Tao Zhiqiang, Lin Yingying, Hu Maotong, Ding Shenghong, Li Jianwei, Qiu Yongming
Department of Neurosurgery, Yiwu Central Hospital, Wenzhou Medical College, Yiwu 32200, Zhejiang Province, People's Republic of China.
Department of Neurosurgery, Renji Hospital, School of Medicine, Shanghai Jiao-Tong University, No. 1630, Dongfang Road, Pudong New District, Shanghai 200127, People's Republic of China.
Med Hypotheses. 2016 Jan;86:43-6. doi: 10.1016/j.mehy.2015.11.027. Epub 2015 Nov 30.
Chronic subdural hematoma (CSDH) is still a mysterious disease. Though great success has been has achieved by neuro-surgery treatment, the origin and development of CSDH remains unknown. Tremendous clinical observations have found the correlation of subdural effusion (SDE) and CSDH. However, systematic elucidation of CSDH's origin and progression is lacking while almost all the current hypothesis only explained partial phenomenon. This hypothesis proposes Interleukin (IL)-8 inducing neutrophil respiratory burst is the crucial impact when SDE evolves into CSDH. IL-8 initially secreted by dural border layer cells, accumulates and the concentration of IL-8 rises in the SDE cavity. Accompanied by the formation of neo-membrane under the dura meninges, IL-8 firstly prompts to establish the neo-vasculature in it, and then attracts lymphocytes aggregation in the neo-membrane. Both the newly recruited lymphocytes and endothelial cells assist the further elevation of local IL-8 concentration. When the IL-8 concentration elevated to a particular level, it attracts neutrophils to the inner wall of neo-vessels and primes them to oxidative burst. Lysosomes and superoxide released by these neutrophils make the fragile neo-capillary became leaky, and subsequently the plasma and blood cells run into SDE. However, as long as the erythrocytes come into the cavity, they shall bind large quantity of IL-8 and decrease IL-8 concentration to a lower level relatively that reduce the neutrophils recruit. When this negative feedback is stagnancy, for example, the SDE space is so large in elder man who is experiencing brain atrophy, the neo-vessels have to release more erythrocytes to bind IL-8, the liquid cavity will expand and the high intracranial pressure symptoms appeared. Our hypothesis holds potential for the proper therapeutic intervention of CSDH. IL-8 antagonist and other anti-inflammation drugs like macrolides antibiotics, glucocorticoid and atorvastatin might be optional to resist the liquid cavity expanding as actually occurs obvious bleeding soon.
慢性硬膜下血肿(CSDH)仍然是一种神秘的疾病。尽管神经外科治疗已取得巨大成功,但CSDH的起源和发展仍不清楚。大量临床观察发现硬膜下积液(SDE)与CSDH之间存在关联。然而,目前几乎所有的假说都只解释了部分现象,缺乏对CSDH起源和进展的系统阐释。本假说提出,白细胞介素(IL)-8诱导中性粒细胞呼吸爆发是SDE演变为CSDH的关键影响因素。IL-8最初由硬脑膜边界层细胞分泌,在SDE腔内积聚,导致IL-8浓度升高。伴随着硬脑膜下新膜的形成,IL-8首先促使在其中建立新血管,然后吸引淋巴细胞在新膜中聚集。新募集的淋巴细胞和内皮细胞都有助于局部IL-浓度进一步升高。当IL-8浓度升高到特定水平时,它会将中性粒细胞吸引到新血管内壁并引发其氧化爆发。这些中性粒细胞释放的溶酶体和超氧化物使脆弱的新毛细血管变得渗漏,随后血浆和血细胞进入SDE。然而,只要红细胞进入腔内,它们就会结合大量IL-8并将IL-8浓度相对降低到较低水平,从而减少中性粒细胞的募集。当这种负反馈停滞时,例如在脑萎缩的老年人中SDE空间很大,新血管就必须释放更多红细胞来结合IL-8,液腔就会扩大并出现高颅压症状。我们的假说为CSDH的适当治疗干预提供了潜力。IL-8拮抗剂和其他抗炎药物,如大环内酯类抗生素、糖皮质激素和阿托伐他汀,可能是抵抗液腔扩大的选择,因为实际上很快就会出现明显出血。