Chronic subdural hematomas (CSDHs) are a common cranial pathology, with an annual incidence of 10.35 per 100,000 in the general U.S. population.1 Incidence is age dependent, with patients over 65 comprising the majority of cases.2, 3 The overall incidence of CSDH is on the rise as the population ages.1, 4 By 2030, CSDH is projected to be the most common cranial neurosurgical disease, with a projected incidence of 17.6 per 100,000, yielding 60,000 new cases per year in the U.S. alone.1
The pathophysiology of non-acute subdural hematomas (NASHs), which comprises both subacute, acute-on-chronic and CSDHs, is driven by a vicious cycle of sustained inflammation, hyperfibrinolysis and angiogenesis.5 The process is usually initiated by a mild traumatic event that damages the dural border cells (DBCs) on the meningeal surface of the dura – a finding first reported in a 1946 histological analysis of CSDH.6 In a misguided repair attempt, DBCs proliferate, forming a fibrocellular membrane that encapsulates subdural blood products. Rapid membrane growth is then driven by the proinflammatory milieu of hematoma lysis products and recruited inflammatory cells within the subdural space, while an overabundance of proinflammatory cytokines and chemokines, procollagens, fibrin degradation products, profibrinolytic factors and angiogenesis mediators encourage ingrowth of an immature microcapillary network into the fragile membrane.5, 7, 8 These highly permeable, delicate vessels become a primary source of fluid exudation and repeated microhemorrhages as locally available fibrinolytic factors prevent reliable hemostasis. This sets in motion a positive feedback loop leading to hematoma expansion over time.5
Conservative management is reserved for patients with small, asymptomatic NASHs; however, as a NASH expands, mass effect on underlying brain parenchyma eventually leads to symptoms such as headache, confusion, pseudodementia, gait difficulty, seizures and focal weakness or hemiparesis.9, 10 Once symptomatic, NASHs are surgically evacuated with burr holes or craniotomy with copious intraoperative irrigation and surgical drain placement. Unfortunately, recurrence is quite common, with estimates between 5 and 30%.11 Additionally, many patients are elderly, harbor comorbidities and/or are dependent on anticoagulation or antiplatelet agents, adding to both immediate risks of surgery and delayed risk of recurrence.
Recent studies have highlighted the role of the middle meningeal artery (MMA) in NASH formation and recurrence.12 This evolving paradigm began with histological studies of CSDH membranes by Tanaka et al. in 1997, who found three types of immature vessels in the outer CSDH membrane that arose from the MMA and crossed the dura.14 These vessels form a scattered, abnormal microcapillary network that is apparent on superselective angiographic studies of the MMA.15 Interestingly, diffuse dilation of the ipsilateral MMA is also seen in CSDH.15, 16,17 Furthermore, NASHs will avidly contrast enhance after MMA embolization, suggesting the MMA does in fact provide the membrane blood supply.18 Together, these early findings suggest a role for MMA embolization in treating CSDH.
The first successful case of MMA embolization for a CSDH was reported in 2000 by Mandai et al. in a 59-year-old male patient with cirrhosis and thrombocytopenia who had a thrice-recurrent CSDH.16 The ipsilateral MMA was embolized with polyvinyl alcohol (PVA) microparticles with near-complete resolution of the CSDH at seven-month follow-up. The ensuing decade saw the publication of many small case series of MMA embolization in intractable CSDHs in patients who were otherwise poor surgical candidates, generally with excellent long-term results reported.19-24
In 2018, both Link et al. and Ban et al. reported on the efficacy of MMA embolization.25-26 The analysis by Link et al. included 42 new, eight recurrent and 10 prophylactically treated postoperative lesions. They reported no procedural complications, an 8.9% recurrence rate and a 91.1% overall long-term success rate defined by lesion stability or size decrease with surgery avoidance. Ban et al. presented their findings in a prospective cohort treated with MMA embolization alone (27/72) or embolization followed by surgical evacuation (45/72). Their pre-specified primary outcome was treatment failure defined by incomplete hematoma resolution or need for surgical rescue. At six-month follow-up, they had no treatment failures in patients treated with embolization alone and 1/45 (2.2%) failure in those treated with embolization followed by surgery. These groups were compared with a historical control cohort of 469 patients with CSDH. Use of MMA embolization was found to have significantly lower treatment failure (1.4% vs 27.5%; p=0.001), less frequent surgical rescue (1.4% vs 18.8%; p=0.005) and no difference in treatment complications (0% vs 4.3%; p=0.182).
A 2018 meta-analysis of available case series comparing embolization with conventional treatment found a lower recurrence rate in embolized groups (2.1% vs 27.7%; p<0.001) with similar complication rates (2.1% vs 4.4%; p=0.497) and similar functional outcomes (modified Rankin Score >2; 12.5% vs 9.1%; p=0.689).27 The authors reported a composite recurrence rate of 3.6% based on six single-arm case series. An excellent review on this topic by Fiorella and Arthur was published in 2019, further clarifying the work that has been done.9
To date, most groups have reported using PVA microparticles as their embosilate of choice.20, 23, 24 Others have used N-butyl cyanoacrylate (nBCA),21 Gugliemi detachable coils (GDCs)20 or Gelfoam with GDCs22 – all with similarly positive results. We have successfully treated NASHs using Embosphere® Microspheres (Merit Medical, Salt Lake City). We recently treated a left-sided NASH in a 62-year-old female patient with history of antiphospholipid syndrome, pulmonary embolism treated with warfarin and leukemia treated with chemotherapy who presented with an international normalized ratio (INR) of 4.2 and complaint of headache with right sided pronator drift. Because of her comorbidities and ongoing anticoagulation requirements, we elected to treat with MMA embolization alone using 100- to 300-micron Microspheres. The anterior and middle branches of the left MMA were embolized without complication (Figure 1). She was restarted on her anticoagulation two weeks following the MMA embolization. Her NASH was nearly resolved by four weeks and completely resolved by her eight-week follow-up. She also experienced clinical improvement, with resolution of headaches and her pronator drift.
Another technical consideration is understanding dangerous vascular anastomotic pathways between the MMA and eloquent regions such as the retina, cranial nerves and posterior intracranial circulation.12, 28 Interventionalists should carefully inspect anterior-directed tributaries for a retinal blush. Branches directed inferomedial to the petrous bone should also be avoided because of the risk of facial nerve injury. Posterior MMA branches should be inspected for anastomosis with the inferolateral trunk at the petrocavernous region or the meningohypophyseal trunk at the petroclival region. Lastly, care should be taken to ensure no transcalvarial routes contribute to upper cervical feeders into the vertebrobasilar system supplying the posterior intracranial circulation.
MMA embolization is a promising, less-invasive method to target the underlying pathophysiology of NASH formation and recurrence. Early studies indicate it is a safe procedure with better treatment efficacy in treating this difficult disease. We anticipate that well-designed, randomized trials will better elucidate the utility of MMA embolization in NASH management.
Figure 1: This left-sided NASH in a 62-year-old female patient on anticoagulation on presentation (a) was treated by embolization of anterior and middle branches of the MMA (d, e) using 100- to 300-micron Embosphere® Microspheres (Merit Medical, Salt Lake City). At four-week follow-up (b), her hematoma was nearly resolved, with complete resolution at eight-week follow-up (c).
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