their alarm bells begin to ring. The alarm bells are discomfort and pain, which go off to signal and prevent you from stretching further and injuring the muscle. So... if you spend your day sitting at a desk, those hamstrings will be “short”, which means have a decreased range of motion (unable to touch your toes easily) before the stretch on the muscle becomes uncomfortable. If you get out on a basketball court and make a heroic leap to snatch a rebound, you might over stretch those “short” hamstrings and strain (tear) the muscle. That injury does not mean your hamstring muscles are either “tight” or “short” as a pathology, it just means they've adapted to your long term desk sitting. If you begin to exercise and stretch those hamstrings (like the dancer), in time they will adapt to their new length/functional requirements, and you'll be able to touch your toes and jump without straining and tearing the muscle.
So, we have disposed with the concepts of “tight” and “short” as being simplified and not particularly helpful from a physiologic (how things work) standpoint. What could cause the QL to be tight, to be actively contracted? This is where my presentation gets interesting, and complicated. Like a guy wire for a tower, the QL is a core stabilizing muscle, bracing the lumbar spine to the pelvis. There is a reflex for balancing the body that occurs when the head is moved away from vertical called the tonic neck reflex (TNR). A reflex is automatic - you don't have to think about it - like pulling your finger back from a hot stove. This reflex is there because the head weighs 10-12 pounds and is out on a relatively long lever arm (the neck). To illustrate, try inserting a broom handle into a 12 pound bowling ball. Grab the broom handle and hold the ball vertically. See how much energy it takes. Now move the ball a few degrees off vertical, note how much more muscular energy it takes to keep the ball balanced out of the neutral vertical position. Same thing happens with your body balance relative to you head. So what does the head and neck and these body balancing reflexes have to do with the lumbo-pelvic QL? If the head and neck are laterally flexed (towards the shoulder) the body is thrown out of balance to that side. Your balance centers think you are going to tip over sideways. To keep from tipping over to that side, the TNR reflex actively (among other things) contracts (tightens) the QL "guy wire" opposite the lateral flexion of the head, stiffening the spine to keep us upright. THIS is how you can get a “tight”, “short” QL.
To test this idea, I did a study which involved combining two procedures: vibration of the posterior upper cervical (UC) (neck) triangle and a QL muscle fatigue test (Biering-Sorensen test). Lengthening of muscles in the UC spine causes muscle spindles (neuromuscular receptors inside muscles) to fire, signaling body balance control center that the head is moved off vertical. Vibration also stimulates muscle spindles to fire. So, I was stimulating the UC spine via vibration with the head and neck in a neutral (vertical) position. After said stimulation, the subject immediately performed the Biering-Sorensen test. This test measures the fatigability of the QL muscle (to learn more about these two procedures, please read https://drgaryknutson.weebly.com/uploads/2/3/5/2/2352396/vib8.pdf). The energy reserves of an actively contracting muscle are partially used up. As such, that muscle will fatigue more quickly relative to the opposite side QL. What I found was this, vibration of the right UC spine resulted in quicker fatigability of the opposite (left) QL vs the right QL, and the opposite, stimulation of the left UC spine caused quicker fatigue of the right QL vs the left. This makes sense vis-a-vie the tonic neck body balance reflex which is controlled by signals from spindles in the muscles of the upper cervical spine.
What this indicates to me is that neuro-muscular dysfunction (what chiropractors call subluxation or joint dysfunction) in the UC spine initiates and perpetuates a balance control reflex that causes a hypertonic (“tight”, “short”) QL muscle in the lumbo-pelvic spine. Muscles want to contract and then relax. A muscle under tonic (prolonged) contraction soon becomes quite painful. You can demonstrate this to yourself easily: stand up with your arms at your side. Move your right arm away from your body till you are holding it up at a 90 degree angle. Hold it there. Within a minute or two the muscles holding the arm up (deltoid mainly) will begin to be painful. That is the kind, and reason for the pain associated with chronic QL hypertonicity – prolonged contraction. So, yeah, the QL is involved in some causes of back pain, but the ultimate cause of the QL “tightness” or, my preferred term, hypertonicity, is joint dysfunction in the upper cervical spine. You can stretch, poke, shake and bake the QL to reduce its hypertonicity, but until you address the cause of the QL “tightness”, the “tight” QL and the back pain will recur. I have seen many cases of patients with chronic back pain being blamed for their problem because they were not regularly doing all the stretches and exercises assigned by their physiotherapist. It's not the patients fault, the cause of the problem is not being addressed, so the problem comes back. I don't believe the UC spine is the only cause for QL hypertonicity (see Knutson G. The Sacroiliac Sprain; Neuromuscular Reactions, Diagnosis and Treatment with Pelvic Blocking. JACA 2004;41(8):32-39), but I do think it is a major, and most overlooked, cause.
Interestingly, one of the signs that many in the arena of manual therapies look for as an indication of a problem is a functional “short leg”. I use quotation marks around “short leg” because the leg is not anatomically short, but there is a problem that, when the subject is in an unloaded position (prone (on the belly) or supine (on the back)) one leg *appears* to be shorter than the other. The muscle associated with the appearance of the unloaded leg length inequality (LLI) is our friend, the QL. A hypertonic (“tight”) QL, because of its insertion in the crest of the pelvis, lifts/twists (torsions) the pelvis. This pelvic torsion, in an unloaded (prone/supine) position, makes the legs appear to be uneven. When an unloaded LLI is found, the QL muscle and UC joint/neuro-muscular dysfunction should be considered as the cause.
After I did the above noted study on the effects of UC vibration and the Biering-Sorensen test, it occurred to me to try using the UC vibration on patients who demonstrated an unloaded LLI. I have done this several times with interesting results. If a patient has a right functional LLI, and I know from examination that the UC dysfunction is on the left (the body balance mechanism feels like the head is falling off the the left, so increases tension on the right QL resulting in a right LLI. Vibration of the UC spine of that patient on the left side would (it seems) cause hypertonicity of, and/or reciprocal inhibition of, the right QL, balancing out the QL tension and, hypothetically, eliminating the appearance of the LLI. This is exactly what I have observed many times. (NOTE: this is not a hard and fast rule as there are many aspects of UC neuro-muscular dysfunction that need to be taken into account. For example, I have found is that this works best in patients with atlas laterality but minimal rotation (sorry to lapse into technical jargon, but those who understand UC joint dysfunction will get it)).
All this outlined above is why I believe that UC joint dysfunction is a (major) cause of QL hypertonicity and back pain. So, those of you who've been told you have a “tight” or “short” QL, get thee to a chiropractor who is knowledgeable about UC joint dysfunction. Yes, the whole hypothesis is somewhat complex, the evidence is weak and based on my own (potentially biased) studies and observations, but it is biologically plausible and there is some interesting evidenciary results. I would like to see these ideas explored more, but I am old, tired and not associated with any group that could organize such studies and get the blessing of the almighty independent review board. I do hope some investigation into this will be done in the future, which is one of the reasons why I am writing them out now.
The recent writing on the QL is mostly in relation to its involvement in low back pain. This is probably due to the QL being a core or stabilizing muscle, and working core stability is the current treatment du jour. Great! I've been hypothesizing (and endeavoring to test those hypotheses) a relationship between the QL and low back pain for years. A problem I have is that most of these newer articles refer to the QL as being “tight” or “short”. While these terms may be potentially useful in explaining to the lay public, they are woefully imprecise for the audience these articles are written: physiotherapists, medical doctors, massage therapists, chiropractors, osteopaths, etc.. A “tight” muscle is one in which the tone of the muscle - defined by resistance of the muscle to stretch - is higher than when the muscle is resting. There are a couple of ways to increase muscle tone, or “tightness” if you prefer; by 1) active contraction and by 2) increasing thixotropy. (If you disagree, or wish to read more about these concepts, see Knutson G, Owens E. Active and Passive Characteristics of Muscle Tone and their Relationship to Models of Subluxation/Joint Dysfunction. Part I. J Can Chiropr Assoc 2003;47(3):168-79, Knutson G, Owens E. Active and Passive Characteristics of Muscle Tone and their Relationship to Models of Subluxation/Joint dysfunction. Part II. J Can Chiropr Assoc 2003;47(4):269-83. While I understand that it is considered poor sport to refer to your own research, these were literature review articles. If you have a problem, you'll have to take it up with the citations noted and/or my interpretation. Finally, the article I'm writing here is about how I came to my beliefs or conclusions, and so my previous work, I think, is fair game).
Let's dispense with #2 first. Most have never heard of and have no idea of what thixotropy is. Thixotropy is a property of muscles that allows them to keep the length/tension they were during a prolonged period of time. This property is useful when a muscle has to hold a length-tension for a prolonged period of time. Thixotropy allows the muscle to do this without active contraction, which can only be held for a short period of time. Ketsup has the property of thixotropy, if left to sit, it does not want to pour, and has to be shaken to allow it to pour (anticipation). Muscle (the actin-myosin filaments) tend to reform to the length-tension of the state the muscle is in. This occurs in a resting condition, as well as during contraction. For example, you've been sitting for some time, say driving the car a long distance. When you get out you are stiff, slightly bent as if still sitting. This is your muscles adapting, via thixotropy, to the long term sitting position. You stand up, stretch, and loosen up, the active stretching breaks the passive “stuckness” (for lack of a better word), actin-myosin bonds reducing the muscle tension and allowing the muscle to move through its normal range of motion. Active thixotropy can be demonstrated by doing the following: stand in a doorway with your arms at your side. Move your arms laterally away from your torso so they contact the doorway. Push on the doorway for as long as you can, then move out of the doorway and relax your arms to drop to your side. If this is done correctly, your arms will try to rise by themselves, without you trying to lift them. This is because the muscle actin-myosin bonds have locked into the short/contracted position when you were pushing out on the doorway, and those bonds tend to stay that way (thixotropy) making your arms seem to rise up by themselves. Regardless, a muscle (the actin-myosin bonds) stuck in a short, tight condition due to thixotropic changes can be broken quite easily by stretching or actively moving the muscle. As such, hypertoncity of the QL muscle would easily be broken down via stretching or moving the spine laterally.
If the QL is “tight” by means #1, then you need to explain why the muscle is *actively* contracting. This is what most theorizing about the QL, core stability and low back pain fails to do. They start with the given that the muscle is “tight” and then outline methods to “loosen” it. Fine, but tell me why it's “tight” or, more precisely, hypertonic, in the first place. What is the cause of the “tightness”? Explaining that, to me, is what we need to know. You can stretch or do massage or trigger point therapy on a hypertonic (“tight”) QL, but unless you understand why the QL is tight, you are not treating causes, but effects. A QL problem is often diagnosed as being “short”, again a nebulous concept. Yes, a muscle can be “short”, which means, as I take it, the range of motion of that muscle is restricted. These descriptive terms are often combined as “short” and “tight”. What causes a “short” muscle? Active contraction is one method, but again, as noted above, why is the muscle actively contracted? Treat the cause not the symptom. The main cause of “shortness” and reduced range of motion, in my opinion, is adaptation to ones environment. If you sit behind a desk all day, those hamstrings rest at a shortened length. Over time, this makes it more difficult to touch your toes. Most of the day those muscles are not actively contracting, but resting comfortably in a shortened state. They may be “short” (compared to younger or more athletic people), but not “tight”. A dancers hamstrings will be much “looser” - greater range of motion – as they spend their day repetitively in full range of motion. Muscles adapt to the length at which they are most often kept. They adapt by resetting tension sensors (called golgi tendon organs) and other neuro-receptors in the muscle that govern how much stretch can be applied to the muscle before their alarm bells begin to ring. The alarm bells are discomfort and pain, which go off to signal and prevent you from stretching further and injuring the muscle. So... if you spend your day sitting at a desk, those hamstrings will be “short”, which means have a decreased range of motion (unable to touch your toes easily) before the stretch on the muscle becomes uncomfortable. If you get out on a basketball court and make a heroic leap to snatch a rebound, you might over stretch those “short” hamstrings and strain (tear) the muscle. That injury does not mean your hamstring muscles are either “tight” or “short” as a pathology, it just means they've adapted to your long term desk sitting. If you begin to exercise and stretch those hamstrings (like the dancer), in time they will adapt to their new length/functional requirements, and you'll be able to touch your toes and jump without straining and tearing the muscle.
So, we have disposed with the concepts of “tight” and “short” as being simplified and not particularly helpful from a physiologic (how things work) standpoint. What could cause the QL to be tight, to be actively contracted? This is where my presentation gets interesting, and complicated. Like a guy wire for a tower, the QL is a core stabilizing muscle, bracing the lumbar spine to the pelvis. There is a reflex for balancing the body that occurs when the head is moved away from vertical called the tonic neck reflex (TNR). A reflex is automatic - you don't have to think about it - like pulling your finger back from a hot stove. This reflex is there because the head weighs 10-12 pounds and is out on a relatively long lever arm (the neck). To illustrate, try inserting a broom handle into a 12 pound bowling ball. Grab the broom handle and hold the ball vertically. See how much energy it takes. Now move the ball a few degrees off vertical, note how much more muscular energy it takes to keep the ball balanced out of the neutral vertical position. Same thing happens with your body balance relative to you head. So what does the head and neck and these body balancing reflexes have to do with the lumbo-pelvic QL? If the head and neck are laterally flexed (towards the shoulder) the body is thrown out of balance to that side. Your balance centers think you are going to tip over sideways. To keep from tipping over to that side, the TNR reflex actively (among other things) contracts (tightens) the QL "guy wire" opposite the lateral flexion of the head, stiffening the spine to keep us upright. THIS is how you can get a “tight”, “short” QL.
To test this idea, I did a study which involved combining two procedures: vibration of the posterior upper cervical (UC) (neck) triangle and a QL muscle fatigue test (Biering-Sorensen test). Lengthening of muscles in the UC spine causes muscle spindles (neuromuscular receptors inside muscles) to fire, signaling body balance control center that the head is moved off vertical. Vibration also stimulates muscle spindles to fire. So, I was stimulating the UC spine via vibration with the head and neck in a neutral (vertical) position. After said stimulation, the subject immediately performed the Biering-Sorensen test. This test measures the fatigability of the QL muscle (to learn more about these two procedures, please read https://drgaryknutson.weebly.com/uploads/2/3/5/2/2352396/vib8.pdf). The energy reserves of an actively contracting muscle are partially used up. As such, that muscle will fatigue more quickly relative to the opposite side QL. What I found was this, vibration of the right UC spine resulted in quicker fatigability of the opposite (left) QL vs the right QL, and the opposite, stimulation of the left UC spine caused quicker fatigue of the right QL vs the left. This makes sense vis-a-vie the tonic neck body balance reflex which is controlled by signals from spindles in the muscles of the upper cervical spine.
What this indicates to me is that neuro-muscular dysfunction (what chiropractors call subluxation or joint dysfunction) in the UC spine initiates and perpetuates a balance control reflex that causes a hypertonic (“tight”, “short”) QL muscle in the lumbo-pelvic spine. Muscles want to contract and then relax. A muscle under tonic (prolonged) contraction soon becomes quite painful. You can demonstrate this to yourself easily: stand up with your arms at your side. Move your right arm away from your body till you are holding it up at a 90 degree angle. Hold it there. Within a minute or two the muscles holding the arm up (deltoid mainly) will begin to be painful. That is the kind, and reason for the pain associated with chronic QL hypertonicity – prolonged contraction. So, yeah, the QL is involved in some causes of back pain, but the ultimate cause of the QL “tightness” or, my preferred term, hypertonicity, is joint dysfunction in the upper cervical spine. You can stretch, poke, shake and bake the QL to reduce its hypertonicity, but until you address the cause of the QL “tightness”, the “tight” QL and the back pain will recur. I have seen many cases of patients with chronic back pain being blamed for their problem because they were not regularly doing all the stretches and exercises assigned by their physiotherapist. It's not the patients fault, the cause of the problem is not being addressed, so the problem comes back. I don't believe the UC spine is the only cause for QL hypertonicity (see Knutson G. The Sacroiliac Sprain; Neuromuscular Reactions, Diagnosis and Treatment with Pelvic Blocking. JACA 2004;41(8):32-39), but I do think it is a major, and most overlooked, cause.
Interestingly, one of the signs that many in the arena of manual therapies look for as an indication of a problem is a functional “short leg”. I use quotation marks around “short leg” because the leg is not anatomically short, but there is a problem that, when the subject is in an unloaded position (prone (on the belly) or supine (on the back)) one leg *appears* to be shorter than the other. The muscle associated with the appearance of the unloaded leg length inequality (LLI) is our friend, the QL. A hypertonic (“tight”) QL, because of its insertion in the crest of the pelvis, lifts/twists (torsions) the pelvis. This pelvic torsion, in an unloaded (prone/supine) position, makes the legs appear to be uneven. When an unloaded LLI is found, the QL muscle and UC joint/neuro-muscular dysfunction should be considered as the cause.
After I did the above noted study on the effects of UC vibration and the Biering-Sorensen test, it occurred to me to try using the UC vibration on patients who demonstrated an unloaded LLI. I have done this several times with interesting results. If a patient has a right functional LLI, and I know from examination that the UC dysfunction is on the left (the body balance mechanism feels like the head is falling off the the left, so increases tension on the right QL resulting in a right LLI. Vibration of the UC spine of that patient on the left side would (it seems) cause hypertonicity of, and/or reciprocal inhibition of, the right QL, balancing out the QL tension and, hypothetically, eliminating the appearance of the LLI. This is exactly what I have observed many times. (NOTE: this is not a hard and fast rule as there are many aspects of UC neuro-muscular dysfunction that need to be taken into account. For example, I have found is that this works best in patients with atlas laterality but minimal rotation (sorry to lapse into technical jargon, but those who understand UC joint dysfunction will get it)).
All this outlined above is why I believe that UC joint dysfunction is a (major) cause of QL hypertonicity and back pain. So, those of you who've been told you have a “tight” or “short” QL, get thee to a chiropractor who is knowledgeable about UC joint dysfunction. Yes, the whole hypothesis is somewhat complex, the evidence is weak and based on my own (potentially biased) studies and observations, but it is biologically plausible and there is some interesting evidenciary results. I would like to see these ideas explored more, but I am old, tired and not associated with any group that could organize such studies and get the blessing of the almighty independent review board. I do hope some investigation into this will be done in the future, which is one of the reasons why I am writing them out now.