Development Of Chronic Subdural Hematoma Research Articles

Spontaneous chronic subdural hematoma associated with arachnoid cyst in children and young adults

Arachnoid cysts are clear, colorless fluid-filled cysts that arise during brain and skull development from the splitting of the arachnoid membrane. Chronic subdural hematoma (CSDH) is an encapsulated collection of old blood, mostly or totally liquefied and located between the dura mater and the arachnoid mater. Trauma is an important factor in the development of CSDH. Here, we report four patients, previously asymptomatic, revealing CSDH with AC on computed tomography (CT) and magnetic resonance imaging (MRI) of the brain. All patients underwent craniotomy with evacuation of hematoma and resection of the cystic membrane that was then connected to the basal cistern under the operating microscope. Postoperatively, all patients were symptom-free. Presentation of an AC with chronic subdural hematoma in the absence of preceding head trauma is considered to be rare in children and young adults.

Risk factors for development of significant chronic subdural hematoma following conservative treatment of acute subdural hemorrhage

Objective. One of the complications of untreated acute subdural hemorrhage (aSDH) is the late development of chronic subdural hematomas (cSDH). cSDH may cause major neurologic deficits, requiring their surgical evacuation. The aim of our work was to find risk factors for the development of significant cSDH requiring surgery following conservative treatment of trauma-related aSDH. Methods. In a retrospective manner, we analyzed the data of 95 adult patients admitted with a non-surgical, traumatic aSDH. The patients were divided into two groups. The first group contained 52 patients who did not, on follow-up, develop cSDH requiring surgery. The second group contained 43 patients who ended up with a significant cSDH, based on clinical and radiological criteria, requiring surgical evacuation. Data acquisition and comparison between the two groups was performed by analyzing the patients’ charts for diverse medical conditions and other trauma-related parameters. Results. The operation rate was significantly higher in patients with medical history of ischemic heart disease (IHD) or hypertension (66.7% vs. 38%, p = 0.019 and 56.9% vs. 20%, p < 0.01, respectively), with a 4-fold increase in the risk for developing surgical cSDH in patients with IHD and a 6-fold increase in the risk in patients with hypertension (odds ratio 4.2 [95% CI for odds, 1.3–13.1] and 5.9 [95% C.I for odds, 1.6–21.5], respectively). Among 21 patients, 20 (95%) patients, who were either on more than 1 anti-aggregant agents (AAA), used Clopidrogrel, or took anti-coagulant drug were in the operative group (OG). A larger initial thickness of the aSDH was statistically significant in the OG as compared to the non-OG (8.9 mm ± 4.6 vs. 5.5 mm ± 2.1, p < 0.001). Conclusion. Head-trauma patients with a medical history of IHD or hypertension, patients on more than one AAA or anti-coagulant agents and patients with worse initial CT scan parameters are at risk of developing significant cSDH requiring surgery after conservative treatment of aSDH and consequently should have closer follow-up.

Mini-craniotomy as the primary surgical intervention for the treatment of chronic subdural hematoma—a retrospective analysis

The incidence of chronic subdural hematoma (CSDH) is increasing, but optimal treatment remains controversial. Recent meta-analyses suggest burr hole (BH) drainage is the best treatment because it provides optimal balance between recurrence and morbidity. Mini-craniotomy may offer supplementary technical advantages while maintaining equal or better outcomes. This study investigates the outcome of mini-craniotomy as the sole treatment in patients with CSDH. We analyzed all patients operated on for CSDH with mini-craniotomy in our neurosurgical center between 2005-2010. Baseline patient characteristics (age, sex, comorbidities, imaging characteristics, known risk factors for development of CSDH and neurological examination at presentation) and outcomes (mortality, complications, recurrence and neurological examination at discharge) were recorded. One hundred twenty-six adult patients were included, mean age was 73.9 (range 18 to 95) years old, and the sex ratio (M:F) was 2:1. Eighty-four percent of the patients showed clinical improvement at discharge, as shown by a decrease in the Markwalder score postoperatively (with 57% Markwalder 0 and 23% Markwalder 1). Recurrence rate was 8.7%. Overall complication rate was 34.1% (27.8% medical complications and 6.3% surgical complications). In-hospital mortality was 13.5% (8.7% due to pulmonary infections and 1.6% to surgical complications). Preoperative Markwalder grade correlated significantly with complication rate, as did the presence of a neurodegenerative disease (p = 0.018). Factors significantly related to mortality in univariate analysis were arterial hypertension (p = 0.038), heart failure (p = 0.02), renal failure (p = 0.017), neurodegenerative disease (p = 0.001), cerebrovascular accident (p = 0.008) and coagulopathy (p = 0.019). Multivariate analysis was not able to confirm any significant relationship. This is the first published series of CSDH in which all consecutive patients were operated on by mini-craniotomy. The invasiveness and complication rate of mini-craniotomy are equal to those of burr hole treatment, but visualization is superior, resulting in lower recurrences. A randomized controlled trial is indicated to identify the best surgical strategy for the treatment of CSDH.

Vascular Endothelial Growth Factor Concentration in Chronic Subdural Hematoma Fluid Is Related to Computed Tomography Appearance and Exudation Rate

Chronic subdural hematoma (CSH) is characterized by a net increase of volume over time. Major underlying mechanisms appear to be hemorrhagic episodes and a continuous exudation, which may be studied using labeled proteins to yield an exudation rate in a given patient. We tested the hypothesis that the concentration of vascular endothelial growth factor (VEGF) in hematoma fluid correlates with the rate of exudation. Concentration of VEGF was determined in 51 consecutive patients with CSH by the sandwich immune enzyme-linked immunosorbent assay technique. Mean values were correlated with exudation rates taken from the literature according to the appearance of CSH on computed tomography (CT) images. The CT appearance of each CSH was classified as hypodense, isodense, hyperdense, or mixed density. Mean VEGF concentration was highest in mixed-density hematomas (22,403±4173 pg/mL; mean±standard error of the mean; n=27), followed by isodense (9715±1287 pg/mL; n=9) and hypodense (5955±610 pg/mL; n=18) hematomas. Only 1 patient with hyperdense hematoma fulfilled the inclusion criteria, and the concentration of VEGF found in this patient was 24,200 pg/mL. There was a statistically significant correlation between VEGF concentrations and exudation rates in the four classes of CT appearance (r=0.98). The current report is the first to suggest a pathophysiological link between the VEGF concentration and the exudation rate underlying the steady increase of hematoma volume and CT appearance.With this finding, the current report adds another piece of evidence in favor of the pathophysiological role of VEGF in the development of CSH, including mechanisms contributing to hematoma growth and CT appearance.

Prediction of Chronic Subdural Hematoma in Minor Head Trauma Patients.

ObjectiveChronic subdural hematoma (CSDH) is relatively common in neurosurgical field. However not all patients develop CSDH after minor head trauma. In this study, we evaluate the risk factors of post-traumatic CSDH.MethodsTwo-hundred and seventy-seven patients were enrolled and analyzed in this study from January 2012 to December 2013. Of those, 20 participants had minor head trauma developed CSDH afterward. We also included 257 patients with minor head trauma who did not develop CSDH during the same follow-up period as the control group. We investigated the risk factors related to the development of CSDH after minor head trauma.ResultsOld age (p=0.014), preexisting diabetes mellitus (p=0.010), hypertension (p=0.026), history of cerebral infarction (p=0.035), antiplatelet agents (p=0.000), acute subdural hematoma in the convexity (p=0.000), encephalomalacia (p=0.029), and long distance between skull and brain parenchyma (p=0.000) were significantly correlated with the development of CSDH after trauma. Multivariate analysis revealed that only the maximum distance between the skull and the cerebral parenchyma was the independent risk factor for the occurrence of CSDH (hazard ratio 2.55, p=0.000).ConclusionWe should consider the possibility of developing CSDH in the post-traumatic patients with the identified risk factors.

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.

Anticoagulation therapy a risk factor for the development of chronic subdural hematoma

ObjectiveChronic subdural hematoma (CSDH) is a common disease among the elderly and with increasing incidence we have chosen to focus on associations between development and recurrence of CSDH and anticoagulation and/or antiplatelet agent therapy. MethodsWe conducted a retrospective review of 239 patients undergoing surgery for CSDH over a period of six years (2006–2011). Risk factors such as age, head trauma, anticoagulant and/or antiplatelet agent therapy and co-morbidity were investigated along with gender, coagulation status, laterality, surgical method and recurrence. ResultsSeventy-two percent of the patients were male and the mean age was 71.8 years (range 28–97 years). Previous fall with head trauma was reported in 60% of the patients while 16% were certain of no previous head trauma. The majority of patients (63%) in the non-trauma group were receiving anticoagulants and/or antiplatelet agent therapy prior to CSDH presentation, compared to 42% in the trauma group. Twenty-four percent experienced recurrence of the CSDH. There was no association between recurrence and anticoagulant and/or antiplatelet agent therapy. ConclusionAnticoagulant and/or antiplatelet aggregation agent therapy is more prevalent among non-traumatic CSDH patients but does not seem to influence the rate of CSDH recurrence.

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.

Cerebral atrophy is associated with development of chronic subdural haematoma

Objective: To test that cerebral atrophy is associated with increased risk for development of chronic subdural haematoma (cSDH), this study performed volumetric analysis of computed tomography (CT) brain scans from patients who were diagnosed with cSDH on subsequent CT scans and their age-matched controls.Methods: Volumetric analysis was performed on CT scans acquired a mean of 209 days prior to cSDH diagnosis in 19 patients. Cerebral atrophy present on these scans was then compared to 76 age-matched control patients randomly selected from cSDH-free subjects.Results: There was a higher degree of atrophy in cSDH patients (n = 19, 14.3% ± 5.4%) than in age-matched control patients (n = 76, 11.9% ± 5.5%; p = 0.044). Logistical regression demonstrated that atrophy was found to be a significant predictor of cSDH at all ages (OR = 1.11, 95% CI = [1.01, 1.23], p = 0.05). For younger subjects ≤65 years of age (n = 50), atrophy was an even stronger predictor of cSDH (OR = 1.17, 95% CI = [1.02, 1.34], p = 0.026).Conclusions: Cerebral atrophy is associated with the development of cSDH and this association is greater in patients ≤65 years of age.

Factors Affecting Postoperative Recurrence of Chronic Subdural Hematoma

Chronic subdural hematoma (CSDH) is a relatively common disease, especially in the geriatric population, frequently encountered in neurosurgical practice. Formation of the outer membrane with an interior containing hyperosmolar blood collection causes development of CSDH, and the outer membrane has abnormally permeable microcapillaries leading to accumulation of exudation from the macrocapillaries in the outer membrane, therefore enlarging the area of the subdural hematoma. CSDHs have been reported to show good postoperative prognosis with relatively simple method of surgical treatment including burr hole trephination. Traditionally, burr hole trephination and evacuation of hematoma with closed drainage system has been widely accepted as the optimal treatment for CSDH. It is agreeable that surgical decompression offers a dramatic improvement of symptoms, and the procedure is relatively noninvasive and safe with satisfactory postoperative outcome in the majority of patients with CSDH. However, considerable recurrence rates have been reported ranging from 3 to 20% following surgical management. This clinical analysis evaluated the postoperative course of CSDH and the factors correlated with recurrence.

Massive Spontaneous Acute-on-Chronic Subdural Hematoma Following Coumadin Administration: A Case Report.

The routine use of oral anticoagulation after total joint arthroplasty procedures to prevent deep venous thrombosis (DVT) and symptomatic pulmonary embolism (PE) has become the current standard of care. However, intracranial hemorrhage remains among the most feared and fatal complications of oral anticoagulation. The majority of intracranial hemorrhages associated with oral anticoagulation are traumatic in nature. Intracranial subdural hematomas typically result from the tearing of bridging veins within the subdural space after varying degrees of trauma1. The hematomas are usually classified temporally as acute, subacute, or chronic. Risk factors for the development of chronic subdural hematomas include increasing age, trauma, and anticoagulant use with coagulopathy2. Subdural hematoma in patients receiving oral anticoagulation therapy, first described in 19643 to the best of our knowledge, is a well-known entity. With the increased use of anticoagulants such as warfarin and aspirin, the incidence of intracranial hemorrhage has also increased4. Even in the setting of well-controlled oral anticoagulation administration with routine international normalized ratio (INR) levels, there is a seven to tenfold increased risk of intracranial hemorrhage1, with one study demonstrating that 15% of patients with spontaneous intracranial hemorrhage had been taking Coumadin (warfarin)5. In a cohort of patients with acute subdural hematoma in another study, 11% had been administered Coumadin or heparin for anticoagulation. In the same study, 13% of patients with chronic subdural hematoma had been taking aspirin, and 21% of the patients had been taking Coumadin6. Despite increased awareness of the greater risk of intracranial bleeding with oral anticoagulation therapy, intracranial hemorrhage is clinically devastating, with a thirty-day mortality rate of approximately 50%7. Among the survivors, high morbidity remains with a high incidence of disability8. Common symptoms of chronic subdural hematomas include altered mental …

Chronic Subdural Hematoma in a Patient With Congenital Afibrinogenemia Successfully Treated With Fibrinogen Replacement -Case Report-

A 37-year-old woman with congenital afibrinogenemia presented with chronic subdural hematoma (CSDH) manifesting as severe headache, nausea, and somnolence after a minor head trauma. Brain computed tomography scans showed a right subdural hematoma associated with midline shift. Laboratory studies showed prolongation of prothrombin time, activated partial thromboplastin time, and undetectably low level of fibrinogen. Until the present episode, she had received plasma-derived fibrinogen concentrate around menstruation and pregnancy. She had also suffered from spinal cord infarction due to vertebral artery occlusion. Burr-hole evacuation and drainage of CSDH was successfully performed using fibrinogen concentrate. The development of CSDH with afibrinogenemia is very rare. Although the past repeated administrations of fibrinogen concentrate were suspected to generate CSDH, paradoxical thrombotic complications caused by upregulation of prothrombin activation, thrombin generation, and growth factors released from platelets might be related to the development of CSDH with congenital afibrinogenemia.

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.

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.

ANGIOTENSIN CONVERTING ENZYME INHIBITION FOR ARTERIAL HYPERTENSION REDUCES THE RISK OF RECURRENCE IN PATIENTS WITH CHRONIC SUBDURAL HEMATOMA POSSIBLY BY AN ANTIANGIOGENIC MECHANISM

Chronic subdural hematoma (CSH) is characterized by pathological vascularization of the parietal membrane. Plasma leakage from immature vessels may be involved in hematoma enlargement and recurrence. We tested the hypothesis that the antiangiogenic side-effect of angiotensin converting enzyme (ACE)-inhibitor treatment for the control of arterial hypertension reduces the risk of recurrence in CSH. We analyzed the data of 438 patients with CSH treated by a standard surgical procedure for hematoma evacuation in our department between 1995 and 2003. Patients with coagulopathies, malignancies, and independent neurological disorders were excluded from this study. Patient records were screened for age, sex, pre- and postoperative Markwalder score, arterial hypertension, medication with ACE-inhibitors, and recurrence of CSH. The rate of ACE-inhibitor treatment in our CSH patients was compared with an age-matched control group treated for herniated lumbar disc at the same time. The concentration of vascular endothelial growth factor was analyzed in hematoma samples and corresponding venous blood in 40 consecutive patients. A total of 310 patients were included in this study. The demographic data of Group A (with ACE-inhibition) and Group B (without ACE-inhibition) were comparable. In Group A, 5% (four out of 81) of the patients experienced recurrence as opposed to 18% (42 out of 229) in Group B (P = 0.00345). A negative correlation was found between the yearly rates of medication with ACE-inhibitors and recurrence (r = -0.8488; P = 0.0044). The rate of ACE-inhibitor treatment was lower in the CSH patients (25%) than in the control group (40%). The VEGF content was significantly lower in the hematoma in patients with ACE-inhibition (mean, 8891 pg/ml; range, 4300-18,300 pg/ml) than in patients without (mean, 22,565 pg/ml; range, 4200-89,650 pg/ml; P = 0.0116). Our data suggest that ACE-inhibitor treatment for the control of arterial hypertension lowers the risk of recurrence in patients undergoing operation for CSH and possibly even the development of CSH. This effect might be the result of an antiangiogenic mechanism of ACE-inhibitors.

NS07 CHRONIC SUBDURAL HAEMATOMAS AND ANTICOAGULATION OR ANTI‐THROMBOLYTIC THERAPY

Purpose The use of anticoagulant therapy as a causative agent in the development of chronic subdural haematomas (CSDH) was investigated. We suspected a high incidence of anticoagulant therapy or anti‐thrombotic therapy in patients who presented with CSDH.Methodology Retrospective analysis of charts of eighty‐one cases of CSDH admitted to the neurosurgical unit of the Royal Hobart Hospital (RHH), Tasmania, Australia, over a 5‐year period were reviewed. A database of neurosurgical procedures performed at RHH was examined to retrieve these patients undergoing surgery for CSDH. We found that anticoagulant therapy was used by a significant percentage of CSDH patients.Results/Conclusions In the patient group presenting to our unit the risk of developing a CSDH was at least 42.5 times higher in warfarinised patients and also increased for patients on aspirin, although the risk could not be quantified.

Chronic subdural haematomas and anticoagulation or anti-thrombotic therapy

Eighty-one cases of chronic subdural haematomas (CSDH) admitted to the neurosurgical unit of the Royal Hobart Hospital, Tasmania, Australia, over a 5-year period were reviewed. The use of anticoagulant therapy as a causative agent in the development of CSDH was investigated. We suspected a high incidence of anticoagulant or anti-thrombotic therapy. We found that anticoagulant therapy was used by a significant percentage of CSDH patients. In the patient group presenting to our unit the risk of developing a CSDH was at least 42.5 times higher in warfarinised patients and also increased for patients on aspirin, although this risk could not be quantified.

Idiopathic chronic subdural hematoma in the newborn: case report

Evidence of intrauterine development of chronic subdural hematoma (CSH) is extremely rare. A very limited number of cases with known and acceptable etiological explanation are reported. We were able to find out only four presented cases of intrauterine development of CSH without known etiology. We present our case with a newborn baby with CSH without known etiology. Short literature review and possible etiological factors are observed.

Infantile head injury, with special reference to the development of chronic subdural hematoma

An infantile head injury has unique features in that infants are totally helpless and dependent on their parents, and biomechanical characteristics of the skull and brain are very different from those of other age groups. The authors reviewed a total of 16 infant head injury patients under 12 months of age who were treated in our hospital from 1989 to 1997. Birth head injury was excluded. The most common age group was 3-5 months. Early seizures were noted in 7 cases, and motor weakness in 6. Three patients with acute intracranial hematoma and another 3 with depressed skull fracture were operated on soon after admission. Chronic subdural hematomas (SDHs) developed in 3 infants. Initial CT scans showed a small amount of SDH that needed no emergency operation. Resolution of the acute SDH and development of subdural hygroma appeared on follow-up CT scans within 2 weeks of injury. Two of these infants developed early seizures. Chronic SDH was diagnosed on the 68th and 111th days after the injuries were sustained, respectively. The third patient was the subject of close follow-up with special attention to the evolution of chronic SDH in view of our experience in the previous 2 cases, and was found to have developed chronic SDH on the 90th day after injury. All chronic SDH patients were successively treated by subduro-peritoneal shunting. In conclusion, the evolution of chronic SDH from acute SDH is relatively common following infantile head injury. Infants with head injuries, especially if they are associated with acute SDH and early development of subdural hygroma, should be carefully followed up with special attention to the possible development of chronic SDH

Expression of matrix metalloproteinases in the chronic subdural haematoma membrane.

To study the role of matrix metalloproteinases (MMP) in the development of chronic subdural haematoma, we investigated the expression and activity of MMPs (MMP-1, -2, -3, -7 and -9) and tissue inhibitors of MMP (TIMP-1 and -2) in capsules of chronic subdural haematoma from 10 patients. Outer membranes of chronic subdural haematoma were immunostained for MMP-1, MMP-2, MMP-9, TIMP-1 and TIMP-2. Moreover, we confirmed MMP activity in membranes by SDS-PAGE zymography and in situ zymography. These results suggest that MMP degrades extracellular matrix in outer membranes of chronic subdural haematoma, which is thought to decrease their integrity followed by direct haemorrhage and exudation of oedematous fluid from membrane vessels into the haematoma cavity.