Stabilizers and movers

[BB]

A good portion of this I already typed and I somehow made it dissapear, so if this shows up twice my apologies!

I was reading a discussion on another forum regarding how when in pain we seem to inhibit our stabilizers and our movers become hypertonic.

Mechanically, I often look for this situation..or a version of it.

I look for if the distal attaching movers have become dominant over the proximal attaching stabilizers.

An example:
Often deltoids (distal attaching) try to do too much and begin to overpower the rotator cuff muscles (proximal attaching) which then become weak and lazy and soon are painful because the deltoids are pulling them into the acromion and causing impingement.

I see this often as a consequence of overusing the deltoids for a long period of time functionally, and the pattern also follows throughout the rest of the body.

What I had not thought about, was this same scenario brought about instantaneously by acute injury or pain onset. The example used in the other thread was concerning low back pain and the resulting inhibition of the lumbar stabilizers and hypertonicity of the movers.

I had reasoned that the pattern was probably present prior to pain, and likely contributed to the eventual onset of pain. If this is not the case, what are the implications for those in chronic pain, because their mechanical presentations don't not necessarily result from specific functional movements prior to injury.

Anybody have any thoughts about this?

Maybe this is part of the reason that people in this situation become so fearful of movement and turn out to have chronic pain. Since the problem did not develop gradually and therefore the pain was less likely to have increased gradually, they don't have the opportunity to get used to the idea of having some pain with their motions and therefore don't have the chance to develop the necessary awareness of movement.

I'm mostly thinking out loud here, so sorry if the question is not developed well, but hopefully it will spark discussion which will help me organize my thoughts.

Cory

[nari]

BB

I will throw in another thought - what of those people who have no obvious injury, no history of sudden acute pain? They still develop chronic pain, and when we go hunting for a cause, we will find something - be it a past whiplash, or a divorce, or a long-forgotten fall.

Why does 'frozen shoulder' appear for no clear reason? It starts insidiously and eventually goes away, leaving no blatant residual signs.
But the history of such shoulder signs suggest the stabilisers are inhibited and the primary movers 'on guard', producing very dysfunctional movements.
With back pain, the large erectors are often tense. but can be placated - temporarily. So we might leap in and facilitate the stabilisers - then what?
Activating Trans Ab and the multifidus does relieve pain, but I wonder if we have got to the stage where there is a light in the end of the tunnel.
Somewhere we need to 'hook in' on the brain reprogramming in a non-mechanical way...


Nari

[nari]

Bernard

If we think of the 'mechanical' process in relieving pain as we were all taught, ie local applications of manual therapy, electrotherapy, exercises and heat, we are treating the periphery. This will relieve pain, for a while, but it will not get to the heart (read brain) of the issue unless we educate well as to why only the distal part should move, if the neural tests are positive. Should the lumbar spine be very painful, move the foot. If the patient does not understand why this is so, there wil be no compliance, and poorer outcomes.
This is what I mean - the way to the brain is with words, and then the mechanical means will work.
It fits in well with the theme of simple therapy.

I know few people agree, but I find this has worked quite well over the last year. There have been quite a few people who have presented with global pain and have had their quality of life 60-70% restored.

Nari

[bernard]

Nari,

the way to the brain is with words

I must suggest the way to brain is communication and communication could take many forms?

[nari]

OK, I'll buy that one.



N

[emad]

yes Nari:

i absouletly agree with you , if we do not address the patient meaning (his understaning) of the problem, we can not manage properly.

where is it sold?

cheers
emad :)

[Diane]

Bernard,
You said the first "normal" movment hurts, and the next slowed down one doesn't. There are probably lots of factors:
1. Closer attention the second time, less "thoughtless"
2. Slower speed = better chance for painless adaptation of peripherals
3. It was the second time, maybe some fading of some cranky feedback in the system occured
4. Different bloodflow the second time, probably better prepared, and because slower, more time to keep tissue fed

Nari, you said:
"Should the lumbar spine be very painful, move the foot." I was reminded of a couple of occasions in my life when I awoke to find myself "paralyzed", by that I mean my forebrain seemed to wake up before any other part. It happened when I was young, and it was scary. I panicked a bit. I sort of scanned through the body looking for something that I could move. All I could move were my eyelids. So I squeezed those and the "body" (action neuromodules) magically woke up. Weird but true.

I totally see the point of your statement. The person has to "wake up" their body from its painful nighmare. And the way to do that is to "move" something that DOESn't hurt, so the brain can feel "successful" and build on that.

Often when I'm treating hands-on/in I can feel the tissues soften as they "wake up." But there's no point in waking them up if one doesn't leave time for movement, if that person's brain doesn't experience right away, before they leave, the freedom of motion and what the body awakened from the nightmare "feels" like, and be taught ways to keep it that way.
Two cents,
Diane

[bernard]

Hello Diane,

I think that velocity (speed) is certainly relevant and the differences you note are to take in count. If we got a painful movement and a painfree one and the unique difference in the two is speed of accomplishment, then celerity did something.

Remember the abstract given by Emad about motor centers activity;
1/ a such simple activity seems complex.
2/ a simple motor activity involves the two sides.
3/ the velocity induces inertia and inertia must induce anticipation.
4/ quicker the movement more anticipation involved?

5/ movement is ever corrected by a kind of phase looked loop! There is a constant flow of inputs/outputs.
6/ how is translated an asynchronous relation in these two flows?
7/ how is translated an event that is added of an asynchronous manner => flow of nociception that is masked normally by the inputs of motion?

[bernard]

I found that one relevant of the thread?

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=14689133

Exp Brain Res. 2003 Dec 19 [Epub ahead of print]
Pain differs from non-painful attention-demanding or stressful tasks in its effect on postural control patterns of trunk muscles.

Moseley GL, Nicholas MK, Hodges PW.

Department of Physiotherapy, Royal Brisbane Hospital, 4029, Herston, Queensland, Australia.

Pain changes postural activation of the trunk muscles. The cause of these changes is not known but one possibility relates to the information processing requirements and the stressful nature of pain. This study investigated this possibility by evaluating electromyographic activity (EMG) of the deep and superficial trunk muscles associated with voluntary rapid arm movement. Data were collected from control trials, trials during low back pain (LBP) elicited by injection of hypertonic saline into the back muscles, trials during a non-painful attention-demanding task, and during the same task that was also stressful. Pain did not change the reaction time (RT) of the movement, had variable effects on RT of the superficial trunk muscles, but consistently increased RT of the deepest abdominal muscle. The effect of the attention-demanding task was opposite: increased RT of the movement and the superficial trunk muscles but no effect on RT of the deep trunk muscles. Thus, activation of the deep trunk muscles occurred earlier relative to the movement. When the attention-demanding task was made stressful, the RT of the movement and superficial trunk muscles was unchanged but the RT of the deep trunk muscles was increased. Thus, the temporal relationship between deep trunk muscle activation and arm movement was restored. This means that although postural activation of the deep trunk muscles is not affected when central nervous system resources are limited, it is delayed when the individual is also under stress. However, a non-painful attention-demanding task does not replicate the effect of pain on postural control of the trunk muscles even when the task is stressful.

PMID: 14689133 [PubMed - as supplied by publisher]

[BB]

I have been reading the book that RIN recommended in another thread-"Change your brain change your life" by daniel amen---Thanks for the recommendation RIN, I'm enjoying it!

In the book, he describes his use of SPECT studies to look at brain activity
He describes problems associated with the basal ganglia including anxiety, physical sensations of anxiety, muscle tension and soreness, fine motor control, among others.

He goes on to give some exercises to effect the basal ganglia which he supports with his SPECT studies.
One of his exercises is diaphragmatic breathing.

It seems that maybe postral muscles and movers are affected by the basal ganglia in similar ways to what we have been describing:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12763089
Basal ganglia efferents to the brainstem centers controlling postural muscle tone and locomotion: a new concept for understanding motor disorders in basal ganglia dysfunction.

Takakusaki K, Habaguchi T, Ohtinata-Sugimoto J, Saitoh K, Sakamoto T.

Department of Physiology, College of Medicine, Asahikawa Medical College, Midorigaoka-Higashi 2-1, Asahikawa 078-8510, Japan. kusaki@asahikawa-med.ac.jp

The present study is designed to elucidate how basal ganglia afferents from the substantia nigra pars reticulata (SNr) to the mesopontine tegmental area of the brainstem contribute to gait control and muscle-tone regulation. We used unanesthetized and acutely decerebrated cats (n=27) in which the striatum, thalamus and cerebral cortex were removed but the SNr was preserved. Repetitive stimulation (50 Hz, 10-60 microA, for 5-20 s) applied to a mesencephalic locomotor region (MLR), which corresponded to the cuneiform nucleus, and adjacent areas, evoked locomotor movements. On the other hand, stimulation of a muscle-tone inhibitory region in the pedunculopontine tegmental nucleus (PPN) suppressed postural muscle tone. An injection of either glutamatergic agonists (N-methyl-D-aspartic acid and kainic acid) or GABA antagonists (bicuculline and picrotoxin) into the MLR and PPN also induced locomotion and muscle-tone suppression, respectively. Repetitive electrical stimuli (50-100 Hz, 20-60 microA for 5-20 s) delivered to the SNr alone did not alter muscular activity. However stimulating the lateral part of the SNr attenuated and blocked PPN-induced muscle-tone suppression. Moreover, weaker stimulation of the medial part of the SNr reduced the number of step cycles and disturbed the rhythmic alternation of limb movements of MLR-induced locomotion. The onset of locomotion was delayed as the stimulus intensity was increased. At a higher strength SNr stimulation abolished the locomotion. An injection of bicuculline into either the PPN or the MLR diminished the SNr effects noted above. These results suggest that locomotion and postural muscle tone are subject to modulation by GABAergic nigrotegmental projections which have a partial functional topography: a lateral and medial SNr, for regulation of postural muscle tone and locomotion, respectively. We conclude that disorders of the basal ganglia may include dysfunction of the nigrotegmental (basal ganglia-brainstem) systems, which consequently leads to the production of abnormal muscle tone and gait disturbance.

PMID: 12763089 [PubMed - indexed for MEDLINE]


Am J Psychiatry. 2003 May;160(5):904-10. Related Articles, Links

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12727694
Personality traits and striatal dopamine synthesis capacity in healthy subjects.

Laakso A, Wallius E, Kajander J, Bergman J, Eskola O, Solin O, Ilonen T, Salokangas RK, Syvalahti E, Hietala J.

Department of Pharmacology and Clinical Pharmacology, University of Turku, Kiinamyllynkatu 4-8, 20520 Turku, Finland.

OBJECTIVE: Neuroimaging and genetic studies suggest that individual differences in the brain dopaminergic system contribute to the normal variability of human personality (e.g., social detachment and novelty seeking). The authors studied whether presynaptic dopamine function is also associated with personality traits. METHOD: Presynaptic dopamine synthesis capacity in the brain was measured with positron emission tomography and [(18)F]fluorodopa in 33 healthy adults, and personality traits were assessed with the Karolinska Scales of Personality. Associations were studied by using a linear regression model controlling for the effects of age and gender on both variables. RESULTS: High scores on two of the anxiety-related personality scales, somatic anxiety and muscular tension, and on one aggressivity-related scale, irritability, were significantly associated with low [(18)F]fluorodopa uptake in the caudate. No statistically significant associations were observed between [(18)F]fluorodopa uptake and the detachment scale or scales related to novelty-seeking behavior (impulsiveness and monotony avoidance). CONCLUSIONS: The results suggest a role for the dopaminergic system in the regulation of anxiety in healthy subjects. Together with previous studies, they also indicate differential involvement of various components of the dopaminergic system in normal and pathological personality traits.

PMID: 12727694 [PubMed - indexed for MEDLINE]

The great reference that bernard provided adds weight to stress and pain contribution to imbalance between movers and stabilizers.

Is it possible or likely that many of the people who develop chronic pain could be those who already have problems with basal ganglia regulation, and are at a hightened anxiety level and therefore may already be at an imbalance between movers and stabilizers. Then when stress and or pain are thrown into the picture this imbalance is pushed further into imbalance. Where for most of us this creates an imbalance that we are able to withstand or re-organize, maybe for those who are starting at an already imbalanced state it pushes them past a threshold into an the various imbalances that we tend to see.

The imbalance in the CNS becomes manifest in the periphery?

Cory

[BB]

Oops!

Forgot to include the actual journal reference for the first abstract.

Neuroscience. 2003;119(1):293-308.

Basal ganglia efferents to the brainstem centers controlling postural muscle tone and locomotion: a new concept for understanding motor disorders in basal ganglia dysfunction.

Takakusaki K, Habaguchi T, Ohtinata-Sugimoto J, Saitoh K, Sakamoto T.


Cory

[BB]

Bernard,

I have been trying to organize my thoughts on this in context with the ideas Diane has been presenting us...

Neurosignature-
If the person's basal ganglia is in imbalance causing higher anxiety levels, then the signature would be "anxious"
I'm picturing it as every outgoing signal is tagged with this anxious signature and the outside presentation is general anxiety.

Sensoryneuromodule-
A stress input is recieved which must now be processed by this brain which is tagging all outputs "anxious"

Actionneuromodule-
Normally, in the absence of the anxious neurosignature, this input would cause a muscle tone imbalance as was demonstrated by your reference bernard. However, since this brain is additionally tagging every output with "anxious", it would make sense that effective output would be that of exagerated anxiety. Like the brain is giving a ball rolling down hill an extra push to make it roll down hill even faster.

I'm interested to hear your thoughts on this!
Cory

[Diane]

Cory,
Like squeal of microphone feedback..

Bernard, Given how innervated the skin is, with both sensory input mechanisms and sympathetic output mechanisms, it makes total sense to me that it is the best place to:
1. Respectfully contact the patient's brain
2. Create a new "major sensory event" which the brain will then be challenged to process into a "neuromodule" ..
3. ..Which will in turn "impress a subsignature" onto the overall "neurosignature"(the continuous outflow from the neuromatrix)..
4. ..Which will affect the sentient neural hub and change/add to the stream of awareness.
Cheers,
Diane

[BB]

Bernard,
You said, "A divergent system has no way to a stable state other than saturated."

Could you explain this a bit more? I'm not sure I follow you.

Thanks!
Cory

[Diane]

Thanks for explaining that stuff about microphones Bernard, love the technical jargon and you are great at explaining it in English. Never knew about Larsen's effect before, just that microphones sound awful sometimes..
Diane

[bernard]

Thanks Diane,

About the thought of Cory, there is another possibility. The explanations of Cory bring an associative solution. It needs almost 2 systems but here we have many ones, so, no problems.

The divergent system is controlled by a convergent one (an inhibiter). If movement is becoming too painful, then the movement is stopped. That is what we are seeing in reality?

The realization speed is lowered if pain is present.

A major question haunts me: if we take, for an example, the frozen shoulder where muscles have had no direct injuries and we assume normally that a muscle is not painful while moving and more, that normally fast inputs, as A fibers cover (mask) the delta and C-ones (pain) => gate control theory!!! We return to our natural mystery because in that case pain has to be explained in CNS.

But since pain is found only while moving, what is the muscular neurosignature generating pain?

Is it a big shift between the neuroaction order and the waited neuroaction feedback?:roll: :?:

[Diane]

"what is the muscular neurosignature generating pain? " The armpit/axilla has many sensitive structures within it, lots of "tubing", a sympathetic supply that is different from that of the leg (I'll dig up the stuff I've been reading about that, to post here later) and no "pelvis" to restrict its motion. Nearby is the heart, and a lot of primitive embryology (branchial arch or 'gill' material) that has turned into throat and vascular structure, like the arch of the aorta and the subclavian arteries. Plus some of the UNmyelinated sympathetic fibres travel through the sternomastoid muscle. Any movement of the shoulder will tilt the clavicle will affect SCM...

So...perhaps some prehistorical "action neuromodule" takes over to inhibit movment by producing pain, because of some perceived threat to tissue in the armpit or under the clavicle. And it rights itself eventually by ceasing to worry about it/learning to move 'around' it.

(This is, of course, just wild, free form clinical speculation of the most un-verified and creative sort!)
:wink:
Diane

[bernard]

I must add this one to the evidences given by Cory.

The role of the serotonergic and noradrenergic neurotransmitter systems in the treatment of psychological and physical symptoms of depression (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=14552653)

[BB]

Thanks for the clarification bernard, that helped me a lot. And thanks for the embryology and neural circuitry Diane.

Let me add more from Daniel Amen's book "Change your brain, change your life"
The only time he mentions chronic pain is in discussion of the cingulate gyrus, which he lumps in with the prefrontal cortex.

He talks about the cingulate gyrus, when imbalanced, causes "getting stuck on ideas." He says that it makes it hard for the brain to move on from an idea.

He then states that the prefrontal cortex regulates the basal ganglia, and when the cortex is not functioning properly the basal ganglia imbalances (which we have already discussed earlier) occur.

This is interesting for application to chronic pain,
-The anxiety neurosignature from is present from the basal ganglia
- A stressor occurs causing further increase in anxiety and the closed loop circuit is in process (bernard?)
- Pain results
- The person is fixated on (stuck on the idea of) thier pain because of the effect, or lack thereof, from the cingulate gyrus (convergent circuit?)

Cory

[bernard]

Hi Cory,

Actually it is known that chronic pain does not activate the same neuromatrix than in acute one. In my view almost two circuits are involved in our situation?
A chronic one created with the imbalances and situations we said.
An acute one since at the beginning of movement, often, there is no or already some chronic pain and pain increases while moving!

Is it the cingulated gyrus, I do not know but we have to think deeply to the patterns that could create acute pain in chronic conditions?

[bernard]

Hi Somasimplers,

I tried some experiments on myself and the shoulders. I think, even if it is a single case, it brings some fine clues?
My right shoulder is still in pain => neurogenic!

The movement is simple => lift up and forward the two arms. No care of compensations!

1/ eyes closed, but I lifted them with trying to feel the same resistance (strength) left > right. (more than 50°)
2/ with awareness to movement, left > right but difference is < 20°.
3/ while thinking to something, result better than 1/ but <2
4/ while thinking to something stressful <3
5/ while thinking to pain in my shoulder <4
6/ adding speed to movement decreases in all cases the results and increases pain!

[bernard]

Hi Somasimplers,

I think that we missed a crucial term in the abstracts => delayed reponse.

It will be great if you'll try to focuss on this word?

[emad]

Hi Bernard and Cory ;'

I am trying to catch the discussion .

i think in chonic pain ,the brain (Cortex) changes are more than in the acute pain ,the map presentation changing is more .
cheers
emad

[BB]

Hi bernard and emad,

I'll have to be brief,

I look at delayed onset (I havn't looked back at the abstracts yet, but I'm assuming that you are talking about after activity and/or therapy sessions) as 2 possibilities, although I'm sure there are lots more.

1- do they still have the improved movement only soreness with it? I tell them this could be appropriate workout-like soreness. And try to help them become more aware of the quality of the sensation, ie. is it "muscular type" pain or is the deep aching pain that you had been getting?

2- did they go home and the movement regressed and the pain increased? I think often the anxiety and other emotional involvements are enough entrenched that the fear of the pain returning might in fact help it to return.

Those are my quick thoughts.

Cory

[bernard]

Hi Cory,

I must admit that I did not think to your explanations that makes sense to me.

3/ delayed onset is delayed because speed of transmission is decreased by anxious neurosignature.

4/ delayed response crosses a longer way before acting, another neurosignature.

[bernard]

Hi Cory,

I must confess that I missed your point of view in a first lecture. My delayed response was the one during the tests in the abstracts. And the reply of my precedent post may be totally irrelevant to your.

If in a painful state the movement starts later I was saying that a possibility is the action neuromodule is perhaps longer (number of neurons activated) or another possibility is that neumodule is less active (by neurotransmitters) then the same program is delayed?

[emad]

Sorry Bernard :

i have lost the topic.

what do you mean exactly , by delayed response .


cheers
emad

[bernard]

Emad,

In painful conditions, the muscle response come a bit later than in normal condition => there is a delay.

[BB]

Hi Bernard,

Sorry for my own "delayed response" to your post!

I think you are right that my thought #1 was on something different than you were talking about...
But thought 2 I would like to discuss...

It seems to me that often when I see people in pain who are demonstrating fear and anxiety about their pain, one of their first statements is always "sure it feels good now, but when I go home it is probably going to hurt even worse because I have used it." And, often it does.

I think maybe the fear and anxiety about the return of pain may trigger some of the imbalance mechanisms that we have been discussing. Also, I think the "virtual self "discussion is very relevent here. If they are "seeing" thenselves in pain maybe that is what the output becomes? The result then is delayed pain onset.

Cory

[BB]

Bernard,
Well stated!
I find often that patients have a hard time totally accepting what I am teaching them about controlling their own pain. Then, after a couple of sessions it becomes more clear when they ask, "why aren't you using the ultrasound like my friends have told me they received in physical therapy?"

I now tell patients right away if I get the sense of the "fix me" attitude, that I intend to be a guide to help them fix themselves and the "gadgets" aren't available to them at home. They need to be able to help themselves when we are not around.

Cory

[nari]

I am sure we all get many patients who have expectations of what we do; due to various factors, they can be 'won' over, but still expect the hands-on and the machines. That is largely because that is all they have had in the past on their many visits to physiotherapists.
This expectation of passive treatment ("you fix me" is the silent message) is a problem for me but I can usually strike a deal - ten minutes of hands-on, and the rest is up to them.
When they come back and say they did not have time to do their 'homework', I stress that it is essential. Seeing me every ten to fourteen days will not be as useful nor as long lasting compared with what they can do.


Nari

[Diane]

"they come back and say they did not have time to do their 'homework', I stress that it is essential. Seeing me every ten to fourteen days will not be as useful nor as long lasting compared with what they can do."

Agree totally Nari. In fact I tell people they have to be their own therapist between visits, just a few minutes or seconds even, hourly, so that their body gets the attention it requires. And that it's a wise investment of time, since they are the ones living in that body 24/7.. I use mild humor and kidding to get them to realize it's their body, not 'mine' somehow, that I have my own to look after, thanks... Make them take back ownership of their tissue/issues.

It is interesting to watch them as they actually "get" what I mean, and go,....oh...yes, I see what you're saying..

Really, I feel that a large portion of my day is spent if not overtly teaching at least modeling to people how to live in, work in, and most importantly relate to, their own body. I use metaphors a lot, body as ecosytem, body as city, etc., body as animal, a large friendly loyal animal that we get to live within for our whole life, that can read us so well that it relates to us usually perfectly, but sometimes we don't learn to relate to IT, we boss it around or just take it completely for granted (and back that up by discussing different parts of the brain and how they can get out of synch with each other..)

There are different spinoffs from that story lead-in, like, "often people would never dream of abusing their dog, but yet they'll drive their bodies to exhaustion with no warmup, no rest breaks..", or, "if your dog caused you grief with its behavior, would you not devote some regularly spaced contact time with it to help it learn new manners?"..etc..

Teaching people how to be kind to themselves rather than uneven, (overindulging then cruel) is a large part of my day. I like to think that my hands-on work gets this message to them in all the non-verbal ways too.

Diane

[Green Hornet]

Cory, you wrote:
I think maybe the fear and anxiety about the return of pain may trigger some of the imbalance mechanisms that we have been discussing. Also, I think the "virtual self "discussion is very relevent here. If they are "seeing" themselves in pain maybe that is what the output becomes? The result then is delayed pain onset.

I agree on that. and I am taking David Butler's course this weekend -- He is in Seattle! He mentions that any physical, emotional, and spiritual threats (including anxiety and fear) create changes in cellular level in the neuron, which generates sensitized and adrenal-activated receptors. So, we get easily pain-cycle activated. The changes happen in our neuromatrix!

So, now education comes into such a very important role that patients feel comfortable with what they do and with their own pain-management.

He said that he spends so much time on education about pain mechanism, before he introduces movement therapies to his patients. They will know why they are in pain and self management strategies they learn from PT make sense to them. Knowing the pain mechanism, they can increase their confidence level and decrease anxiety and fear.

Manual therapists like to put hands-on. But, we sometimes can make a mistake by focusing too much on making patients feel better without educating about reasoning behind behavior. We seem to have to maintain a good balance between hands-on and hands-in (first person learning).

[Green Hornet]

Another comment:

Japanese used to have an excellent body-mind culture. Up to 200 years ago, almost every Japanese are an expert in the area. Connecting with their own mind and body was a part of daily routine, as the word "culture" represents. They all could know how to reach their inner self and seldom had to rely on others for "fixing" (unless they have a huge medical problem).

Connecting with self is a key to become independent in rehabilitation, health, and wellness. It requires an effort and sometimes hard-work, but reward is big. People want to have an easy fix, because it is easy and passive and it make them feel they don't have to take responsibility for their health.

[nari]

Takao,

Precisely! Which is why I became a more hands-off PT over the last year or so. I have not touched interferential for years, primarily because I do not understand how or why it works (if it works...sorry Bernard).

Exercises, as they are listed on endless sheets, are minimally useful, because each patient (particularly the persistent pain people) is individual.
I do heaps of drawings to explain the movements I want them to do.

I can appreciate Diane's hands-on, though, because that can establish the intrapersonal relationships she mentions.

I think the Eastern cultures and attitudes to health and wellbeing are something the West needs to take very serious note of. Unfortunately, with the impact of the West, these may gradually be lost - unless Western medicine sees the light before then.

Nari

[BB]

I think that maybe the common theme between effective treatment, hands on and hands off, is that the person needs to become more actively in control of their situation.

For myself it tends to be more hands off as I have not developed the skills needed to guide and educate with my hands as Diane has. But I think that as long as the awareness of the movement is increasing, and active learning is occurring, the hands on approach is great as is evidenced by Diane's great results.

I also agree that sheets of exercises are rarely useful. (I use alot of hand drawings too Nari! My stick figure art gallery) Every persons movement patterns are like a finger print and different to that individual, although identifyable patterns exist that are similar from person to person.

Takao,
I tried to get into the seattle course but it sold out too quickly! I am going to take the portland course instead, but unfortunately it won't be taught by David Butler (one of his colleagues instead).

Cory

[nari]

Cory

Hope you can get to Portland to do the course. David actually keeps you wide awake even after 6 hours per day of cognitive slog!!!

It changed my entire perspective on our role in physiotherapy, but that started in 1991, with his first course (Adverse Mechanical Tension) and the course has changed greatly since then, after Wall and Melzack had done heaps more research.


Nari

[Green Hornet]

Cory,
Bob Nee is probably the one who teaches the Portland course (when do you go to the course?). He assisted this Butler's course in Seattle and he is excellent, too. You will enjoy it. He is one of the faculties at Pacific University in Forest Grove, Oregon and teaches there.

Yes, this course has deepened my perspective of pain and would help me understand much better what is going on under the patient's skin.

I think that David will come back to the US in October (in New York) to teach Level II course " Explain Pain." He just finished two-month long trip (South Africa, Canada, and US) and headed back to Australia. He was a fun and excellent speaker. And his handling technique was wow and very elegant.

[bernard]

Well Somasimplers,

There is already Forum for Courses :idea: . It would be great if you put your announce in the good place? :wink: It is opened to formers and trainers and members too.