Sarcopenia in stroke—facts and numbers on muscle loss accounting for disability after stroke

Abstract

Stroke is the third leading cause of death and the leading cause of disability in Western countries. More than 60% of patients remain disabled, 50% of patients suffer from some hemiparesis and 30% remain unable to walk without assistance. The skeletal muscle is the main effector organ accountable for disability in stroke. This disability is, however, traditionally attributed to the brain injury itself and less attention is paid to structural, metabolic and functional aspects of muscle tissue. Hemiparetic stroke leads to various muscle abnormalities. A combination of denervation, disuse, inflammation, remodelling and spasticity account for a complex pattern of muscle tissue phenotype change and atrophy. While the molecular mechanisms of muscle degradation after stroke are only incompletely understood, a stroke-related sarcopenia may be concluded. Reinnervation, fiber-type shift, disuse atrophy and local inflammatory activation are only some of the key features to be addressed. Despite the importance for optimum post stroke recovery, stroke-related sarcopenia is not recognised in current guidelines for stroke therapy and rehabilitation. A total of not more than 500 patients forms the basis for all available evidence on clinical muscle changes after stroke. A lack of robust evidence on muscle pathology after stroke and on treatment strategies becomes apparent that needs to be addressed in an interdisciplinary integrated approach.

Stroke-Related Sarcopenia: Specific Characteristics

“…26 Markers of inflammation have been found in the musculature of the paretic and nonparetic limbs. 27,28 Ongoing inflammation, intramuscular lipid deposition, and sympathetic activation affect the insulin sensitivity and the consequence is muscle wasting.…”

Body Weight After Stroke

“…41 Generally, paretic stroke leads to loss in muscle mass, intramuscular fat deposition, and reduction of cross-sectional area. 21,22 However, what are the mechanisms underpinning muscle wasting after stroke?…”

Evaluation of C-terminal Agrin Fragment as a marker of muscle wasting in patients after acute stroke during early rehabilitation

“…A combination of mechanisms, including immobilization, disuse, inflammation, metabolic, and neurovegetative imbalance after stroke, results frequently in muscle wasting and may progress to the stroke‐related sarcopenia 1, 7. The presence of stroke‐specific sarcopenia has been proposed from experimental8 and clinical data 9, 10…”