Changes in muscle architecture in people with muscle contracture after stroke
Muscle contracture is a major cause of disability and deformity after stroke. It results in a stiffening of the muscles that limits normal joint movement or causes deformity. Contractures arise when brain lesions produce paralysis or spasticity, which cause muscles to experience different patterns of activity, different changes in length, and different forces. The muscles adapt by becoming stiffer, and the joints become less mobile.
Many people who have had a stroke or traumatic brain injury develop contractures of the calf muscles. Contractures impede ankle motion, making it difficult to stand or walk normally. Similarly, contractures of shoulder muscles can impair the ability to reach, and contractures of wrist and finger muscles can impair grasp. For many people, contractures become a much greater impediment to normal movement than the paralysis or spasticity that initially caused the contracture to develop.
There has been surprisingly little research into the mechanisms of contracture. Studies on models have shown that the stiffening of muscles occurs either because of changes in the muscle tissue, or because of changes in the tendons. However, it is still not clear whether contractures in people with certain injuries and illnesses are due to changes in the muscle fibres, tendons or a combination of both.
We are currently seeking volunteers to learn more about the mechanisms of contracture and test new treatments. One study is looking at how muscle tendons and fibre bundles change shape during movement, which will inform subsequent clinical studies in people with contracture. This study uses diffusion tensor imaging (a type of MRI) to identify architectural changes (such as changes in length and arrangements of muscle fibres and the lengths of tendons) in people who have muscle contracture after stroke.
If you are interested or are aware of someone who might be interested in participating in this study click here