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The Performance Lab A place to discuss the role of physical exercise on health in diseased and non-diseased states.

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Old 16-12-2007, 06:39 AM   #301
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Quote:
Originally Posted by anoopbal View Post
Is there any use of motor control exercises when the pain has "moved up" the nervous system? I am assuming pain which lasts for more than 3-6 months have caused changes in the nervous sytem irrespective of the initial biomechanical issues.

Or when you are doing motor control exercises its positively affecting the CNS too and therby relieving pain?

Anoop
well, i would say that if the pain is there since a while, it depends of some factors. yes, the exercises have a chance to help the person to regain confidence in the movements, to give more neuromuscular control, awareness, and thereby relieving pain. with a chronic lbp, if there is some evidence that there is an 'instability' i would definitively teach some stability exercises. but if the person already have seen an other therapist and already did some exercises, i will not spend much time to teach more about core stability. and, personally, if i treat someone with manual therapy (read orthopedic), and there is absolutely no change with whatever i do, i think central. but i do see chronic patient that manual therapy/core exercises did help a lot, so i think it must be teached, whatever the reason why it may help.
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Old 16-12-2007, 03:48 PM   #302
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On a side note, another purported test for lumbar instability:
http://www.thefreelibrary.com/A+new+.....-a0156552654

Anders.
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Old 16-12-2007, 04:50 PM   #303
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but i do see chronic patient that manual therapy/core exercises did help a lot, so i think it must be teached, whatever the reason why it may help.
But do't you think all the manual therapy and core exercise has an inevitable affect on the CNS too in the form of tactile, propioreceptive fedback, positive expectation and so on?

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Old 16-12-2007, 06:29 PM   #304
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Hi pht3k,

Quote:
with a chronic lbp, if there is some evidence that there is an 'instability' i would definitively teach some stability exercises.
You put instability in quotes which indicates that you have some reservation yourself whether there is indeed instability present. Shouldn't there then be quotes around the word stability as in 'stability' exercises?

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if i treat someone with manual therapy (read orthopedic)
manual therapy is not exclusively orthopedic and it is arguable that depending on the "manual" technique, there is no direct relevant orthopedic impact whatsoever.

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but i do see chronic patient that manual therapy/core exercises did help a lot, so i think it must be teached,
Would it be a catastrophe to not teach these specific stability exercises?
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Old 16-12-2007, 07:12 PM   #305
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Ph3k,

My understanding as well is that the function of 'stability' exercises is moreso for motor control improvements thereby reducing mechanical deformation of neural tissue. Nonetheless, McGill et al. have come up with a CPR to determine which populations would most benefit from 'stabilization' exercises. So, it's not a catch all a majority of people seem to think.

As a Kinesiologist/Exercise Physiologist it's more important to groove proper motor patterns and begin correcting neuromucular imbalances that likely contribute to chronic/recurrent/acute mechanical pain.

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Old 16-12-2007, 07:45 PM   #306
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The stabilization CPR only includes one test that contends to assess "stability" and that is the prone instability test. The recent study posted in the red file thread demonstrated how such a test was not able to reliably locate a segmental abnormality.

The prone test, in which a P/A force is applied to the spine causing pain which when repeated with the pt. engaging the lumbar extensors no longer causes pain thus is not a test of instability but instead a test whether or not pain can be modified by engaging extensors. That's it. Instability is only one possible mechanism and it is less and less supported as an explanation.

McGill likes to point to a one time shot when he observed an increased movement of one segment which happened along with pain on one repetition out of many. A problem is that if this observation was of an "unstable segment" then why would it not occur on every repetition.

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the exercises have a chance to help the person to regain confidence in the movements, to give more neuromuscular control, awareness
I think you've nailed it here, ph3tk. In a graded fashion the person learns that they are OK to move and gain an increase in awareness which likely coincides with changes in cortical mapping.
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Old 16-12-2007, 07:49 PM   #307
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it's more important to groove proper motor patterns and begin correcting neuromucular imbalances that likely contribute to chronic/recurrent/acute mechanical pain
How likely might that be?
Although I'm glad to see the word "likely" inserted between "that" and "contribute", I wonder how much pain science has really, actually, managed to find its way into motor control paradigms and practices, constructs and concepts.
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Old 16-12-2007, 08:43 PM   #308
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pht3k,

What kind of manual therapy would you do, assuming the presence of 'instability', along with the core exercises?

CPR or no CPR, it all rather seems like shots in the dark to me; searching for a cause and hoping to find one which works for a certain group of people with LBP. What about the rest who don't fit the CPR?

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Old 16-12-2007, 08:58 PM   #309
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And what exactly is a "neuromuscular imbalance"? If I could be convinced that such a thing actually existed, I'd wonder how this was determined, and then I'd wonder why such a thing would contribute to any origin of pain.

Reasonable questions?
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Old 16-12-2007, 10:06 PM   #310
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And what exactly is a "neuromuscular imbalance"? If I could be convinced that such a thing actually existed, I'd wonder how this was determined, and then I'd wonder why such a thing would contribute to any origin of pain.

Reasonable questions?
Sure.

Neuromuscular imbalances, implies a lack of motor control/efficiency resulting in physiologically inefficiient recruitment and movement patterns of agonists, antagonists and synergists.

Simply, it has to do with excessive facilitation patterns of certain groups and inhibition of others. Repetitive movement tasks or patterns resulting in increased synaptic strength and plastic changes at the sensorimotor cortex and cerebellar levels. Hence, these movement patterns, become facilitated, as a result of motor learning, and over time, can effective change the gamma bias of the spindle system. Consequently, mechanical deformation can occur resulting in relative hypoxic conditions of the nervo nervorium, small afferent in the skin, fascia, muscle, ligaments and other movement sensors. So, function alters structure which then impedes function and a positive feedback sort of loop ensues. The brain, trying to maintain a degree of allostasis/homeostatis from a kinetic standpoint begins to develop compensation and substitution strategies to the overly inhibited and facilitated muscles. Synergists then become overfacilitated as a means of compensation and can then become subject to strains. When tissue load exceeds tissue tolerance, tissue breakdown ensues.

Consequently we had the pre-cursor conditions ripe for nociception, and if the brain decides, pain. I could go on about how inflammation (chemical) and other means are involved in mechanical pain syndromes, but that seems to have been well established here.
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Old 16-12-2007, 10:24 PM   #311
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This is a description of something that stems from neuroplasticity gone wrong, is it not? Surely "neuromuscular imbalance" is not an actual entity in and of itself, "contributing" to "pain"... surely not..

It isn't "pain" until/unless the brain "decides" it's "pain".
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Old 16-12-2007, 10:52 PM   #312
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Of course I know the theory. Wouldn't it be nice to see some evidence that it's close to reality? This is nothing more than a regurgitation of a decades-old idea, an idea that hasn't panned out.

Am I off base here?
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Old 16-12-2007, 10:58 PM   #313
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Neuromuscular imbalances, implies a lack of motor control/efficiency resulting in physiologically inefficiient recruitment and movement patterns of agonists, antagonists and synergists
I would add, for example, a double amputee who runs a with prosthetics. His body is at the height of neromuscular "imbalance or inefficiency".

Only problem is that he has no pain whatsoever and runs faster than most of the healthy 100 m sprinters in the world.

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Old 16-12-2007, 11:10 PM   #314
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The brain, trying to maintain a degree of allostasis/homeostatis from a kinetic standpoint begins to develop compensation and substitution strategies to the overly inhibited and facilitated muscles. Synergists then become overfacilitated as a means of compensation and can then become subject to strains.
How would one go about to seperate this "defensive" neuromuscular imbalance from the original "defect" one? What about maladaptive pain behaviour on top aswell?

Anders.
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Old 17-12-2007, 12:04 AM   #315
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Hi there,

I have a few questions.

Quote:
Hence, these movement patterns, become facilitated, as a result of motor learning, .....
What is the difference between this process of motor learning etc etc, as it relates to exercise (ie repetitive movements) and thus improved function with supposedly less pain, compared with the idea that the same process leads to NM imbalance and thus pain?

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Consequently, mechanical deformation can occur resulting in relative hypoxic conditions of the nervo nervorium, small afferent in the skin, fascia, muscle, ligaments and other movement sensors.
I'm not sure I can see how the "consequently" fits here - the former statement doesn't seem to lead at all naturally to the later (unless, perhaps, the tissues have hypertrophied considerably - possible, but an unlikely contributor for most patients)

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Consequently we had the pre-cursor conditions ripe for nociception,
I'm not sure I understand the position ascribed to nociception on this continuum. "Excessive facilitation patterns of certain groups and inhibition of others", "plastic changes at the sensorimotor cortex", "the brain trying to maintain a degree of allostasis/homeostatis" and "develop[ment of] compensation and substitution strategies" may in fact occur as a result of nociception, instead of the other way round.

Re:
Quote:
it's more important to groove proper motor patterns
It now seems evident that something else is going on besides 'proper motor control'.
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Old 17-12-2007, 12:07 AM   #316
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Originally Posted by Barrett Dorko View Post
Of course I know the theory. Wouldn't it be nice to see some evidence that it's close to reality? This is nothing more than a regurgitation of a decades-old idea, an idea that hasn't panned out.

Am I off base here?
Well, in all due respect, the evidence presented in motor learning theories greatly surpasses the depth and breadth of evidence that you bring for SC. Also, the aforementioned "theory" is of known neurophysiological processes. It also provides a tenable concept of how "insidious" mechanical deformation occurs with potential concomittant chemical irritation. Am I off base here? What exactly is your argument? That mechanical deformation cannot cause pain?
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Old 17-12-2007, 12:13 AM   #317
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Originally Posted by kongen View Post
How would one go about to seperate this "defensive" neuromuscular imbalance from the original "defect" one? What about maladaptive pain behaviour on top aswell?

Anders.
That's the million dollar question. When you have a nerve that isn't functioning properly without obvious signs of classical pathology (i.e. NCV tests, neurodynamics etc) and there's a lack of proper sensorimotor integration it's clear that the information being provided to and/or from the brain to the rest of the CNS/PNS/ANS isn't reliable.

I would assume that the defense and defect can be occuring simultaneously and be indistinguishable. Hard to say clinically. What do you do figure this out?
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Old 17-12-2007, 12:19 AM   #318
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Originally Posted by Luke Rickards View Post
Hi there,

I have a few questions.

What is the difference between this process of motor learning etc etc, as it relates to exercise (ie repetitive movements) and thus improved function with supposedly less pain, compared with the idea that the same process leads to NM imbalance and thus pain?

I'm not sure I can see how the "consequently" fits here - the former statement doesn't seem to lead at all naturally to the later (unless, perhaps, the tissues have hypertrophied considerably - possible, but an unlikely contributor for most patients)
Why would that have to be hypertrophied? You're simply changing length-tension relationships of the muscles which impacts and the surrouding neurovascular bundles. A shortened, tonic muscle with increased gamma bias is more likely to "squish"/compress/narrow the tunnels that the nerves travel in and affect motor units, etc.

Quote:
I'm not sure I understand the position ascribed to nociception on this continuum. "Excessive facilitation patterns of certain groups and inhibition of others", "plastic changes at the sensorimotor cortex", "the brain trying to maintain a degree of allostasis/homeostatis" and "develop[ment of] compensation and substitution strategies" may in fact occur as a result of nociception, instead of the other way round.
Classic case of chicken or the egg. My personal opinion is that in absence of blunt trauma, functional losses precedes pain states.

Re: It now seems evident that something else is going on besides 'proper motor control'.[/QUOTE]

One study would hardly prove conclusive. I would also say that the best motor learning strategies were also likely not found to be used thus negating the validity, at least to a degree, the conclusions of this study.
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Old 17-12-2007, 12:41 AM   #319
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Hi dswayze,

Quote:
My personal opinion is that in absence of blunt trauma, functional losses precedes pain states.
Can you provide an example of this for us?
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Old 17-12-2007, 01:31 AM   #320
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the evidence presented in motor learning theories greatly surpasses the depth and breadth of evidence that you bring for SC.
I think you may have a narrow view of what motor control is. It takes into account goals, end state comfort, context, etc and I think SC can fit nicely into the explanation. My issue with motor control is therapists who like the control part.
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Old 17-12-2007, 01:56 AM   #321
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I think you may have a narrow view of what motor control is. It takes into account goals, end state comfort, context, etc and I think SC can fit nicely into the explanation. My issue with motor control is therapists who like the control part.
I realized that I may have touched on a sacred cow there so I'll leave it at that. At the very least it seems like SC therapists are trying to facilitate the "inhibited" nonconcious movements which I would say is more in the realm of OT or psychology.

I'd say with 4 university courses in motor learning/lifespan development, 6 courses in exercise physiology, fitness testing and training, external (envrionmental) influences on exercise physiology and 5 years of clinical experience that I know my motor control and exercise physiology theory vey well.

Jon

It's difficult to provide evidence of my opinion on the matter, but what about EMG testing of supraspinatus, for example, that shows inhibition (greater than 10% which would typically account for dominance) and is substantially weaker than the opposite side? Loss of function occurs, could result in a strain, subsitution strategies requiring increased deltoid/trapezius action, loss of vector forces stabilization the humerus in the glenoid, etc... (end result is mechanical deformation or a decrease in tissue tolerance which would "break" under seemingly unchanged loads (work, exercise, blag blah)
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Old 17-12-2007, 02:10 AM   #322
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Hello dswayze,

Your credentials are wonderful but it would be more useful for readers here if you apply them. Knock over any sacred cows (as you see them) you can; don't back off now. It's sort of the credo here.

Can you expand on the inhibition aspect of your example?
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Old 17-12-2007, 02:34 AM   #323
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Last I heard, there is no gamma bias in human beings. Among many other things, I find your actual knowledge of the deep model rather mystifying.

Now you're trying to compare your work, whatever it may be, to Simple Contact - something you obviously don't understand to speak of.
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Old 17-12-2007, 02:40 AM   #324
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At the very least it seems like SC therapists are trying to facilitate the "inhibited" nonconcious movements which I would say is more in the realm of OT or psychology
Do you think "unconscious" and "nonconscious" are the same thing?
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Old 17-12-2007, 02:51 AM   #325
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Hi,
Quote:
You're simply changing length-tension relationships of the muscles which impacts and the surrouding neurovascular bundles.
Doesn't that happen every time you contract a muscle under load?

Again- What is the difference between this process of motor learning etc etc, leading to NM imbalance and thus pain, compared with exercise (ie repetitive movements) and thus improved function with supposedly less pain?

Quote:
functional losses precedes pain states.
Really? The reason my patients stop bending over is because it hurts. Are you talking about function here, or impairments (which are often of indeterminate clinical significance)?
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Old 17-12-2007, 02:53 AM   #326
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It wasn't my intention to imply you do or do not know about motor control, rather it needs to be taken into a broader context... pain and the science of.
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Old 17-12-2007, 03:54 AM   #327
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If control and muscular balance, or lack thereof, caused pain wouldn't ballet dancers be free from mechanical pain?

These people need an enormous movement reportoire and have an obvious abundance of control to perform their art. I've been told that this is a population that experiences a high degree of mechanical pain, however, sometimes even having their own PTs on staff.
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Old 17-12-2007, 07:15 AM   #328
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Hi,
Doesn't that happen every time you contract a muscle under load?
Yes. But it usually doesn't stay at that length and returns to its pre-contracted state. In deafferented states or overfacilitation the gamma bias of the spindle is set so that the tension remains constant and the mechanoreceptors and such are "reset" to a new normal resting length. This in turn leads to the aforementoned hypoxic states to important neurovascular bundles which starts to irritate the tissues as cell transport functions become comprimised as well leading to a cascade of changes cellularly leading to eventual inflammation and or lysis. Mechanical and chemical irritation ensues. Whether or not this manifests itself perceptually as pain or clinically significant depends on a lot of factors naturally, not the least being the general health of the person.

Quote:

Again- What is the difference between this process of motor learning etc etc, leading to NM imbalance and thus pain, compared with exercise (ie repetitive movements) and thus improved function with supposedly less pain?

Really? The reason my patients stop bending over is because it hurts. Are you talking about function here, or impairments (which are often of indeterminate clinical significance)?
I'm a little confused by the nature of the question. Neuromuscular imbalances can be caused by and CORRECTED by therapeutic exercises/movement patterns depending on a good clinical assessment and objective data tracking (videography, EMG, VO2max levels, RQ values, etc). And, it makes sense that the correct PRESCRIPTION of exercise could help alleviate mechanical pain on a lot of levels, one of them being increasing overall tissue tolerance. Did that answer your question?
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Old 17-12-2007, 07:17 AM   #329
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Originally Posted by BB View Post
If control and muscular balance, or lack thereof, caused pain wouldn't ballet dancers be free from mechanical pain?

These people need an enormous movement reportoire and have an obvious abundance of control to perform their art. I've been told that this is a population that experiences a high degree of mechanical pain, however, sometimes even having their own PTs on staff.
Because in this case, the amount of training, performance exceeds amount of rest and recovery. Again, coming down to tissue mechanics, when tissue load exceeds tissue tolerance will result in tissue failure -->mechanical deformation, chemical irritation etc.
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Old 17-12-2007, 07:18 AM   #330
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but what about EMG testing of supraspinatus, for example, that shows inhibition (greater than 10% which would typically account for dominance) and is substantially weaker than the opposite side?
That is all the problem with strengthening: inhibition doesn't equate with weakness. An inhibited muscle is not weak. Strengthening will create a typical and greater imbalance, IMHO.
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Old 17-12-2007, 07:29 AM   #331
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Originally Posted by bernard View Post
That is all the problem with strengthening: inhibition doesn't equate with weakness. An inhibited muscle is not weak. Strengthening will create a typical and greater imbalance, IMHO.
What is your understanding of inhibition, Bernard? It doesn't have to be just strength but endurance too.

An overfacilitated muscle be weak too, due to poor length-tension mechanics resulting in too gross of an overlap of the sarcomeres. Gross ROM and palpation of tissue tension under that ROM could help distinguish between the two.
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Old 17-12-2007, 07:35 AM   #332
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Originally Posted by Barrett Dorko View Post
Last I heard, there is no gamma bias in human beings. Among many other things, I find your actual knowledge of the deep model rather mystifying.
This can easily be found in the literature.

Quote:

Now you're trying to compare your work, whatever it may be, to Simple Contact - something you obviously don't understand to speak of.
I'm not comparing "my work" to yours. And I understand the premise and excution of SC quite well. I would say it's the closest thing I've seen to a human ouija board. Clever, that ideomotor effect.
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Old 17-12-2007, 07:38 AM   #333
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An overfacilitated muscle be weak too, due to poor length-tension mechanics resulting in too gross of an overlap of the sarcomeres.
Does it happen frequently with LBP? They have often tight and short muscles.

Inhibition is the contrary of activation. A muscle is inhibited by higher centers or nerve problems.
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Old 17-12-2007, 07:38 AM   #334
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Originally Posted by anoopbal View Post
But do't you think all the manual therapy and core exercise has an inevitable affect on the CNS too in the form of tactile, propioreceptive fedback, positive expectation and so on?
sure

Quote:
Originally Posted by Jon Newman
You put instability in quotes which indicates that you have some reservation yourself whether there is indeed instability present. Shouldn't there then be quotes around the word stability as in 'stability' exercises?
I simply put instability in quotes because there is a controversy around this term.

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Originally Posted by Jon Newman
Would it be a catastrophe to not teach these specific stability exercises?
maybe for me, since i don't know yet the skin stretch treatment, ideomotion, etc - my background is mainly orthopedic. i think it's useful. but if some1 else use other techniques and relieves the patient's pain, then that's fine.

Quote:
Originally Posted by nari
What kind of manual therapy would you do, assuming the presence of 'instability', along with the core exercises?
if there is something instable, i will definitively look around to see if there is hypomobility, hip restrictions, plantar fascia tightness, etc... and if there is any neurodynamic findings.

btw, there were some concerns about the fact of having the core muscles always contracted to stabilize the unstable segments. this is not my point of view. i hope to have the csa back (giving more passive resistance to movement) and having an automated motor control. according to o'sullivan, there is some evidence that changes to automatic patterns of muscle recruitment can be achieved by core stab is supported by surface EMG data.

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Old 17-12-2007, 07:50 AM   #335
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Quote:
Originally Posted by O'sullivan
On physical examination, active spinal movement
revealed good ranges of spinal mobility, with the
presence of `through range' pain or a painful arc
rather than end of range limitation, and the inability
to return to erect standing from forward bending
without the use of the hands to assist this motion.
Quote:
Originally Posted by =O'sullivan
It appears that these patients
develop compensatory movement strategies which
`stabilize' the motion segment
Here is two quotes that defines the "instability". That is not kind because patients use different strategies they thought helpful for movements.

In fact, these strategies do not work because these compensations increase the problem.
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Old 17-12-2007, 08:00 AM   #336
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Originally Posted by bernard View Post
Does it happen frequently with LBP? They have often tight and short muscles.
In fact, yes. See Sorensen test results. They lack endurance in the extensors relative to the normal population which was an indicator of future/current back pain as opposed to people who had longer endurance times.

Quote:
Inhibition is the contrary of activation. A muscle is inhibited by higher centers or nerve problems.

What kind of nerve problems? Furthermore, a muscle can be activated and inhibited at the same time. Whether or not it is functioning at peak capacity is all together a different story.
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Old 17-12-2007, 08:20 AM   #337
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They lack endurance in the extensors relative to the normal population
Is it a normal and daily activity? BTW, a fatigue appears for sure but fatigue is not a proof of weakness.

Quote:
What kind of nerve problems?
Many!

Quote:
Furthermore, a muscle can be activated and inhibited at the same time
How?
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Old 17-12-2007, 09:15 AM   #338
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Thanks for the reply, pht3k. If there is instability, I am wondering why you would expect hypomobility in nearby joints? Compensatory effects?


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Old 17-12-2007, 01:43 PM   #339
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I think this fits here.

Quote:
Journal of Rehabilitation Research & Development; Mar/Apr2005, Vol. 42 Issue 2, p235-249
Electromyographic activity imbalances between contralateral back muscles: An assessment of measurement properties.
Lariviëre, Christian; Gagnon, Denis; Arsenault, A. Bertrand; Gravel, Denis; Loisel, Patrick.

Electromyographic (EMU) contralateral imbalances of back muscles are often interpreted as an aberrant back muscle pattern related to back pain. This study assessed different measurement properties (influence of the control of asymmetric efforts and of the force level, reliability, and sensitivity to low back status) of EMU imbalance parameters. Healthy controls (ii = 34) and chronic low back pain subjects (n = 55) stood in a dynamometer measuring the principal (extension) and coupled (lateral bending, axial rotation) L5IS 1 moments during isometric trunk extension efforts. The results showed that back pain subjects did not produce higher coupled moments than controls. Providing feedback of the axial rotation moment to correct asymmetric efforts during the task did not reduce EMU contralateral imbalances, except for some extreme cases. Normalized EMU imbalance parameters remain relatively constant between 40% and 80% of the maximal voluntary contraction. The reliability of EMU imbalance parameters was moderate, at best. Finally, neither low back status nor pain location had an effect on EMU contralateral imbalances. We conclude that the clinical relevance of EMU contralateral imbalances of back muscles remains to be established.
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Old 17-12-2007, 01:48 PM   #340
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Nari,

well there might be hypomobility because there is less movement occuring there since there is instability. with time mobility will be restricted. and hypomob can also be a cause for the instability, because of compensations. so, it's the egg or the chick, depending the patient and the articulation.
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Old 17-12-2007, 02:52 PM   #341
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because there is less movement occuring there since there is instability
A simpler answer: There is hypomobility because it hurts.
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Old 17-12-2007, 05:54 PM   #342
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Last I heard, there is no gamma bias in human beings.
Barrett,
I take it you were pointing out the challenges to maintained gamma bias as it relates to the theory being presented here.

For more on that-

Quote:
Muscle Nerve. 1993 Jul;16(7):693-705.
Microneurography and applications to issues of motor control: Fifth Annual Stuart Reiner Memorial Lecture.
Hagbarth KE.

Among the hypotheses regarding fusimotor functions based on earlier animal experiments some are inconsistent, others are in conformity with microneurographic observations in man. The human data provide evidence against the following two theories: (1) the length follow-up servo theory; and (2) the theory that fusimotor neurons can be selectively activated to produce spindle sensitization and stretch reflex reinforcements. The human data support the theory of alpha-gamma coactivation. In particular, in the early phase of isometric voluntary contractions fusimotor-driven afferent spindle activity assists in autogenetic activation of alpha motoneurons and in reciprocal relaxation of antagonists. As muscle fatigue develops, the autogenetic reflex drive via the fusimotor route declines. The fusimotor bias during contraction provides for maintenance of spindle sensitivity to minute perturbations and for load-compensating reflex adjustments to such perturbations. Reflex overcorrections may lead to uncontrollable oscillations of the type seen in enhanced physiological tremor.
Quote:
Exp Brain Res. 1991;86(3):673-8.
Post-contraction changes in human muscle spindle resting discharge and stretch sensitivity.
Ribot-Ciscar E, Tardy-Gervet MF, Vedel JP, Roll JP.

The activities of human muscle spindle primary endings were recorded in the lateral peroneal nerve using the microneurographic method. The aim of the study was to test whether voluntary isometric contraction causes any after-effects, first in the resting discharge of muscle spindle primary endings and secondly in their responses to a slow ramp stretch...... The results were as follows: (1) most of the units did not exhibit the "post-contraction sensory discharge" reported to occur in numerous animal experiments; this means that the muscle spindle resting discharge was essentially the same before and after isometric voluntary contraction. ......The results are discussed with reference to the theory according to which the processing by the CNS of muscular proprioceptive messages deals mainly with signals arising from muscles stretched during movement, and it is concluded that the coactivation of alpha and gamma motoneurones during the contraction facilitates the coding of the parameters of forthcoming stretching movements, by the muscle spindles.
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Old 17-12-2007, 09:36 PM   #343
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Originally Posted by bernard View Post
A simpler answer: There is hypomobility because it hurts.
I cannot agree with this affirmation. Studies show clearly that there is findings within asymptomatic population. And what about the stiff cyphotic dorsal spine?
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Old 17-12-2007, 09:53 PM   #344
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pht3k,
If by this:
Quote:
Studies show clearly that there is findings within asymptomatic population.
you mean that asymptomatic individuals show signs of hypomobility too, I agree.

Quote:
what about the stiff cyphotic dorsal spine?
What about it? Maybe you could expand on this further. My take on this is that it's a common finding in asymptomatic people as well.
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Old 17-12-2007, 10:25 PM   #345
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Originally Posted by EricM View Post
If by this you mean that asymptomatic individuals show signs of hypomobility too, I agree.
that's exactly what i mean.

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Originally Posted by EricM View Post
What about it? Maybe you could expand on this further. My take on this is that it's a common finding in asymptomatic people as well.
yes it is a common finding in asymptomatic people.

...it shows that it's not hypomob because it hurts.
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Old 17-12-2007, 10:28 PM   #346
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pht3k,

If there is pain, there is likely to be hypomobility (a defence). However, hypomobility does not = pain.

So 'correcting' a hypomobile segment may or may not resolve the pain. Encouraging active movement with pain education would be far more effective in resolving pain.

Many people have a stiff kyphotic spine and are fully functional and painfree; which to me indicates that stiffness and weakness are, by themselves, not really associated with pain. Passive resolution of a hypomobility can help for a while, but active movement + education is better in the long term.

Active neurodynamics can definitely help with pain resolution, if you are not familiar with ideomotion and DNM.

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Old 18-12-2007, 12:21 AM   #347
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yes it is a common finding in asymptomatic people.

...it shows that it's not hypomob because it hurts.
Of course, the other implication of this is that hypomobility doesn't cause pain, ie hypomobility may not be a clinically relevant finding in low back pain, and treatment directed at 'fixing' this is unjustifiable.
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Old 18-12-2007, 12:40 AM   #348
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usually i don't think of hypomobs as pain producers, except in some situations, but are definitively not helpful for the other unstable vertebrae. i think of hypomob as a potential culprit (among other), not as the painful victim vertebrae.
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Old 18-12-2007, 12:54 AM   #349
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usually i don't think of hypomobs as pain producers, except in some situations, but are definitively not helpful for the other unstable vertebrae. i think of hypomob as a potential culprit (among other), not as the painful victim vertebrae.
If it is not a pain producer what is the point of thinking about it at all? I suspect your answer is, 'because they will cause exacerbation unstable segments'.

BTW, Bernard was saying that hypomobility may occur as a result of pain (ie, guarding). This is not the same as saying pain may occur as a result of hypomobility, which is the argument you are actually countering with the comment on asymptomatic people.
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Old 18-12-2007, 01:00 AM   #350
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I think this quote by Louis Gifford is apt for this discussion about pain and dysfunction, “It is important to note that we are full of dysfunctions whether we are not in pain or not. If we are in pain it is easy to find something wrong relevant to a precise tissue model but which may not be relevant at all to the patients state”

And forget abt hypomoblity: Disc protrusions, said to be one of THE definite cuases of low back pain, have been extensively found in asymptomatic population. Also Sahrmann thinks that it is due to the hypomobilty of the hip, and thereby the HYPERMOBILTY of the spine, that causes low back pain.

This is was my question for David Butler:

My second questions is: It seems like chronic pain can be treated by focussing just on the brain, like miror therapy and motor imagery without much attention to the periphery ( even if could be impaired). So could it mean that hypoxic nerves or nerve damage or ectopic signals DO NOT neccasirly cause pain unless the brain decides to? Or most of the these impairemnts are common in a healthy person and sometimes for unknown reasons trigger pain?

And his answer was: YES.


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