Controversies in preterm brain injury

Penn, Anna A.; Gressèns, Pierre; Fleiss, Bobbi; Back, Stephen A.; Gallo, Vittorio

doi:10.1016/j.nbd.2015.10.012

Cited by 58 publications

(49 citation statements)

References 149 publications

(194 reference statements)

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“…Some of the increased risk might reflect vulnerability of cerebral maturation processes, 49 paucity of neuroprotective factors, 50 postnatal physiologic instability, 51 and/or inflammatory phenomena that appear to increase the risk of brain damage in very preterm newborns. 52 …”

Section: Discussionmentioning

confidence: 99%

Extremely low gestational age and very low birthweight for gestational age are risk factors for autism spectrum disorder in a large cohort study of 10-year-old children born at 23-27 weeks’ gestation

Joseph¹,

Korzeniewski²,

Allred³

et al. 2017

American Journal of Obstetrics and Gynecology

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BACKGROUND No prospective cohort study of high-risk children has used rigorous exposure assessment and optimal diagnostic procedures to examine the perinatal antecedents of autism spectrum disorder (ASD), separately among those with and without cognitive impairment. OBJECTIVE To identify perinatal factors associated with increased risk for ASD with and without intellectual disability (ID: IQ < 70) in children born extremely preterm. STUDY DESIGN This prospective multi-center (14 institutions in 5 states) birth cohort study included children born at 23-27 weeks gestation in 2002-2004 who were evaluated for ASD and ID at age 10 years. Pregnancy information was obtained from medical records and by structured maternal interview. Cervical-vaginal ‘infection’ refers to maternal report of bacterial infection (n = 4), bacterial vaginosis (n = 30), yeast infection (n = 62), mixed infection (n = 4) or other/unspecified infection (n=43; e.g., chlamydia, trichomonas or herpes, etc.). We do not know the extent to which ‘infection’ per se was confirmed by microbial colonization. We use the terms ‘fetal growth restriction’ and ‘small for gestational age’ interchangeably in light of the ongoing challenge to discern pathologically from constitutionally small newborns. Severe fetal growth-restriction was defined as a birth weight Z-score for gestational age at delivery < - 2 (i.e., 2 standard deviations or more below the median birth weight in a referent sample that excluded pregnancies delivered for preeclampsia or fetal indications). Participants were classified into four groups based on whether or not they met rigorous diagnostic criteria for ASD and ID (ASD+/ID−, ASD+/ID+, ASD−/ID+ and ASD−/ID−). Temporally-ordered multinomial logistic regression models were used to examine the information conveyed by perinatal factors about increased risk for ASD and/or ID (ASD+/ID−, ASD+/ID+ and ASD−/ID+). RESULTS 889 of 966 (92%) children recruited were assessed at age 10 years, of whom 857 (96%) were assessed for ASD; of these, 840 (98%) children were assessed for ID. ASD+/ID− was diagnosed in 3.2% (27/840), ASD+/ID+ in 3.8% (32/840), and ASD−/ID+ in 8.5% (71/840). Maternal report of presumed cervical-vaginal ‘infection’ during pregnancy was associated with increased risk of ASD+/ID+ (odd ratio [OR], 2.7; 95% CI, 1.2-6.4). The lowest gestational age category (23-24 weeks) was associated with increased risk of ASD+/ID+ (OR, 2.9; 95% CI, 1.3-6.6) and ASD+/ID− (OR, 4.4; 95% CI, 1.7-11). Severe fetal growth restriction was strongly associated with increased risk for ASD+/ID− (OR, 9.9; 95% CI, 3.3-30), whereas peripartum maternal fever was uniquely associated with increased risk of ASD−/ID+ (OR, 2.9; 95% CI, 1.2-6.7). CONCLUSION Our study confirms that low gestational age is associated with increased risk for ASD irrespective of intellectual ability, whereas severe fetal growth restriction is strongly associated with ASD without ID. Maternal report of cervical-vaginal infection is associated with increased risk of ASD with ID, and per...

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Section: Discussionmentioning

confidence: 99%

Extremely low gestational age and very low birthweight for gestational age are risk factors for autism spectrum disorder in a large cohort study of 10-year-old children born at 23-27 weeks’ gestation

Joseph¹,

Korzeniewski²,

Allred³

et al. 2017

American Journal of Obstetrics and Gynecology

View full text Add to dashboard Cite

show abstract

“…There are also regional vulnerabilities to brain dysmaturation; for example, the frontotemporal lobes and hippocampi are highly vulnerable 73, 74 . Historically, cystic PVL and intraventricular hemorrhage were the most common forms of brain injury seen in preterm patients; however, the incidence of PVL has declined and diffuse WM injury is now more commonly present 16, 70, 75–77 . Importantly, as seen in CHD, WM injury identified with neuroimaging techniques is associated with, and predictive of, worse motor and cognitive outcomes following premature birth 78–80 .…”

Section: Similarities and Differences To The Preterm Populationmentioning

confidence: 99%

Neurodevelopmental Abnormalities and Congenital Heart Disease

Morton

Ishibashi

Jonas

2017

Circulation Research

158

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In the past two decades it has become evident that individuals born with congenital heart disease (CHD) are at risk of developing life-long neurological deficits. Multifactorial risk factors contributing to neurodevelopmental abnormalities associated with CHD have been identified; however the underlying etiologies remain largely unknown and efforts to address this issue have only recently begun. There has been a dramatic shift in focus from newly acquired brain injuries associated with corrective and palliative heart surgery to antenatal and preoperative factors governing altered brain maturation in CHD. In this review, we describe key time windows of development during which the immature brain is vulnerable to injury. Special emphasis is placed on the dynamic nature of cellular events and how CHD may adversely impact the cellular units and networks necessary for proper cognitive and motor function. In addition, we describe current gaps in knowledge and offer perspectives about what can be done to improve our understanding of neurological deficits in CHD. Ultimately, a multidisciplinary approach will be essential in order to prevent or improve adverse neurodevelopmental outcomes in individuals surviving CHD.

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“…By contrast, a proinflammatory status with cytokine imbalance has been reported in PVL (124, 126, 127). In this regard, LPS-induced inflammation mouse, rat, rabbit, and sheep models and an IL-1β administration mouse model are also useful for studies of preterm brain injury (125, 128). …”

Section: Clinical Relevance Of Basic Studies Of the Structure And Funmentioning

confidence: 99%

Histological Architecture Underlying Brain–Immune Cell–Cell Interactions and the Cerebral Response to Systemic Inflammation

Shimada

Hasegawa-Ishii

2017

Front. Immunol.

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Although the brain is now known to actively interact with the immune system under non-inflammatory conditions, the site of cell–cell interactions between brain parenchymal cells and immune cells has been an open question until recently. Studies by our and other groups have indicated that brain structures such as the leptomeninges, choroid plexus stroma and epithelium, attachments of choroid plexus, vascular endothelial cells, cells of the perivascular space, circumventricular organs, and astrocytic endfeet construct the histological architecture that provides a location for intercellular interactions between bone marrow-derived myeloid lineage cells and brain parenchymal cells under non-inflammatory conditions. This architecture also functions as the interface between the brain and the immune system, through which systemic inflammation-induced molecular events can be relayed to the brain parenchyma at early stages of systemic inflammation during which the blood–brain barrier is relatively preserved. Although brain microglia are well known to be activated by systemic inflammation, the mechanism by which systemic inflammatory challenge and microglial activation are connected has not been well documented. Perturbed brain–immune interaction underlies a wide variety of neurological and psychiatric disorders including ischemic brain injury, status epilepticus, repeated social defeat, and neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease. Proinflammatory status associated with cytokine imbalance is involved in autism spectrum disorders, schizophrenia, and depression. In this article, we propose a mechanism connecting systemic inflammation, brain–immune interface cells, and brain parenchymal cells and discuss the relevance of basic studies of the mechanism to neurological disorders with a special emphasis on sepsis-associated encephalopathy and preterm brain injury.

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Controversies in preterm brain injury

Cited by 58 publications

References 149 publications

Extremely low gestational age and very low birthweight for gestational age are risk factors for autism spectrum disorder in a large cohort study of 10-year-old children born at 23-27 weeks’ gestation

Extremely low gestational age and very low birthweight for gestational age are risk factors for autism spectrum disorder in a large cohort study of 10-year-old children born at 23-27 weeks’ gestation

Neurodevelopmental Abnormalities and Congenital Heart Disease

Histological Architecture Underlying Brain–Immune Cell–Cell Interactions and the Cerebral Response to Systemic Inflammation

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