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复旦大学:《儿科学》课程教学资源(PPT课件讲稿,双语版)第二讲 新生儿神经

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1. Causes Hypoxia Perinatal asphyxia, apnea, respiratory failure, right to left shunt Ischemia Heart arrest, Heart failure, Shock
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Neonatal Neurological Diseases 陈超 Childrens Hospital, Fudan University

Neonatal Neurological Diseases 陈 超 Children’s Hospital,Fudan University

Neonatal Hypoxic-Ischemic Encephalopathy 新生儿缺氧缺血性脑病 (HIE)

Neonatal Hypoxic-Ischemic Encephalopathy 新生儿缺氧缺血性脑病 (HIE)

l。 Causes Hypoxia Perinatal asphyxia, apnea, respiratory failure, right to left shunt schemia Heart arrest, Heart failure, Shock

Hypoxia Perinatal asphyxia, apnea, respiratory failure, right to left shunt Ischemia Heart arrest,Heart failure, Shock 1. Causes

Onset of he Timing of Insults Percentage Antepartum 20 Intrapartum 35 Antepartum t antepartum 35 Postnatal 10

Onset of HIE Timing of Insults Percentage Antepartum 20 Intrapartum 35 Antepartum  antepartum 35 Postnatal 10

Pathogenesis 1. Cerebral hemodynamic alteration 脑血流重分布 Initial changes: redistribution of circulation ( diving reflex)→> cerebral blood flow↑ Continue insult: loss of vascular autoregulation, systemic hypotension, cerebral blood flow cerebral ischemia

1. Cerebral hemodynamic alteration: 脑血流重分布 Initial changes:redistribution of circulation (diving reflex) → cerebral blood flow↑ Continue insult:loss of vascular autoregulation, systemic hypotension, cerebral blood flow↓ cerebral ischemia Pathogenesis

Pathogenesis(Cont's) 2. Effects of Hypoxic-Ischemic Insults on Energy Metabolism(能力代谢) (1) Brain glucose√ (2)Lactate production T (3)ATP↓ (4)Energy failure (5)Neuronal death

Pathogenesis (Cont’s) 2. Effects of Hypoxic-Ischemic Insults on Energy Metabolism(能力代谢) (1) Brain glucose  (2) Lactate production  (3) ATP  (4) Energy failure (5) Neuronal death

Pathogenesis(Cont's) 3 Role of free radicals(自由基) (1) Perioxidation(过氧化) of membrane phospholipids 2)Damage to DNA (3) Activation of proapoptotic(促凋亡) genes

Pathogenesis (Cont’s) 3. Role of Free Radicals (自由基) (1) Perioxidation (过氧化) of membrane phospholipids (2) Damage to DNA (3) Activation of proapoptotic (促凋亡) genes

Pathogenesis(Cont's) 4. Calcium Reflux(钙内流) (1) Activate phospholipases(磷脂酶) (2) Activate proteases(蛋白酶) (3) Activate nucleases(核酸酶) (4)T neurotransmitter release (5)钙内流,导致细胞死亡

Pathogenesis (Cont’s) 4. Calcium Reflux(钙内流) (1) Activate phospholipases (磷脂酶) (2) Activate proteases (蛋白酶) (3) Activate nucleases (核酸酶) (4)  neurotransmitter release (5) 钙内流,导致细胞死亡

Pathogenesis(Cont's) 5. Neurotoxicity of Excitatory Amino Acids 兴奋性氨基酸) (1)Nat entry: with H2o cell swelling and lysis (2) Cat entry: Cat-mediated events to cell death

Pathogenesis (Cont’s) 5. Neurotoxicity of Excitatory Amino Acids (兴奋性氨基酸) (1) Na+ entry: with H2O cell swelling and lysis (2) Ca+ entry: Ca+ -mediated events to cell death

Pathogenesis(Cont's) 6. Delayed Cell Death(迟发性神经元死亡) (1) Cell death: Necrosis(坏死) and Apoptosis(凋亡) (2) Necrosis: occurs in minutes (3) Apoptosis: delayed cell death occurs over hours or days, or months

Pathogenesis (Cont’s) 6. Delayed Cell Death (迟发性神经元死亡) (1) Cell death: Necrosis (坏死) and Apoptosis (凋亡) (2) Necrosis:occurs in minutes (3) Apoptosis: delayed cell death occurs over hours or days, or months

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