We read the interesting article by Kim et al. [2] in Journal of Korean Neurosurgical Society. It contextualizes the significance of chronic subdural hematomas (cSDHs), including their prevalence, etiology, and treatment challenges [1]. The comprehensive literature review sets a strong foundation for the study objectives and hypotheses, demonstrating a clear understanding of the existing research landscape.

The authors organized the study well and provided a detailed description of the experimental procedures, including tissue sampling, tissue clearing, immunostaining, and volume measurement of vessels. Additionally, the incorporation of advanced imaging techniques, such as confocal microscopy and transmission electron microscopy, which added depth to the histopathological analyses.

They demonstrated compelling evidence of neovascularization in the outer membrane (OM) of cSDHs, highlighting the structural differences between normal and pathological dura mater samples. The quantitative analysis of vascular volume density and the comparison of laminin-positive vessels further supported their findings, underscoring the role of neovascularization in cSDH recurrence.

Overall, the study contributes significantly to our understanding of cSDH pathophysiology and offers a rationale for middle meningeal artery embolization as a potential therapeutic approach.

This paper presents new facts in a well-organized manner, but there are some shortcomings. It might be better to describe the rationale for the selection of specific immunostaining markers (laminin, α-smooth muscle actin, podoplanin) and discuss their relevance to the study objectives. Providing additional context on why these markers were chosen will enhance the interpretability of their immunohistochemistry results.

The readers would benefit from new insights if the impact of the study on future treatment strategies for cSDHs were presented. Consider addressing potential challenges or limitations in translating their research findings into clinical practice.

Additionally, I would like to know the potential mechanisms underlying the neovascularization in the OM of cSDHs. Exploring possible connections with known pathways involved in angiogenesis and vascular remodeling and discussion on how these mechanisms may contribute to cSDH recurrence will be a great help.

Another point we would like to mention is the large discrepancy in the recurrence rate for primary cSDHs. While the manuscript mentions a recurrence rate of 2-37% for primary cSDHs, this figure appears to deviate from the range typically cited in previous studies referred to in the text. It would be better to present the various figures for the recurrence rate observed in different studies or reconcile this discrepancy with the existing literature to ensure the accuracy and consistency of the reported data.