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.