Abstract
Children surviving preterm birth have a high risk of disability, particularly cognitive and learning problems. There is extensive clinical and experimental evidence that disability is now primarily related to dysmaturation of white and gray matter, defined by failure of oligodendrocyte maturation and neuronal dendritic arborization, rather than cell death alone. The etiology of this dysmaturation is multifactorial, with contributions from hypoxia-ischemia, infection/inflammation and barotrauma. Intriguingly, these factors can interact to both increase and decrease damage. In this review we summarize preclinical and clinical evidence that all of these factors trigger secondary or chronic inflammation and gliosis. Thus, we hypothesize that these shared pathological features play a key role in a final common pathway that leads to the impaired neural maturation and connectivity and cognitive/motor impairments that are commonly observed in infants born preterm. This raises the possibility that secondary or chronic inflammation may be a viable therapeutic target for delayed interventions to improve neurodevelopmental outcomes after preterm birth. What this paper adds: Hypoxia-ischemia, infection/inflammation, and barotrauma/volutrauma all contribute to preterm brain injury. Multiple different triggers of preterm brain injury are associated with central nervous system dysmaturation. Secondary brain inflammation may be a viable target to improve neurodevelopment after preterm birth.
| Original language | English |
|---|---|
| Pages (from-to) | 126-133 |
| Number of pages | 8 |
| Journal | Developmental Medicine and Child Neurology |
| Volume | 60 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - 1 Feb 2018 |
| Externally published | Yes |
Cite this
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Complex interactions between hypoxia-ischemia and inflammation in preterm brain injury. / Galinsky, Robert; Lear, Christopher A.; Dean, Justin M.; Wassink, Guido; Dhillon, Simerdeep K.; Fraser, Mhoyra; Davidson, Joanne O.; Bennet, Laura; Gunn, Alistair J.
In: Developmental Medicine and Child Neurology, Vol. 60, No. 2, 01.02.2018, p. 126-133.Research output: Contribution to journal › Review Article › Research › peer-review
TY - JOUR
T1 - Complex interactions between hypoxia-ischemia and inflammation in preterm brain injury
AU - Galinsky, Robert
AU - Lear, Christopher A.
AU - Dean, Justin M.
AU - Wassink, Guido
AU - Dhillon, Simerdeep K.
AU - Fraser, Mhoyra
AU - Davidson, Joanne O.
AU - Bennet, Laura
AU - Gunn, Alistair J.
PY - 2018/2/1
Y1 - 2018/2/1
N2 - Children surviving preterm birth have a high risk of disability, particularly cognitive and learning problems. There is extensive clinical and experimental evidence that disability is now primarily related to dysmaturation of white and gray matter, defined by failure of oligodendrocyte maturation and neuronal dendritic arborization, rather than cell death alone. The etiology of this dysmaturation is multifactorial, with contributions from hypoxia-ischemia, infection/inflammation and barotrauma. Intriguingly, these factors can interact to both increase and decrease damage. In this review we summarize preclinical and clinical evidence that all of these factors trigger secondary or chronic inflammation and gliosis. Thus, we hypothesize that these shared pathological features play a key role in a final common pathway that leads to the impaired neural maturation and connectivity and cognitive/motor impairments that are commonly observed in infants born preterm. This raises the possibility that secondary or chronic inflammation may be a viable therapeutic target for delayed interventions to improve neurodevelopmental outcomes after preterm birth. What this paper adds: Hypoxia-ischemia, infection/inflammation, and barotrauma/volutrauma all contribute to preterm brain injury. Multiple different triggers of preterm brain injury are associated with central nervous system dysmaturation. Secondary brain inflammation may be a viable target to improve neurodevelopment after preterm birth.
AB - Children surviving preterm birth have a high risk of disability, particularly cognitive and learning problems. There is extensive clinical and experimental evidence that disability is now primarily related to dysmaturation of white and gray matter, defined by failure of oligodendrocyte maturation and neuronal dendritic arborization, rather than cell death alone. The etiology of this dysmaturation is multifactorial, with contributions from hypoxia-ischemia, infection/inflammation and barotrauma. Intriguingly, these factors can interact to both increase and decrease damage. In this review we summarize preclinical and clinical evidence that all of these factors trigger secondary or chronic inflammation and gliosis. Thus, we hypothesize that these shared pathological features play a key role in a final common pathway that leads to the impaired neural maturation and connectivity and cognitive/motor impairments that are commonly observed in infants born preterm. This raises the possibility that secondary or chronic inflammation may be a viable therapeutic target for delayed interventions to improve neurodevelopmental outcomes after preterm birth. What this paper adds: Hypoxia-ischemia, infection/inflammation, and barotrauma/volutrauma all contribute to preterm brain injury. Multiple different triggers of preterm brain injury are associated with central nervous system dysmaturation. Secondary brain inflammation may be a viable target to improve neurodevelopment after preterm birth.
UR - http://www.scopus.com/inward/record.url?scp=85036509002&partnerID=8YFLogxK
U2 - 10.1111/dmcn.13629
DO - 10.1111/dmcn.13629
M3 - Review Article
VL - 60
SP - 126
EP - 133
JO - Developmental Medicine and Child Neurology
JF - Developmental Medicine and Child Neurology
SN - 0012-1622
IS - 2
ER -