Dr. Fred Clary's Functional Analysis Chiropractic Technique

Any discussion of the Bobath Concept requires a common understanding of what the Bobath Concept is. In an interview almost twenty years ago, Bobath explained it this way: "......... A whole new way of thinking, observing, interpreting what the patient is doing, then adjusting what we do in the way of techniques- to see and feel what is necessary, possible for them to achieve. We do not teach movements, we make them possible........." (Bobath, 1981). It was also made clear that Bobath was not a method or technique, not limiting, but fluid; was not rigid but changing, and still changing. The Concept can be summarised as follows: It is primarily a way of observing, analysing and interpreting task performance. This also includes the assessment of the client's potential, which was considered to be that task or those activities which could be performed by the person with a little help, and therefore possible for that person to achieve independently where possible. Of course the Concept also involves the use of various techniques, and Bobath always advocated that the therapist should- "do what works the best" (Bobath, 1978). In the present day, this should mean, that therapy is based on sound evidence when it is available, while recognising that currently much of what therapists do has not been evaluated. This does not mean that these therapy strategies should be discarded, but does mean that they require investigation and possibly an alternative explanation of their effect. There is evidence to support some of what therapists do, but there are still many unanswered questions. For the Bobath therapist, there is also the dilemma of what it means to be a Bobath therapist. A study by Davidson and Waters (2000) showed that 88% of neurological physiotherapists in the UK use the Bobath approach. But, it depends on when you trained, where and who with. I very much doubt that those 88% of the therapists surveyed would explain or clinically apply the Bobath Concept with any degree of similarity.

When therapists attending the paediatric course at the Bobath Centre are asked what Bobath, the reply usually concerns the use of techniques of inhibition of abnormal tone and movement patterns, facilitation of more normal movement, and possibly stimulation in cases of hypotonia or muscle inactivity. These techniques should not be considered to be Bobath, and yet for most therapists Bobath these techniques are Bobath. Given the diverse understanding of the Bobath Concept, it seems important to ask this question: Is Bobath a relevant therapy approach in the year 2000? It might be, but only if it is based on current scientific evidence, is actively finding ways to produce such evidence, and additionally an agreement to leave old ideas, such as the inhibition of spasticity, in the past. We need to have the courage to challenge our current practise and clinical reasoning. With this in mind, several of the assumptions underlying the Bobath Concept need to be re-evaluated. The following questions are intended in part to address some of the current issues facing therapists.

1. Is tone relevant? Bobath proposed that the main reason for reduced functional ability resulted from abnormalities of tone e.g. spasticity was thought to be due to abnormally increased tonic reflex activity and therefore could be inhibited. It is necessary to define what normal tone is in order to understand any deviation from that norm.

Tone is the resistance offered by muscles to continuous stretch (Brooks, 1986)

......... at complete rest a muscle has not lost its tone although there is no neuromuscular activity in it (Basmajan & De Luca, 1985)

Normal tone can be defined as a slight constant tension of healthy muscles (Kandel, Schwarz & Jessell, 1991)

A state of readiness (Bernstien, 1967)

These definitions suggest that tone comprises both neural (eg. Proprioceptive reflexes, and arousal level of the CNS) and non-neural (eg. visco-elastic properties of muscle) components. Commensurate with this idea, any abnormal tone will also demonstrate neural and non-neural changes. For many years, spasticity has been clearly defined by Lance (1980) as a velocity-dependent increase in stretch reflexes with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex, as one component of the upper motor neurone syndrome. The UMN which consists of positive symptoms (exaggeration phenomena such as hyperreflexia, extensor plantar response) and negative symptoms (functional deficits such as weakness, loss of dexterity) was described by Hughlings-Jackson (1954), and subsequently explained by Burke (1988) and Carr and Shepherd (1998). When viewed in this context, spasticity is often only a small component of the movement disorder, and in some cases can even be of functional value to the client, e.g. standing. We should conclude from the preceding discussion that spasticity and hypertonia are not the same. Spasticity is a part of hypertonia and of course they co-exist, but velocity dependent hyperreflexia does not usually in itself explain the clients movement disorder, and therefore simply reducing spasticity is not the solution for providing effective, evidence-based intervention. Therapists can reduce hypertonia, but can they by handling inhibit spasticity? The term inhibition was introduced by Bobath as a physiological explanation for the effect of handling on spasticity, based on the assumption that spasticity resulted from exaggerated / released, abnormal tonic reflexes and subsequently abnormal tonic reflex activity (Mayston 2001a). Although on passive movement spasticity is shown to be present by evidence of hyperreflexia, on voluntary movement there is usually an inability to generate sufficient electrical activity in the muscle (Ibrahim et al 1993). Inhibition physiologically is defined as a decrease in transmitter release, a way of moulding excitation and shaping the firing of action potentials, and is present at all levels of the CNS. But suggesting inhibition is a physiological explanation for what therapists achieve by handling is not scientifically correct. Therapists are effecting changes in both inhibitory and excitatory synapses simultaneously, but their "inhibition" also affects visco-elastic properties of muscle and by improving muscle length can gain a better biomechanical advantage for more efficient muscle action for the performance of functional tasks. Handling via stretch will of course affect and reduce muscle spindle firing and resultant abnormal reflex activity, but for any lasting effect of spasticity to be obtained the therapist must enable the client to perform more effective, efficient functional activity.

2. Muscle weakness is secondary to the problems of abnormal tone. For all their working life, the Bobaths considered that muscle weakness was a secondary problem to that of abnormal tone in the management of the neurologically impaired person. They assumed that when hypertonia was reduced the client would have near normal activity with which to function. This may be potentially true, but any person will know that disuse and lack of opportunity to activate muscles results in atrophy and weakness. More significantly, the person with an UMN lesion will most likely lose some of their voluntary drive onto the motoneurone pools in the spinal cord resulting in a lack of activation of muscles for action, despite exhibiting hyperreflexia at rest. Even those with significant velocity dependent hyperreflexia encounter difficulty in generating sufficient voluntary activity, rather than being limited by an exaggeration of abnormal muscle activity on attempts at self-generated activity.

Recent evidence suggests that weakness is a problem for the neurologically impaired adult and child (Bourbonnais & van der Noven 1989; Giuliani 1992). While therapists can work to increase strength by the use of activity, repetition and weight bearing, it has been shown that when used appropriately, strengthening can improve function and does not increase spasticity (Miller and Light 1997; Damiano and Abel 1998). This evidence suggests that therapists must direct more attention to the role of muscle strength and ways of improving it, for the rehabilitation / habilitation of the neurologically impaired person, of course with the proviso that the individual has sufficient muscle activity to participate in a strengthening regime.

3. Bobath proposed that working for normal movement patterns would lead to function. This idea has been misinterpreted by some to the extent that it is thought that the person with neurological impairment can become normal if only they receive the "right" therapy and do not make themselves spastic by overactivity or activity too early. Firstly, the CNS is highly task oriented in its organisation (Flament et al 1993; Ehrsson et al 2000), therefore movement patterns will not automatically lead to function- the function must be practised in the correct context. Secondly, there is no evidence to suggest that stopping a client from moving will stop the development of spasticity. My experience of working with Mrs Bobath was that the therapists role was to help the person function in the best way possible, helping them to counteract any unwanted increase in tone, not to stop them moving. While certain activities are not encouraged in some cases, the idea of stopping a client from moving, especially if they are motivated to do so, cannot be supported on financial, moral or scientific grounds.

Although learning movement patterns might be a part of the re-learning process, clients need the opportunity to practise functional, meaningful tasks if therapy is to be effective.

4. Related to this is the question of compensation. If the CNS is damaged, there will of necessity be a compensation by other parts of the system, which can be either positive or negative, and can be shaped by experience. Compensation means to take the place of that which is lost, but is understood in a variety of ways. For example, the person with hemiplegia will have to compensate with the sound side for the loss of function on the affected side if recovery is less than optimal. The person with spastic diplegia will overuse their upper body and limbs to compensate for the lack of useful activity of their lower limbs. The critical questions to ask are the following: how much of that compensation is necessary and how much can be avoided by training the affected body parts to function more effectively. It has long been part of the Bobath approach to restrain use of the less affected body parts manually during a therapy session to try and activate the affected body parts, e.g. Hold back the sound arm to force the use of the affected arm, providing there is activity for the person to work with. For the person with diplegia, it might mean, activating the legs without overuse of the upper body and arms e.g. to sit to stand without pushing on the arms. Support for this idea is found in the recent work of Taub (Taub, et al 1993; Taub & Wolf, 1997), described as Constraint Induced Therapy, or forced use. One of the basic ideas underlying the Bobath Concept is that each person with a neurological lesion has the potential for improved functional performance- this is one way that it might be achieved for clients who meet the criteria for inclusion in such a regime. I very much doubt that therapy can make a person normal- if so, their CNS had the potential for recovery and they would have been normal anyway (whatever normal is!). The CNS if damaged has to compensate, it is the therapists' job to guide the persons recovery so that they can achieve their maximal functional potential within the constraints of the damaged CNS. How soon and how much is unclear, but Tardieu (1988) states that a muscle must be stretched for 6 hours a day in order for length to be maintained; the clients receiving forced use therapy were trained for at least three hours a day. The work of Nudo (1996) and colleagues indicates that specifically training activity can enhance behavioural recovery and reduce the loss of secondary areas around the infarct. Forced use of the lower limbs by treadmill training has also been shown to be effective in improving function for both adults and children (Hesse et al 1994; Schindl et al, 2000). The caveat is of course, that the person can only enter this kind of regime if they have sufficient activity to utilise. Forced use in clients who have little or no activity may drive negative changes in the CNS and result in further loss of neural tissue around the original lesion site.

These are only a few of the considerations for the Bobath therapist in the light of changes in our understanding of the control of movement and changes in the clinical presentation of clients. It is essential to continuously read the available literature and to review our mode and frequency of therapy intervention. Carr and Shepherd (1998) have contributed much by their aggressive encouragement that we read the literature and act upon it. Their motor learning approach to optimise functional performance is of value in clients with a reasonable level of ability. But what about the less able client, and is the emphasis on training and biomechanics sufficient? It should be noted that their ideas for motor re-learning are predominantly based on data from healthy individuals. It is not known if those same principles can be directly applied to the neurologically impaired person.

I would like to propose some factors that we might take into account when planning an intervention programme.

Muscles need to be at the best length for activation. It is known that muscles generate the most efficient active force at a mid-length. For this reason alone it would seem important to gain alignment (see Fig. 1., Mayston 2001a). This may involve muscle stretching to achieve length, perhaps we could call it tone reduction, the judicious use of equipment and /or orthoses. Sustained muscle stretch may also prepare for more efficient muscle activity by reducing the effect of hypersensitive muscle spindles.

The muscle needs sufficient activity to generate force for action. In the case of reduced drive onto the motoneurone pool, there might need to be stimulation of muscle activity through the use of weight bearing, resistance, sensory stimulation in appropriate postures and patterns to enable the person to have a sufficient basis for the training of functional tasks. Splinting and orthoses may also be indicated to gain alignment, or a good weight-bearing base for improved proximal and truncal activity (Mayston 2001b).

This activity needs to be translated into functional, meaningful goals for that person. Bobath advocated specific preparation for specific function, which is another way of stating this principle of translating activity into function.

There needs to be opportunity for practise for learning/ re-learning to occur, either by the individual or with the help of carers.

Goals need to be realistic according to the client's potential and appropriate to the environment encountered during daily life.

These principles integrate with the main ideas of motor learning theory, which requires the active participation of the client. This is not new. Bobath in the 1960s stated that "unless you stimulate or activate your patient in the way in which new activities are possible, you have done nothing at all. So the handling techniques as such are only the very first step in treatment, though they are very important" (Bobath, 1965).

Secondly, motor learning emphasises the need for practise, also advocated by Bobath though perhaps less rigorously, by stressing the importance of home activities for the client. Thirdly, learning requires that there be meaningful goals, relevant to the client. This aspect of motor learning is now important, and at the Bobath Centre goals are set in collaboration with the client and their family (at least for each child) and their achievement is monitored using a variety of outcome measures.

In summary, the Bobath Concept states that each client has the potential for improved function and that we should work with our clients doing "what works the best". This requires an ongoing knowledge of current scientific motor control and rehabilitation literature, and courage to put old ideas in the past.

References:

Basmajan JV and De Luca, Carlo J 1985 Muscles Alive.

Their Functions Revealed by Electromyography Williams and Wilkins.

Chapter 10 and 11

Bernstein, N 1967 The Co-ordination and Regulation of Movements.

Oxford : Pergamon

Bobath B 1965 Notes on Reflex Inhibiting Postures.

Archival material, Bobath Centre, London.

Bobath B 1978 Course notes, Bobath paediatric 8-week course.

Bobath B & Bobath K 1981 Interview for NDTA. Baltimore.

Bourbonnais D & Van den Noven S 1989 Weakness in patients with hemiparesis.

American Journal of Occupational Therapy: 43: 676-685.

Brooks, Vernon (1986): Neural Basis of Motor Control.

Oxford University Press. Chapter 1,8

Burke D 1988 Spasticity as an adaptation to pyramidal tract injury.

Advances in neurology. Vol 47. Raven Press NY.

Carr J, Shepherd R 1998 Neurological Rehabilitation - optimizing motor performance.

Butterworth Heinemann, Oxford.

Damiano DL and Abel MF. 1998 Functional outcomes of strength training in spastic cerebral palsy.

Archives of Physical Medicine and Rehabilitation; 79: 119-25.

Davidson I, Waters K 2000 Physiotherapists working with stroke patients:

A national survey. Physiotherapy 86: 69-80.

Ehrsson HH, Fagergren A, Jonsson T, Westling G Johansson RS, Forssberg H. 2000 Cortical activity in precision versus power grip tasks: an fMRI study. Journal of Neurophysiology; 83: 528-536.

Flament D, Goldsmith P, Buckley CJ, Lemon RN. 1993 Task dependence of responses in first dorsal interosseous muscles to magnetic brain stimulation in man. Journal of Physiology (London); 464: 361-378.

Giuliani CA. 1992 Dorsal rhizotomy as a treatment for improving function in children with cerebral palsy. In: Movement Disorders in Children, ed. Forssberg H, Hirschfeld H. 247-254.

Hesse S, Bertelt CH, Schaffrin A, Malezik M, Mauritz KH. 1994 Restoration of gait in non-ambulatory patients by treadmill training with partial body-weight support. Archives of Physical Medicine and Rehabilitation; 75: 1087-1093.

Ibrahim IK, Berger W, Trippel M, Dietz V. 1993 Stretch-induced electromyographic activity and torque in spastic elbow muscles. Brain; 116:971-989.

Lance JW. 1980 Symposium synopsis. In: Spasticity: disordered motor control. Ed. Feldman RG, Young RR, Koella WO. Chicago: Year Book of Medical Publishers; 485-495.

Mayston MJ. (2001a) Setting the scene. In: Edwards S, ed, Neurological Physiotherapy - a Problem Solving Approach. 2nd edition, Churchill Livingstone. (in press).

Mayston MJ. (2001b) People with cerebral palsy: effects of and perspectives for therapy. Neural Plasticity (in press).

Miller GJT and Light KE 1997 Strength training in spastic hemiparesis: should it be avoided? Neurorehabilitation, 9, 17-28.

Nudo RJ, Wise BM, SiFuentes F, Milliken GW 1996 Neural substrates for the effects of rehabilitative training on motor recovery after ischaemic infarct. Science 272:1791- 1794

Schindl MR, Forster C, Kern H, Hesse S. 2000 Treadmill training with partial body weight support in nonambulatory patients with cerebral palsy. Archives of Physical Medicine and Rehabilitation; 81: 301-306.

Tardieu C, Lespargot A, Tabary C, Bret MD. For how long must the soleus be stretched each day to prevent contracture? Developmental Medicine Child Neurology 1988; 30: 31-10.

Taub E, Miller NE, Novack TA 1993 A technique for improving chronic motor deficit after stroke. Archives of Physical Medicine and Rehabilitation, 74, 347-354

Taub E and Wolf SL 1997 Constraint induced techniques to facilitate upper extremity use in stroke patients. Topics in Stroke Rehabilitation 3: 38-61