Causes of CTS
There is a natural human inclination to want to know why something has happened to us, and an understanding of the causation of disease can help in treatment and prevention. Causation is rarely simple - a fall leading to a wrist fracture appears simple enough at first glance but even then one might ask, at a slightly deeper level - “Why did I fall?” and “Is there anything about my bones which might make them break more easily?” Many medical disorders result from the interaction of several patient and environmental factors and rarely do we fully understand all of them.
In the case of carpal tunnel syndrome the one thing that is in no doubt at all is that there is a problem with the median nerve at the wrist. This is part of the definition of CTS so there can be no argument but that does not mean that problems somewhere else could not also be contributing to the overall symptoms. People who argue that CTS is frequently due to nerve compression further up the median nerve are misusing the term - there are perfectly good medical terms to describe nerve compression in the forearm, at the brachial plexus or in the neck and it does not aid the choice of appropriate treatment if these disorders are confused with CTS. Most cases of CTS do not have an immediately obvious 'cause' and this discussion relates mainly to these 'idiopathic' CTS cases.
The immediate cause of the median nerve injury is generally believed to be raised pressure in the carpal tunnel which obstructs the circulation to the nerve. Most people are familiar with the symptoms which result from direct pressure on a nerve for a few minutes, for example the numbness and tingling of the little and ring fingers which results from leaning on the ulnar nerve at the elbow for too long, and such symptoms are similar in character to those experienced in the early stages of CTS. The pressure in the carpal tunnel has been measured experimentally and been shown to be higher in CTS patients than in asymptomatic individuals (Gelberman 1981) but this observation immediately begs the further question -
Why is the pressure elevated?
Maintaining a pressure in a space usually requires that there are some boundaries to that space. These can be obvious and physical - a bicycle tyre holds air inside so that it can be pumped up to a high pressure - or more subtle - the maintenance of atmospheric pressure requires the gravitational attraction of the earth to provide a virtual boundary to the atmosphere. The carpal tunnel does not possess a complete surround of physical barriers - it is literally a tunnel which is open at both ends like a railway tunnel and just as, in a railway tunnel, the air pressure is much the same inside the tunnel as outside it, one would normally expect the tissue pressure in the carpal tunnel to be much the same as that in the forearm or the hand. The first thing we therefore need to understand is how this odd observation can be explained.
For such an explanation we have to turn to the physical properties of the stuff inside the tunnel. In a railway tunnel the air inside is a very mobile substance which can easily flow in and out of the ends and thus, if a pressure imbalance does arise, air flows from the area of higher pressure to that of lower pressure and the two equalise. The contents of the carpal tunnel are a complex mixture of tissues which are not, overall, as fluid as air or water. Even the water content of biological tissue is not entirely free to move around in order to equalise pressure, much of it being compartmentalised inside cells or bound up with other larger molecules in gel structures. It is this property of the carpal tunnel contents which allows us to have a higher pressure in the tunnel than just outside it, essentially the stuff inside cannot get out, not because there is no way out, but because its mobility is restricted by its physical and chemical properties. Now that we have a grasp of how the pressure in the carpal tunnel can be raised we need to ask...
What is different about the carpal tunnels of sufferers as opposed to that of normal individuals?
Traditionally this has been reduced to a very simple idea, either there must be more stuff in the tunnel, or the tunnel itself must be smaller, or some combination of the two. In a minority of patients there turns out to be an obvious reason why the carpal tunnel pressure is high based on this model. Fractures of the wrist bones can physically narrow the tunnel, patients with inflammatory disorders can get swelling of the tendons inside the tunnel and occasional patients turn out to have something inside the tunnel which would normally not be there - muscle, tumour, gouty deposit, infection etc. Such cases may be considered 'Secondary CTS' caused by other disease. However most cases of CTS do not have such an obvious cause.
Much experimental work has been devoted to studies of carpal tunnel dimensions and contents based on this concept and as early as 1980 it was suggested on the basis of computed tomography studies that women with CTS had smaller carpal tunnels than female controls and that women had smaller carpal tunnels than men (Dekel 1980) but subsequent answers have been surprisingly inconclusive, in particular when the size of the carpal tunnel is compared with the size of the contents - a smaller tunnel in absolute terms does not matter if structures within it are also smaller in a smaller individual. Overall there is no clear consensus that CTS is caused simply by having a congenitally smaller tunnel. We can however suggest an alternative possibility - perhaps all that is needed for the carpal tunnel pressure to increase is a change in the physico/chemical properties of the tissues in the tunnel which reduce their fluidity, thus providing an invisible barrier to equalisation of pressure with that outside the tunnel.
Some evidence is available which gives further clues about causation. A good explanation of the cause of CTS would satisfactorily explain all the clinical, epidemiological and experimental observations, so the next few pages will summarise much of what we know about CTS under four headings:
Revision date - 5th May 2012