Hemiparetic stroke leads to various muscle abnormalities: A combination of denervation, disuse, inflammation, remodelling and spasticity accounts for a complex pattern of muscle tissue phenotype change and atrophy. The molecular mechanisms of muscle degradation after stroke are only incompletely understood. Reinnervation, fibre-type shift, disuse atrophy, and local inflammatory activation are only some of the key features yet to be explained. Only limited data is available today on clinical muscle changes after stroke that results from few studies in a mere 500 patients. Despite its importance for optimum post stroke recovery, stroke-related sarcopenia is not considered in current guidelines for stroke therapy or rehabilitation and measurement tools to address sarcopenia are infrequently used. This lack of robust evidence on muscle pathology after stroke and on treatment strategies needs to be addressed in an interdisciplinary integrated approach.
This review provides an overview on current pathophysiologic insights and on clinical relevance of sarcopenia in stroke patients and on measurement tools to address the problem in the clinical setting.