类淋巴系统和硬膜淋巴管在颅内出血后脑积水的病理及治疗中的潜在作用

doi:10.3877/cma.j.issn.1673-9248.XXXX.XX.XXX

脑积水是一种由脑脊液循环障碍引起的脑室系统异常扩张性疾病，其病理过程复杂，涉及脑脊液生成、流动及吸收的紊乱。颅内出血后脑积水尤为复杂，核心机制围绕脑脊液循环障碍和颅内压力失衡。近年来，类淋巴系统和硬膜淋巴管作为脑脊液清除的新通路受到关注，参与脑脊液和代谢废物的清除。颅内出血后，游离血红蛋白通过氧化应激下调星形胶质细胞水通道蛋白-4（AQP4）表达，铁离子沉积诱导硬膜淋巴管内皮细胞焦亡，导致类淋巴引流效率下降。此外，炎症激活和脑脊液通路阻塞进一步损害硬膜淋巴管的清除功能，共同加重脑室压力负荷，促进脑积水形成。类淋巴功能障碍可能不仅是继发改变，亦可能是脑积水的早期驱动因素，挑战了传统发病机制。未来研究需结合临床与动物模型，进一步阐明颅内淋巴系统在脑积水中的作用，并探索其作为潜在治疗靶点的可行性。

关键词: 颅内出血, 脑积水, 类淋巴系统, 硬膜淋巴管

Hydrocephalus is a neurological disorder characterized by abnormal dilation of the ventricular system, resulting from impaired cerebrospinal fluid (CSF) circulation. Its pathophysiology involves complex disturbances in CSF production, flow, and absorption. Post-hemorrhagic hydrocephalus (PHH) represents a particularly complex form, where disrupted CSF circulation and intracranial pressure imbalance play central roles. Recent studies have identified the glymphatic system and meningeal lymphatic vessels (mLVs) as important alternative pathways for CSF clearance, facilitating the removal of CSF and metabolic waste. After intracranial hemorrhage, free hemoglobin triggers oxidative stress, which downregulates aquaporin-4 (AQP4) expression in astrocytes, while iron deposition induces ferroptosis in mLVs endothelial cells. These processes jointly reduce glymphatic drainage efficiency and impair CSF and interstitial fluid clearance. In addition, inflammatory activation and CSF pathway obstruction further compromise the clearance function of mLVs, exacerbating ventricular pressure and accelerating hydrocephalus progression. Evidence suggests that dysfunction of the glymphatic and meningeal lymphatic systems may act not only as a secondary consequence but also as an early driving factor in hydrocephalus development, challenging traditional pathophysiological models. Future research should integrate clinical and animal studies to clarify the role of intracranial lymphatic pathways in hydrocephalus and explore their potential as therapeutic targets.

Key words: Intracranial hemorrhage, Hydrocephalus, Glymphatic system, Meningeal lymphatic vessels

表1 PHH分类及总结

分类	常见原因	发病特点	好发人群
阻塞性脑积水^[9,10]	中脑导水管狭窄、脑室出口阻塞（如肿瘤、血肿、囊肿）、先天性畸形（如Chiari畸形）、颅脑外伤。	CSF循环通路机械性阻塞、脑室系统明显扩张、颅内压升高症状显著。	各年龄段均可发生、常见于青壮年和儿童。
交通性脑积水^[9,10]	SAH、脑膜炎导致的脑膜粘连、脑室出血引发CSF循环障碍。	CSF循环未完全阻塞、脑室扩大伴蛛网膜下腔扩张、颅内压变化不一。	脑外伤或感染后患者。
急性脑积水^[11]	症状迅速发展，病程短。	严重颅脑创伤、急性脑出血（SAH、脑室内出血）、急性脑膜炎或感染。	急性创伤后患者、卒中患者、感染性疾病患者。
慢性脑积水^[12,13]	症状逐渐出现，病程较长。	慢性脑病如正常压力脑积水、长期脑萎缩后代偿性脑积水。	老年人，伴有慢性脑功能退化的患者，如记忆障碍或运动障碍患者。

表1 PHH分类及总结

分类	常见原因	发病特点	好发人群
阻塞性脑积水^[9,10]	中脑导水管狭窄、脑室出口阻塞（如肿瘤、血肿、囊肿）、先天性畸形（如Chiari畸形）、颅脑外伤。	CSF循环通路机械性阻塞、脑室系统明显扩张、颅内压升高症状显著。	各年龄段均可发生、常见于青壮年和儿童。
交通性脑积水^[9,10]	SAH、脑膜炎导致的脑膜粘连、脑室出血引发CSF循环障碍。	CSF循环未完全阻塞、脑室扩大伴蛛网膜下腔扩张、颅内压变化不一。	脑外伤或感染后患者。
急性脑积水^[11]	症状迅速发展，病程短。	严重颅脑创伤、急性脑出血（SAH、脑室内出血）、急性脑膜炎或感染。	急性创伤后患者、卒中患者、感染性疾病患者。
慢性脑积水^[12,13]	症状逐渐出现，病程较长。	慢性脑病如正常压力脑积水、长期脑萎缩后代偿性脑积水。	老年人，伴有慢性脑功能退化的患者，如记忆障碍或运动障碍患者。

图1 CSF在GS中的循环示意图注：Aquaproin-4为水通道蛋白-4；CSF为脑脊液；GS为类淋巴系统。

表2 基于影像学的早期诊断和治疗监测标准

标准	DTI-ALPS指数	SWI铁沉积
早期诊断	DTI-ALPS指数值低于某个预设阈值（例如：相对扩散率低于正常范围的30%）时，提示CSF流动受到明显阻碍，可视为GS功能障碍的早期指标^[49]。	SWI图像显示脑组织中铁沉积的区域和程度，当铁沉积量超过一定阈值（例如：铁沉积区面积占脑室系统面积的5%以上）时，提示CSF清除的能力受损，可能发展为脑积水^[50]。
治疗监测	治疗后DTI-ALPS指数的改善可作为治疗效果的标志。若治疗能够有效改善CSF流动，DTI-ALPS指数应显著上升，表明GS功能正在恢复^[51]。	随着治疗的进行，如果铁沉积区域的大小和强度有所减少，则表明CSF清除效率有所恢复，GS功能得到改善^[52]。

表2 基于影像学的早期诊断和治疗监测标准

标准	DTI-ALPS指数	SWI铁沉积
早期诊断	DTI-ALPS指数值低于某个预设阈值（例如：相对扩散率低于正常范围的30%）时，提示CSF流动受到明显阻碍，可视为GS功能障碍的早期指标^[49]。	SWI图像显示脑组织中铁沉积的区域和程度，当铁沉积量超过一定阈值（例如：铁沉积区面积占脑室系统面积的5%以上）时，提示CSF清除的能力受损，可能发展为脑积水^[50]。
治疗监测	治疗后DTI-ALPS指数的改善可作为治疗效果的标志。若治疗能够有效改善CSF流动，DTI-ALPS指数应显著上升，表明GS功能正在恢复^[51]。	随着治疗的进行，如果铁沉积区域的大小和强度有所减少，则表明CSF清除效率有所恢复，GS功能得到改善^[52]。

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Potential role of the glymphatic system and meningeal lymphatic vessels in the pathology and treatment of post-hemorrhagic hydrocephalus

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Potential role of the glymphatic system and meningeal lymphatic vessels in the pathology and treatment of post-hemorrhagic hydrocephalus