Expression of and correlational patterns among neuroinflammatory, neuropeptide, and neuroendocrine molecules from cerebrospinal fluid in cerebral palsy

Abstract

Background The underlying pathogenesis of cerebral palsy (CP) remains poorly understood. The possibility of an early inflammatory response after acute insult is of increasing interest. Patterns of inflammatory and related biomarkers are emerging as potential early diagnostic markers for understanding the etiologic diversity of CP. Their presence has been investigated in plasma and umbilical cord blood but not in cerebrospinal fluid (CSF). Methods A clinical CP sample was recruited using a single-time point cross-sectional design to collect CSF at point-of-care during a standard-of-care surgical procedure (intrathecal pump implant). Patient demographic and clinical characteristics were sourced from medical chart audit. Results Significant (p ≤ 0.001) associations were found among neuroinflammatory, neuroendocrine, and nociceptive analytes with association patterns varying by birth status (term, preterm, extremely preterm). When between birth-group correlations were compared directly, there was a significant difference between preterm and extremely preterm birth subgroups for the correlation between tumour necrosis factor alpha (TNFα) and substance P. Conclusion This investigation shows that CSF can be used to study proteins in CP patients. Differences in inter-correlational patterns among analytes varying by birth status underscores the importance of considering birth status in relation to possible mechanistic differences as indicated by biomarker signatures. Future work should be oriented toward prognostic and predictive validity to continue to parse the heterogeneity of CP’s presentation, pathophysiology, and response to treatment.

Electroacupuncture activates the peroxisome proliferators‐activated receptor pathway to improve the phenotype of cerebral palsy

“…32 Neuroinflammatory responses play a crucial role in this process, releasing numerous pro‐inflammatory factors and lipid peroxidation products, leading to neuronal death, delayed brain cell differentiation, and myelination, ultimately progressing to CP. 33 Therefore, finding effective means to suppress post‐ischemic–hypoxic brain inflammation and promote neural functional recovery is key to treating CP. Current research indicates that Ros's primary mechanism in treating neurodegenerative diseases is through inflammation suppression for neuroprotection.…”

“…Ischemic–hypoxic brain injury, a primary pathological feature of CP, involves brain tissue changes due to partial or complete lack of oxygen, reduced or halted cerebral blood flow 32 . Neuroinflammatory responses play a crucial role in this process, releasing numerous pro‐inflammatory factors and lipid peroxidation products, leading to neuronal death, delayed brain cell differentiation, and myelination, ultimately progressing to CP 33 . Therefore, finding effective means to suppress post‐ischemic–hypoxic brain inflammation and promote neural functional recovery is key to treating CP.…”