1. Epidemiology

Chronic subdural haematoma is an abnormal collection of blood products in the subdural space. Its overall incidence is 1.72 - 20.6 / 100000 persons / year. There has been an increase in its incidence due to longer life expectancy, increased use of antiplatelet drugs and/or anticoagulants. It is more frequent in males (3:1), mainly due to the higher rates of alcoholism and epilepsy associated with this sex. In 20% of cases it is bilateral. 

2. Clinic

It usually has an indolent course. Manifestations are variable and mainly caused by intracranial compression mediated by the expansion of the haematoma.

Its clinical progression comprises three stages: Initial period of the traumatic event, latency period of the expanding haematoma and clinical period of manifestations. 

3. Diagnosis 

The radiological test of choice is CT of the skull without IV contrast, visualised as extra-axial collections of crescentic morphology in the hemispheric convexity, which may cross suture lines. Their attenuation is variable depending on the time of evolution, being more hyperdense in the acute process and of less attenuation when they evolve over time. 

  3. Pathophysiology

The aetiology of chronic subdural haematoma has been a controversial subject for 350 years (Table 1). 

The origin of chronic subdural haematomas resulting from ruptured bridging veins is nowadays dismissed and the inflammatory theory of the ‘dural border cell layer’ is taken as a reference.

In 1946, it was described that the dura mater was lined internally by a layer of modified and specialised connective tissue cells with two main functions, that of phagocytosis and that of becoming fibrocellular connective tissue, named ‘’dural border cells‘’, becoming the interface layer between the dura mater and arachnoid. Due to its high flattened fibroblasts with little collagen and poor adhesion to the underlying meninges. Because it consists mainly of flattened fibroblasts, low collagen and poor cell junctions, it is a weak stratum tending to form membranes in the subdural space under any insult. ''Border dural cells'' are considered to be the place where CSHs initially develop (Figure 1).   

After a certain injury mechanism (from minor trauma, coagulation disorder, etc...) a reparative response is triggered by this interphase layer, thus triggering a complex process of interrelated inflammatory mechanisms (inflammation of the dura mater, formation of neomembranes, fibrinolysis and neoangiogenesis). 

Pathological delamination of the ‘dural border layer’ occurs, forming two membranes (outer and inner) enclosing the new subdural cavity. This cavity fills with fluid and blood due to fluid exudation and migration of erythrocytes and platelets through fragile neoangiogenesis within the outer membrane, thus enlarging and perpetuating the haematoma (Figure 1).   

The main blood supply to the dura mater comes from the meningeal arteries. There is a rich anastomotic layer of superficial vessels that give rise to other smaller arterial structures, forming the internal dural plexus, with the penetrating arteries of 5-15 microns being the most relevant in the formation of the haematoma. This internal dural plexus establishes connection with the neovessels present in the outer membrane of the SDH, causing intermittent haemorrhages within the subdural space (Figure 2). 

4. Anatomy of Middle Meningeal Artery 

The middle meningeal artery (MMA) is an ascending branch of the proximal portion of the internal maxillary artery originating from the external carotid artery. It enters the cranial cavity through the foramen spinosum. Its main branches are the frontal, parietal and petrosquamosal branches. It can give rise to other branches such as the cavernous and petrosal branches. (Figure 3).

It is important to review the possible anatomical variants of the MMA, especially the meningeal origin of the Ophthalmic Artery (0.5-2%). (Figure 4).

5. Treatment 

Most of them are indolent and their treatment is asymptomatic. When clinical symptoms are present, the treatment of choice is surgery with the aim of evacuation through trephines or with decompression craniotomy. However, there are two drawbacks to surgery:- It does not act on the pathophysiological mechanism, it only serves to alleviate symptoms secondary to the intracranial mass effect.- Complications and a high rate of recurrences (9-28%). 

The recurrence factors for chronic subdural haematomas are: increased CT density and heterogeneity (membranes, loculations...), cerebral atrophy, bilateral haematomas, midline shift > 5 mm, haematoma thickness > 10 mm and taking antiplatelet or / and anticoagulant drugs. 

With the aim of seeking an aetiological treatment for chronic subdural haematomas, embolisation of the middle meningeal artery (MMAE) is proposed in order to achieve devascularisation of the subdural membrane and favour absorption of the haematoma by means of a biological process of capsular necrosis. The first endovascular treatment of subdural haematomas for prophylactic purposes was carried out in 2000 by Mandai et al. 

Since then, several experimental studies of endovascular treatment of chronic subdural haematomas by embolisation of the middle meningeal artery have been carried out. (Table 2). 

The results of the latest published studies show:

- The MMAE alone is, although not immediately, as effective as evacuation surgery alone in reducing haematoma.

- The combined treatment has a lower recurrence rate than evacuation surgery alone.

- The MMAE is a safe procedure with high resolution rates and low recurrence and surgical salvage rates, that should be considered for patients at high risk of recurrence.

5.1 Indications of embolisation of MMA:

- Curative or prophylactic (1st choice) as an aetiological treatment to prevent perpetuation of the haematoma and thus avoid surgical intervention.

Failure of conservative treatment, asymptomatic / paucisymptomatic patients (including headache), advanced age, use of antiplatelet or anticoagulant medication, > 8-10 mm thickness associated or not with midline displacement. 

- Adjuvant to surgery as a preventive treatment for rebleeding after surgical evacuation of the haematoma. It depens on imaging criteria after post-surgical follow-up CT scan: persistence of collection (>8-10 mm thick), presence of membranes in the CSH or foci of rebleeding in the CSH. 

5. 2 Endovascular technique:

Procedure under anaesthetic requirement, usually general anaesthesia. Patient in supine position on the angiography table. Femoral or radial vascular access, preferably ultrasound-guided. (Figure 5-6).  Systemic heparinisation (4000 IU) and a calcium antagonist: nimodipine (15 ml 3 mg) in a guide catheter flush.  No need to suspend antiplatelet or anticoagulation therapy. 

Diagnostic catheterisation (diameter of 4 - 6 F) on a guidewire, we navigate through the femoral / radial artery to the aortic arch (Figure 7), and from there we go to the common carotid artery, and the origin of the external carotid artery (ECA) and internal carotid artery (ICA). 

At this point, a selective angiographic study is performed for both the internal carotid artery and the external carotid artery, with the aim of assessing possible anastomoses or vascular malformations. 

The distal ECA was catheterised and a new diagnostic series was performed to determine its anatomy. Subsequently, supraselective microcatheterisation (1.3 and 1.5 F) of the proximal middle meningeal artery is performed. (Figure 8). 

It can be embolised with the microcatheter positioned in the main trunk in the absence of anastomosis, or more distally, in each of its frontal and parietal branches (of choice in our team).

• To avoid unintentionally embolising potentially dangerous collateral branches.
• To administer the embolising agent selected by the microcatheter.

5.3 Embolisation equipment

• Particles (PVA 40 - 300 microns)
• Coils (better if anastomosis)
• Liquid agents: EVOH (Etilen-Vinil-Alcohol) or cyanocrylate. (Figure 9). These are of choice for more distal branches, but caution should be taken against microcatheter obstruction if there is reflux from the tip of the microcatheter.

Final control angiographic series should be performed at the origin of the ECA and ICA in order to:

- Check the result of embolisation. 

- To rule out the presence of vascular occlusion or other iatrogenic intracranial complications. 

It is recommended to perform an ‘in situ’ cranial CT scan in the interventional room. Radiological control with skull CT scan at 24h, 1-3-6 months and at one year. 

We provide examples from our centre in (Figures 10 - 15).

5.5 Complications (0,86 - 1 %)

• Optic (Figure 16), Facial or Trigeminal nerves involvement.
• Intracranial arterial or venous thromboses.
• Intracranial haemorrhages.
• Vascular injury in MMA, ECA, CCA.
• Epidural abscess.
• Complications related to the femoral or radial puncture site.

5.6 Experience in our hospital (Table 3).