Serban Nicoleta-Larisa, Ungureanu Gheorghe, Florian Ioan Stefan, Ionescu Daniela
Department of Neurosurgery, Cluj County Clinical Emergency Hospital, 400347 Cluj-Napoca, Romania.
Department of Neurosciences, "Iuliu Hatieganu" University of Medicine and Pharmacy, 400012 Cluj-Napoca, Romania.
Life (Basel). 2025 Sep 18;15(9):1470. doi: 10.3390/life15091470.
Traumatic brain injury (TBI) is a major global health concern and a leading cause of long-term disability and mortality. While the primary mechanical insult is often the focus of acute care, secondary injury mechanisms-particularly cerebrovascular dysfunction-play a critical role in ongoing neural damage and poor outcomes. Increasing research highlights the role of neurovascular changes in TBI pathophysiology. This narrative review compiles evidence from the past decade on mechanisms, diagnostic methods, and treatments related to cerebrovascular dysfunction after TBI. A structured search of PubMed and Embase identified relevant clinical and preclinical studies. Key mechanisms include blood-brain barrier disruption, impaired cerebral autoregulation, microthrombosis, and oxidative stress. Diagnostic tools discussed include perfusion imaging, cerebrovascular reactivity testing, and blood-based biomarkers of vascular injury. Therapeutic strategies targeting the neurovascular unit are categorized by mechanism: anti-inflammatory agents (e.g., celecoxib, minocycline), mitochondrial protectors (e.g., Tanshinone IIA), and vasomodulators (e.g., sildenafil). We propose an integrated therapeutic approach for a multimodal treatment plan that integrates these interventions. The findings emphasize the importance of patient-specific vascular therapies to reduce secondary ischemic injury and enhance neurological recovery. Although promising preclinical data exist, clinical application remains limited. More well-designed trials are needed to confirm the safety and effectiveness of emerging therapies.
创伤性脑损伤(TBI)是一个重大的全球健康问题,也是长期残疾和死亡的主要原因。虽然原发性机械损伤通常是急性护理的重点,但继发性损伤机制,尤其是脑血管功能障碍,在持续的神经损伤和不良预后中起着关键作用。越来越多的研究突出了神经血管变化在TBI病理生理学中的作用。这篇叙述性综述汇编了过去十年中关于TBI后脑血管功能障碍的机制、诊断方法和治疗的证据。对PubMed和Embase进行结构化检索,确定了相关的临床和临床前研究。关键机制包括血脑屏障破坏、脑自动调节受损、微血栓形成和氧化应激。讨论的诊断工具包括灌注成像、脑血管反应性测试和基于血液的血管损伤生物标志物。针对神经血管单元的治疗策略按机制分类:抗炎药(如塞来昔布、米诺环素)、线粒体保护剂(如丹参酮IIA)和血管调节剂(如西地那非)。我们提出了一种综合治疗方法,用于整合这些干预措施的多模式治疗计划。研究结果强调了针对患者的血管治疗对于减少继发性缺血性损伤和促进神经恢复的重要性。尽管存在有前景的临床前数据,但临床应用仍然有限。需要更多设计良好的试验来证实新兴疗法的安全性和有效性。