Our understanding of the underlying pathophysiology of cSDH has undergone substantial evolution in the last decade. By definition, cSDH is an extra-axial collection of blood and related products encapsulated by an outer vascularized and an inner non-vascularized membrane in the subdural potential space [11, 15, 68]. This encapsulated collection is formed and expanded by a self-perpetuating cycle of inflammation, hypervascularization, exudation, and rebleeding initiated by inciting injury to the innermost dural layer [11, 15, 29, 68]. Shear stress injury disrupts the loose connectivity of dural border cells and activates a pro-inflammatory and pro-angiogenic response cascade resulting in neomembrane and microcapillary formation [15, 21, 24, 64]. These neocapillaries form preferentially in the outer membrane with anastomotic channels directly connecting to middle meningeal artery (MMA) perforating branches [11, 15, 52]. Their fragile structure with fenestrated basement membranes, absent smooth muscle layers, and numerous gap junctions makes them prone to leaking into the intramembranous collection space and producing chronic microhemorrhages [11, 15, 17]. In response, fibrinolytic activity is stimulated and additional pro-inflammatory and pro-angiogenic signals further sustain cycles of membrane formation and expansion, microvessel formation, and microhemorrhage [15, 16, 21, 24, 64]. Growth of the cSDH ensues for as long as accumulation of blood products outpaces physiologic reabsorption (Fig. 2) [11, 15].

Schematic representation of subdural hematoma

Age over 65 years is the single greatest risk factor for development of cSDH. Brain atrophy is a known age-related phenomenon that results in altered tension mechanics along the dura and creates a potential space for extra-axial collections to develop. Additionally, anticoagulation and antiplatelet medication use is prevalent among older patients and polypharmacy in the setting of multiple medical comorbidities may further increase the risk of medication-induced coagulopathy [2, 4, 11, 14, 36, 39, 41]. Another significant factor is the increased risk of ground level falls and other age-related trauma in this patient population. Finally, Weigel et al. described multiple age-dependent cellular and molecular alterations in the immune and angiogenic pathways of cSDH pathophysiology that create a more favorable setting for its formation [68].

Overall, cSDHs are the product of a self-sustained process of chronic inflammation and angiogenesis that result in extra-axial collections within a dual-membrane capsule supplied by the MMA [11, 68]. Age is a multifactorial risk factor [4, 11, 14, 68]. Surgical evacuation involves the removal of the extra-axial collection and decompression of the underlying brain parenchyma, but surgery alone may not sufficiently disrupt the underlying pathophysiology [11, 48, 62]. Pharmacologic interventions targeting this process including dexamethasone, atorvastatin, angiotensin-converting enzyme inhibitors, selective COX-2 inhibitors, and tranexamic acid have yielded variable and non-definitive results [11, 55]. MMAE, however, is a promising, minimally invasive intervention that will disrupt further cSDH formation and expansion by occluding the MMA perforating branches supplying the leaky neocapillaries, the main source of repetitive microhemorrhages [6, 11, 15, 26, 52].

MMAE for cSDHs is still an active area of clinical research. However, many studies are suggesting a safe and efficacious role for MMAE as a minimally invasive adjunct or alternative procedure. A selected list of important neurosurgical studies on MMAE for cSDH is included in Table 1 [3, 5, 7,8,9, 19, 22, 25,26,27, 31,32,33,34, 37, 40,41,42,43,44,45,46, 50, 51, 54, 56, 58, 60, 65, 69].

Across all published studies to date, the most common outcomes of interest include recurrence rate, re-intervention or re-operation rate, mortality rate, procedure-related complication rate, and length of hospital stay and/or intensive care unit stay [1, 12, 20, 23, 35, 53, 63, 67]. MMAE has been shown to significantly reduce recurrence rates, prevent hematoma enlargement, and reduce SDH size with minimal mortality or procedure-related complications [11]. A recent systematic review by Martinez-Perez et al. reported a pooled recurrence rate of 6.7% for primary and adjunct MMAE with a complication rate of 6% [35]. Similarly, a large meta-analysis in 2021 by Ironside et al. reported a recurrence rate of 4.8% and a re-operation rate of 4.4%, which were significantly reduced compared to their medically managed comparison group (21.5% and 16.4%, respectively) [20]. Mortality is reported at 1% or less across these systematic studies. Numerous additional systematic reviews reinforce these general findings for MMAE with recurrence and treatment failure in less than 10% of patients and favorable neurological outcomes in greater than 75% of patients [1, 12, 20, 23, 35, 53,