Department of Neurology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Department of Neurology, Mayo Clinic College of Medicine and Science, Rochester, MN, USA.
Curr Neuropharmacol. 2024;22(14):2330-2352. doi: 10.2174/1570159X22666240528160237.
Cerebral Edema (CE) is the final common pathway of brain death. In severe neurological disease, neuronal cell damage first contributes to tissue edema, and then Increased Intracranial Pressure (ICP) occurs, which results in diminishing cerebral perfusion pressure. In turn, anoxic brain injury brought on by decreased cerebral perfusion pressure eventually results in neuronal cell impairment, creating a vicious cycle. Traditionally, CE is understood to be tightly linked to elevated ICP, which ultimately generates cerebral hernia and is therefore regarded as a risk factor for mortality. Intracranial hypertension and brain edema are two serious neurological disorders that are commonly treated with mannitol. However, mannitol usage should be monitored since inappropriate utilization of the substance could conversely have negative effects on CE patients. CE is thought to be related to bloodbrain barrier dysfunction. Nonetheless, a fluid clearance mechanism called the glial-lymphatic or glymphatic system was updated. This pathway facilitates the transport of cerebrospinal fluid (CSF) into the brain along arterial perivascular spaces and later into the brain interstitium. After removing solutes from the neuropil into meningeal and cervical lymphatic drainage arteries, the route then directs flows into the venous perivascular and perineuronal regions. Remarkably, the dual function of the glymphatic system was observed to protect the brain from further exacerbated damage. From our point of view, future studies ought to concentrate on the management of CE based on numerous targets of the updated glymphatic system. Further clinical trials are encouraged to apply these agents to the clinic as soon as possible.
脑水肿（CE）是脑死亡的最终共同途径。在严重的神经疾病中，神经元细胞损伤首先导致组织水肿，然后颅内压（ICP）升高，导致脑灌注压降低。反过来，脑灌注压降低引起的缺氧性脑损伤最终导致神经元细胞损伤，形成恶性循环。传统上，CE 被认为与升高的 ICP 密切相关，而升高的 ICP 最终会导致脑疝，因此被认为是死亡率的一个危险因素。颅内压增高和脑水肿是两种常见的神经科疾病，通常用甘露醇治疗。然而，应该监测甘露醇的使用，因为不恰当地使用这种物质可能会对 CE 患者产生负面影响。CE 被认为与血脑屏障功能障碍有关。然而，一种被称为胶质淋巴或糖质系统的液体清除机制得到了更新。该途径促进了脑脊液（CSF）沿着动脉周围间隙进入大脑，并随后进入脑间质。将溶质从神经胶中清除后，该途径将流向脑膜和颈淋巴引流动脉，然后再流入静脉周围和神经周间隙。值得注意的是，糖质系统的双重功能被观察到可以保护大脑免受进一步恶化的损伤。从我们的角度来看，未来的研究应该集中在基于更新的糖质系统的多个靶点来管理 CE。鼓励进一步的临床试验尽快将这些药物应用于临床。
