Expression Of And Correlational Patterns Among Neuroinflammatory
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Expression Of And Correlational Patterns Among Neuroinflammatory
Goracke‑Postle et al. BMC Neurol (2021) 21:384 https://doi.org/10.1186/s12883‑021‑02333‑2
R E S E A R C H A R T I C L E
Expression of and correlational patterns among neuroinflammatory, neuropeptide, and neuroendocrine molecules from cerebrospinal fluid in cerebral palsy Cory J. Goracke‑Postle1, Chantel C. Burkitt2, Angela Panoskaltsis‑Mortari3, Michael Ehrhardt3, George L. Wilcox4, Patrick Graupman2, Michael Partington5 and Frank J. Symons6*
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 biomark‑ ers 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 nocicep‑ tive 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, pathophysiol‑ ogy, and response to treatment.
Keywords: Cerebral palsy, Neuroinflammation, Neuroendocrine, Nociceptive, Biomarkers, CSF, Children
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Background Cerebral palsy (CP) is a neurodevelopmental disorder of movement, muscle tone or posture caused by an insult to the developing brain before birth, at birth, or before the
age of two years. CP is the most common motor disabil- ity in childhood, affecting an estimated 500,000 Ameri- can children and occurring in approximately 2 children per 1,000 live births. The pathogenesis of CP is not fully understood. CP risk factors predominantly involve peri- natal factors such as anoxia and ischemia and prenatal factors such as young gestational age, intrauterine viral infections, and maternal thyroid abnormalities. Intrau- terine infection and inflammation are of particular
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*Correspondence: symon007@umn.edu 6 Department of Educational Psychology, College of Education and Human Development, Minneapolis, MN 55455, USA Full list of author information is available at the end of the article
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interest with both maternal response (chorioamnionitis) and fetal response (funicitis or elevated interleukin-6 in fetal plasma) being associated with white matter dam- age (WMD) and CP [1]. Injury and related inflammatory processes may persist for considerable periods of time (years) leading to hypotheses and emerging models of tertiary-like mechanism of damage including epigenetic regulation and inflammatory relevant changes [2].
Work investigating infection- and neuroinflammatory- related biomarkers related to WMD in neonates has generated evidence mostly supporting a pathway from intrauterine infection to placental inflammation then to systemic fetal circulation and the preterm newborn brain [3]. The specifics of the infection-inflammation-brain damage link have been described and documented and are an active area of investigation [4] particularly given cautions about what level of inference is or is not sup- ported by high quality evidence [5]. What is less clear, however, is the robustness of the inference supporting an infection-inflammation-WMD link with CP as an inevi- table outcome. There is some evidence for such a link [6], but it may be conditioned on whether the infant was born term or preterm. From a more general perspective, the emerging viewpoint on the role of neuro-inflammation as a pathophysiological contributor to CP has created the possibility of a new therapeutic window through which to view the condition [7, 8].
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