This study^{Reference Hansen, Tursø-Finnich, Olsen, Binderup, Fugleholm and Jensen1} aims to determine if there is a correlation between C-reactive protein (CRP) and chronic subdural hematoma (cSDH). The assertion from the paper is that cSDH has an inflammatory pathophysiology; thus, biomarkers of inflammation may be useful in predicting hematoma recurrence and potentially lead to a possible target for treatment.

The etiology of cSDH was initially described as “delayed apoplexy” by Wepfer in 1657.^{Reference Wepfer2} Most in keeping with this paper, the etiology was described as “pachymeningitis hemorrhagica interna” by Virchow in 1857.^{Reference Virchow3} This chronic inflammation that develops after the inciting factor of trauma drives the growth of new vessels and fibrin exudation. The basis of this study is therefore sound and reflected in the literature.

The objective in finding a marker that predicts recurrence would be critical in combating cSDH as a whole. The incidence of cSDH in the general population is 1.7–20.6 per 100,000 persons per year, with an extremely high incidence of 7.35 in the 70–79 years age group.^{Reference Foelholm and Waltimo4} Morbidity for cSDH is estimated to range from 0% to 25%, mortality from 0% to 32% and reoperation rates for recurrence from 10% to 20%.^{Reference Feghali, Yang and Huang5} Therefore, with the aging worldwide population, the medical burden of cSDH is quite large. The management of cSDH has evolved over the years, from craniotomy, simple burr hole or combination of burr holes, copious irrigation, use of a subdural drain and tranexamic acid, to more minimally invasive techniques such as twist drill and endoscopic procedures, and more recently, middle meningeal artery embolization has also been done.^{Reference Mandai, Sakurai and Matsumoto6}

The authors have shown great insight to conduct this research given the medical burden that cSDH poses. The paper is very well written. The methodology was well outlined, and the statistical analysis was comprehensively presented. Alhough the CRP result was negative in predicting recurrence, there was still an increase in CRP levels during the second operation. Perhaps more research in timing and trends of CRP levels may help determine if there is indeed a correlation.

One flaw in the study is perhaps the sample size of 24 patients with recurrence. Chances are that this sample size is too small to detect a significant difference in CRP levels (absolute effect size). It is quite possible with a larger study population, different conclusions may be drawn.

Overall, the authors should be congratulated on their well-presented paper.