Pathogenesis Of Chronic Subdural Hematoma Research Articles

Acute-to-chronic subdural hematoma: radiographic and clinical progression from acute subdural hematoma

Introduction: The pathogenesis of chronic subdural hematoma (CSDH) has not been completely understood. However, different mechanisms can result in space-occupying subdural fluid collections, one pathway can be the transformation of an original trauma-induced acute subdural hematoma (ASDH) into a CSDH. Materials and Methods: All patients with unilateral CSDH, requiring burr hole trephination between 2018 and 2023 were included. The population was distributed into an acute-to-chronic group (group A, n = 41) and into a conventional group (group B, n = 282). Clinical and radiographic parameters were analyzed. In analysis A, changes of parameters after trauma within group A are compared. In analysis B, parameters between the two groups before surgery were correlated. Results: In group A, volume and midline shift increased significantly during the progression from acute-to-chronic (p < 0.001, resp.). Clinical performance (modified Rankin scale, Glasgow Coma Scale) dropped significantly (p = 0.035, p < 0.001, resp.). Median time between trauma with ASDH and surgery for CSDH was 12 days. Patients treated up to the 12th day presented with larger volume of ASDH (p = 0.012). Before burr hole trephination, patients in group A presented with disturbance of consciousness (DOC) more often (p = 0.002), however less commonly with a new motor deficit (p = 0.014). Despite similar midline shift between the groups (p = 0.8), the maximal hematoma width was greater in group B (p < 0.001). Conclusion: If ASDH transforms to CSDH, treatment may become mandatory early due to increase in volume and midline shift. Close monitoring of these patients is crucial since DOC and rapid deterioration is common in this type of SDH.

The pathogenesis of chronic subdural hematoma in the perspective of neomembrane formation and related mechanisms

The pathogenesis of chronic subdural hematoma in the perspective of neomembrane formation and related mechanisms

Subdural Lesions Linking Additional Intracranial Spaces and Chronic Subdural Hematomas: A Narrative Review with Mutual Correlation and Possible Mechanisms behind High Recurrence.

The purpose of this study was two-fold. The first was to investigate the pathologic mechanisms underlying the formation of subdural fluid collection, an umbrella term referring to a condition commonly seen in the clinical setting. Accumulation of the cerebrospinal fluid (CSF) in the subdural space can be referred to in this disease category, disregarding the underlying source of the subdural fluid. However, in these two clinical situations, especially after trauma or brain surgery, fluid collection from the subarachnoid space (subdural hygroma) or from the ventricle to the subarachnoid space and infusion into the subdural space (external hydrocephalus), surgical management of critical patients may adopt the strategies of burr-hole, subduroperitoneal shunt, or ventriculoperitoneal shunt, which present distinctly different thoughts. Crucially, the former can be further transformed into chronic subdural hematoma (CSDH). The second significant theme was the pathogenesis of CSDH. Once the potential dural border cell (DBC) layer is separated such as if a wound is formed, the physiological mechanisms that seem to promote wound healing will resume in the subdural space as follows: coagulation, inflammation, fibroblast proliferation, neovascularization, and fibrinolysis. These aptly correspond to several key characteristics of CSDH formation such as the presence of both coagulation and fibrinolysis signals within the clot, neomembrane formation, angiogenesis, and recurrent bleeding, which contribute to CSDH failing to coagulate and absorb easily. Such a complexity of genesis and the possibility of arising from multiple pathological patterns provide a reasonable explanation for the high recurrence rate, even after surgery. Among the various complex and clinically challenging subdural lesions, namely, CSDH (confined to the subdural space alone), subdural hygroma (linked in two spaces), and external hydrocephalus (linked in three spaces), the ability to fully understand the different pathological mechanisms of each, differentiate them clinically, and devote more interventional strategies (including anti-inflammatory, anti-angiogenic, and anti-fibrinolysis) will be important themes in the future.

Glucocorticoides en el tratamiento del hematoma subdural crónico

Se revisan cincuenta y tres pacientes adultos consecutivos tratados por hematoma subdural crónico con el agregado de glucocorticoidesen su plan de tratamiento. El concepto actual de la patogenia del hematoma subdural crónico y el mecanismo por el cual los glucocorticoides podrían mejorar el pronóstico de esta condición son discutidos. Se presentan los resultados clínicos de este régimen terapéutico y si se comparan con los resultados de otras series en las cuales el hematoma subdural crónico fue tratado sin el agregado de glucocorticoides. Da la impresión que los glucocorticoides merecen un lugar en el tratamiento del hematoma subdural crónico.

Hematoma within the Outer Membrane of the Arachnoid Cyst Located in the Middle Fossa: A Mechanism of Development of Chronic Subdural Hematoma Associated with Arachnoid Cysts

It is well known that chronic subdural hematoma (CSDH) occasionally arises in patients harboring an arachnoid cyst (AC) located in the middle fossa. Although the pathogenesis of CSDH associated with ACs remains unknown, several possible mechanisms have been proposed. In many reported cases, the patients with ACs in the middle fossa would be symptomatic according to development of CSDH. A 9-year-old girl presenting with a headache, nausea, and diplopia was referred to our department. Magnetic resonance imaging showed an AC in the left-side middle fossa and ipsilateral CSDH with a remarkable mass effect. Irrigation of the CSDH, partial removal of the outer membrane of the AC and CSDH, and endoscopic cystocisternostomy were performed to relieve her symptoms. Postoperative clinical course was excellent. Histopathological examination of the outer membrane of the CSDH demonstrated an arachnoid cell layer and hemorrhage from the granulation inside the membrane, and collagen fibers outside the membrane. These findings strongly suggested that the membrane and the content of the CSDH were derived from the outer membrane of the AC, and the CSF including the hemorrhage within the membrane, respectively. Laceration and hemorrhage from granulation tissue within the outer membrane of the AC are considered as one of the developmental mechanisms of the CSDH associated with AC in the middle fossa.

Characterization of Chronic Subdural Hematoma Fluid Proteome

Chronic subdural hematoma (CSDH) is commonly caused by head injury, but the progression of CSDH is recognized as an inflammatory process. The protein composition of the CSDH fluid has not been fully elucidated, nor has the contribution of its components to the enlargement of the hematoma cavity and to its chronic manifestation. To characterize the protein content of CSDH fluid and study the differences between CSDH fluid and serum to identify proteins putatively involved in the pathogenesis of CSDH. CSDH fluid and serum of 5 patients were investigated with 2-dimensional gel electrophoresis followed by glycosylation-specific fluorescence staining and mass spectrometry. Two-dimensional gel electrophoresis revealed approximately 1100 protein spots in the CSDH fluid. We identified 213 spots representing 57 different proteins, most of which were glycosylated. The comparison with serum revealed 11 proteins with elevated levels in the CSDH fluid including carbonic anhydrase I, catalase, ferritin light chain, fibrinogen (α, β, γ), hemoglobin (α, β), malate dehydrogenase, peroxiredoxin 2, and transforming growth factor-β-induced protein ig-h3. The levels of haptoglobin and a fragment of complement C4 were decreased. Changes in spot positions were detected for apolipoprotein A1 and a fragment of complement C3. The hematoma fluid originates mainly from blood and the results suggest the involvement of coagulation and fibrinolysis cascades. However, proteins with a potential role in CSDH pathogenesis were detected including carbonic anhydrase I, transforming growth factor-β-induced protein ig-h3, and the altered components of the complement system. Inflammation and fibrosis indicate targets for further studies in the pathogenesis of CSDH.

Chronic subdural hematoma associated with the middle fossa arachnoid cyst: pathogenesis and review of its management

The pathogenesis of chronic subdural hematoma (CSDH) associated with an arachnoid cyst (AC) is still not clear. We propose an origin of initial bleeding of CSDH in patients with AC based on our experience and discuss the management of this disease. The total number of operations included in this study was 23. Eleven cases were indicated because of associated CSDH (group 1), and the other cases were due to different reasons (group 2). The relationship of the AC and dura was evaluated in patients who did not have CSDH (group 2) because patients with CSDH would have had structural changes of AC due to hematoma. In group 1, the age distribution was from 8 to 61years (mean 23.0). The development of CSDH was not related with Galassi types. The hematomas were located outside of the outer cyst membrane in six patients and both inside and outside in three patients. In two patients, the location could not be reviewed. After suspicion of the outer cyst membrane as the origin of the bleeding site, we found small bridging vessels between the dura and outer cyst membrane in three of five consecutive patients in group 2. Based on our surgical experience of AC cyst, we found small bridging vessels between the dura and outer membrane of the AC. We suggested that these small vessels are the source of initial bleeding leading to CSDH in AC.

Corticosteroid Suppression of Vascular Endothelial Growth Factor and Recurrence of Chronic Subdural Hematoma

We read with interest the article by Berghauser et al1 in which the authors described that in surgical treatment of chronic subdural hematoma (CSDH) with burr hole craniostomy, a longer period of preoperative dexamethasone administration is associated with a lower recurrence rate of CSDH and that dexamethasone administration seems to be unrelated to the higher incidence of complications and treatment-related deaths compared with the current literature. However, the authors mentioned that the mechanism of action of dexamethasone in CSDH has not been fully clarified. We wish to provide further comments on the issue of the effect of preoperative dexamethasone administration on CSDH recurrence. The involvement of vascular endothelial growth factor (VEGF), a potent inducer of angiogenesis and vascular permeability, in the pathogenesis of CSDH and the mechanism of recurrent CSDH has been reported.2-4 Weigel et al2 reported that 5% (4 of 81) of the patients with angiotensin-converting enzyme (ACE) inhibition experienced recurrence as opposed to 18% (42 of 229) of patients without ACE inhibition (P = .00345) and that VEGF content was significantly lower in the hematomas of patients with ACE inhibition than in those without. Greenberger et al5 reported that systemic treatment with dexamethasone led to dose-dependent inhibition of vasculogenesis in an in vivo model of infantile hemangioma and that dexamethasone suppressed VEGF production in hemangioma-derived stem cells in vitro. On the basis of these reports, we consider that the effect of preoperative dexamethasone administration on the recurrence of CSDH might be dependent on the corticosteroid suppression of VEGF. Additionally, Funai et al3 recently reported that phosphatidylinositol 3-kinase/Akt signaling is activated in CSDH outer membranes and that the phosphatidylinositol 3-kinase/Akt pathway might be activated by VEGF in outer membranes. A previous study by Nanko et al4 also revealed that VEGF expression in the outer membrane of 30 patients with CSDH was significantly correlated with VEGF concentration in the hematoma (r[s] = .654, P = .0013) and that VEGF concentration in layered hematomas, which have an intrahematoma membranous structure, was significantly higher than in nonlayered hematomas (P < .01), suggesting that the high concentration of VEGF in the hematoma can originate from the hematoma membrane. We previously reported recurrence rates in 64 consecutive patients after CSDH evacuation.6 Recurrence was noted in 7 of the 64 patients (10.9%) after burr-hole craniostomy with drainage, and layered hematoma was seen in 3 of the 7 recurrent cases (42.9%). Therefore, we consider that preoperative dexamethasone administration might be effective in the prevention of recurrent CSDH, especially in the case of layered-type CSDH. Further investigations on the relationship between preoperative dexamethasone administration and VEGF concentration in the hematoma and the correlation of preoperative dexamethasone administration and preoperative radiological findings of hematomas with CSDH recurrence will provide additional insights into the recurrence of CSDH after preoperative dexamethasone administration. Disclosure The authors have no personal financial or institutional interest in any of the drugs, materials, or devices described in this article.

Dural metastases in chronic myeloid leukemia presenting as subdural hematoma”

Subdural hematoma (SDH) has been reported in 0.5-4% of all intracranial metastatic tumors. Chronic SDH has been reported in intracranial metastases from both solid and haematological malignancies. Here we report recurrent SDH in a patient with chronic myeloid leukaemia (CML) following dural metastases. An elderly male patient a known case of CML was admitted to our casualty with symptoms of headache and altered sensorium and imaging revealed a large right fronto temporo parietal chronic SDH. This was surgically managed and histopathology of the duramater and subdural membrane confirmed infiltration with leukemic cells. The pathogenesis of chronic SDH in malignancies is multifactorial and this case report throws light on leukemic infiltration of duramater as a cause for chronic SDH other than coagulopathy.

Prolonged drainage reduces the recurrence of chronic subdural hematoma

Recurrence of chronic subdural hematoma (CSH) is a significant problem in neurosurgical practice. Various risk factors associated with patient's characteristics and the pathogenesis of CSH have been investigated in many studies, but controversial findings are not uncommon. Therefore we made a retrospectively investigation focusing mainly on the factors associated with surgical techniques. in order to find out the factors that may affect the recurrence rate of CSH. The medical records of 97 consecutive patients with 121 CSHs, who were treated with burr-hole craniostomy and continuous drainage, were retrospectively reviewed. The relationships between the recurrence rate and some factors associated with surgery, such as location of burr-hole, thickness of residual hematoma, location of drainage catheter, intracapsular air postsurgery, duration of drainage were investigated. The average recurrence rate was 6.6% in this whole series. For patients with less than three days of drainage, the recurrence rate was16.3%, whereas for those with 3 and more days of drainage, the recurrence rate was only 1.3%. The duration of drainage significantly related to recurrence rate. In addition, a higher recurrence rate seemed to be associated with more intracapsular air postsurgery, but it did not reach statistically significant level in this study. Prolonged duration of drainage did not increase the frequency of infection in this series. We found in this study that the duration of drainage play an important role in the treatment of CSH and 3 full days of drainage seems to be necessary, especially for patients of 60 years and over. We presumed that it takes at least 3 days of drainage for outer membrane of CSH to get the restoration of a normal balance between coagulation and fibrinolysis after surgery, which is necessary for termination of the vicious cycle and resolution of the hematoma.

Chronic subdural hematoma preceded by traumatic subdural hygroma

Patients with traumatic subdural hygroma (SDG) are at an increased risk of developing chronic subdural hematoma (CSDH). However, the mechanism by which this occurs is still not fully understood. The purpose of this paper is to investigate the clinical characteristics and pathogenesis of CSDH, as well as the relationship between CSDH and SDG. We review the pertinent literature and retrospectively examine a series of cases in which CSDH had been preceded by SDG to understand the natural history and developmental mechanisms of these lesions. We discuss the cases of 24 patients in whom CSDH developed from traumatic SDG between 2001 and 2005. Headache was the most common symptom, and the mean Glasgow Coma Scale score was 14.1. Increases in SDG volume were observed in CT scans of 17 patients, and increased density and volume was observed in five patients. The mean interval between the two diseases was 57.6 days, and 13 patients developed new symptoms after the development of CSDH. The most common symptoms at that time were headache and hemiparesis. All patients underwent an operation, which resulted in good recovery in all but one case. The cycle of persistent SDG, rebleeding, coagulation and fibrinolysis contributes to the development of CSDH from SDG. It is important to understand the natural history of CSDH and carefully follow up patients with head injury, especially if it is associated with SDG, and the potential for the development of CSDH should be considered.

Cerebrospinal fluid leakage into the subdural space: possible influence on the pathogenesis and recurrence frequency of chronic subdural hematoma and subdural hygroma

The purpose of this study was to clarify whether cerebrospinal fluid (CSF) leakage into the subdural space is involved in the genesis of chronic subdural hematoma (CSDH) and subdural hygroma (SH) and to clarify whether this leakage of CSF into the subdural space influences the postoperative recurrence rate of CSDH and SH. In this prospective observational study, 75 cases involving patients treated surgically for CSDH (67 patients) or SH (8 patients) were evaluated with respect to clinical and radiological findings at presentation, the content of beta -trace protein (beta TP) in the subdural fluid (betaTPSF) and serum (betaTPSER), and the CSDH/SH recurrence rate. The betaTPSF was considered to indicate an admixture of CSF to the subdural fluid if betaTPSF/betaTPSER>2. The median beta TPSF level for the whole patient group was 4.29 mg/L (range 0.33-51 mg/L). Cerebrospinal fluid leakage, as indicated by betaTPSF/betaTPSER>2, was found to be present in 93% of the patients with CSDH and in 100% of the patients with SH (p=0.724). In patients who later had to undergo repeated surgery for recurrence of CSDH/SH, the betaTPSF concentrations (median 6.69 mg/L, range 0.59-51 mg/L) were significantly higher (p=0.04) than in patients not requiring reoperation (median 4.12 mg/L, range 0.33-26.8 mg/L). As indicated by the presence of betaTP in the subdural fluid, CSF leakage into the subdural space is present in the vast majority of patients with CSDH and SH. This leakage could be involved in the pathogenesis of CSDH and SH. Patients who experience recurrences of CSDH and SH have significantly higher concentrations of betaTPSF at initial presentation than patients not requiring reoperation for recurrence. These findings are presented in the literature for the first time and have to be confirmed and expanded upon by further studies.

Local elevation of the anti-inflammatory interleukin-10 in the pathogenesis of chronic subdural hematoma

We investigated the relationship between inflammatory and anti-inflammatory cytokines in the pathogenesis of chronic subdural hematoma (CSDH) by measuring the plasma and subdural fluid levels of interleukin-6 (IL-6), interleukin-8 (IL-8), and interleukin-10 (IL-10). The levels of IL-6, IL-8 and IL-10 were measured in the subdural fluid obtained from 34 patients with CSDH, using the enzyme-linked immunosorbent assay. The patients were classified into a high IL-10 group and a low IL-10 group according to the level of IL-10 in their subdural fluid samples. The subdural fluid levels of IL-6 and IL-8 were significantly higher in the high IL-10 group than in the low IL-10 group (P<0.05). A tendency for the patients in the low IL-10 group to show the separated or layer type of pattern on the CT scans was noted.

Electrophoretic demonstration of high molecular weight fibrin degradation products persisting in chronic subdural hematomas.

Local hyperfibrinolysis plays an important role in the pathogenesis of chronic subdural hematoma (CSH). The purpose of this study is to elucidate the nature of the local hyperfibrinolysis in CSH, by comparing the pattern of fibrin/fibrinogen degradation product (FDP) of hematomas with that of purified fibrin clots digested by plasmin in vitro. Forty-seven hematoma samples were subjected to the analysis. FDPs of CSH and the purified fibrin clots digested by plasmin for different incubation times were identified using sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and immuno-blotting, and then quantified by densitometry. The effect of alpha-2 plasmin inhibitor (A2-PI) on the degradation process was also studied. The FDP pattern of CSH was similar to those of purified fibrin digested by plasmin for 0.75-2 h. The FDP composition of CSH was closest to that of purified fibrin digested for 1 h. By adding the physiological concentration of A2-PI at the second hour, further degradation of high molecular weight FDPs was inhibited and the early FDP pattern persisted after 24 h. Local hyperfibrinolysis in CSHs is characterized by incomplete fibrinolysis, which occurs only on the solid fibrin clot, and is arrested in the liquid hematoma. As a result, high molecular weight FDPs persist in CSHs for weeks or months in the hematoma. A2-PI seems to play an important role in producing this unique FDP pattern in CSH.

Degradation of fibrinogen and fibrin by plasmin and nonplasmin proteases in the chronic subdural hematoma: evaluation by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunoblot.

To characterize local hyperfibrinolysis in the pathogenesis of chronic subdural hematoma (CSDH), fibrin degradation products (FDPs) were separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) to identify each FDP fragment (fragments HMW, YY, DY and DD) by immunoblotting. The electrophoretic patterns of FDP in 40 hematomas from 33 patients could be categorized into 3 patterns; (i) type 1, the sharp DY and DD bands; (ii) type 2, the broad DY and DD bands; and (iii) type 3, the sharp DY and DD with two bands with higher molecular weights than fragment DY and DD. The broadening of DY and DD bands was reproduced by incubating the sample containing sharp DD and DY bands with the hemolyzed peripheral blood cells. These results indicated that the hyperfibrinolysis in CSDH could be characterized by the constant and incomplete proteolysis of fibrinogen and fibrin by plasmin and further degradation of FDPs by non-plasmin proteases released from hemolyzed blood cells.

Chronic subdural hematoma: Pathophysiological basis for treatment

Fifty-three consecutive adult patients treated surgically for chronic subdural hematoma are reviewed. The current understanding of the pathogenesis of chronic subdural hematoma is discussed. In the current neurosurgical literature, wide discrepancies exist, in patients treated by burr-hole evacuation, regarding the rate of subdural recollection. Possible factors responsible for these discrepancies include (1) failure to recognize and properly treat multiloculated chronic subdural hematomas, (2) too aggressive a surgical approach toward persistent CT-demonstrated but asymptomatic subdural residual or recurrent collections, and (3) failure to use corticosteroids in the post-operative management of patients with persistent or recurrent symptoms as a step prior to re-operation. A prospective controlled clinical trial of glucocorticoids in chronic subdural hematoma is needed to establish their place in the management of this condition.

Coagulation and Fibrinolysis in Chronic Subdural

The pathogenesis of chronic subdural hematoma is not fully understood. It is thought that fibrinolytic hyperactivity within the hematoma capsule plays an important role. However, since this hyperactivity has not been found in the systemic blood, accelerated fibrinolysis is thought to occur only locally. To evaluate coagulant and fibrinolytic activities in the peripheral blood, the authors measured fibrinopeptide A (FPA) and fibrinopeptide B beta 15-42 (FPB beta), which are relatively sensitive hematologic factors, in 14 patients with chronic subdural hematoma. Peripheral venous blood was collected within 24 hours before surgery and FPA and FPB beta levels were determined. In the eight cases followed for more than 1 month after surgery, pre- and postoperative FPA and FPB beta values were compared. The possible relationship between preoperative FPB beta and hematoma density as well as elevated intracranial pressure (judged by preoperative computed tomography) was also examined. The following results were obtained: 1) Preoperative FPA and FPB beta values were both statistically significantly elevated suggesting systemic acceleration of coagulant and fibrinolytic activities. FPB beta levels exceeded those of FPA in almost all cases, indicating that fibrinolysis was more dramatically enhanced. 2) Many patients with high FPB beta values had high-density areas on computed tomography scans. 3) Patients with choked disc had high FPB beta values, suggesting a correlation between chronic intracranial hypertension and FPB beta. 4) Postoperatively, there was a marked decrease in FPA values, whereas FPB beta values remained above normal, which may reflect persistence of accelerated systemic fibrinolytic activity in patients with chronic subdural hematoma.

Steroid receptors in the pathogenesis of chronic subdural hematoma.

Chronic subdural hematoma (CSDH), located between the dura mater and the arachnoid and usually characterized by a well-vascularized external capsule (HEM), has a higher incidence in male patients with elevated urinary estrogens than in female patients. In an attempt to increase our understanding of the physiopathogenesis of CSDH, total estrogen receptor (ER) was measured in HEM specimens from four male patients by a sodium thiocyanate exchange assay and cytosol progesterone receptor (PRc) in three specimens by a dextran-coated charcoal adsorption assay. Although no nuclear ER could be detected, ERc and PRc were found in all three specimens examined. The presence of ER in a mesenchymal tissue like HEM could suggest that, in addition to inducing vascular changes, estrogens might act directly on HEM through a receptor-mediated mechanism more pronounced in men than in women, whose vascular network is adapted to high estrogen values.

Subdural tapping and irrigation for the treatment of chronic subdural hematoma in adults.

A new technique for the treatment of chronic subdural hematoma by tapping and irrigation was shown by computed tomography to be safe and reliable in 39 patients. The basis for such treatment is discussed in light of the current theories of the pathogenesis of chronic subdural hematoma.

Chronic subdural hematoma after lumbar-subarachnoid analgesia for a cesarean section

The following case report illustrates the occurrence of a chronic subdural hematoma as a consequence of lumbar-subarachnoid analgesia for a caesarean section. The pathogenesis of chronic subdural hematoma is discussed briefly.