Cerebral Palsy and Stroke—Early and Late Brain Lesion Present Differences in Systemic Biomarkers and Gene Expression Related to Muscle Contractures

Abstract

Background: CNS lesions that are acquired early in life e.g. cerebral palsy (CP) \ndisturb muscle development and growth, while CNS injuries acquired later in \nlife e.g. stroke, affect fully matured muscles and cause paresis and atrophy. These differences may result in different contracture \nphenotypes. Aim: The purpose of this study was to compare systemic \nbiomarkers and gene expression levels in muscle of individuals with CNS lesions \nacquired early and later in life. Methods: Blood samples and muscle \nbiopsies were analyzed using Enzyme-linked immunosorbent assay and Real-time \nPCR from n = 24 control participants, n = 14 individuals with cerebral palsy, \nand n = 12 stroke survivors. Results: Systemic markers: Myostatin was significantly decreased in both the cerebral palsy (p = 0.0051), and the stroke group (p = 0.036). Creatine \nKinase-MB and C-Reactive Protein were significantly elevated in stroke patients \nonly (p 0.034 respectively). Gene expressions: The expression of myostatin (MSTN) was significantly lower in both the ST and \nthe CP group when compared to Ctrl (p = 0.02). In \naddition, collagen type 4A1 (COL4A1) was significantly lower in the CP \ngroup compared to the other groups (p = 0.015). Finally, the troponin 1 slow \nskeletal muscle type was significantly increased in the ST group when compared \nto both CP and Ctrl (p = 0.03). Conclusion: The downregulation of \nmyostatin in individuals with both early and late CNS injury is likely a \ncompensatory reaction to muscle weakness, reduced muscle mass and/or muscle atrophy. Changes in gene \nexpression may reflect a specific alteration depending on when in life the CNS lesions were acquired.