Enlargement Of Chronic Subdural Hematoma Research Articles

Middle meningeal artery embolization for the treatment of unilateral large chronic subdural hematoma patients with significant midline shift: A single-center experience.

The amount of midline shift (MLS) considered safe for middle meningeal artery embolization (MMAE) in patients with chronic subdural hematoma (CSDH) has not been established. Whether MMAE could be used as upfront treatment for unilateral large CSDH patients with significant MLS (>1 cm) has not been reported. To investigate the efficacy and safety of MMAE in unilateral large CSDH patients with MLS > 1 cm. Eleven carefully selected CSDH patients with mild or moderate symptoms and significant MLS > 1 cm from 1 May 2021 to 31 August 2022 were included in the study. All patients were treated with MMAE using polyvinyl alcohol (PVA) particles. Outcomes were assessed clinically and with interval imaging studies at follow-up. All 19 MMAs (unilateral embolization in three patients and bilateral embolization in eight patients) were successfully embolized. All 11 patients were followed for subsequent months, and there was no recurrence and enlargement of CSDH. Procedural adverse events, mortality, or complications were not observed. The average time to achieve a 50% reduction in MLS was approximately four weeks, while it took approximately eight weeks to achieve a 50% reduction in maximal volume. All 11 patients showed improvement in their neurological symptoms at three days post-operation, including four hemiplegic patients. MMAE may demonstrate safety in carefully selected CSDH patients with significant midline shift (MLS > 1 cm), particularly in those who are not suitable for surgery, thus providing a potential alternative approach.

Chronic Subdural Hematoma: Role of Vascular Endothelial Growth Factor and Craniotomy in Pathophysiology and Prevention of Recurrence

AbstractCurrent body of evidence suggests that the maintenance or enlargement of chronic subdural hematoma (cSDH) is caused by multiple factors. Inflammatory and vascular endothelial growth factor (VEGF)–induced accumulation of hematoma plays an important role in pathophysiology of cSDH. If neomembrane is implicated in the propagation of inflammatory mediators, excision of the culprit membrane becomes essential to treat and prevent recurrence of cSDH. This retrospective study was conducted in a service hospital where 48 cases of cSDH were operated in 2 years. Patients were evaluated clinically and radiologically. Surgical procedure offered included burr hole craniotomy (BHC), twist drill craniotomy (TDC), or craniotomy (Cr) with excision of neomembrane. Cr was offered whenever there was suspicion or evidence of reaccumulation, solid or calcified hematoma formation, nonobliteration of the subdural space, or numerous thick membranes as were demonstrated in imaging. In Cr maximum part of outer neomembrane was excised and margins were coagulated. The excised outer neomembrane was sent for immunohistochemical examination to assess the VEGF expression. Depending on the VEGF expression as seen on the microscope, these expressions were grouped into weak, moderate, or strong VEGF expression. The study showed that cSDH patients with neomembrane formation benefit from Cr. The strong VEGF expression from the excised neomembrane further strengthens the proinflammatory VEGF theory propagation of cSDH. It further proves that excision of the culprit membrane is essential to prevent recurrences.

Expression of the TGF-β–ALK-1 Pathway in Dura and the Outer Membrane of Chronic Subdural Hematomas

Neovascularization of the outer membrane plays a critical role in the development and enlargement of chronic subdural hematomas (CSHs) and vascular endothelial growth factor (VEGF) may promote their progression. However, the precise mechanisms remain to be determined. We focused on the signaling pathway upstream of VEGF, transforming growth factor β (TGF-β), and activin receptor-like kinase 1 (ALK-1) to identify the mechanisms underlying the neovascularization of the outer membrane of CSH. Retrospective comparative study was conducted on 15 consecutive patients diagnosed as CSH with burr-hole drainage. Dura and the outer membrane were collected. We immunohistochemically examined the expression of VEGF, integrin-α, TGF-β, and ALK-1 on the outer membrane and dura of CSH and compared our findings with control samples and the signal intensity of hematomas on computed tomography (CT) scans. VEGF and integrin-α expression was markedly up-regulated in both the dura and outer membrane of CSH, the expression of TGF-β and ALK-1 in the dura was slightly increased in the dura and markedly up-regulated in the outer membrane. There was no significant correlation between their expression and CT density. Here we first report the expression of TGF-β and ALK-1 in the outer membrane and dura mater of CSH. We suggest that the TGF-β–ALK-1 pathway and VEGF affect neovascularization and the progression of CSH.

Involvement of Hypoxia-Inducible Factor-1.ALPHA. and Vascular Endothelial Growth Factor in the Mechanism of Development of Chronic Subdural Hematoma

Vascular endothelial growth factor (VEGF), a potent inducer of angiogenesis and vascular permeability in diverse physiological and pathological conditions, may be involved in the pathophysiology of chronic subdural hematoma (CSDH). The present study investigated the source and mechanisms for the induction of VEGF in CSDH by measuring the concentration of VEGF in the hematoma of 102 patients (122 hematomas) using the enzyme-linked immunosorbent assay technique. The relationship between the VEGF concentration in hematoma and the intrahematoma membranous structure confirmed by preoperative T(2)(*)-weighted magnetic resonance image was examined in 46 of these patients. VEGF and hypoxia-inducible factor-1alpha (HIF-1alpha) expression was immunohistochemically studied and microvessel density (MVD) in the outer membrane was identified using anti-CD31 antibody in 30 patients. VEGF and HIF-1alpha were positive in the outer membranes of all 30 patients. VEGF expression was significantly correlated to HIF-1alpha expression (r(s) = 0.651, p = 0.0084) and VEGF concentration in the hematoma (r(s) = 0.654, p = 0.0013). VEGF concentration in layered hematomas, which have intrahematoma membranous structure, was significantly higher than in non-layered hematomas (p < 0.01). Although MVDs of the outer membranes were comparable to those described in tumors, there was no significant relationship with VEGF expression. The present study suggests that VEGF in CSDH, which may be induced in the neomembrane by HIF-1 release, may give rise to the excessive development of fragile microvessels and hyperpermeability, resulting in the enlargement of CSDH.

The role of exudation in chronic subdural hematomas

Chronic subdural hematomas (SDHs) are a local inflammatory process that causes the formation of a granulation tissue often referred to as the external or outer membrane. This membrane has abnormally permeable macrocapillaries. Therefore, exudation from the macrocapillaries in the outer membrane of chronic SDH may play an important role in the enlargement of chronic SDH. In this study the authors investigated the role of exudation in chronic SDH. The authors examined 24 patients (16 men and eight women; age range 38-86 years [mean age 61.4 years]) with 27 chronic SDHs. The clinical status of the patients was evaluated according to the classification described by Markwalder. The diagnosis was established on computed tomography (CT) scans in all cases. The authors also used the Nomura Classification for judging the lesion's appearance on CT scans. Immediately after the diagnosis, all patients were administered 20 mCi (740 mBq) technetium-99m human serum albumin. Four hours later, blood and SDH samples were taken and radioactivity levels were measured in each. The ratio of activity of the samples taken from chronic SDH to the radioactivity of blood was determined as a percentage and defined as the exudation rate. On the follow-up CT scan obtained on postoperative Day 20, subdural collections thicker than 5 mm were determined to be a reaccumulation. The correlations between the exudation rate and age of the patients, clinical grades, CT appearances, and amount of reaccumulation were investigated. In this series the average exudation rate was 13.24% (range 2.05-28.88%). The mean exudation rates according to the clinical grades assigned to patients were as follows: Grade 0, 8.67 +/- 5.64% (three patients); Grade 1, 5.07 +/- 1.43% (eight patients); Grade 2, 17.87 +/- 3.73% (seven patients); and Grade 3, 19.65 +/- 7.67% (six patients). Exudation rates in patients with Grades 2 and 3 were significantly higher than those in Grades 0 and 1 (p < 0.05). The mean exudation rates according to the lesion's appearance on CT scans were found as follows: hypodense appearance, 6.55 +/- 4.52% (eight patients); isodense appearance, 11.07 +/- 6.32% (five patients); hyperdense appearance, 19.47 +/- 13.61% (three patients); and mixed-density appearance, 17.40 +/- 5.80% (nine patients). The differences among the groups were significant (p < 0.05). The average exudation rate was statistically higher in the patients with reaccumulation (16.30 +/- 8.16%) than that in the patients without reaccumulation (9.96 +/- 6.84%) (p < 0.05). The exudation rate in chronic SDH is correlated with a higher clinical grade (Markwalder Grade 2 or 3), mixed-density CT appearance, and reaccumulation. Therefore, exudation from macrocapillaries in the outer membrane of chronic SDH probably plays an important role in the pathophysiology and the growth of chronic SDH.

What are the Causative Factors for a Slow, Progressive Enlargement of a Chronic Subdural Hematoma?

PurposeTo test the hypothesis that chronic subdural hematoma (CSDH) enlarges by the causative factors, this study has performed.Materials and MethodsIn 10 patients with CSDH, coagulation factors in venous blood taken at the time of surgery and hematomic contents aspirated from the CSDH were studied, using both laboratory assays and microscopy.ResultsWhen compared to the range of normal plasma, the hematoma fluids demonstrated a marked reduction in factor II, V, VII, VIII, and X, moderate reduction of factors IX and XI, and slight reduction of factor XII. Activated protein C and antithrombin III levels were decreased. The FDP (Fibrinogen Degradation Product) levels in chronic subdural hematoma were extremely high. The endothelial cells of the macrocapillaries (also called "sinusoid") showed numerous gap junctions between adjacent endothelial cells and a thinness or absence of the basement membrane, suggesting that the macrocapillaries are very fragile and susceptible to bleeding.ConclusionExcessive coagulation in the hematoma, predominantly via the extrinsic clotting pathway, local hyperfibrinolysis, transmitted pulsations, and characteristics of the macrocapillaries play an important role in the leakage of blood and the enlargement of CSDH.

Tissue-type plasminogen activator in the chronic subdural hematoma

We measured the concentrations of tissue-type plasminogen activator (t-PA) in 92 patients with chronic subdural hematoma involving 102 sites. The t-PA level in the normal plasma was 4.0 ± 1.8 ng/mL (mean ± SD), while that in the hematoma content of these patients was 11.2 ± 6.2 ng/mL. Patients showing stupor (grade 3) and coma (grade 4) had higher t-PA levels than those showing headache (grade 1) and somnolence (grade 2) or psychiatric disorder (grade 5). Also, those with the layer-type hematoma on computed tomographic images had higher t-PA levels than those with any other types. The t-PA level in the draining fluid decreased after surgery. In three patients showing a gradual increase of t-PA, subdural fluid reaccumulated and the general condition remained unchanged after surgery. Overproduction of t-PA is considered to initiate intermittent hemorrhage by conversion of plasminogen to plasmin and results in persistence or enlargement of chronic subdural hematoma.

The role of endothelial gap junctions in the enlargement of chronic subdural hematomas.

The structure of macrocapillaries (also called 'sinusoids") in the outer membrane of chronic subdural hematomas was investigated by electron microscopy, with particular attention paid to vascular permeability. One characteristic of macrocapillaries is the frequent formation of gap junctions between adjacent endothelial cells. In endothelial gap junctions 0.6 to 8 microns in diameter, numerous blood components, including red blood cells and plasma, can be seen squeezing or spilling into the interstitial space of the outer membrane. Irregularly deformed erythrocytes are located around the macrocapillaries, and amorphous material is seen among scattered thin collagen fibers. It is suggested that endothelial gap junctions of macrocapillaries play an important role in the leakage of blood, causing enlargement of chronic subdural hematomas.