Diane
24-09-2006, 07:42 PM
I decided to start a thread here instead of under general discussion, because it involves Evidence in Motion (http://blog.evidenceinmotion.com/evidence/2006/09/marketing_and_t.html), which prides itself on being THE most evidence based interactive PT site on the planet just now, and the attempt of PT marketers to promote ATM2.
Currently under discussion is something called an ATM2 device, huge and looming, to which standing patients get strapped in various ways that have been ascertained to work well, whereby some of their parts (i.e., pelvis) are fixed while other parts (i.e., upper body) are left moveable. You can check out a little video (http://www.backproject.com/) on this, while photos of various clinicians who seem to want to be in on all the goodies that may rain down from its sale, by lending their combined weight to its marketing, are shown in an adjacent window. Curiously, Weiselfish, another mesodermalist of a different sort, is also there. Nice touch. The bone mesodermalists have usually been allergic to the fascia mesodermalists, even though neither camp speaks ectodermese, so you'd think they'd be allies.. so maybe this is showing that they finally are. Becoming allies I mean.
The discussion was begun by Jason, who responded to the manner in which the device was being pushed onto... I mean, introduced to the rehab world. The lack of actual evidence in its favor, and lack of underlying concept, was noted; the various flimsy, promotive, and transparent marketing strategies were analyzed.
Here is a quote from an Aussie researcher who is working on this, bolds mine:
The ATM2 has taken a bit of a battering in this discussion. While I am not prepared to comment on the marketing of the ATM2 that started this discussion, I feel compelled as a physiotherapist (PT) and academic to provide some input into this discussion. Wearing many ‘hats’ – a clinician, an academic, a sceptic of ‘new’ devices, but also possessing an open mind that says to me – just because I do not know or understand how something works doesn’t mean that it doesn’t work. While I am firmly entrenched in the world of evidence-based practice with clinical reasoning forming the basis of teaching and clinical practice, I must also be forward thinking about ‘how can I contribute to the future of the clinical professions’ by my clinical practice, knowledge and preparedness for participation in research. My introduction to the ATM2 was not in clinical practice, but a series of single-case research designs that followed the clinical guidelines for use of the unit in cooperation with a colleague (Max Zusman) who has an interest in the neurophysiology of pain. Yes, I agree that a series of single-case research designs are not an RCT and do not provide robust cause and effect relationships, nor explore the theoretical concepts behind clinical practice, but the results were encouraging from a clinical perspective to encourage more research. That led to a pilot study in a group of young active sports people with chronic movement related back pain in which we investigated changes in muscle activation patterns during a controlled perturbation to the trunk before, immediately after, and then following a time-course of interventions (along with a control group). This is being prepared for submission to a peer-reviewed journal. Our study cannot answer all the questions that this discussion has posed but to have seen abdominal/trunk muscle activation patterns change closer to, or before, the onset of the perturbation, has provided support for the use of the ATM2 in changing muscle activations with respect to anticipatory postural adjustments. Concurrently, the subjects all self-reported decreased pain into their previously painful movement pattern and on video (no - not 3D kinematics, unfortunately) appeared to have an increased ROM and maintained that on follow-up. This of course poses another set of questions related to issues that may be captured within areas of ‘fear avoidance beliefs’ inherent within the biopsychosocial model of low back pain. So while each of us can propose concepts as to how the use of the ATM2 may or may not work, which may all vary based on our own ‘belief’ and knowledge systems, the use in a clinical and research setting encourages me to find out more.
I am also conscious, perhaps a little embarrassed but also encouraged that the winners of the 2005 Nobel Prize for Medicine were not able to pursue their belief in their research here in Australia back in the 1980’s; found it extremely difficult to get their ‘discovery’ published; and their claim was almost considered heresy in the 1980’s but set the example by going ahead and providing the evidence. I am prepared to accept the clinical and research results I see, while investigating ways in which to provide the evidence for the concept of its use that may encompass mechanical, neurophysiological, motor control and neurobehavioural domains of pain. From concepts, we can develop theories from which hypotheses can drive research.
Prof. Peter Hamer,
DipPT, BPE(Hons), MEd, PhD, FASMF
The University of Notre Dame Australia
Hmmnn. Correct me if I'm wrong, but does not the good doctor contradict himself in his own post? I mean, the last sentence sounds good, but he just wrote a whole post rationalizing why he didn't do exactly that. Shouldn't the concepts come before the research? Is this not a backwards way to do science? Is it just me?
My pet theory about this, about how it "works", based on everything I know, is that the belts are providing dermoneuromodulation while the patient is encouraged to move at the same time. They've got the skin pulled one way in the upper pelvis and the other way in the lower pelvis, pulling the long cutaneous nerves, iliohypogastric and lateral cutaneous, etc, into different directions relative to one another in addition to immobilizing the pelvis. But note that it isn't just immobilizing the mesoderm that is important; it's the direction in which the belts are pulled or ratcheted, relative to each other.
What are they pulling on? Skin obviously, through clothing.. What happens when they get the patient to bend forward? Neurodynamics of cutaneous nerves. What happens to pain if you move nerves? They get fed and watered, less hypoxic, and less nocioceptive. What happens when nerves are sending less nocioception up? The brain's level of perceived threat decreases and motor output increases. Hello, do we need some huge machine to do this? Hm, I doubt it. I can do that with my hands, move skin relative to mesoderm, with or without the patient moving, and they'll move better after.
The ONLY possible use I can imagine for a contraption like this is to do more Balnibarian research with it. I'm so glad Cory is building his Unified Theory thread (http://www.somasimple.com/forums/showthread.php?t=2823). It's like scaffolding for building a new cognitive reality for PT, not the cognitive hemi-neglect we currently ..um, enjoy. :rolleyes:
Currently under discussion is something called an ATM2 device, huge and looming, to which standing patients get strapped in various ways that have been ascertained to work well, whereby some of their parts (i.e., pelvis) are fixed while other parts (i.e., upper body) are left moveable. You can check out a little video (http://www.backproject.com/) on this, while photos of various clinicians who seem to want to be in on all the goodies that may rain down from its sale, by lending their combined weight to its marketing, are shown in an adjacent window. Curiously, Weiselfish, another mesodermalist of a different sort, is also there. Nice touch. The bone mesodermalists have usually been allergic to the fascia mesodermalists, even though neither camp speaks ectodermese, so you'd think they'd be allies.. so maybe this is showing that they finally are. Becoming allies I mean.
The discussion was begun by Jason, who responded to the manner in which the device was being pushed onto... I mean, introduced to the rehab world. The lack of actual evidence in its favor, and lack of underlying concept, was noted; the various flimsy, promotive, and transparent marketing strategies were analyzed.
Here is a quote from an Aussie researcher who is working on this, bolds mine:
The ATM2 has taken a bit of a battering in this discussion. While I am not prepared to comment on the marketing of the ATM2 that started this discussion, I feel compelled as a physiotherapist (PT) and academic to provide some input into this discussion. Wearing many ‘hats’ – a clinician, an academic, a sceptic of ‘new’ devices, but also possessing an open mind that says to me – just because I do not know or understand how something works doesn’t mean that it doesn’t work. While I am firmly entrenched in the world of evidence-based practice with clinical reasoning forming the basis of teaching and clinical practice, I must also be forward thinking about ‘how can I contribute to the future of the clinical professions’ by my clinical practice, knowledge and preparedness for participation in research. My introduction to the ATM2 was not in clinical practice, but a series of single-case research designs that followed the clinical guidelines for use of the unit in cooperation with a colleague (Max Zusman) who has an interest in the neurophysiology of pain. Yes, I agree that a series of single-case research designs are not an RCT and do not provide robust cause and effect relationships, nor explore the theoretical concepts behind clinical practice, but the results were encouraging from a clinical perspective to encourage more research. That led to a pilot study in a group of young active sports people with chronic movement related back pain in which we investigated changes in muscle activation patterns during a controlled perturbation to the trunk before, immediately after, and then following a time-course of interventions (along with a control group). This is being prepared for submission to a peer-reviewed journal. Our study cannot answer all the questions that this discussion has posed but to have seen abdominal/trunk muscle activation patterns change closer to, or before, the onset of the perturbation, has provided support for the use of the ATM2 in changing muscle activations with respect to anticipatory postural adjustments. Concurrently, the subjects all self-reported decreased pain into their previously painful movement pattern and on video (no - not 3D kinematics, unfortunately) appeared to have an increased ROM and maintained that on follow-up. This of course poses another set of questions related to issues that may be captured within areas of ‘fear avoidance beliefs’ inherent within the biopsychosocial model of low back pain. So while each of us can propose concepts as to how the use of the ATM2 may or may not work, which may all vary based on our own ‘belief’ and knowledge systems, the use in a clinical and research setting encourages me to find out more.
I am also conscious, perhaps a little embarrassed but also encouraged that the winners of the 2005 Nobel Prize for Medicine were not able to pursue their belief in their research here in Australia back in the 1980’s; found it extremely difficult to get their ‘discovery’ published; and their claim was almost considered heresy in the 1980’s but set the example by going ahead and providing the evidence. I am prepared to accept the clinical and research results I see, while investigating ways in which to provide the evidence for the concept of its use that may encompass mechanical, neurophysiological, motor control and neurobehavioural domains of pain. From concepts, we can develop theories from which hypotheses can drive research.
Prof. Peter Hamer,
DipPT, BPE(Hons), MEd, PhD, FASMF
The University of Notre Dame Australia
Hmmnn. Correct me if I'm wrong, but does not the good doctor contradict himself in his own post? I mean, the last sentence sounds good, but he just wrote a whole post rationalizing why he didn't do exactly that. Shouldn't the concepts come before the research? Is this not a backwards way to do science? Is it just me?
My pet theory about this, about how it "works", based on everything I know, is that the belts are providing dermoneuromodulation while the patient is encouraged to move at the same time. They've got the skin pulled one way in the upper pelvis and the other way in the lower pelvis, pulling the long cutaneous nerves, iliohypogastric and lateral cutaneous, etc, into different directions relative to one another in addition to immobilizing the pelvis. But note that it isn't just immobilizing the mesoderm that is important; it's the direction in which the belts are pulled or ratcheted, relative to each other.
What are they pulling on? Skin obviously, through clothing.. What happens when they get the patient to bend forward? Neurodynamics of cutaneous nerves. What happens to pain if you move nerves? They get fed and watered, less hypoxic, and less nocioceptive. What happens when nerves are sending less nocioception up? The brain's level of perceived threat decreases and motor output increases. Hello, do we need some huge machine to do this? Hm, I doubt it. I can do that with my hands, move skin relative to mesoderm, with or without the patient moving, and they'll move better after.
The ONLY possible use I can imagine for a contraption like this is to do more Balnibarian research with it. I'm so glad Cory is building his Unified Theory thread (http://www.somasimple.com/forums/showthread.php?t=2823). It's like scaffolding for building a new cognitive reality for PT, not the cognitive hemi-neglect we currently ..um, enjoy. :rolleyes: