How to do Bobath? Part 6 Compensation, motor control and muscle activity

Introduction – the usual explanation and caveats – see previous posts.

NB Italics are direct quotes and BB = Bobath!

In the icsp a discussion, compensation has come up several times – about how much of a problem it is and whether it should be discouraged. There are mixed views. Jackie W feels the reason BB appears to be ineffective is because the trials have failed to measure compensation. She feels (I have paraphrased) that the essential element of BB is to find a way to get the patient to move without compensating.

Bobath tutors have contributed, saying how BB never involves preventing function. But then one way or another go on to contradict themselves by saying it is OK to prevent compensatory movement to achieve “a longer term functional outcome”. In the Bobath book, although stating that patients should be encouraged to practice functional tasks, this is with the caveat that practice functional tasks should only happen once the patient is able to do so withappropriate activity”.

Like the book, the Vaughan-Graham et al paper makes many statements about what Bobath is, and isn’t. Here are some that relate to compensation and motor control; again I have paraphrased to keep the word count down (they can be a bit wordy)

  • Clinicians practicing BB facilitate task-specific patterns of muscle activation, minimize unnecessary compensatory movement strategies, and identify potential secondary impairments which enable tasks to be completed successfully.
  • Successful completion of tasks refers to doing a task in a certain way (normally/ with ‘quality’ movement) and indicators of this quality movement relate to efficiency, the muscle activity/ motor patterns used, speed, balance strategies, strength, endurance.
  • Compensations may prevent recovery or prevent function in the long term if they “become established”.
  • Improvements in task performance extend beyond practicing the task [presumably this refers to carry –over into functional improvements].

As ever, the statements and descriptions are presented alongside evidence about how motor control and sensory systems work, and how neuroplasticity and motor learning are promoted. But there is nothing actually connecting the evidence to Bobath. It generically applicable to any neurological physiotherapy, it is not specific to Bobath. There is no evidence that Bobath actually achieves the effects to claims, or uses the mechanisms the authors associate it with.

There is however considerable evidence that refutes the beliefs that BB appears to be based on, and the statements describing BB (above). So let’s have a look at that. Now this is easier said than done as the jargon used in BB is voluminous, ever-changing and largely undefined. It is difficult to pin down what is meant and what is done. The rest of the world has no idea what is meant by ‘selective movement’, ‘dynamic stability’, ‘arrested mobility’ or ’up against gravity’ [isn’t that just, up?]. The Bobath tutors don’t offer definitions and everyone uses terminology inconsistently. When the jargon is considered with a critical eye, much of it is pretty meaningless. It is often unclear whether folk are talking about different things, or if they are saying the same thing in a slight different way. This is probably a factor in the lack of consensus about Bobath and those famous misunderstandings about it. The excessive and inconsistent use of pseudo-scientific babble is one of the criticisms of Bobath that is most damaging to its credibility. Why not use plain English and the same clinical language as the rest of the physio world and our clinical colleagues?

Much of the discussion about compensations and motor control overlap with topics covered in the previous posts on ‘How to do Bobath’ so I won’t repeat them here. But here are a few key points. The available evidence shows:

  • facilitation does not improve quality of movement
  • Quality of movement is not directly related to function
  • Bobath practitioners focus on impairments at the expense of activity.
  • There is no automatic transfer / carry-over of the type of activities practiced in BB treatment sessions (abstract movements, practice of movement components > whole tasks, therapist- led with patients inactive, low repetition, excessive guidance, etc, etc) to sustained change after the session ends (or the hands are taken off). Ie any changes are merely practice effects, without carry-over into changes in function.
  • the types of activity used in BB treatment sessions are not those that are known to promote neuroplasticity and motor learning

What I would like to pick up here, is the statement that BB facilitates task-specific patterns of muscle activation. Because the notion of task-specific patterns of muscle activation is a misunderstanding of how motor control works. The BB tutors says that the systems model of motor control underpins the BB Concept, and there is quite a good explanation of the systems model in the BB book [Steady, headline writers, steady]. Essentially, the systems model explains how and why there are many different ways to achieve a task, and how the brain does not control movement by specifying the muscle activity needed to achieve a task, but by monitoring whether the task has been achieved. Even if the task is exactly the same, then people do not move in exactly the same way to achieve it every time (especially when they are (re)learning how to do the task). So there is no such thing as task-specific patterns of muscle activation. The whole point is that the muscle activation used to achieve a task is not specific, it is variable and able to adapt to changes in task, environment and the patients ability (by compensating). Adaptation/ compensation happen automatically to ensure the patient achieves the task safely, consistently and as easily as possible.

To give a simple example, the muscle activity and movement patterns used to walk changes all the time – depending where you walking (flat, hills uneven ground, around crowds etc), what shoes you are wearing (think about the differences between walking in flat or heeled shoes) or if there is an impairment. For example, if you get a stone in your shoe and it hurts, then your movement pattern and muscle activity automatically changes to reduce weight-bearing on the part that hurts. That adaptation/ compensation is a good thing. It enables you to achieve your task/ goals in a variable world with a variable body. That principle continues if the body becomes impaired, whether something minor like a stone in the shoe, or something major, like a stroke. The motor control system will automatically adapt to enable the patient to achieve their goals as well as they are able. If a patient is able to do something (eg walk), however they do it, is the best way they can.

So compensation is a good thing. It enables patients to continue to function even with impairments. Patients can function BECASE they compensate, not despite it.

I had better provide some evidence to support this assertion that compensation is not a bad thing…. In my first ever research project I looked at quality of movement of gait after stroke (and the effect of walking aids thereon). The results showed that asymmetry (the compensation/ impairment/ marker of poor quality movement du jour) was not related to gait function. Ie people with asymmetric gait were not less able to walk that those with a more symmetric gait. Some people were able to walk BECAUSE they used an asymmetric gait pattern, not despite it. These were not the results I was expecting (I was a bit of a Bobath groupie and aspiring tutor at the time! Yes, I too have “fabulous handling skills”). But these findings have been replicated many times since.

  • Tyson SF (1999) Trunk kinematics during hemiplegic gait and the effects of walking aids Clinical Rehabilitation 1999;13;295-300
  • Tyson SF (1994) Hemiplegic gait symmetry and walking aids. Physiotherapy Theory and Practice 1994;10;153-159
  • Tyson SF & Ashburn A (1994) The influence of walking aids on hemiplegic gait. Physiotherapy Theory and Practice 1994;10;77-86

There have also been some influential papers investigating changes over time as patients recover (or not). The examples below all investigate balance and mobility, but there is no reason to believe that the take home messages illustrated here don’t apply just as much to other areas of motor activity. Here are the references

  • de Haart et al. Recovery of standing balance in post-acute stroke patients; a rehabilitation cohort study. APMR 2004;85;886-95
  • Geurts et al. A review of standing balance recovery after stroke. Gait & Post 2005;22;2;267-281
  • Kirker et al. Changing patterns of postural hip muscle activity during recovery from stroke. Clin Rehab 2000;14(6):618-26
  • Kirker et al. Stepping before standing: hip muscle function in stepping and standing balance after stroke. JNNP 2000:68(4):458-64
  • Garland et al. Recovery off standing balance and functional mobility after stroke. APMR 2003;84;1753-1759

And this is a summary of what they tell us:

    • impairments improve with time & rehabilitation but show MUCH LESS improvement than disability/ function/ activity
    • Impairment (in the form of compensations) persists even in people who can function.
    • Some people function because of their compensations/ impairments
    • Recovery is not associated with changes in timing of muscle activity
    • Timing of motor activity does not become ‘more normal’ as the patient recovers function
    • The way in which patients changes with time & rehab is variable. Four different responses have been identified:

Group1 demonstrate increases function & more normal motor responses in the weak limb with time. Ie they become more normal. This is a relatively small proportion of stroke survivors with the mildest impairments. Many of whom would not usually get access to physio

Group 2 show increases in function & changes in motor responses of the weak limb(s) with time but the changes are much less that Group 1.They become able to use their weak limb less abnormally (ie using compensation strategies but less ‘severe’).

Group 3 show increases in function but NO changes in the muscle activity of the weak leg BUT they do show increases in the muscle activity in the sound leg. So they become more able because they compensations more with their sound limb, not because they recover activity in the weak limb

Group 4 (who have the most severe strokes) initially had no activity or very abnormal activity in the weak and the sound limbs. They improve function by increasing activity in the sound leg (but still none in the weak limb) and thus join group 3.

These groups could be considered stages, or a continuum, of recovery as patients tend to progress through them (to a greater or lesser extent)as they recover. So those in group 4 who show some recovery, progress from no activity –> using compensations in the sound leg (group 3) to function. Those in Group 3 tend to progress –> using compensation in both legs to function (group 2). And group 2 sometimes progress –> Group 1, when compensations start to approach normal movement.

This evidence contradicts many of the statements about BB and how it works. It

  • questions the importance of minimising compensations and ‘restoring ‘normal movement’ in order for patients to function
  • shows that using compensation is not a barrier to developing more ‘normal’ movement or muscle activity
  • shows that increase in motor activity, rather than the timing/pattern of motor activity, is what is important to regain function. Ie most patients get better at using their compensations, rather than restoring a particular pattern of muscle activity.
  • Some patients became functional BECAUSE they used their sound limb to compensate and/or use compensations/ abnormal activity in their weak limb

Our professional challenge as physiotherapists is to work out how to manipulate the tasks and environment (by using aids and equipment for example) to enable patients to do as much as they can, safely, comfortably and as easily as possible. And then to work out how they can learn to get better at doing that so they are able to do more, or do the same but more easily. The evidence is that using exercise and task-specific exercise to promote motor learning and neuroplasticity is the way to go.

It is much better to get folk doing something and then train them to get better at it, than to stop folk doing something. I would suggest that the legacy of Bobath is that we have tended to focus much too much on how patients are doing things (impairments) at the expense of what they can do (function). In doing so we have inadvertently made our patients more disabled/ less active than they could be, in the mistaken beliefs that improving impairments this will automatically carry over into improvements in activity and that ‘normal’ or ‘quality’ movement is needed to function/ be active.  Which isn’t saying that we shouldn’t work on impairments at all (especially if it is the impairment that is limiting the function) or try to improve someone’s movements towards becoming’ more normal’(if they are at that stage). I’m saying we have given it more prominence than is helpful for many of our patients.

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15 thoughts on “How to do Bobath? Part 6 Compensation, motor control and muscle activity

  1. I am afraid Sarah, I just cannot agree with the conclusions you have expressed in the last 2 paragraphs.
    “Our professional challenge as physiotherapists is to work out how to manipulate the tasks and environment (by using aids and equipment for example) to enable patients to do as much as they can, safely, comfortably and as easily as possible. And then to work out how they can learn to get better at doing that so they are able to do more, or do the same but more easily.”
    Emphasis of treatment in the early days really does need to be on quality non compensatory function. By allowing a patient to use only the good arm to get from lying to sitting or doing any functional activity enables compensatory postural habits to become very easily established. Trunk posture thus becomes asymmetrical and one sided. Abnormal plastic adaptions thus begin to take place in the neurones muscles and fascia with inappropriate fascia and muscle shortening. Shortened muscles and fascia accordingly changes the nature of normal pressure and stretch stimuli onto the sensory neurone endings. It is much better to work on quality movement from the start of rehabilitation than to work on apparent impairments in the latter stages of rehabilitation. It is much more difficult to unlearn abnormal compensatory habits and lengthen shortened structures in the latter stages of rehabilitation.
    “It is much better to get folk doing something and then train them to get better at it, than to stop folk doing something.”
    Yes help patients to be active but Compensatory function needs to be strongly discouraged. By using Berta Bobath’s “Placing” handling technique patients can be helped to use their own automatic postural re-actions in functional activities such as rolling over in bed, moving from lying to sitting and from sitting to standing. By guiding patients to move in normal non compensatory patterns of movement, the appropriate proprioceptors are activated which accordingly activate the appropriate non compensatory automatic postural reactions. Yes I agree it is not enough to just facilitate postural reactions. Patients do need to learn to facilitate their own postural reactions. I however find that once patients experience normal posture and movement they are strongly motivated to practice for themselves in between physiotherapy sessions.

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  2. Cheers Bobath (and thanks)

    One of the advantages of long service leave is that it gives me time to write on posts such as these! I also owe a great deal to the Bobath Concept. It introduced me to client-centred care, detailed movement analysis, hands-on palpation, handling and facilitation skills, teamwork, motor control theories, movement neuroscience and so much more. As a result, I decided to study neuroscience further in the UK and pursued research into balance and gait movement analysis. BB also introduced me to mental imagery, CIMT and task specific practice!

    Now as a clinician I use any arsenal at my disposal.The more ideas I have the better for my patients. However I, like so many others (of my ilk) we would be far less effective if it wasn’t for BB. BB remains popular for many reasons, however we all seem to agree that it does fill a huge void in the education needs of neuro therapists. BB has an effective teaching style , using real patient demos, plenty of intense practice and constant problem solving. Deciding to pursue a career as a Bobath Tutor would therefore be a huge commitment and personal sacrifice as there is much to learn. For the rest of us, BB allows for an opportunity to learn skills in assessment using a combination of visual observation and manual handling. It explores the relationship between postural movements, balance and all body parts, and enables the patient to actively move. If you think it is passive, then perhaps you should be facilitated yourself!

    Now, I find myself in a position that presents an enormous challenge. As coordinator of a Neurological Physiotherapy Masters program, I need to get a feel for where all of these concepts, approaches, skillsets and techniques fit into the future picture. What does a Neurological Physiotherapist of today need to know? What is the future of service delivery funding? When do we need to learn about and implement new technologies such as Robotics and FES? Do we wait for the evidence? When I worked in London in 2003-05 we used a BWS treadmill before any decent evidence was available. At our current teaching hospital we are using UL and gait robotics despite little to no evidence.

    The next generation of Physiotherapists are expected to appraise evidence far more than ever before. And let’s not kid ourselves, the evidence for many key areas of neurological rehabilitation remains very weak – all of it. So where do we go from here?

    At this stage the direction we have taken is to provide multiD and interD learning opportunities for our Neurological Physiotherapy students to update on the latest knowledge about the rehabilitation needs and key rehab developments for a number of adult population groups including Stroke. MS, Parkinsons, MND and electives on TBI, SCI and others. There is more on the horizon such as the many dementias and other movement disorders such as dystonia. We do not cover paediatrics unfortunately. It is essential to explore the individual presentations and plights of our patients that may include, sensory, perceptual, biomechanical and psychological factors that challenge both clinical practice and research methodology. In addition, we devote a topic to explore neuroscience and motor control theories and how this relates to the retraining of our patients. This way we expect our students to draw upon and critique both clinical and neuroscientific evidence to become better therapists, coaches and researchers. We do not promote nor reject any ‘approach’, but encourage careful scrutiny.

    It’s true that research rules the roost in terms of university funding. Clinical trials, RCTs, systematic reviews and PhD students bring in the bacon for sure, however the reality is such that the strong research gets stronger. This is why simple and clearly defined techniques lead the way, such as treadmills, Task Practice, CIMT (although ‘shaping’ can be quite variable), FES, TMS, tDCS, Robots, strengthening and aerobic fitness. These interventions spit out data for all kinds of colourful and often biased analysis. And don’t get me wrong, I really love this stuff (and research it myself), but it is such a small part of the overall rehabilitation picture. Unfortunately, it will take a long time to research the areas of physiotherapy that we often crave such as movement analysis, developing more specific and valid outcomes measurements for impairment and function, and perhaps more relevant issues of quality of life, self-efficacy and cost.

    We have such a long way to go, yet clinicians and patients need some reassurance that we are providing best practice NOW! This is why I understand the temptation to push aside Bobath and others (especially manual techniques), where it seems (and may well be) impossible to research, despite the important contributions from my colleague Sheila Lennon and others(Lennon & Ashburn, 2000). I agree with Margaret Mayston and Lewis Rosenboom in that we should ‘Please proceed with caution’.(Mayston & Rosenbloom, 2014) I also agree that NDT/Bobath should have been excluded according to Novaks exclusion criteria.(Novak et al., 2013)

    We are also investing time and money to explore the best ways to deliver clinically focussed CPD at university. In doing so, we should look at the strengths of the Bobath teaching style and use it (and acknowledge it despite fear of being labelled a heretic in some parts of Australia). We will explore a combined eclectic approach that reflects the real practice of so many therapists. I am hopeful, (but remain doubtful) that Universities across the globe can provide high level CPD. Young, enthusiastic and intelligent physiotherapists with an interest in neurology are often attracted to the challenges and clear career structure within universities, and are directed toward these clearly defined, funded research opportunities such as those that involve Transcranial Magnetic Stimulation, Robotics. gait labs or Body Weight Support Treadmill training. All great stuff, but these young guns with a PhD and only one or two years real clinical experience will be teaching the next crop of physiotherapists! This means that Bobath and other CPD providers play an important role in teaching our young physios.

    Further research into the role of sensation and movement will help determine where, when and for whom facilitation can play a role in skill acquisition and retraining is possible. We can explore how certain handling techniques might allow for improving movement performance, and how it can be combined with additional protocols such as CIMT (this is happening with more severely impaired adults and children in the US), FES, functional strengthening programs and balance re-training. If we do cross fertilize like this, I realise the intervention can no longer be called ‘Bobath’ – an issue that may well be the key challenge for Bobath as it continues to evolve. I am a strong believer in ‘cross-fertilization’ and do not see it as ‘contamination’ like so many researchers. It might sound melodramatic, but there is a bigger issue here. If we over-simplify our practice, the future of neurological physiotherapy will be threatened. Health assistants, occupational therapists and exercise physiologist will be more than happy to stick our patients on robots, FES, treadmills or bikes based on available best evidence. This already happening believe me! Evidence and information can always be misunderstood and misused.

    The Bobaths were ahead of their time, which means that criticism comes with the territory. They attempted to explain their observations based on very the limited neuroscientific knowledge at the time, yet were more than happy for it to evolve with time. I agree with others that research evidence and Bobath are not incompatible, (Cott, Graham, & Brunton, 2011; Mayston, 2008) we just have a way to go. If you have been taught that Bobath is evil and outdated, perhaps you should ask yourself what motivates such extreme hatred, because the limited evidence against it just does not stack up. If you don’t know much about Bobath, I suggest you find out what all the fuss is about!

    Cheers Bobath (and thanks)

    James.

    Dr James McLoughlin
    BAppSc (Physio) MSc (Clinical Neuroscience), PhD
    Director JMNP Pty Ltd
    Senior Lecturer, Flinders University
    APA Neurological Physiotherapist
    Accredited Vestibular Physiotherapist

    Cott, C. A., Graham, J. V., & Brunton, K. (2011). When will the evidence catch up with clinical practice? Physiotherapy Canada. Physiotherapie Canada, 63(3), 387–390.
    Lennon, S., & Ashburn, A. (2000). The Bobath concept in stroke rehabilitation: a focus group study of the experienced physiotherapists’ perspective. Disability and Rehabilitation, 22(15), 665–674.
    Mayston, M. (2008). Bobath Concept: Bobath@ 50: mid-life crisis—What of the future? Physiotherapy Research International: The Journal for Researchers and Clinicians in Physical Therapy, 13(3), 131–136.
    Mayston, M., & Rosenbloom, L. (2014). Please proceed with caution. Developmental Medicine and Child Neurology, 56(4), 395–396.
    Novak, I., McIntyre, S., Morgan, C., Campbell, L., Dark, L., Morton, N., … Goldsmith, S. (2013). A systematic review of interventions for children with cerebral palsy: state of the evidence. Developmental Medicine and Child Neurology, 55(10), 885–910.

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    1. Hello Dr McLoughlin
      Welcome to the blog and thank you for sharing your thoughts.
      I’m intrigued about how BB introduced you to mental imagery, CIMT and task specific practice. Could you elaborate? Also that you hadn’t, apparently, come across client-centred care, movement analysis, palpation or handling skills, teamwork, motor control theories, movement neuroscience etc before discovering Bobath. I always had the impression that PT training in Oz was very comprehensive and academically rigorous but now I’m wondering. But you raise a good point about where/ how one gains one’s knowledge, there has been some discussion of this in the icsp discussion, but I guess you don’t have access, assuming that you aren’t a MCSP. In summary we agreed that we all gain for our basic UG training (the biggest influence); experience; patients, colleagues and peers and post-graduate training. Yes, I’ve done many BB courses in my time and would like to think that some of it rubbed off, after paying for it! And indeed for many years I explained my assessment in terms of the Bobath du jour – but Bb is seems to be something else now. Does that mean that the BB of my day was never BB? Is it now wrong? Or is it the same thing but with different jargon?

      In response to your comment about facilitation: Yes I have done, and received, plenty of facilitation in my time, and I can confirm that it is a largely passive experience (possibly active-assisted, on a good day) on the receiver/ patients’ part, although often v active for the deliverer. You say that BB “explores the relationship between postural movements, balance and all body parts, and enables the patient to actively move”. Is there a physio approach that doesn’t claim to do that? What is about BB that makes it unique?
      I agree that part of the reason that BB continues is that the courses fill something of a gap in the market, and the format are familiar which is another appeal. I disagree that there aren’t alternatives. We have discussed this in the EBP and CPD thread https://sarahtphysioblog.wordpress.com/2015/10/22/ebp-and-cpd-alternatives-to-bobath-courses/ which gives several examples and I imagine similar opportunities are available in Oz (many of the suggested are available electronically and so have no geographical boundaries).

      You ask what a neurological physiotherapist of today need to know? I would suggest they need to know about the evidence base and to gain the skills and knowledge to understand the state of evidence and how to apply it for themselves. As you say, the issue of when the accumulating evidence is sufficient to implement, is of growing importance as the breadth and depth of evidence grows. It isn’t a clear cut process. Clearly there is no point in waiting until the definitive Phase III trials and completely positive Cochrane review (which never happens) has been published, but then one would not want to be chasing every interesting new idea (most of which turn out to be a red herring). I think the key is to equip students with the skills to be critical, evaluative discriminating and open minded.

      You ask whether we should wait for the evidence before using FES and robotics. There has been a previous thread about how much evidence is needed to change practice. https://sarahtphysioblog.wordpress.com/2015/10/22/ebp-and-cpd-alternatives-to-bobath-courses/ I agree it is a difficult and nuanced call. But that is what modern-day clinical reasoning is about. It is about when and how to apply the evidence so it meets individuals’ needs and it ‘fit-for-purpose’ in one’s local context. Specifically regarding FES and robotics, I would say that there is already abundant evidence to support their use for the lower limb/ mobility. The research on LL robotics is called electromechanical gait training and 2 Cochrane Reviews have shown that it enables people regain independent mobility. The NNT (numbers needed to treat) is 5. That means for every 5 people treated one more patient will become independently mobile. How good is that? To be able to get 20% more people out of a wheelchair and on to their feet?? True, it doesn’t work for people who can already walk (but then it isn’t intended to, treadmill training is effective for them) and is more effective for acute/ sub-acute strokes than chronic (but then so is pretty much everything else). FES for the LL/ foot drop has been recommended in national clinical guidelines and NICE guidelines for years; I’ve added references to a couple of systematic reviews. I agree the evidence for UL robotics and FES is much less developed and decidedly mixed. So I would advise holding off implementation until stronger evidence and/ or more user-friendly devices are available, which may be a v long time coming.

      If I may, I must pull you up on the claim that there was no evidence for BWSTT in the early 00’s. Stephan Hesse published his first paper on BWSTT in the early 90’s (reference below). An avalanche of research followed as folk realized what a good idea it was. By 2003 there was enough evidence for systematic reviews, and the focus of the research had moved on to details of application, such as the need to increase the incline to produce a CV effect; to work at the patient’s fastest safe speed, and that it worked for those who were already ambulant but not those who were yet mobile. Your senior physios at St Georges were definitely aware of this evidence as I remember many discussions in the later 90’s and early 00’s about the evidence and how it could/should be implemented when I was a lecturer at Brunel University and we collaborated in research projects. I suspect they would be rather miffed by the implication that they were using new interventions without awareness of the evidence base.

      Also it’s a tad harsh to say that the evidence for neurological rehabilitation is very weak. The content of this blog, clinical guidelines, top quality RCTS, and systematic reviews and meta-analyses show very strong evidence to the contrary: exercise and intensive task-specific practice (which includes treadmill training, electromechanical gait training, CIMT), AFOs, FES, botox etc work; the time has come to use them. Why use something that might, but probably doesn’t work, like Bobath when there are others that do work?

      The direction your MSc is taking sound spot-on. Your next paragraph is in contrast with the evidence based approach you profess to promote. It is simply incorrect to dismiss RCTs of the EB interventions you list as biased analyses. Again, this has been discussed before in the blog in When Should EB change Practice Thread. https://sarahtphysioblog.wordpress.com/2015/11/02/when-should-evidence-change-practice-part-3-levels-of-evidence/ Of course I’m happy to discuss the ins and outs of whichever trials you think are so biased that their results should be negated and change the direction of evidence if you provide the details.

      It is also incorrect to imply there isn’t a relevant evidence base for movement analysis, specific and valid outcomes measurements for impairment and function, quality of life, self-efficacy and cost. It is huge (except the evidence for cost-effectiveness of rehab, which is small but growing and positive). Perhaps when you talk about “research [into] the areas of physiotherapy that we often crave” you just mean research that gives you the answers you want, which is probably never going to happen. Please don’t dismiss a huge body of evidence because you are either unaware of it, or because it does not give the answers you want.

      Im glad that you recognise the “the temptation to push BB aside”, because best practice is to do just that. Best practice is to use exercise, intensive task-specific practice etc because that is what works. As I have asked before, why do something that probably doesn’t work, like BB, rather than something that does?

      You say that further research is needed into the role of sensation and movement to determine where, when and for whom facilitation can play a role. There has been some work in to facilitation (but not very much) which we have discussed at length in the How to do BB Part 5 facilitation thread and the reader’s comments that followed https://sarahtphysioblog.wordpress.com/2015/10/19/how-to-do-bobath-part-5-the-facilitation-thing/ The problem is that the evidence shows that facilitation doesn’t work. Agreed, further research might produce a convincing case, but probably not. So why hasn’t this work been done? It would be perfectly possible to get funding for hypothesis driven mechanisms research and/or RCTs of BB if the applications for funding were written with a sound theoretical basis and methodology. So why hasn’t this work been done? Perhaps proponents of BB don’t have the skills to do this (but as the Sheila’s collaboration with the BBTA shows it is possible to work with people who do), or perhaps they don’t want to do the research in case it gives the ‘wrong results’ (Lennon et al 2006 for example). Even some audit data from BB practitioners’ own practice (which would be easy, given that they say they use objective, standardised measurement tools) would be a start. As you say, BB has been practiced for decades, so … come on, show us the results of that practice.

      You also suggest combining BB with EB interventions such as CIMT, FES, strengthening programs and balance re-training. The notion of ‘cross-fertilisation’ is appealing but the logical things to cross –fertilise would be interventions that have evidence of effectiveness to see if the sum of parts is greater than the individual components. This is already being done in gait rehab- looking at combining FES with other EB interventions (with mixed results, but it is early days, some examples below). But what is the rationale or logic for adding BB? Why add something which probably doesn’t work (or at best doesn’t work very well) to one that does? The most likely outcome is that the ineffect of BB will just dilute the effect of the EB intervention, by reducing the dose of the EB intervention, if nothing else.

      You raise the spectre of our professional practice being overtaken by OTs, exercise professionals and PTAs who will be “more than happy to stick our patients on robots, FES, treadmills or bikes based on available best evidence”. This raises two points. Firstly if professionals other than PTs (and even stroke survivors themselves cf the ARNI programme) can deliver EB interventions that enable stroke survivors to recover more, do more and be happier, then great. Bring it on. Access to PT is very limited and most stoke survivors receive woefully inadequate amounts of PT, so enabling survivors to get access to treatment that work is a good thing.

      Secondly, there have been many references in these icsp, blog and twitter discussions referring “just sticking patients on machines”, “EBP being for Monkeys” (thanks @Wigmore-Welsh, classy) and that is EBP doesn’t “take the patient into account”, and the like. I can only think such comments are made by people who have never tried using these interventions (or if they have, they have done them very badly). Applying EB interventions require just as much skill and expertise as any other aspect of physiotherapy. As I said earlier, modern-day clinical reasoning and professional skill is about knowing when and how to apply the evidence so it meets individuals’ needs and is ‘fit-for-purpose’ in one’s local context. I can understand that this means learning a new skill set for PTs who have gained experienced, skill and status in ‘traditional clinical reasoning’ and that that may be threatening to many. This is probably a factor for many ‘late changers’ and ‘change resistors’ groups when it comes to implementing new interventions, but that doesn’t make it right

      Finally, I’ve been wondering how to take your final comments that “If you have been taught that Bobath is evil and outdated, perhaps you should ask yourself what motivates such extreme hatred”. It is often difficult to give and take the wrong impression in text. So I’m wondering if you are letting your over-weening enthusiasm overtake you, or whether you are joking. Hopefully the latter, as if the former, you are just being silly. Of course no-one is taught that BB is evil (it isn’t) but it is ineffective and has been superseded by other treatments that work much better. And no-one is demonstrating extreme hatred, life is much too short for such things. As I have noted before, it should possible for adult professionals to be able to disagree and discuss those differences without arguing or resorting to such over-emotional nonsense.

      REFERENCES
      Hesse et al. Restoration of gait in non-ambulatory hemiparetic patients by treadmill training with partial body weight support. Arch Phys Med Rehabil. 1994;75:1087-1093
      Moseley et al. Treadmill training and body weight support for walking after stroke. Stroke 34.12 (2003): 3006-3006.
      Mehrholz et al. Electromechanical-assisted training for walking after stroke. Cochrane Database Syst Rev 4.4 (2007).
      Mehrholz et al. Electromechanical-assisted training for walking after stroke. Cochrane Database Syst Rev 7 (2013).
      Kottink et al. The orthotic effect of functional electrical stimulation on the improvement of walking in stroke patients with a dropped foot: a systematic review. Artificial organs 28.6 (2004): 577-586.
      Robbins et al. The therapeutic effect of functional and transcutaneous electric stimulation on improving gait speed in stroke patients: a meta-analysis. Archives of physical medicine and rehabilitation 87.6 (2006): 853-859.
      Lennon et al. “Gait outcome following outpatient physiotherapy based on the Bobath concept in people post stroke.” Disability and rehabilitation 28.13-14 (2006): 873-881.
      Daly et al. “Recovery of Coordinated Gait Randomized Controlled Stroke Trial of Functional Electrical Stimulation (FES) Versus No FES, With Weight-Supported Treadmill and Over-Ground Training.” Neurorehabilitation and neural repair 25.7 (2011): 588-596.
      Tong et al. Effectiveness of gait training using an electromechanical gait trainer, with and without functional electric stimulation, in subacute stroke: a randomized controlled trial. Archives of physical medicine and rehabilitation 87.10 (2006): 1298-1304.
      Kesar et al. Combined effects of fast treadmill walking and functional electrical stimulation on post-stroke gait. Gait & posture 33.2 (2011): 309-313.

      Liked by 1 person

  3. Things Bobath tutors taught me that are untrue :-

    1. “Proximal Hamstrings”.
    We were told by the tutor that hamstring muscles could pull more at one end than the other. When questioned the tutor explained that although this was contrary to conventional theories of biomechanics it was a Bobath fact and she could feel it with her advanced handling skills. This is impossible.

    2. Core stability and proximal before distal
    Presumable based on the original model of infant development I was taught that core trunk stability was fundamental and that activity progressed in a proximal to distal pattern from this stable core. However, the research demonstrates that activity moves from base of support first (refs 1-3). The obsession with the core is misplaced, thus a stroke patient struggles to walk or sit because they lack control of their BoS (ankle/leg in gait, hip in sitting) not core trunk (which is relatively unaffected after stroke). Compensatory core activity is a symptom of this lack of BoS control.

    3. High tone muscles are an important impairment.
    I would spend hours each week manipulating high tone muscles and go to great lengths to suppress this demon. We now know that muscle weakness and lack of sensation are much more important than altered tone (refs 4-6).

    4. RCTs are not relevant to Bobath.
    I was taught that RCTs were invented for simplistic research like drug trials and that Bobath was so individualised, multifaceted and complex that research outcome measures cannot demonstrate its benefits.
    Firstly RCTs were invented to deal with agricultural field trials which, in my experience of both, are more complex and full of uncontrolled variables than neurorehab research.
    If Bobath worked it would produce changes in outcome that can be measured, to blame the lack of this on the RCT rather than Bobath is to start with the answer you want and then alter reality to fit. This is the defence used by homeopaths, who also honestly “know” what they do must work.

    All the above led me to finally conclude that Bobath tutors lacked fundamental knowledge of biomechanics and were unaware or ignored research that was contrary to their teaching (they do however quote the very few RCTs that support Bobath on their website, so obviously some RCTs are less inappropriate than others)

    If Bobath were invented today it would have to demonstrate its efficacy in RCTs, and it would fail this test and therefore would not be adopted. So why do we all follow it so religiously? Is it an easy all included package course to go on, rather than attend a series of courses on the techniques that are recommended in national guidelines? For some it does seem to be a quasi religious / faith process and these people do become very defensive if their habits of practice are challenged. For the sake of our patients we need to step back and objectively look at the evidence and in the light of this honestly assess our treatment habits. It is not being “holistic and balanced” to promote Bobath as an equal to alternative treatments that do have an objective evidence base. Why promote a treatment that, even after 60 years, is still not recommended in independent reviews and national guidelines?

    Refs

    1. Bozec & Bouisset (2004) Does postural chain mobility influence muscular control in sitting ramp pushed? Exp Brain Res 158 427-437. (available at :-http://www.researchgate.net/publication/8509104_Does_postural_chain_mobi…).
    2. Mercer & Sahrmann (1999) Postural synergies associated with a stepping task. Physical Therapy 79 1142-1152. (available at :-http://ptjournal.apta.org/content/79/12/1142.full).
    3. Misiaszek (2003) Early activation of arm and leg muscles following pulls to the waist during walking. Exp Brain Res. 151 318-329. (abstract available at :-http://link.springer.com/article/10.1007%2Fs00221-003-1501-x).
    4. Harris & Eng (2007) Paretic Upper-Limb Strength Best Explains Arm Activity in People With Stroke. Physical Therapy Volume 87 Number 1 88-97. (available at :-http://ptjournal.apta.org/content/87/1/88.full.pdf+html).
    5. Disa et al.(2004) Spasticity After Stroke: Its Occurrence and Association With Motor Impairments and Activity Limitations. Stroke 35, 134-139. (available at :-http://stroke.ahajournals.org/content/35/1/134.long).
    6. Ross SA, Engsberg JR. Relationships between spasticity, strength, gait, and the GMFM-66 in persons with spastic diplegia cerebral palsy. Arch Phys Med Rehabil 2007; 88:1114-20. (available at :-http://www.fizjoterapeutom.pl/files/29/Ross%20SA%202007%20Re

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  4. Roger you identify 4 points which you believe are untrue and which were taught to you by Bobath Tutors. I comment on each point: –
    1. “Proximal Hamstrings”
    Could not the Bobath Tutor have been correct to detect extra muscular tension in the proximal part of the hamstring muscles? Is not protective muscle spasm localised to a specific area of a muscle? After key hole surgery to my right knee I was amazed to see so much tension in the distil end of the Vastus Lateralis Muscle.
    2. “Core Stability and proximal before distal”.
    You state Compensatory Core activity is a symptom of this lack of BOS control. I agree. But where I disagree with you is that muscle weakness is caused by brain injury and is an impairment. Could not the muscle weakness be simply caused by some form of inhibitory control at the alpha motor neurone?
    3. “High Tone muscles are an important impairment”
    To a point I agree with you Roger. All abnormal symptoms of a stroke such as muscle weakness and poor sensory awareness need to be addressed not just hypertonus. The skill in rehabilitation however comes with establishing the true underlying causes to movement dysfunction. Selecting Compensatory movement can often be the main contributory cause.
    4. “RCTs are not relevant to Bobath”
    Rather than compare Bobath Therapists with another group of Therapists, I do believe we need to be much more specific in what we compare. For instance in the Lennon et al (2006) trial would it not have been better to compare “Facilitation of Gait” rather than the overall gait outcome. Yes there was no difference in the overall outcome but was the gait any better whilst being handled by a Bobath Trained therapist?

    Ref
    Lennon et al. “Gait outcome following outpatient physiotherapy based on the Bobath concept in people post stroke.” Disability and rehabilitation 28.13-14 (2006): 873-881.

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    1. Hello Jackie
      Thank you for your comments, which i will now try to address.

      Regarding proximal hamstrings.
      I do not know if muscle spasm is localised, but I do know that all standard biomechanics texts state that tension in the muscle body produces an equal and opposite tension on the tendons at each end. My point is that if Bobath tutors have found something that refutes such a basic principle of biomechanics they need to back it up with better evidence than “it’s what I think I can feel”.
      The tutor then told up that she could feel very weak proximal hamstring activity in the leg of one of my colleagues. This seemed odd to me as the woman concerned was in her twenties and had no injuries or deficits of mobility. My conclusion was firstly if proximal hamstrings existed they were of no consequence and that the Bobath tutor’s lacked a basic knowledge of biomechanics was compounded by an exaggerated faith in her own handling skills.

      Regarding core stability & proximal before distal
      I think we will disagree on the cause of muscle weakness, for me damage to the motor cortex seems like a good explanation, but I’m happy to also accepts there are also other factors involved. My point is that because Bobath tutors were ignorant of or choose to ignore the published evidence regarding BoS activity first, they have caused huge amounts of effort to be incorrectly concentrated on core stability and proximal control.

      “RCTs are not relevant to Bobath”
      RCTs compare treatment A to treatment B, the complexity or otherwise of each treatment package is irrelevant. We just want to know if there is a difference between A and B, if so there will be a difference in outcome measures, it really is that simple. I think it is also important to not think we are comparing Bobath therapist with other therapists, we are comparing treatments not therapists.
      The Lennon paper was not an RCT, it was a before and after study, which showed that even under idealised conditions with unlimited therapy to cherry picked patients from advanced trained therapist that the Bobath approach has no effect on quality of gait. Are you suggesting that the quality of gait was only better when the therapist were handling the patients? These therapist themselves decided when to stop treatment and thus the patients had many more weeks of rehab than usual. Even then there was no carry over into quality of gait.
      In this study improving gait was the main objective, yet patients only spent 10% of their therapy time actually walking! Based on my observations of Bobath therapists I suspect the remaining 90% of therapy time was occupied with their obsessions of normalising tone, core stability and proximal control. The results show how useful that was.

      BBTA hide evidence.
      One more point I have noticed is that the BBTA website contains a rebuttal of criticism of their approach, but does not tell us where the criticism is published. I presume it is a rebuttal of this blog and previous comments on iCSP. They then reprint the supportive comments of James McLoughlin from this blog, but again do not tell people where they can read the comments that are critical of them. Sarah Tyson in contrast is happy to openly debate all the evidence in an open manner, the BBTA only want to talk about what supports their position.
      This desire to hide anything that is negative about them is also evident in the way they only quote the minority of research that support their approach. It is a sign of a defensive and closed attitude to best evidence and seems to put the interests of the BBTA before anything else. Is this really the best way forwards for our profession and patients?

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  5. Further to Roger’s point of ‘it’s what I think I feel’ – look at Cranial Osteopathy

    As Ben Goldacre points out, practitioners claim to feel a subtle pulse in the fluid surrounding the brain’. Cranial osteopaths don’t think the pulses are blood pressure; their theories revolve around the “inherent rhythmic motility” of the brain and spinal cord, mixed with breath and cardiac cycles, causing rhythmic fluctuation of the brain and surrounding fluid, which they think they can feel through the bones of your skull, and fix up with a bit of wiggling. They write long articles about actin and myosin (the things in muscle cells that make them move) being present in brain cells; unfortunately, they always forget to mention that brain cells lack the dense arrays of those filaments which are necessary to generate any significant movement. But are there real “cranial pulses” to be felt, however they may be generated? It’s easy to find out: ask a couple of cranial osteopaths to write down the frequency of the pulses on the same person’s skull, and then see if they give the same answer. There have been five papers published doing just this, and in none of them did the osteopaths give similar answers. Which suggests to me that (a) this is not a reliable biological phenomenon, and (b) perhaps these cranial osteopaths are, er, imagining it. So: the discipline is based on a misunderstanding, they can’t measure what they claim to measure and work with, and there’s no evidence to say it works. And they charge pots of £ for doing it…

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  6. Thank you for your reply Roger. Yes I am suggesting gait could be better with the patients handled by Bobath Therapists.
    That there was no “carry over” I also believe can be explained. For instance did the nurses handling patients for the remaining 23 hours of the day have the same Bobath handling skills? Were the patients encouraged/allowed to use compensatory tactics whilst being helped to roll over in bed, get from lying to sitting and from bed to chair. Were the patients discharged home using a compensatory gait?
    In the distant past I used to work in a General Hospital for a short time. I used to discharge my stroke patients in a wheel chair. Fortunately I was lucky enough not to be challenged by senior physiotherapists or by medical staff. These very same patients that I saw as an Inpatient then came to see me as an outpatient. Perhaps it is wishful thinking, but I do recall the out comes as very good!
    “Regarding proximal hamstrings”
    Roger you refer to your knowledge of standard biomechanics texts that tension in the muscle body produces an equal and opposite tension on the tendons at each end. I question whether the tension can go in more than one direction. By examining cadavers Willem Fourie http://www.wayforward.co.za has observed collagenous tissue (fascia) to be distributed in all directions within a muscle belly. I also question the nature of protein molecular binding. I do feel Science has a long way to go.
    Tom Balchin you challenge the cranial suture theory of movement as proposed by Cranial Osteopaths. I find it difficult to fully agree with your argument as I do believe we can palpate cranial plate movement. Rafferty and Herring (1999 ) investigations on young pigs and collagen distribution within different sutures does seem to suggest that different cranial sutures are designed for different movement strains. http://onlinelibrary.wiley.com/doi/10.1002/(SICI)1097-4687(199911)242:2%3C167::AID-JMOR8%3E3.0.CO;2-1/abstract;jsessionid=C9552A12F5711E7F250E068D30975018.f04t01

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  7. Hello Jackie

    Re; Sheila Lennon’s paper

    I feel you are making too many excuses for these advanced trained Bobath therapists, they did their best and were confident it would improve the quality of gait. These cherry picked patients had far more therapy than usual, more than that is unrealistic and impractical. In the real world this as good a Bobath gets.

    I think a better explanation for their failure to alter quality of gait is that they were using their out-dated model of core stability first and proximal activity before distal as so:-

    “The therapists in this study hypothesised that improving selective control of the pelvis would improve weight transference over the hemiplegic leg, thus improving the movement patterns (both proximally at the hip and distally at the knee and foot) in both the stance and the swing phases of the gait cycle.”

    This model does not now fit the research which, as I referenced above, indicates that activity works from base of support first (ankle in this case) to trunk. How many of us have spent hours using the Bobath model to work on proximal / core stability and hip control of patients who actually cannot walk because they lack control of their BoS.
    I imagine it would be very difficult for the BBTA to abandon such a fundamental teaching and likewise I do not expect any therapist to just take my word for it. BUT I would urge anyone interested to read the papers concerned and form their own opinion. These BoS first papers (links above) and the paper by Lennon et al. could make a very good IST.

    Why are the Bobath tutors so reluctant to justify their teachings in open an detailed debate?

    The BB tutor who taught us proximal hamstrings would not explain the theory behind it or give us any objective evidence to support it. It seemed that the teachings of a Bobath tutor were there to be accepted and not discussed.

    Likewise, when I tried to initiate a discussion of the Novak review (ref 1) onto the CSP website the Bobath -CP staff removed it on the grounds that they (British Association of Bobath Trained Therapists) owned that part of the site and its was there to promote Bobath rather than discuss it.

    This was a deliberate attempt to hide evidence critical of Bobath from UK therapists. It sits very oddly with the statement that “The BBTA encourages an informed and respectful dialogue”. Luckily the CSP over ruled them.

    In my experience (unless their hand is forced, as by the CSP above) Bobath tutors are very reluctant to discuss specific issues and prefer to talk in generalities on their own websites / blogs, where they will block any critical comments.

    So it really is up to them to justify their theories of both proximal hamstrings and core stability first plus proximal before distal (in the light of the evidence that activity starts from the BoS). Just where is the objective evidence?

    They could always prove me wrong and add Prof. Tyson’s reply to the criticisms of this blog to their website. But as the primary motive of the BBTA seems to be to promote their courses and themselves (rather than the best neurorehabilitation) I somehow think they will try to avoid that!

    Ref
    Novak et al. (2013) 55 885-910. A systematic review of interventions for children with cerebral palsy: state of the evidence. Dev. Med. Child Neurol. Available at :- http://onlinelibrary.wiley.com/doi/10.1111/dmcn.12246/pdf

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  8. Hi Roger
    Re Sheila Lennon Paper
    Thank you for pointing out the Bobath Hypothesis. I have to agree with you, I too feel the theoretical logic does not make much sense. I feel the problem lies with the differences in understanding between “Facilitating an instant physiological change” and a slower learning/plasticity change.
    My personal understanding is that it is possible to facilitate normal postural learned reflexes at spinal cord level. A physiotherapist inhibits abnormal postural activity and facilitates normal postural activity by guiding/ placing the trunk and limbs into normal alignment.
    I do believe Karl and Berta argued over this very same point of learning versus facilitation. I went to a seminar given by both the Bobaths. They agreed with each other not to be present while the other person was lecturing. They feared they might interrupt each other!

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  9. Well I agree with Sarah.
    and thought I’d add my opinion here on one strand of this piece

    “Some patients became functional BECAUSE they used their sound limb to compensate and/or use compensations/ abnormal activity in their weak limb”

    yes

    But then there has been a fair bit of banter on twitter between various folk, and I couldn’t work out what was about this blog or something else.

    I realised probably a bit too late that the use of the word ‘compensation’ has a positive use in my world of neuropsychological rehabilitation, but that for some, this is a kind of perjorative word, as if by compensating for deficits you might impede recovery. I don’t think there’s much evidence for that position, and it seems to me a kind of urban myth or meme that perpetuates in different aspects of rehab.

    In memory rehab we hear patients (/or their relatives) say something like “if i/they use a diary – and i/they never needed one before – that’ll stop my/their memory getting better”. In my view and experience a pragmatic approach to _impaired_ memory is to use a strategy such as a date-book to compensate, improve participation in life and generally live more successfully. This is what I think of when i read the word compensation.

    In PT the C word also exists in the plural, seemingly describing something else and us. I have always thought that in physiotherapy, particularly in the care of people who are a long time post injury (which after all is what we do at OZC), there comes a point where I think adjustment and acceptance has to come in – “this is a paralysed body part, therefore to be successful I will compensate by doing … (_fill in the compensatory strategy_). It’s not in my view a failure of rehabilitation to help someone live successfully with paralysis (an impairment). However it does seem to me that some think this would be a failure?

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  10. Your comment Andrew challenges me to reply! We definitely seem to have differing views to what is impairment and to what has caused the impairment.
    I subscribe to the view point (hypothesis) that it is only the higher centres of the Central Nervous System (CNSS) that is damaged following a Cerebral Vascular Accident (CVA) and that the lower centres perform normally to peripheral input. Namely, the postural reflexes and automatic movement patterns, such as walking, are still intact and are functioning correctly.
    I thus maintain that the main early disabling factors to CVA recovery are pain and stress inhibition. Thus rehabilitation needs to be about coaxing patients to overcome their inhibitions and compensations.
    As to research outcomes, I can only say I have witnessed many good recoveries over my working life and I strongly suspect they are not spontaneous. The reason why there are so few good results today, I feel is due to the fact that there is too much emphasis on compensatory function and not enough on quality movement.

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  11. well Jackie that’s an interesting point. I certainly don’t dispute that amazing recoveries do happen.
    I do disagree and can assure you that I am seeing many good rehab results today all around the world. Of course how we define and measure these results becomes the topic of many blogs in their own right.

    so I think you are saying that aiming to achieve automatic movements can be a useful focus of therapy. this seems reasonable to me.
    however- and –
    There is so much of movement that does require processing that happens above the foramen magnum (eg planning, initiating, monitoring, adjusting, guiding to the right location in space, adapting to the cognitive demands/affordances of the environment or an object that is being interacted with) – that I am suggesting that compensation is a necessary and good thing. So this still leaves me trying to understand in which way the term “compensation” may be an unwanted thing.

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  12. How does Bobath suggest treatment when the functional control area in the motor cortex is dead? No movement. It seems Bobath is making an assumption that it is just faciltating spontaneous recovery in the penumbra. I’m just a survivor who had NDT in the first year although I doubt anything could be attributed to NDT vs. spontaneous recovery. My therapist never saw any of my scans.

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    1. Due to being away on holiday, I have been slow to reply. I do apologise.
      I agree with you Andrew that there is a lot of movement processing above the foramen magnum and that the neurones responsible for this function are often destroyed following a CVA. But because the brain has spare neurones in other undamaged parts of the brain movement loss need not be so devastating. Also, as I stated previously, automatic movement can still function normally in certain situations. Higher centre sensory awareness is not essential for normal automatic movement function.
      Personal observation and experience has led me to reason that the main disabling factor to CVA and hemiplegia is sensory/general information inattention and not movement loss. An injured brain just cannot do too many functions at one time. It has to forego one function to compensate for another lost function. Thus functions such as visual attention, auditory attention and kinaesthetic attention can be temporarily lost in the process of neuronal compensation and one area of neurones compensating for the loss of function in another area.
      I thus see this aspect of neuronal compensation as essential and a normal healing process to CVA rehabilitation.
      The form of compensation that I usually refer to when I talk about compensation is joint stability. I work on a personal hypothesis that an injured brain is unable to cope with too much sensory information. Therefore to minimise this afferent neuronal information, patients compensate by using the structural mechanical forces and properties of bone, fascia and the principles of tensegrity.
      When patients use this form of compensation they lose their normal dynamic base of support and normal dynamic joint stability. Thus when handling a patient or observing a patient move, a Bobath therapist will state a patient is “fixing” when they notice movement has changed from fluid dynamic movement to a state of rigidity. Associated Reactions (ARs) can usually be observed at this moment of time.
      This type of compensation, I strongly feel needs to be discouraged. It only leads to abnormal plasticity, shortened and distorted muscles, loss of normal proprioceptor firing and loss of automatic movement.
      To answer your question oc1dean I can only state that Berta Bobath herself strongly felt that patients had a “potential” to move more normally and that it was all too easy to destroy this potential by allowing a patient to compensate. She wrote a very strong letter in “Physiotherapy”.
      When using the word “potential” I believe she was talking about the normal automatic postural re-actions that she was able to facilitate through her good sensitive handling. Having observed Mrs Bobath handle patients herself, I was just amazed at what she could do. She managed to help a lady straighten a strongly flexed hemiplegic arm and facilitate a normal supporting reflex through a beautifully straightened arm and open hand.

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