In the last blog we established that tendon injuries are caused by focal overload. The overload can come about through poor mechanics, poor equipment, poor training load/frequency, or acute overload.
Once this occurs we start the cascade!
Weaker tendon fibers start to yield, tenocytes (specialised cells) are triggered and start producing more matrix to make more fibers and things get a bit messy. It is important to note that this load and response is a normal function. In fact, it is one of the aims of training to incite this increased production. Unfortunately we can get into issues if this relationship is lop-sided. If production can't keep up with demand, then we end up with lower quality, more easily damaged fibers; hence the mess.
Interestingly, most of this is completely asymptomatic; you wont feel a thing! Furthermore, the VAST MAJORITY of these tendon issues will self resolve without ever producing symptoms, and certainly without limiting function.
Then, there are the ones that bark. For reasons that are still under investigation, some tendinopathies do become symptomatic. The presentation is varied and does not correspond reliably with the level of damage seen on scans.
Scans can be useful in helping to clarify a tricky diagnosis, but most of the time a clinical diagnosis is sufficient, and scans can actually complicate the situation. One of the reasons for this is the prevalence of asymptomatic tendinopathies in the general and sporting public.
What becomes more important than pathology, is the impact of the injury on quality of life. The level of reported pain and disability and is more important than the results of a scan.
It becomes the physio's job to establish where the patient is currently in regards to these factors, where they want to be, and work with the patient to work out how to get there.
To help demonstrate this process, we will go through a case study in part 3, illustrating the stages of tendon change, and how we deal with them.
- James Sincock