Cerebrospinal fluid leak as a driving factor in chronic subdural hematoma formation: A histological study

xlomafota13 shared this article with you from Inoreader Cerebrospinal fluid leak as a driving factor in chronic subdural hematoma formation: A histological study Via leak of cerebrospinal fluid Surg Neurol Int. 2021 Nov 23;12:578. doi: 10.25259/SNI_950_2021. eCollection 2021. ABSTRACT BACKGROUND: Chronic subdural hematoma (CSDH) represents the most common neurosurgical disease. Given the demographic shift toward an aging population, the overall incidence of this condition is increasing. Nevertheless, clarity in the pathophysiological process is yet to be made. Several etiological mechanisms have been proposed to initiate and consequently promote fluid collection in the subdural space. Traumatic injury of the bridging veins has long been considered the primum movens of the pathology but increasing evidence shows that trauma is not the only factor involved. Along with recent advances we sought to understand the role of the cerebrospinal fluid (CSF) in the buildup of the intense inflammatory reaction that characterizes CSDH. METHODS: In the present study, we examined histological features of reactive membranes secondary to extrac ranial CSF leakage with CSDH-related membranes. Similarity and differences between the specimens were examined by means of light microscopy. RESULTS: Histological similarities were consistently found between CSDH membranes and reactive membranes secondary to CSF leakage in the extracranial space. Activated histiocytes were highlighted in all specimens along with an intense inflammatory reaction. CONCLUSION: CSDH is most likely the result of a complex interaction among different pathophysiological events resulting from both traumatic and inflammatory etiologies. In the present work, we highlight how CSF leakage could be an early factor that leads to a cascade of events that culminates in CSDH formation. PMID:34877064 | PMC:PMC8645496 | DOI:10.25259/SNI_950_2021 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.