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

Background: CNS lesions that are acquired early in life e.g. cerebral palsy (CP) disturb muscle development and growth, while CNS injuries acquired later in life e.g. stroke, affect fully matured muscles and cause paresis and atrophy. These differences may result in different contracture phenotypes. Aim: The purpose of this study was to compare systemic biomarkers and gene expression levels in muscle of individuals with CNS lesions acquired early and later in life. Methods: Blood samples and muscle biopsies were analyzed using Enzyme-linked immunosorbent assay and Real-time PCR from n = 24 control participants, n = 14 individuals with cerebral palsy, and 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 Kinase-MB and C-Reactive Protein were significantly elevated in stroke patients only (p < 0.007 & p > 0.034 respectively). Gene expressions: The expression of myostatin (MSTN) was significantly lower in both the ST and the CP group when compared to Ctrl (p = 0.02). In addition, collagen type 4A1 (COL4A1) was significantly lower in the CP group compared to the other groups (p = 0.015). Finally, the troponin 1 slow skeletal muscle type was significantly increased in the ST group when compared to both CP and Ctrl (p = 0.03). Conclusion: The downregulation of myostatin in individuals with both early and late CNS injury is likely a compensatory reaction to muscle weakness, reduced muscle mass and/or muscle atrophy. Changes in gene expression may reflect a specific alteration depending on when in life the CNS lesions were acquired.