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Extensive Delayed Brain Atrophy after Resuscitation in a Patient with Multiple System Atrophy

机译:多系统萎缩患者复苏后广泛的延迟性脑萎缩

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摘要

Brain magnetic resonance imaging (MRI) of multiple system atrophy (MSA) shows atrophy in the cerebrum, cerebellum, and brainstem. It is also characterized by specific patterns such as hyperintense lateral putaminal rim. MRI of hypoxic encephalopathy shows atrophy mainly in the gray matter, and laminar necrosis in the cerebral cortex is often observed. Here, we report an MSA patient damaged by hypoxic insult and resuscitated after 18-min cardiac arrest. The brain of the patient developed severe atrophy within a period of 10 months. Furthermore, brain atrophy was observed in the white and gray matter, which preserved the brain atrophy pattern in MSA. We assume that alpha-synuclein oligomerization is involved in the neural cell death and brain atrophy. It might have caused further neural cell death in the brain damaged by hypoxia. Alpha-synuclein, which is involved in the pathogenesis of MSA, is suggested to be a prion. Misfolded alpha-synuclein may propagate through cell-to-cell transmission and cause wide pathological change, visible as atrophied MR imaging.
机译:多系统萎缩(MSA)的脑磁共振成像(MRI)显示大脑,小脑和脑干出现萎缩。它的特征还在于特定的图案,例如高强度的侧腹角膜缘。缺氧性脑病的MRI显示萎缩主要在灰质中,并且经常观察到大脑皮层的层状坏死。在这里,我们报道了一名MSA患者,该患者因低氧损伤而受损,并在18分钟的心脏骤停后恢复了生命。患者的大脑在10个月内出现严重萎缩。此外,在白色和灰色物质中观察到脑萎缩,保留了MSA中的脑萎缩模式。我们假设α-突触核蛋白寡聚参与神经细胞死亡和脑萎缩。它可能导致缺氧损伤的大脑中进一步的神经细胞死亡。 MSA发病机理中涉及的α-突触核蛋白被认为是a病毒。错误折叠的α-突触核蛋白可能通过细胞间传播而传播,并引起广泛的病理变化,如萎缩性MR成像所见。

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