Brain and cognitive‐behavioural development after asphyxia at term birth

Haan, Michelle de; Wyatt, John; Roth, Simon; Vargha‐Khadem, Faraneh; Gadian, David G.; Mishkin, Mortimer

doi:10.1111/j.1467-7687.2006.00499.x

Cited by 152 publications

(112 citation statements)

References 86 publications

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“…The lack of reports of amygdala gray matter reductions in previous studies might be accounted for by the statistical threshold applied and/or the fact that apart from hippocampal formation, other medio-temporal lobe regions did not undergo rigorous volumetric quantifications Rosenbaum et al, 2011). In line with other studies showing damage to thalamic areas after episodes of (perinatal) hypoxia (Jacob and Pyrkosch, 1951;Voit et al, 1987;Markowitsch et al, 1997;Cowan et al, 2003;Macey et al, 2005;de Haan et al, 2006), we identified indices of reductions in gray matter density in thalamus, namely in the pulvinar, when we applied a less conservative statistical threshold (p < 0.001, uncorrected).…”

Section: Discussionsupporting

confidence: 63%

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1741 – Social cognition in a case of amnesia with neurodevelopmental mechanisms

Markowitsch

Borsutzky

Staniloiu

2013

European Psychiatry

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Episodic-autobiographical memory (EAM) is considered to emerge gradually in concert with the development of other cognitive abilities (such as executive functions, personal semantic knowledge, emotional knowledge, theory of mind (ToM) functions, language, and working memory). On the brain level its emergence is accompanied by structural and functional reorganization of different components of the so-called EAM network. This network includes the hippocampal formation, which is viewed as being vital for the acquisition of memories of personal events for long-term storage. Developmental studies have emphasized socio-cultural-linguistic mechanisms that may be unique to the development of EAM. Furthermore it was hypothesized that one of the main functions of EAM is the social one. In the research field, the link between EAM and social cognition remains however debated. Herein we aim to bring new insights into the relation between EAM and social information processing (including social cognition) by describing a young adult patient with amnesia with neurodevelopmental mechanisms due to perinatal complications accompanied by hypoxia. The patient was investigated medically, psychiatrically, and with neuropsychological and neuroimaging methods. Structural high resolution magnetic resonance imaging revealed significant bilateral hippocampal atrophy as well as indices for degeneration in the amygdalae, basal ganglia, and thalamus, when a less conservative threshold was applied. In addition to extensive memory investigations and testing other (non-social) cognitive functions, we employed a broad range of tests that assessed social information processing (social perception, social cognition, social regulation). Our results point to both preserved (empathy, core ToM functions, visual affect selection, and discrimination, affective prosody discrimination) and impaired domains of social information processing (incongruent affective prosody processing, complex social judgments). They support proposals for a role of the hippocampal formation in processing more complex social information that likely requires multimodal relational handling.

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Section: Discussionsupporting

confidence: 63%

“…However, the reported difficulties were milder than the ones experienced by ML. Although postulated, a connection between the basal ganglia (and thalamic) damage and motor impairment in cases of developmental amnesia remained unclear (Gadian et al, 2000;Vargha-Khadem et al, 2003;de Haan et al, 2006).…”

Section: Case Reportmentioning

confidence: 99%

1741 – Social cognition in a case of amnesia with neurodevelopmental mechanisms

Markowitsch

Borsutzky

Staniloiu

2013

European Psychiatry

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“…Neonatal encephalopathy due to perinatal asphyxia or hypoxia-ischemia (HI) is an important cause of mortality in the neonatal period and is associated with high morbidity, mainly characterized by neurological deficits such as cerebral palsy, seizures, and sensory and cognitive limitations [1,2,3,4,5]. The prevalence of neonatal HI is about 2-6 per 1,000 live term births in Western countries [1,6,7].…”

Section: Introductionmentioning

confidence: 99%

Cerebral and Hepatic Inflammatory Response after Neonatal Hypoxia-Ischemia in Newborn Rats

Bonestroo¹,

Nijboer²,

Velthoven³

et al. 2013

Dev Neurosci

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Background: Neonatal encephalopathy induced by perinatal asphyxia is a serious condition associated with high mortality and morbidity. Inflammation after the insult is thought to contribute to brain injury. This inflammatory response to hypoxia-ischemia (HI) may not only occur in the brain but also in peripheral organs. The aim of the present study was to investigate the effect of neonatal HI on the inflammatory response in the liver in comparison to inflammation in the brain. Methods: HI was induced in P7 Wistar rats by unilateral carotid artery occlusion and hypoxia. Cytokine and chemokine mRNA levels were determined in the brain and liver by quantitative PCR. Polarization of brain macrophages to the M1/M2-like phenotype and infiltration of neutrophils were characterized by immunohistochemistry. Results: 3 h after HI, an upregulation of the proinflammatory cytokines TNF-α and IL-1β and anti-inflammatory IL-10 was observed in the ipsilateral hemisphere of the brain compared to mRNA levels in sham-operated animals. Additionally, cerebral CINC-1 and MCP-1 mRNA expressions were increased. We also observed increased numbers of macrophages/microglia of the M1-like phenotype as well as a small increase in granulocyte influx in the ipsilateral hemisphere. Conversely, in the liver 3 h after HI, a downregulation of TNF-α, IL-1β, and MCP-1 and a trend towards an upregulation of IL-10 were observed compared to mRNA levels of sham-operated animals. However, hepatic CINC-1 expression was increased compared to levels in sham-operated animals. Following systemic hypoxia only, no significant changes in the expression of TNF-α, CINC-1 or MCP-1 were observed in the liver compared to sham-operated littermates, except for an upregulation in hepatic IL-1β expression 3 h after hypoxia. Twenty-four hours after insult, cerebral ipsilateral TNF-α, MCP-1 and CINC-1 mRNA expression was still increased, together with an increase in TGF-β expression. Moreover, an increase in macrophages/microglia of the M1-like phenotype was observed together with the appearance of macrophages/microglia of the M2-like phenotype around the cerebral lesion as well as an increase in granulocyte influx in comparison to 3 h after HI. In the liver, 24 h after HI, cytokine and chemokine responses were similar to mRNA levels in sham-operated animals except for a decrease in IL-10 and MCP-1. Conclusion: We describe for the first time that brain damage following neonatal HI induces an early downregulation of the proinflammatory response in the liver. HI induces an early proinflammatory response in the brain with a concomitant increase in influx of neutrophils and polarization of macrophages/microglia to the M1-like phenotype starting at 3 h and increasing up to 24 h after HI. The inflammatory state of the brain changes after 24 h, with an increase in the anti-inflammatory cytokine TGF-β together with the appearance of macrophages/microglia of the M2-like phenotype. The downregulation of proinflammatory cytokines in the liver is not due to systemic hypoxia only, but i...

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“…Acute kidney injury (AKI) is a complex syndrome, with various clinical manifestations, from minimal serum creatinine increases to renal failure with anuria. [1][2][3][4][5] Serum creatinine is a biomarker commonly used to diagnose AKI. However, creatinine examination is not particularly sensitive or specific for diagnosing AKI, as other non-renal factors regulate creatinine, distribution volume, and creatinine excretion.…”

Section: Resultsmentioning

confidence: 99%