PDF(Pubmed)
Abstract：
BACKGROUND: Hypoxic-ischemic encephalopathy (HIE) appears in neurological conditions where some brain areas are likely to be injured, such as deep grey matter, basal ganglia area, and white matter subcortical periventricular áreas. Moreover, modeling these brain areas in a newborn is challenging due to significant variability in the intensities associated with HIE conditions. This paper aims to evaluate functional measurements and 3D machine learning models of a given HIE case by correlating the affected brain areas with the pathophysiology and clinical neurodevelopmental.
METHODS: A comprehensive analysis of a term infant with perinatal asphyxia using longitudinal 3D brain information from Machine Learning Models is presented. The clinical analysis revealed the perinatal asphyxia diagnosis with APGAR <5 at 5 and 10 minutes, umbilical arterial pH of 7.0 BE of -21.2 mmol / L), neonatal seizures, and invasive ventilation mechanics. Therapeutic interventions: physical, occupational, and language neurodevelopmental therapies. Epilepsy treatment: vagus nerve stimulation, levetiracetam, and phenobarbital. Furthermore, the 3D analysis showed how the volume decreases due to age, exhibiting an increasing asymmetry between hemispheres. The results of the basal ganglia area showed that thalamus asymmetry, caudate, and putamen increase over time while globus pallidus decreases.
RESULTS: spastic cerebral palsy, microcephaly, treatment-refractory epilepsy.
CONCLUSIONS: Slight changes in the basal ganglia and cerebellum require 3D volumetry for detection, as standard MRI examinations cannot fully reveal their complex shape variations. Quantifying these subtle neurodevelopmental changes helps in understanding their clinical implications. Besides, neurophysiological evaluations can boost neuroplasticity in children with neurological sequelae by stimulating new neuronal connections.
METHODS: A comprehensive analysis of a term infant with perinatal asphyxia using longitudinal 3D brain information from Machine Learning Models is presented. The clinical analysis revealed the perinatal asphyxia diagnosis with APGAR <5 at 5 and 10 minutes, umbilical arterial pH of 7.0 BE of -21.2 mmol / L), neonatal seizures, and invasive ventilation mechanics. Therapeutic interventions: physical, occupational, and language neurodevelopmental therapies. Epilepsy treatment: vagus nerve stimulation, levetiracetam, and phenobarbital. Furthermore, the 3D analysis showed how the volume decreases due to age, exhibiting an increasing asymmetry between hemispheres. The results of the basal ganglia area showed that thalamus asymmetry, caudate, and putamen increase over time while globus pallidus decreases.
RESULTS: spastic cerebral palsy, microcephaly, treatment-refractory epilepsy.
CONCLUSIONS: Slight changes in the basal ganglia and cerebellum require 3D volumetry for detection, as standard MRI examinations cannot fully reveal their complex shape variations. Quantifying these subtle neurodevelopmental changes helps in understanding their clinical implications. Besides, neurophysiological evaluations can boost neuroplasticity in children with neurological sequelae by stimulating new neuronal connections.
摘要：
背景：缺氧缺血性脑病（HIE）出现在某些脑区可能受伤的神经系统疾病中，比如深灰质，基底神经节区，和白质皮质下脑室周围。此外，由于与HIE条件相关的强度存在显著差异,因此在新生儿中对这些脑区进行建模具有挑战性.本文旨在通过将受影响的大脑区域与病理生理学和临床神经发育相关联，评估给定HIE病例的功能测量和3D机器学习模型。
方法：使用来自机器学习模型的纵向3D大脑信息对围产期窒息的足月婴儿进行综合分析。临床分析显示围产期窒息诊断在5和10分钟APGAR<5。脐动脉pH为7.0BE为-21.2mmol/L），新生儿癫痫,和侵入式通风力学。治疗干预：物理，职业,和语言神经发育疗法。癫痫治疗：迷走神经刺激，左乙拉西坦,还有苯巴比妥.此外，3D分析显示了体积如何因年龄而减少，半球之间表现出越来越大的不对称性。基底节区结果显示丘脑不对称,尾状,壳核随时间增加，而苍白球减少。
结果：痉挛型脑瘫，小头畸形,治疗难治性癫痫。
结论：基底神经节和小脑的轻微变化需要3D容积检测，因为标准MRI检查不能完全揭示其复杂的形状变化。量化这些微妙的神经发育变化有助于理解其临床意义。此外,神经生理学评估可以通过刺激新的神经元连接来增强神经后遗症儿童的神经可塑性。
方法：使用来自机器学习模型的纵向3D大脑信息对围产期窒息的足月婴儿进行综合分析。临床分析显示围产期窒息诊断在5和10分钟APGAR<5。脐动脉pH为7.0BE为-21.2mmol/L），新生儿癫痫,和侵入式通风力学。治疗干预：物理，职业,和语言神经发育疗法。癫痫治疗：迷走神经刺激，左乙拉西坦,还有苯巴比妥.此外，3D分析显示了体积如何因年龄而减少，半球之间表现出越来越大的不对称性。基底节区结果显示丘脑不对称,尾状,壳核随时间增加，而苍白球减少。
结果：痉挛型脑瘫，小头畸形,治疗难治性癫痫。
结论：基底神经节和小脑的轻微变化需要3D容积检测，因为标准MRI检查不能完全揭示其复杂的形状变化。量化这些微妙的神经发育变化有助于理解其临床意义。此外,神经生理学评估可以通过刺激新的神经元连接来增强神经后遗症儿童的神经可塑性。
