The prognostic value of multivoxel magnetic resonance spectroscopy determined metabolite levels in white and grey matter brain tissue for adverse outcome in term newborns following perinatal asphyxia

Doormaal, Pieter Jan van; Meiners, Linda C.; Horst, Hendrik J. ter; Veere, Christa N. van der; Sijens, Paul E.

doi:10.1007/s00330-011-2315-z

Cited by 21 publications

(21 citation statements)

References 26 publications

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“…Increased choline levels have been correlated with increased risk of mortality following HIE. 42 HT+EPO treatment had no deaths and had the lowest choline levels. Choline may be a biomarker of response to treatment and/or a prognostic biomarker.…”

Section: Discussionmentioning

confidence: 90%

Concurrent Erythropoietin and Hypothermia Treatment Improve Outcomes in a Term Nonhuman Primate Model of Perinatal Asphyxia

et al. 2013

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Background: Up to 65% of untreated infants suffering from moderate to severe hypoxic-ischemic encephalopathy (HIE) are at risk of death or major disability. Therapeutic hypothermia (HT) reduces this risk to approximately 50% (number needed to treat: 7-9). Erythropoietin (Epo) is a neuroprotective treatment that is promising as an adjunctive therapy to decrease HIE-induced injury because Epo decreases apoptosis, inflammation, and oxidative injury and promotes glial cell survival and angiogenesis. We hypothesized that HT and concurrent Epo will be safe and effective, improve survival, and reduce moderate-severe cerebral palsy (CP) in a term nonhuman primate model of perinatal asphyxia. Methodology: Thirty-five Macacanemestrina were delivered after 15-18 min of umbilical cord occlusion (UCO) and randomized to saline (n = 14), HT only (n = 9), or HT+Epo (n = 12). There were 12 unasphyxiated controls. Epo (3,500 U/kg × 1 dose followed by 3 doses of 2,500 U/kg, or Epo 1,000 U/kg/day × 4 doses) was given on days 1, 2, 3, and 7. Timed blood samples were collected to measure plasma Epo concentrations. Animals underwent MRI/MRS and diffusion tensor imaging (DTI) at <72 h of age and again at 9 months. A battery of weekly developmental assessments was performed. Results: UCO resulted in death or moderate-severe CP in 43% of saline-, 44% of HT-, and 0% of HT+Epo-treated animals. Compared to non-UCO control animals, UCO animals exhibit poor weight gain, behavioral impairment, poor cerebellar growth, and abnormal brain DTI. Compared to UCO saline, UCO HT+Epo improved motor and cognitive responses, cerebellar growth, and DTI measures and produced a death/disability relative risk reduction of 0.911 (95% CI -0.429 to 0.994), an absolute risk reduction of 0.395 (95% CI 0.072-0.635), and a number needed to treat of 2 (95% CI 2-14). The effects of HT+Epo on DTI included an improved mode of anisotropy, fractional anisotropy, relative anisotropy, and volume ratio as compared to UCO saline-treated infants. No adverse drug reactions were noted in animals receiving Epo, and there were no hematology, liver, or kidney laboratory effects. Conclusions/Significance: HT+Epo treatment improved outcomes in nonhuman primates exposed to UCO. Adjunctive use of Epo combined with HT may improve the outcomes of term human infants with HIE, and clinical trials are warranted.

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Section: Discussionmentioning

confidence: 90%

Concurrent Erythropoietin and Hypothermia Treatment Improve Outcomes in a Term Nonhuman Primate Model of Perinatal Asphyxia

et al. 2013

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“…Identification of an early biomarker to diagnose and, even more, if possible to give information on later outcome would be of great interest, helping physicians to improve early diagnosis and prognosis of neonates suffering from HIE. At present the evaluation of a neonate with suspected HIE relies on clinical signs, imaging methods and monitoring of electrocortical activity [2,3]. Several promising laboratory markers have been evaluated including inflammatory cytokines (such as IL-1b, -6 and -8), markers of oxidative stress (e.g.…”

Section: Introductionmentioning

confidence: 99%

Secretoneurin Serum Levels in Healthy Term Neonates and Neonates with Hypoxic-Ischaemic Encephalopathy

Wechselberger

Schmid²,

Posod³

et al. 2016

Neonatology

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Background: Hypoxic-ischaemic encephalopathy is a major cause of neurologic impairment and mortality in neonates. Early knowledge of brain injury is important to guide therapeutic decisions and reliably inform the parents. Increased secretoneurin levels have been detected in adult patients suffering from brain injury and it has also been shown to be a promising early serum biomarker of unfavourable neurological outcome. However, no data are available in neonates. Objective: The aim of this study was to obtain reference values for secretoneurin in healthy term neonates and then to assess the potential of this neuropeptide as a biomarker in the context of hypoxic-ischaemic encephalopathy in asphyxiated term neonates. Methods: A total number of 139 term neonates, of which 7 were asphyxiated and 132 were healthy, were prospectively enrolled. Secretoneurin serum concentrations were assessed by radioimmunoassay. Results: In healthy controls, secretoneurin serum concentrations were influenced by the mode of delivery (highest in infants born per vacuum extraction and lowest in infants born per caesarean section) and abnormal cardiotocography. In asphyxiated term neonates, secretoneurin concentrations were higher in umbilical cord blood and significantly lower 48 h after birth in comparison to healthy controls. Conclusion: Secretoneurin levels are elevated in cord blood in infants suffering from hypoxic-ischaemic encephalopathy following perinatal asphyxia. The potential of secretoneurin as a marker of neonatal hypoxic-ischaemic brain injury should be further evaluated in larger trials.

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“…Экспериментальные данные свидетельствуют о вари-ативности выживания нейронов в период от нескольких дней до нескольких недель после гипоксии-ишемии, т. е. своеобразных «окнах возможностей» [17,18]. Именно в этот патологически сложный промежуток времени тре-буются лечебные мероприятия с целью предотвращения некроза.…”

Section: патофизиологические механизмы гипоксически-ишемических поражunclassified

Recent Information on the Pathogenesis and Treatment of Hypoxic-Ischemic Brain Lesions in Newborns

Каркашадзе¹,

Аникин²,

Зимина³

et al. 2016

Pediatr. farmakol.

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ВВЕДЕНИЕ Общемировой научно-технический прогресс в отно-шении исследовательских технологий за последние де-сятилетия привел к качественному и количественно-му скачку нейронаук. Наиболее активно наполняется новыми данными поле фундаментальных представлений о развитии головного мозга, что обусловливает интересы ученых к таким областям медицины, как перинатальная неврология и неврология раннего возраста. Несмотря на расширение представлений о вкладе генетической составляющей, по-прежнему большое внимание уделяет-ся изучению прямых патофизиологических механизмов гипоксически-ишемических поражений (ГИП) головного мозга у новорожденных. К настоящему моменту накоплен массив новых данных в этой области, что подталкивает медицину к внедрению передовых лечебных технологий.Цель работы -провести литературный обзор совре-менных научных данных о механизмах гипоксически-ише-мических повреждений мозга у новорожденных и разра-батываемых на их основании новых методов лечения. ПАТОФИЗИОЛОГИЧЕСКИЕ МЕХАНИЗМЫ ГИПОКСИЧЕСКИ-ИШЕМИЧЕСКИХ ПОРАЖЕНИЙТрадиционно основные лечебные тактики в острый период гипоксически-ишемических перинатальных поражений головного мозга (ГИППГМ) предусма-тривают медикаментозное поддержание сердечно-легочных функций и противосудорожную защиту [1]. Послед ние достижения в раскрытии патофизиологи-ческих механизмов непосредственно ГИП дают опору для поиска и внедрения новых лечебных технологий. У доношенных детей основным прямым механизмом ГИП является внутриутробная асфиксия, вызванная проблемами кровообращения, в том числе в области плацентарных артерий, отслойкой плаценты или вос-палительным процессом. За этим следуют снижение объема кислорода и углекислого газа в крови и тяже-лый лактат-ацидоз. Выраженное снижение сердечного выброса в условиях гипоксии, называемое гипоксией-ишемией, в течение 12-36 ч приводит к поражению головного мозга [2].

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The prognostic value of multivoxel magnetic resonance spectroscopy determined metabolite levels in white and grey matter brain tissue for adverse outcome in term newborns following perinatal asphyxia

Cited by 21 publications

References 26 publications

Concurrent Erythropoietin and Hypothermia Treatment Improve Outcomes in a Term Nonhuman Primate Model of Perinatal Asphyxia

Concurrent Erythropoietin and Hypothermia Treatment Improve Outcomes in a Term Nonhuman Primate Model of Perinatal Asphyxia

Secretoneurin Serum Levels in Healthy Term Neonates and Neonates with Hypoxic-Ischaemic Encephalopathy

Recent Information on the Pathogenesis and Treatment of Hypoxic-Ischemic Brain Lesions in Newborns

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