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Published on: August 30, 2020
Paradigms in chronic subdural hematoma pathophysiology: Current treatments and new directions
Michael T Bounajem1, Robert A Campbell, Frederik Denorme
1From the Department of Neurosurgery, Clinical Neurosciences Center (M.T.B., R.G.), Molecular Medicine Program (R.A.C., F.D.); and Department of Internal Medicine (R.A.C.), University of Utah, Salt Lake City, Utah.
Insights
Chronic subdural hematomas (CSDHs) have a high recurrence rate due to complex inflammatory processes. Understanding these mechanisms is key to developing better treatments for CSDH.
Area of Science:
- Neurosurgery
- Pathophysiology
Background:
- Chronic subdural hematomas (CSDHs) are a common neurosurgical pathology.
- Despite extensive research, CSDH recurrence rates remain high.
Purpose of the Study:
- To review the pathophysiological mechanisms underlying CSDH recurrence.
- To identify factors contributing to the high recurrence rates of CSDH.
Main Methods:
- Literature review of PubMed and Scopus databases.
- Search terms: "pathophysiology" AND "chronic subdural hematoma" [tiab].
- Included English-language reviews and articles.
Main Results:
- CSDH recurrence involves a complex inflammatory response and neomembrane formation around the clot.
- Proinflammatory mediators promote microbleeding via fragile, leaky vessels and widened gap junctions.
- Simple subdural evacuation does not fully address these pathological factors.
Conclusions:
- The high recurrence rate of CSDHs is linked to unresolved pathophysiological mechanisms.
- Targeted therapies like middle meningeal artery embolization and anti-inflammatory treatments show promise.
- Further prospective studies are needed to validate the efficacy of novel CSDH treatments.
Abstract:
Chronic subdural hematomas (CSDHs) are an increasingly common pathology encountered in a neurosurgical trauma practice. Although the operative and nonoperative management of CSDH has been studied extensively, the recurrence rate of CSDH remains high, with no significant decrease in recent years. We undertook a detailed assessment of the known pathophysiological mechanisms by which CSDHs recur to improve our ability to treat patients with this disease successfully. In this review of the literature from the PubMed and Scopus databases, we used the search terms "(pathophysiology) AND chronic subdural hematoma [tiab]" to identify pertinent reviews and articles in English. The results demonstrated a complex inflammatory response to subdural blood, which begins with the formation of a collagen neomembrane around the clot itself. Proinflammatory mediators, such as vascular endothelial growth factor, interleukin-6, interleukin-8, tissue necrosis factor α, matrix metalloproteinases, and basic fibroblast growth factor, then contribute to chronic microbleeding by promoting the formation of fragile, leaky blood vessels, and widening of gap junctions of existing vessels. It is evident that the lack of improvement in recurrence rate is due to pathological factors that are not entirely alleviated by simple subdural evacuation. Targeted approaches, such as middle meningeal artery embolization and anti-inflammatory therapies, have become increasingly common and require further prospective analysis to aid in the determination of their efficacy.
