The struggle between heat and ice

This debate is one of the oldest in musculoskeletal therapy. To heat or to ice? I have given this a great deal of thought during my studies and continue to investigate the pros and cons of each approach. The following post outlines my views on the subject and ultimately my opinion on which is best used in clinical practice.

The debate between heat and ice invariably looks at the effect each will have on the inflammatory process. 

When considering this effect we need to:

1). Understand the inflammatory process and hence

2). Understand the variables that can be manipulated to alter the inflammatory process.

It would be tedious of me to go through the process of inflammation so I will highlight the variables that can potentially be manipulated by temperature:

1). Vasodilation

2). Vascular permeability

HEAT

Vasodilation

Many would consider that in the case of heat the inflammatory process will be exacerbated. Is this in fact the case? In the circumstance of vasodilation the blood vessels have already expanded and the degree to which they can be further dilated would be marginal. In fact it is worth considering that the superficial blood vessels of the skin will expand resulting in a re-distribution of blood to the superficial tissues and hence the possibility of reduced blood flow to the site of inflammation. However, the effect of this would be extremely small and most likely not clinically relevant.

Vascular permeability 

I am not sure if it is 100% understood how the blood vessels become ‘leaky’ in the event of inflammation. It is most likely a combination of the influence of chemical mediators and the change in structure of the vascular wall following vasodilation (I like to imagine a deflated balloon with holes and visualize the increased size of these holes as the balloon expands). Heat I would imagine has little effect on the permeability of the blood vessels (possible indirect effect through vasodilatory influence).

It would appear that by considering the above that heat has very little influence on the inflammatory process and is therefore not indicated for use in patients suffering from ACUTE inflammation. However, what about chronic inflammation and long-standing musculoskeletal conditions.

In these cases the patient has:

1). Undergone long periods of reduced mobility in a particular articulation (or articulations)

2). Subject to long standing pain

Given these factors with long-term musculoskeletal conditions I will highlight the benefits of heat.

Reduced mobility

In order to understand how heat will benefit the patient in regards to reduced mobility I would like you to watch gil hedley’s fuzz speech. 

 

                                                                      Fuzz Speech

Klingler (Klingler W 2011 IN: Schleip, Findley, Chaitow & Huijing, Fascia in Manual and Movement Therapies, Elsevier IN PRESS) has shown that the thoraco-lumbar fascia extensibility modifies when heated - taking nearly 50 Newtons of pressure to lengthen at 20ºC as against under 40 Newtons, at 50ºC (over a 3 minute period). This would suggest that the application of heat may allow for increased movement and is also I believe an explanation for why exercise is important (our body temperature increases as we exercise).

Long standing pain

This is where the psychological influence of heat application is beneficial. Generally people are comforted by the application of heat. It can be a pleasurable sensation (as opposed to ice) and therefore can play a role in pain relief through psychological and neurological processes.

Based on the above thought processes I would conclude that heat is indicated in long-standing musculoskeletal conditions and also in the presence of low back pain (acute or chronic).

ICE

It is logical that the application of ice would result in reduced vasodilation and therefore reduced blood flow to the area of inflammation. This would in theory reduce oedema and promote increased ROM and also reduce the number of inflammatory mediators thereby reducing vascular permeability and reducing pain sensitivity. In simple terms, ice slows down and in very low grade acute inflammatory states may stop the process. This is probably why ice baths are advocated after sporting activities, also why I would advocate their use.

Therefore I would advocate Ice in the use of more ACUTE injuries as opposed to long-standing conditions.

Conclusion

Much of this may be quite straight forward, but it is a topic that is continually debated and I felt I would provide a post that would attempt to bring some clarity to the subject.

I would welcome and encourage any other ideas and thought on the topic.

The slump test as a myofascial tension test

In recent times I have finally managed to gain hold of a copy of the renowned anatomy trains by Thomas Myers. I recently finished reading the chapter in regards to the superficial back line (SBL). For those of you who have not read the book the SBL is a continuous connection between myofascial structures from the plantar fascia to the galea aponeurotica (scalp fascia). Reading about the continuity of the SBL got me thinking about the Slump Test. From my experience (which is very little at the moment) the Slump test is one of the most commonly performed special tests and possibly the most commonly performed neural tension test (given the prevalence of low back pain). 

                                                                       Slump Test

The slump test is deemed to fall in the category of a neural tension test as each progressive manoeuvre gradually increases tension within the neural tissue of the spinal cord and peripheral nerves of the lower limb. However, in light of the SBL, it would appear that a positive result in this test would not exclusively be a sign of neural tension (given that tension would also accumulate along the course of the SBL). Therefore, the Slump test should also be considered a myofascial tension test with a positive possibly indicating pathology of the myofascial tissues that contribute to the formation of the SBL. I am sure this same thinking can be applied in other ways.

   Superficial Back Line

An alternative view on the function of fascial adhesions

I recently came across this picture which was posted by Leon Chaitow courtesy of Professor Andrzej Pilat. It posed major discussion and got me thinking as to what it is we are actually seeing. The majority conclusion was that we are visualizing an adhesion between fascial planes. It has previously been shown by Helen Langevin PhD that fascial planes of the lumbodorsal fascia slide and glide freely in asymptomatic patients and become stuck in individuals with low back pain. Based on this one may conclude that what we are seeing here is an abnormal connection between fascial planes. Therefore, we should implement a treatment technique designed to ‘break’ the adhesion and allow for free movement.

Fascial Adhesion

However, there are always two sides to the one story and the question needs to be asked, is this in fact abnormal? Or is the connection between these two fascial planes there for a reason and a good one? I proposed the possibility that we are in fact visualizing a compensatory mechanism whereby the body is re-distributing forces from one fascial plane to the other. Much in the same way the tibia re-distributes force to the fibula via the interroseous membrane. This would mean a different treatment approach and one that is more osteopathic in thinking. 

Let us consider we adopted a treatment approach designed to stress this ‘adhesion’. How would the body respond? Would it be beneficial? If the adhesion is there to distribute force, then when it is subjected to increased force it will respond by strengthening it’s connection to cope with the increased stress. Perhaps this is why local treatment in a lot of cases only provides short-term results. Initially you may have elongated the fibres of this connection allowing initial freedom of movement, however the force used to develop this freedom has stimulated a process that reinforces the connection.

I believe the above approach is flawed for the reasons I have given. What then is the right approach? You may not like my answer but it is INDIVIDUAL to the patient. The human body is an extremely complex organ and hence developing the right treatment approaches do not come about easily. The patient will have a biomechanical problem, or multiple biomechanical problems that have lead to this need for force distribution. It is like adding an extra strut to the framework of a building for extra support. 

It would be great to see a large scale dissection study to see if these adhesions are common. If anyone is aware of any I would love to know. I want to end this post by saying that I am merely hypothesizing as I will do with the majority of my posts. I may be completely wrong at times but it is all in the search for a better understanding.

Why the cuboid?

Manipulation of the cuboid

Just a quick post

Something that has come to my attention is the way in which a cuboid manipulation is performed and it occurred to me that this technique is effective due to the mechanical compensations occurring at this articulation in the event of pronation. When the arch flattens the cuneiforms approximate inferiorly, this causes the lateral cuneiform to pull the cuboid into eversion. When performing a manipulation of the cuboid the practitioner places their thumb on the medical aspect of the cuboid to promote inversion, the other hand position is on the 4^th and 5^th met into plantarflexion and adduction (components of supination) resulting in a repositioning of the cuboid and allowing other techniques designed to combat pronation to be more effective. I have found that this technique almost always achieves cavitation in patients with pronated feet and is not effective in supinated or neutral arches. The same philosophy applies with thrusts directed at the cuneiforms (non-effective in the pronated foot and effective in supinated feet).

Perceiving the Imperceptible

Sensing the Imperceptible: The human cranium

You see before you a dreamer – one who had to get away from the texts, as did Dr Still, and follow something he could not explain. Something that kept him digging into his dreams
‘William Garner Sutherland’

This particular post is intended for the reading eyes of the health professional, in particular osteopaths. Having studied osteopathic medicine for the past 5 years it has become obvious that there are contrasting styles in the way in which different individuals treat their patients. The most obvious difference being the divide between those who prefer a more structural approach to those who opt for the ‘gentler’ functional methods. The most controversial of these approaches seems to be techniques aimed at manipulating cranial bones (termed cranial osteopathy). I myself have modelled my treatments to the structural approach and have been highly sceptical of techniques aimed at influencing the articulations of cranial bones. Although I can’t help but wonder if this scepticism is justified, so I have decided to examine the cranial approach to see if it has any merit.

There is no doubting that the articulations between cranial bones (known as sutures) move. This has been proven again and again through research. The problem is that these movements are extremely small in amplitude (1mm and less). The contention of cranial osteopathy is that all of the cranial bones move at their sutures in a rhythmical fashion. This rhythm has been termed the cranial rhythmic impulse (makes sense). This too has been shown through research and even conventional medical textbooks agree that there is the presence of a slow oscillating rhythm. However, the debate begins to arise with the following questions:

What is causing this rhythmical movement?

Can we both palpate and therapeutically alter the movements of the cranial bones and hence influence the rhythm?

An Osteopath by the name of William Garner Sutherland was the first to describe these movements and hence was the first to propose a theory behind its cause. He concluded that a phenomenon known as the ‘Primary Respiratory Mechanism’ was the cause of these movements. The problem is that more than 60 years after Sutherland described the PRM we still don’t know what it actually is. I am also yet to be offered even a proposed theory as to what the PRM (after 3 months of classes). All I have been taught at university are 5 of its effects but nothing of its cause. This is a bit of a problem. If we are going to treat using this theory we need to at least develop a theory as to its cause. Luckily, through a bit of research of my own, I have come across some research papers which have looked at proposed causes for the PRM. It appears that there is a phenomenon in the body known as the traube-herring oscillation which just happens to share the same frequency as the Cranial rhythmical impulse (coincidence I think not). The traube-herring oscillation is defined as follows:

Slow oscillations in blood pressure usually extending over several respiratory cycles; related to variations in vasomotor tone; rhythmical variations in blood pressure.

This explanation for the cause of the PRM makes sense for the following reasons:

The PRM is proposed to be felt anywhere over the body (method of treatment in the field of biodynamics). The traube-herring oscillation is present throughout the entire body not just the cranium. I propose the following theory regarding treatment using cranial manipulation. If the traube-hering oscillation is a reflection of autonomic activity (variations in blood pressure and vasomotor tone reflect autonomic activity) then the PRM and the CRI is an expression of autonomic activity and hence cranial osteopathy deals with the treatment of the autonomic nervous system through manipulation this rhythm.

Ok, so I have attempted to put together an answer for the first question, now the next question. Can we both palpate and therapeutically alter the movements of the cranial bones and hence illicit a change in autonomic activity?

This has been the biggest problem for me to come to grasps with. Initially looking on the surface it would seem unlikely that we can perceive and manipulate such small movements. I can only speak from experience and say that I have definitely felt two rhythms. One that would correlate with pressure changes due to the cardiac cycle and a second more closely resembling the Traube-hering oscillation. Evidence also appears to back up that we can perceive this motion. Can we manipulate it? Given that the proposed contact required to manipulate these sutures are extremely light and small in nature to the normally structurally oriented practitioner it is difficult to grasp the concept of influencing these movements. I mean, if the cranium feels so firm and rigid to forceful contacts how will light contact illicit a change.

In order to better appreciate the possibility of manipulating the sutures let us consider the properties of water and how it may possibly relate to these articulations. When water is met with forceful contact it exhibits a rigid property, however, if we lightly caress the water it assumes a more malleable (and manipulable) state. It would make sense that sutures possess the same qualities. Rigid to force for protective and structural reasons and malleable to small forces for functional and physiological reasons.

The most important question of all is can we use this to illicit a therapeutic change in our patients? How would we do this? There is a current nomenclature in cranial osteopathy that deals with strain patterns and their correction, however, I think there is cause for another approach. This approach would involve illiciting an artificial frequency with our hands to alter the frequency of the traube-hering oscillation. This concept is usually termed entrainment and has been demonstrated in other physiological processes, most notably the menstrual cycle. By increasing frequency we would amplify the activity within the sympathetic nervous system and by decreasing the frequency we would dampen activity within the sympathetic nervous system. There has already been one study which has shown that cranial techniques improve latency to sleep which may be due to its effect on the autonomic nervous system (they did not use methods that would result in entrainment).

Some osteopaths use cranial osteopathy as their only means of treatment, I strongly disagree with this practice. Some osteopaths prefer a strictly structural approach. However, should we be distinguishing between a structural and functional approach? Shouldn’t manipulation of the cranial bones merely be viewed as simply another form of osteopathic technique rather than some specialised field of therapy? The only difference is you are working with the structure of the skull as opposed to the structure of the spine, shoulder, knee, ankle etc. In any case, I think the theoretical evidence behind cranial manipulation cannot be ignored and its acceptance will only come with clinical trial evidence, which for obvious reasons is difficult to obtain. Nevertheless, if you consider yourself to be an osteopathic physician in the true sense of the word, then you should not neglect the reciprocal nature of structure and function expressed by the cranium.