Roos K L
Department of Neurology, Indiana University School of Medicine, Indianapolis, USA.
Clin Neuropharmacol. 1995 Apr;18(2):138-47. doi: 10.1097/00002826-199504000-00005.
The inflammation in the subarachnoid space (SAS) that develops in the course of bacterial meningitis may have a role in eradicating the infection, but also, ultimately, is the cause of the neurological sequelae associated with this infection. The presence of an inflammatory exudate in the SAS leads to alterations in the blood-brain barrier, altered cerebrospinal fluid dynamics, cerebral edema and increased intracranial pressure, and loss of cerebral auto-regulation. Our increasing understanding of the pathophysiology of meningeal inflammation has led to therapeutic interventions to limit the degree of meningeal inflammation and neurologic sequelae. The inflammatory cascade that leads to alterations in central nervous system physiology will be reviewed as well as the experimental evidence and clinical trials demonstrating the efficacy of adjunctive therapy in reducing meningeal inflammation and decreasing the incidence and severity of neurological sequelae in bacterial meningitis.
细菌性脑膜炎病程中发生的蛛网膜下腔（SAS）炎症可能在清除感染方面发挥作用，但最终也是与该感染相关的神经后遗症的原因。SAS中炎性渗出物的存在会导致血脑屏障改变、脑脊液动力学改变、脑水肿和颅内压升高，以及脑自动调节功能丧失。我们对脑膜炎症病理生理学的日益了解促使了旨在限制脑膜炎症程度和神经后遗症的治疗干预措施的出现。本文将对导致中枢神经系统生理学改变的炎症级联反应进行综述，同时也会探讨证明辅助治疗在减轻细菌性脑膜炎脑膜炎症、降低神经后遗症发生率和严重程度方面疗效的实验证据和临床试验。
