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 Ive screwed 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.
The spasticity/ tone thing
The Bobath tutors say: Clinicians practicing the Bobath concept address both neural and non-neural elements of tone to potentiate improved muscle activation patterns, minimize unnecessary compensatory movement strategies, and identify potential secondary impairments.
This is a bit tricky to tackle as ‘tone’ has never been defined, as it is often used (rightly or wrongly) interchangeably with spasticity, so we’ll go with that. The statement above indicates that Bobath-ers believe that tone/spasticity is the primary impairment that gives rise to everything. Presumably, this means that they believe that most, if not all, neurological patients have abnormal tone. The upper motor neuron system is a useful way to understand the component of neurological motor dysfunction. It identifies negative features (ie aspects of motor control that are lost – weakness) and positive features (the aspects which are exaggerated, ie. spasticity). Then there are adaptive changes (soft tissue shortening) which are secondary to both. Probably the best place to read more about the UMN syndrome is in the Carr & Shepherd books, they were the ones who 1st introduced it.
Now the evidence that the BB beliefs are wide of the mark:
A minority of stroke patients are spastic and spasticity has a poor relationship (ie isn’t very important) with function (Sommerfield et al. Spasticity after stroke: Its occurence and association with motor impairments and activity limitations. Stroke 2004; 35:134–139)
The element of the UMNS that is most closely related to function is weakness, not abnormal tone
- Harris & Eng (2007) Paretic Upper-Limb Strength Best Explains Arm Activity in People With Stroke. Physical Therapy Volume 87 Number 1 88-97. (http://ptjournal.apta.org/content/87/1/88.full.pdf+html).
- Disa et al.(2004) Spasticity After Stroke: Its Occurrence and Association With Motor Impairments and Activity Limitations. Stroke 35, 134-139. (http://stroke.ahajournals.org/content/35/1/134.long).
- 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 (http://www.fizjoterapeutom.pl/files/29/Ross%20SA%202007%20Relationships%)
This is why exercise is an effective treatment – it works on the main problem. Exercise improves strength/ weakness, endurance, fatigue, mood, function and doesn’t increase spasticity (in fact it may reduce it)
- Clin Rehab 2004;18:833-862; Lancet Neurol 2009; 8: 741–54; Cochrane reviews of exercise interventions in http://onlinelibrary.wiley.com/cochranelibrary/search
Despite all the assertions by Bobath-ers, there is no objective evidence that treatment using the Bobath Concept has any effect on weakness, muscle activity or spasticity/tone. Nor that altering tone has any has any effect on muscle activation patterns, strength, soft tissue or function. A probable reason for the lack of effect found in the only study of the effects of Bobath (Lennon et al D& R 2006:28;873-881– you must know this reference off by heart by now!) is that by aiming to change tone and quality of moment they were targeting the wrong element. We should be primarily treating weakness not tone. Forget about the tone thing alrighty, and get with the programme – it’s all about the weakness these days.