How to do Bobath? Part 5 The facilitation thing

 

Introduction

There has been a lot of discussion in the icsp threads (found here http://www.csp.org.uk/icsp/topics/rationale-evidence-bobath-neurological-physio and http://www.csp.org.uk/icsp/topics/novak-review-casts-doubt-efficacy-bobath-should-we-embrace-or-ignore-it ) from physios who use Bobath about: what Bobath is, or isn’t, what it aims to do, how and why. Fair to say, I think, that there is considerable uncertainty, despite the earlier posts about the definition of Bobath. So I have tried to collect together the relevant discussions and to chunk them into easily digestible pieces. I hope this makes sense and represents everyone reasonably. You can always go back to the original icsp thread to check it out. If I’ve messed up, I’m happy to be shown the error of my ways. Unfortunately I can’t directly attribute the discussion to the person posting (unless they have specifically said that I can) because that would fall foul of the terms and conditions of icsp and their copyright rules, so I have to summarise the contributions in my own words. I have tried to do this as openly and even-handedly as I can.

In this chunk some of the theoretical beliefs about how Bobath works are considered in the light of evidence. I’ve taken the Vaughan-Graham 2009 paper (Top Stroke Rehabil 2009;16(1):57–68) as a starting point. In the paper there are several statements specifying aspects of the Bobath Concept. I published that list before in the icsp thread a while ago. At the time it didn’t raise a lot of discussion. So I’ve grouped the statements into several sections and will consider how they compare with the evidence. Ive also added some relevant queries, stated beliefs and discussion from the icsp threads and drawn on the Bobath Concept book (pub 2009 – a most illuminating read). There is a sprinkling of references to back up my claims or I have recommended other reading (would hate to be accused of not justifying my claims!) These are by no means a comprehensive indication of the evidence, they are some examples.

 

Part 5. The Facilitation Thing 

The Bobath tutors say that facilitation is a key feature of BB and always has been. They make many statements about facilitation including that it:

  • involves the use of afferent information to effect improvements in motor performance
  • aims to provide appropriate afferent information approximating that usually experienced during performance of the motor task.
  • involves specific manipulation of afferent inputs inclusive of somatosensation, vision, vestibular, and auditory in order to bring motor systems to threshold.
  • enables the Bobath clinician to specify the sequences of movement and specific muscle activity that will produce efficient task performance.
  • is intended to enable the individual to have an experience of movement that is not passive but one that they cannot yet do alone
  • is used to enable successful movement and task performance with regard to aspects such as postural orientation, components of movement, functional sequences of movement, recognition of the task, and motivation to complete the task.

 Which sounds marvellous. Who wouldn’t want to use something that enables patients to move and do things in the way they did before they had their stroke? The problem is that there is no evidence that facilitation does enable patients to move and do things etc, etc, or any of the other things listed above. The limited evidence available suggests that it doesn’t have an effect on movement. The Lennon et al study showed that facilitation did not affect motor performance, movement sequences etc, etc. Hesse et al (Electroencephalogr Clin Neurophysiol 1998;109:515–22) looked at the effect of facilitation on gait in a one-off session, which showed that patients showed some minor changes in gait pattern while facilitated but any effect had worn off half an hour later.

So what little evidence there is, does not support the hypothesis/ belief that facilitation improves motor or task performance. There is no evidence that facilitation manipulates any type of afferent information, nor that manipulating afferent information affects motor performance in a functional way. Now you may well be thinking that the lack of evidence may just be because the research hasn’t been done (after all, lack of evidence isn’t evidence of lack of effect). But why isn’t there any evidence? The Bobath-ers have been using their concept for decades and claim to use objective outcome measures and to be active in research. So why has no evidence of the effect of their treatment ever been published? It wouldn’t even need to be high-powered trial evidence. Even a decent case series or two; detailed small N studies or some before and after reports would be a start. At least that would be something on the first couple of layers of the evidence pyramid. But no, nothing, zilch. Why?

Next blog is all about compensation

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23 thoughts on “How to do Bobath? Part 5 The facilitation thing

  1. Thank you SarahT for clarifying and bullet point listing statements from Bobath Tutors on Facilitation. I have duly made my comments to each bullet point on my own iCSP thread http://www.csp.org.uk/icsp/topics/bobath-research-why-there-none#comment-132556?utm_comment=253829
    In my last post to your blog I asked to be called Granny Jackie. I am now not sure whether I like the name! Would it be possible to change it again to either JackieW or JacquelineWright?
    Best Wishes Jackie

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  2. Hi Jose
    Here are my thoughts

    Both papers were produced by the Bobath Memorial Hospital in Japan and used near Infra-red spectroscopy (NIRS) to measure cerebral blood oxygenation (an increase in oxygenation levels is assumed to indicate increased brain activity) while walking. In the 1st study they recruited 6 young (mean age 57 years) sub-acute stroke survivors with a severe stroke, who were unable to walk in every-day life. They measured NIRS, step frequency (cadence) and swing time symmetry while patients walked on a bodyweight supported treadmill. They walked for 2 mins, divided in to 4x 30 seconds spent walking (with 30s rest in between). During two of the walking phases the participants’ gait was also facilitated at the pelvis and for the other two walks their weak foot or thigh was “held by the therapist to help swing in the swing phase and to ensure stable stand phase”. For an inexplicable reason, they called this mechanical assistance but it sounds very much like facilitation to me.

    They found that the medial sensorimotor cortex, primary, supplementary and pre-supplementary motor areas are activated during hemiplegic gait in patients with severe stroke – as found in healthy patients but the activation was more asymmetrical than healthys. So no real surprise there. They also reported found that the activation levels were higher during the BWSTT+ pelvis facilitation than during BWSTT+Leg facilitation during the 30s that the participant was walking. What does it tell us? Not much. It shows the cortical activation while walking with BWSTT + facilitation for a very short period – much as one would expect. It doesn’t tell us anything about whether facilitation has any effect, or not To test this, one would have to compare with walking while facilitated with walking without facilitation or BWSTT for a feasible period (ie longer than 30s). There may be some limited value of testing whether gait pattern is altered by facilitation while the ‘hands are on’ but in order to make any meaningful claim of a treatment effect then one would also need to demonstrate an enduring change once the facilitation was removed. The paper by Hesse et al (described in the Blog post on facilitation) showed that gait pattern reverted to pre-facilitation levels within half an hour.

    The 2nd paper is a congress abstract so it is very brief. The same team compared NIRS while walking in 6 children (aged 5-11) with 3 healthy children of a different age (9-11 years). This is not a meaningful comparator group; the control group needs to be age and sex matched to the CP group. The children walked for 30s under 3 conditions. Condition 2 was walking while swing phase was facilitated. We don’t know what the other two conditions were. They found no change in cortical activation in the healthy children (which one would expect- the technique didn’t work). In the children with CP, cortical activation was increased during the 1st task and reduced during the 2nd and 3rd. But we don’t know what the 1st and 3rd tasks were. What does this tell us? Nothing really.

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    1. Hi Sarah and Jose.
      The Ichiro Miyai et al paper on restoration of gait sounds very useful. It is interested that the activation levels were higher during BWSTT+ pelvis facilitation than during BWSTT+ leg facilitation.
      Thank you Sarah for summarising the paper. I tried to download the whole article but found I was restricted because I have never had a paper published. I agree with you that “facilitation” is better wording than “mechanical assistance”.
      Using my personal understanding of “compensatory trunk stability” I would hypothesise that the therapist’s hands on the pelvis were facilitating normal weight bearing through the stance leg and were also preventing asymmetrical compensatory trunk stability.
      I do not find Hesse et all’s paper on gait pattern surprising. I too have found that “carry over” is often poor with many patients. I believe it is fear of falling that prevents patients from selecting a non compensatory gait.
      Re Facilitation and learning new movements plasticity etc, I find that most of the practice learning etc occurs between physiotherapy sessions and not during the session. Thus “carry over” is much better when the patient is motivated to practice on his own.
      Best wishes
      Jackie

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      1. Jackie
        Sorry you can’t access the paper, I don’t think I can post it on the blog because of the copyright limitations. I wouldn’t read anything into the differences found in the paper tbh. The sample size is sooo small that many would consider an attempt at statistical comparison meaningless. I was always taught that no statistician worth his/ her salt would get out of bed for less than 10 subjects.
        Another point occurred to me after I had posted yesterday ….. If, as the Bobath’s tutors claim, facilitation manipulates specific afferent/ sensory inputs, then one would expect activity in the sensory cortical areas. But that doesn’t appear to occur …….

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  3. Sarah
    Are you suggesting there should be more sensory cortical activity with hemiplegic patients than with normal healthy subjects not receiving physiotherapy handling?
    If so I disagree. Does not the “Placing” handling/assessing technique as described by Berta Bobath (1990) facilitate normal postural reflex mechanisms? Are not these postural reflexes situated in the lower areas of the CNS such as the spinal cord, cerebellum and basal ganglia?
    My observation with hemiplegic patients is that sensory awareness is not essential to the process of facilitating normal postural reflexes.
    Best wishes Jackie

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  4. Hi Jackie
    I’m saying that if facilitation has its affect (if there is one) by manipulating sensory inputs and some how this improves neuroplasticity and motor learning (the stated underlying mechanism of the Bobath effect), then one would expect to see signs of the brain processing that sensory manipulation and integrating it into their motor activity. But activity in the sensory areas isn’t reported in the above paper. As I’ve said, provide very low level evidence (many would classify it as (pre)-pilot testing) in a very small non-representative sample so I wouldn’t read much in to the results one way or another. But the results such as they are aren’t supporting the idea that facilitation manipulates sensory inputs, and it is the only study (as far as I know) that has attempted to consider the effects of facilitation on neural activity.

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    1. I agree with you Sarah one would expect to see some sort of activity in the sensory cortex where the physiological process entails neuroplasticity and learning. But the physiological processes I am talking about is about sensory stimulus and reflex response. By supplying the correct environment the patient is then subjected to the appropriate sensory stimuli which accordingly activates the appropriate motor response.
      Yes I agree with you that stroke rehabilitation is mainly about neuroplasticity and learning. But could not this physiological activity be occurring between physiotherapy sessions than during a physiotherapy session?
      By the way do you know who first coined the phrase “Sensory Manipulation”? I don’t think Berta Bobath used this phrase.
      Best wishes Jackie

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  5. I agree with you Sarah one would expect to see some sort of activity in the sensory cortex where the physiological process entails neuroplasticity and learning. But the physiological processes I am talking about is about sensory stimulus and reflex response. By supplying the correct environment the patient is then subjected to the appropriate sensory stimuli which accordingly activates the appropriate motor response.
    Yes I agree with you that stroke rehabilitation is mainly about neuroplasticity and learning. But could not this physiological activity be occurring between physiotherapy sessions than during a physiotherapy session?
    By the way do you know who first coined the phrase “Sensory Manipulation”? I don’t think Berta Bobath used this phrase.
    Best wishes Jackie

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  6. Thank you Sarah. This has been a fascinating series to read. I used to be involved in teaching neurological physiotherapy but in recent years have moved onto other things. I find it both disheartening and also most interesting that such “schools of thought” as the Bobath Method still has so much popularity amongst physios.

    My disheartening is when I reflect on the enormous amount of clinical research that has happened over the last two decades; the enormous amount of evidence now for task based approaches and growing evidence for other approaches such as targeted strengthening to name but one; the more-or-less complete failure of trials investigating BB to show benefit. Yet a huge body of therapists just don’t get it and continue to flog a dead horse. And that old tired line of well “we have changed – we truly have and we now incorporate all that is new” while doing basically the same old stuff.

    My interest is more in the sociology that we still seem to be a profession that is prone to cults rather than applied science. When I trained back when pterodactyls were still flying around we students watched as this massive fight between the PNF and Bobath adherents tried win over hearts and minds.

    Not long after that in the 80’s Roberta Shepherd and Janet Carr injected true scientific scepticism into the profession and took a direct aim at the Bobath method in their crosshairs. They presented arguments based mainly on plausibility drawing from the movement sciences; clinical trials weren’t very common then and those that were done weren’t up to much. But that had an unintended effect. Far from assisting the majority of physiotherapists to move on it just created another skirmish and seemed to make the Bobath adherence dig in to their trenches deeper.

    Carr and Shepherd were right to do this but I am not sure that how they went about it helped matters. Cults tend to flourish on acrimony. Now I wonder if this is what still drives the Bobath crowd to carry on this way rather than paying attention to the literature.

    There can be a blurred line between recognising and paying respect to a leader in the profession who advances the development of the profession and a cult. And cults often get named after their leaders. Why are we still littered with names such as the McKenzie approach, the Bobath method, or the Maitland concept?

    Why don’t we just attach a simple label the that describes the function of an approach? When the evidence supports it use it. As the evidence develops, refines, or refutes the approach it is much easier to deconstruct it, or chuck it away rather than having to attack the persona and dogma of the guru.

    A lot of physiotherapy does do this but we haven’t shaken off the gurus and their cults.

    Liked by 1 person

  7. I so enjoyed these blogs! I am so not a bobath fan but I do find I am often in the minority where I work. I work in acute neuroscience unit and usually use a much more functional/impairment/participation approach but recently had a young patient and I felt doing this would be a disadvantage to him…. Now reading these blogs and I am so questioning my practice! Yikes! I need to have the courage of my convictions and stand up for what I (and I know others!) think and need to stop worrying about what my colleagues in the rehab and stroke units think of my practice and I need to challenge their approach! Will re read these blogs and share! Thank you!

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  8. Thanks for your thoughts Zack and JB
    I agree Zack, life would be much easier and more effective if the cults and named approaches were done away with, but a lot of people have invested time, effort, finances and reputation on the named approaches and have gained status and often comfortable living from following and promoting the named approaches so there are many vested interests in keeping them going, which doesn’t make it right but does explain why it happens despite its illogicality.
    The amount of acrimony around how to deliver effective physio has always been something of a mystery to me. This isn’t restricted to neuro physios, it is very prevalent in MSK and sports physio too. And I’ve observed the same sort of weeping and wailing, passive aggression (sometimes not so passive) and tantrums in other AHPs too, when their comfort zones are challenged. I think an important element is that many do not understand the difference between disagreeing and arguing. It is quite possible to do the former without the latter. It isn’t a personal attack or professional practice to hold a different view and express it (further thoughts in the post on EBP and professionalism), but many take it as such. I think it’s something about the maturity of the profession tbh.
    JB, thanks you I’m glad you’re enjoying them. The feedback has been very heartening and it is amazing how many and how far they have reached. There might be something to this social media business after all!
    You describe a common dilemma, and it is a difficult one. At the end of the day most people want an easy, harmonious life and to get on with their colleagues so it is easiest to go with the flow. In the original icsp discussions that were the pre-cursors to this blog some contributors did so anonymously, I suspect for similar reasons to the ones you raise. It is hard work swim against the tide, but if enough folk swim for long enough, others will join and the tide will turn. There has already been massive changes in the last few years; this blog and icsp discussions just would not have happened a few years ago. So keep going and stand by your convictions and the evidence!
    I’m intrigued about why you felt your young patient might be disadvantaged by an EB approach.

    Liked by 1 person

  9. I like your title Sarah for this Part 5 “The Facilitation Thing”. I do believe that “Facilitation” is the key word where there is most disagreement amongst all Neuro Physiotherapists. How can one facilitate normal postural reflex re-actions where spasticity is present?
    Berta Bobath (1990) in her third edition of Adult Hemiplegia page 24 talks about Facilitating and assessing normal non compensatory movement. She calls this movement “Potential”. A patient has the ability to move normally in certain situations but instead chooses to select compensatory movement. But where the desired function is abnormal or very difficult to perform, Berta Bobath talks about spasticity and release of tonic reflex activity. On page 61 Berta Bobath (1990) states that “The patient has to learn to control actively the widespread total patterns of spasticity.”
    But what is Spasticity? How can Neuro physiotherapists teach their patients to control it when we don’t even know its true nature?
    My hypothetical theories “Compensatory Fascial Stability” and “Low Threshold to Sensory Input” I do believe go a long way to explaining these unanswered questions on the true nature of Spasticity. Sarah in previous correspondence you have challenged me to start my own research. This I do not feel I can do alone. I would dearly like someone to help me.
    I apologise Sarah for using your blog to advertise my plea. But I really do believe that stroke patients today have the potential to make far better recoveries.

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    1. Hi Jackie
      Good to hear from you and pleased the blog is being used to promote discussion. Be my guest!
      There seems to be some parallels with your ‘low threshold to sensory input’ and the BB tutors current explanation for what they do – manipulating sensory inputs which they say facilitates more normal movement. Not sure about whether/how the fascial contractions fit in. But the BB tutors have a website http://www.bbta.org.uk/ (and blog type thing that appears as the ‘news’ section). Perhaps they could help with your ideas
      Sarah

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  10. Thank you Sarah for your kind reply and suggestion that I use the BBTA blog.
    You state that you are not sure about whether/how the fascial contractions fit into BB understanding on “Facilitation”. As you use the word “contractions” rather than “contractures”, I assume you are having difficulty with the idea that fascia has a contractile ability.
    In spite of the work of Robert Schleip (2007) on fascia contract-ability, I too believe that the main feature of fascia is its connect-ability and not its contract-ability. I base my understanding of fascial connectedness on Thomas Myers (2001) “Myofascial Meridians”. I do believe these myofascial lines of strain go a long way to explain propriorceptive neuromuscular facilitation (PNF) and patterns of movement, developed by Kabat and Knott and expanded by Voss (Voss et al 1985). The patterns of movement are thus predetermined by fascial lines of strain rather than by higher centre neuronal firing.
    Refs
    Schleip R1, Klingler W, Lehmann-Horn F (2005) “Active fascial contractility: Fascia may be able to contract in a smooth muscle-like manner and thereby influence musculoskeletal dynamics.” Med Hypotheses. 2005;65(2):273-7. http://www.ncbi.nlm.nih.gov/pubmed/15922099
    Myers Thomas W (2001) Anatomy Trains Myofascial Meridians for Manual and Movement Therapists, Churchill Livingstone
    Voss D, Ionata M, Myers B. (1985) “Propriorceptive neuromuscular facilitation patterns and techniques. 3rd ed. Philadelphia: Harper & Row.

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    1. Hi Jackie

      My use of the term ‘contraction’ rather than ‘contractures’ was inadvertent. I’m afraid I hadn’t consciously made a distinction. It a long way back to my 1st year anatomy classes but from what I recall fascia is just collagenous connective tissue that can stretch and recoil but mainly resists strain but doesn’t contract. I don’t think there is anything within fascia that can contract, is there? If so, what? how?

      I also can’t claim any great expertise in PNF, although I find the techniques useful sometimes. However I thought the movement patterns were based on muscle synergies. Possible the muscle fascia has some influence on those movements but I can’t imagine that they are of any significance compared to the influence of joint shape, ligaments and muscles/ tendon.

      I’m afraid I haven’t come across the idea of myofascial meridians (whatever they are) and can’t see how fascia could influence movement. It is muscles that produce movement and nothing else, and the muscles are controlled by the nervous system. Are you saying that muscle activity is controlled by the fascial rather than the nervous system? Really? I’m afraid I’m not buying this idea at all .

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  11. Hi Sarah
    Thank you for your reply. I gather that, from what I have written, I have made a seriously careless mistake.
    In my eagerness to share my understanding of “inhibition/facilitation” at spinal cord level I have completely omitted to describe my theoretical understanding of the fascial stretch reflex.
    Biedert et al (1992) examined the distribution of free nerve endings in the soft tissue of the knee joint. They found that there was a greater distribution in the fascia surrounding the Vastus Medialis Muscle. From these observations I hypothesise that it could be possible for Thomas Myers’ myofascial lines/trains/meridians of force to be activated by the fascial stretch reflex, located at spinal cord level.
    Refs
    BIEDERT, R.M., STAUFFER, E., FRIEDERICH, N.F. (1992); Occurrence of free nerve endings in the soft tissue of the knee joint. Am J Sports Med 20 No.4: 430-433 1992
    Myers Thomas W (2001) Anatomy Trains Myofascial Meridians for Manual and Movement Therapists, Churchill Livingstone

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    1. But free nerve endings are sensory nerves. Its not a great surprise that fascia has a sensory nerve supply. But it doesn’t explain how fascia can contract or have a stretch reflex. There is nothing to contract.

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  12. Yes it is muscles that contract and not fascia. The main properties of fascia is its ability to connect different muscles and different tissues, and its ability to store energy. Thus a line of muscles can be connected together through the fascia surrounding them and through them.
    By fascia’s ability to be pre-stressed, a stretch at any one point in the line of taut fascia will activate all the muscles in the chain to fire. Thus alpha motor neurone firing will be activated by the type 1V free sensory nerve endings situated in the fascia surrounding the relevant muscle bellies; and firing will not be activated by higher centre motor activity.

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    1. Ahh, OK. That makes more sense. But is there any evidence that the free nerve endings in the fascia connect to anterior horn cells/ alpha motor neurones to influence the stretch reflex? Or that it happens independent of the higher centres? My understanding is that any muscle activity has some higher centre input. After all we don’t move by reflex actions in every-day life, it is always modulated.

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  13. The exact part that Type IV free nerve ending neurons play in the stretch reflex and what exact part the muscle spindle plays, I hesitate to begin to explain; but as the muscle spindle sensory neuron axon is larger in diameter than the type IV sensory neuron axon, conduction speed will be faster in the muscle spindle afferent. So it is more likely that the stretch reflex is initiated from the muscle spindle, than from the type IV free nerve endings.
    As to the number of synapses in a spinal reflex and to whether the synaptic modulations are initiated from the higher centres or from the peripheral sensory organs, I again hesitate to explain.
    I do however work on the theories of Magnus(1926), Melzack and Wall (1965) that synaptic connections are gated and pre-set to whether they are open or closed; and that this gating control can either come from the higher centres or from peripheral sensory organs.
    Thus the nature of spinal reflex motor output (flexor pattern or extensor pattern) will be largely predetermined by the postural set and limb position.
    An example of whether we first move into a flexor pattern of mobility or extensor pattern of mobility can perhaps be illustrated by what position we sit in a chair. If we are slouched and flexed at the lumbar spine our reaction to a loud frightening noise will be to flex further and protect our abdomen. But if we are alert and have an extended back our first reaction will be to jump out of the chair or just throw our arms into the air.
    Refs
    Magnus R (1926) “Some results of studies in physiology of Posture” Lancet ii, 531-6, 585-8
    Melzack R, Wall PD (1965) “Pain mechanisms: a new theory”, Science. 1965;150 (3699):971–9

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  14. Hello again Sarah
    From re-reading our dialogue on the nature of fascia, I see some clarification is needed. I thus make the following points.
    1. “Fascia is a collagenous connective tissue that can stretch and recoil but mainly resists strain but doesn’t contract.” I agree with this statement of yours.
    2. Because Fascia has this tensile ability to stretch and recoil, it also has the ability, together with bone to create structural stable tensegrity shapes, with the compressional forces of bone counteracting the tensile forces of fascia.
    3. Whereas the selection or the making of the tensegrity structural shapes may well be neuro-muscular in nature, the maintenance of the stable structure is not. The energy forces used here are the natural compressional forces of bone and tensile forces of fascia.
    4. This understanding of tensegrity stability is based on the work of Donald Ingber (1998), Kenneth Snelson and Buckminster Fuller.
    5. It is important to define the difference between energy forces that both creates and maintains a tensegrity structure/shape and the extra movement forces that create “rebound energy”.
    6. A tennis ball bouncing is a good illustration to explain how the combination of a tensegrity structure and an extra outside force creates bounce or elastic rebound. On impact after landing on the ground the outside rubber surface becomes distorted. This in turn creates greater internal air pressure pushing outwards. This rebound energy lifts the ball off the ground.
    7. The similarity between Thomas Myers mapped lined forces of fascial tension and PNF patterns of movement is that the energy forces released (rebound energy) can be channelled along Thomas Myers mapped lines of fascial tension. Thus efficient movement is both created by neuro muscular energy and fascial rebound energy

    Refs
    INGBER, D. (1998) The Architecture of Life. Scientific American. January 1998.

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