Chronic subdural hematoma

Chronic subdural hematoma

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.

They are arbitrarily defined as those hematomas presenting 21 days or more after injury. These numbers are not absolute, and a more accurate classification of a subdural hematoma usually is based on imaging characteristics.

The first description of a chronic subdural hematoma was made in 1658 by J.J. Wepfer, followed in 1761 by Morgagni. A possible case was described by Honoré de Balzac in 1840 including its traumatic origin and surgical treatment.

Virchow, in 1857, denied a traumatic origin, and gave the name of “pachymeningitis hemorrhagica interna” to this pathology which he explained by inflammatory processes.

The traumatic etiology of chronic subdural hematoma was recognized in the XXth century, especially by Trotter in 1914. Pathophysiology was considered later on in the XXth century.

It was first described by Rudolf Ludwig Karl Virchow, in 1857, as “an internal hemorrhagic pachymeningitis” 1).

Later, in 1914, Trotter launched the theory of traumatic brain injury and the consecutive lesion of the “bridging veins”, as being the cause of what he called “hemorrhagic subdural cyst” 2).

Chronic subdural hematoma epidemiology.

see Chronic subdural hematoma etiology.

Chemokines in Chronic Subdural Hematoma

see Chronic subdural hematoma classification.

Chronic subdural hematoma pathophysiology.

cSDHs have a tendency to persist and gradually increase in volume over time. The disease is thought to be related to a cycle of chronic inflammation and angiogenesis. An original hemorrhage forms and fibrinolysis ensues with the liquefaction of the initial clot. The subsequent blood breakdown products stimulate inflammation and thickening of the inner dural layer (ie, ‘dural border cells). This process incites angiogenesis with the ingrowth of immature capillaries, which chronically leak blood. These microhemorrhages result in the progressive enlargement of the collection with increased fibrinolytic activity, inflammation, and further angiogenesis, membrane formation, and vessel proliferation. The rate of accumulation of blood products outpaces physiological reabsorption and the collection gradually enlarges. Thus the entire basis for the pathology is the formation of leaky vascular membranes, which incite a positive feedback cycle of continued hemorrhage, inflammation, and angiogenesis 3) 4)


Chronic subdural hematoma (CSDH) is characterized by an “old” encapsulated collection of blood and blood breakdown products between the brain and its outermost covering (the dura).

It is delimited by an outer and inner membrane. In between are bloodplasmacerebrospinal fluid, membranes, and a mixture of inflammatory angiogenic fibrinolytic and coagulation factors. These factors maintain a self-perpetuating cycle of bleeding, lysis, and growing of neo-membranes and neo-capillaries 5).

see Chronic subdural hematoma clinical features.

Glasgow Coma Scale.

Markwalder grading score.

Modified Rankin Scale.

Chronic subdural hematoma diagnosis

The association between the biomarkers of inflammation and angiogenesis, and the clinical and radiological characteristics of CSDH patients, need further investigation. The high number of biomarkers compared to the number of observations, the correlation between biomarkers, missing data and skewed distributions may limit the usefulness of classical statistical methods.

Pripp et al. explored lasso regression to assess the association between 30 biomarkers of inflammation and angiogenesis at the site of lesions, and selected clinical and radiological characteristics in a cohort of 93 patients. Lasso regression performs both variable selection and regularization to improve the predictive accuracy and interpretability of the statistical model. The results from the lasso regression showed analysis exhibited lack of robust statistical association between the biomarkers in hematoma fluid with age, gender, brain infarct, neurological deficiencies and volume of hematoma. However, there were associations between several of the biomarkers with postoperative recurrence requiring reoperation. The statistical analysis with lasso regression supported previous findings that the immunological characteristics of CSDH are local. The relationship between biomarkers, the radiological appearance of lesions and recurrence requiring reoperation have been inclusive using classical statistical methods on these data, but lasso regression revealed an association with inflammatory and angiogenic biomarkers in hematoma fluid. They suggest that lasso regression should be a recommended statistical method in research on biological processes in CSDH patients 6).

Chronic subdural hematoma (CSDH) is a disease of the meninges and is to be distinguished from hygroma and subdural empyema.

Subdural effusion in the setting of dural metastases is very rare and may be difficult to be distinguished from chronic subdural hematoma. Such lesions could be missed and could be the cause of recurrence in CSDH. A contrast-enhanced brain CT scan is recommended to diagnose dural metastases.

Rosai–Dorfman disease may be mistaken for a CSDH on imaging. This disease is an uncommon, benign systemic histioproliferative disease characterized by massive lymphadenopathy, particularly in the head and neck region, and is often associated with extranodal involvement. CSDH can also develop in multifocal fibrosclerosis (MFS) which is a rare disorder of unknown etiology, characterized by chronic inflammation with dense fibrosis and lymphoplasmacytic infiltration into the connective tissue of various organs. The mechanism of the formation of CSDH is presumed to involve reactive granular membrane together with subdural collection. On the other hand, the extramedullary erythropoiesis within CSDH can be confused with metastatic malignant tumors, such as lymphoma, carcinoma, and malignant melanoma 7).

A 44-year old woman with gastric adenocarcinoma was presented with headache and a hypodense subdural collection in right fronto-parietal in brain CT. Burr-hole irrigation was performed with the impression of chronic subdural hematoma, but nonhemorrhagic xantochromic fluid was evacuated without malignant cell. Brain CT on the 11th day depicted fluid re-accumulation and noticeable midline shift, necessitating craniotomy and removing the affected dura.

Because the affected dura can be supposed as the main source of subdural effusion, resection of the involved dura is obligatory for the appropriate palliative management of such patients 8).

see Chronic subdural hematoma treatment.

Routine postoperative CT

Routine post-operative CT brain for burr hole drainage of CSDH may be unnecessary in view of the good predictive value of pre-operative volume, and also because it is not predictive of the clinical outcome 9).

Scheduled postoperative cranial imaging with indwelling drains was not shown to be beneficial and misses information of intracranial damage inflicted by removal of drains. Brokinkel et al recommend CT-scanning after drainage removal 10).

see Chronic subdural hematoma surgery complications.

see Chronic subdural hematoma recurrence.

see Chronic subdural hematoma outcome.

A study aimed to quantify the heterogeneity of data elements in the pre-operative, operative, and post-operative phases of care, and build the basis for the development of a set of common data elements (CDEs) for CSDH. This systematic review adhered to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement and was registered with the PROSPERO register of systematic reviews (CRD42014007266). All full-text English studies with more than 10 patients (prospective) or more than 100 patients (retrospective) published after 1990 examining clinical outcomes in CSDH were eligible for inclusion. One hundred two eligible studies were found. Only 40 studies (39.2%) reported the main presenting symptom/feature and 24 (23.5%) reported additional symptoms/features. Admitting neurological/functional status was classified by the Glasgow Coma Scale (25 studies; 24.5%), the Markwalder Score (26 studies; 25.5%) and the modified Rankin Scale (three studies; 2.9%). Fifty-four studies (52.9%) made some mention of patient comorbidities and 58 studies (56.9%) reported the proportion or excluded patients on anticoagulant medication. Eighteen studies (17.6%) reported baseline coagulation status. Sixty-four studies (62.7%) stratified or assessed severity based on radiological findings, although the methods used varied widely. There was variable reporting of surgical technique and post-operative care; 32 studies (31.4%) made no mention of whether the operations were performed under general or local anesthetic. This study, a part of the Core Outcomes and Common Data Elements in CSDH (CODE-CSDH) project, confirms and quantifies the heterogeneity of data elements collected and reported in CSDH studies to date. It establishes the basis for the consensus-based development of a set of common data elements, facilitating robust cross-study comparisons and resulting improvements in patient outcomes 11).

see Chronic subdural hematoma case series.

see Chronic subdural hematoma case reports.

Attempts to create CSDH have been made in mice, rats, cats, dogs and monkeys. Methods include injection or surgical implantation of clotted blood or various other blood products and mixtures into the potential subdural space or the subcutaneous space. No intracranial model produced a progressively expanding CSDH. Transient hematoma expansion with liquification could be produced by subcutaneous injections in some models. Spontaneous subdural blood collections were found after creation of hydrocephalus in mice by systemic injection of the neurotoxin, 6-aminonicotinamide. The histology of the hematoma membranes in several models resembles the appearance in humans. None of the models has been replicated since its first description.

D’Abbondanza et al. did not find a report of a reproducible, well-described animal model of human CSDH 12).


1) 
Weigel R, Krauss JK, Schmiedek P. Concepts of neurosurgical management of chronic subdural haematoma: historical perspectives. Br J Neurosurg. 2004 Feb;18(1):8-18. PubMed PMID: 15040710.
2) 
Guénot M. [Chronic subdural hematoma: historical studies]. Neurochirurgie. 2001 Nov;47(5):461-3. French. PubMed PMID: 11915757.
3) 
Ito H , Yamamoto S , Komai T , et al . Role of local hyperfibrinolysis in the etiology of chronic subdural hematoma. J Neurosurg 1976;45:26–31.doi:10.3171/jns.1976.45.1.0026
4) 
Edlmann E , Giorgi-Coll S , Whitfield PC , et al . Pathophysiology of chronic subdural haematoma: inflammation, angiogenesis and implications for pharmacotherapy. J Neuroinflammation 2017;14:108.doi:10.1186/s12974-017-0881-y
5) 
Frati A, Salvati M, Mainiero F, Ippoliti F, Rocchi G, Raco A, Caroli E, Cantore G, Delfini R (2004) Inflammation markers and risk factors for recurrence in 35 patients with a posttraumatic chronic subdural haematoma: a prospective study. J Neurosurg 100:24–32
6) 
Pripp AH, Stanišić M. Association between biomarkers and clinical characteristics in chronic subdural hematoma patients assessed with lasso regression. PLoS One. 2017 Nov 6;12(11):e0186838. doi: 10.1371/journal.pone.0186838. eCollection 2017. PubMed PMID: 29107999.
7) 
Yadav YR, Parihar V, Namdev H, Bajaj J. Chronic subdural hematoma. Asian J Neurosurg. 2016 Oct-Dec;11(4):330-342. Review. PubMed PMID: 27695533; PubMed Central PMCID: PMC4974954.
8) 
Mirsadeghi SM, Habibi Z, Meybodi KT, Nejat F, Tabatabai SA. Malignant subdural effusion associated with disseminated adenocarcinoma: a case report. Cases J. 2008 Nov 18;1(1):328. doi: 10.1186/1757-1626-1-328. PubMed PMID: 19019205; PubMed Central PMCID: PMC2611978.
9) 
Ng HY, Ng WH, King NK. Value of routine early post-operative computed tomography in determining short-term functional outcome after drainage of chronic subdural hematoma: An evaluation of residual volume. Surg Neurol Int. 2014 Sep 19;5:136. doi: 10.4103/2152-7806.141299. eCollection 2014. PubMed PMID: 25298918.
10) 
Brokinkel B, Ewelt C, Holling M, Hesselmann V, Heindel WL, Stummer W, Fischer BR. Routine postoperative CT-scans after burr hole trepanation for chronic subdural hematoma – better before or after drainage removal? Turk Neurosurg. 2013;23(4):458-63. doi: 10.5137/1019-5149.JTN.7269-12.0. PubMed PMID: 24101264.
11) 
Chari A, Hocking KC, Edlmann E, Turner C, Santarius T, Hutchinson PJ, Kolias AG. Core Outcomes and Common Data Elements in Chronic Subdural Hematoma: A Systematic Review of the Literature Focusing on Baseline and Peri-Operative Care Data Elements. J Neurotrauma. 2016 Sep 1;33(17):1569-75. doi: 10.1089/neu.2015.4248. Epub 2016 Jan 28. PubMed PMID: 26541092.
12) 
D’Abbondanza JA, Loch Macdonald R. Experimental models of chronic subdural hematoma. Neurol Res. 2014 Feb;36(2):176-88. doi: 10.1179/1743132813Y.0000000279. Epub 2013 Dec 6. Review. PubMed PMID: 24172841.

Interhemispheric subdural hematoma

Interhemispheric subdural hematoma

Interhemispheric acute subdural hematomas (ASDHs) were first described by Aring and Evans 1).

Interhemispheric Subdural Hematoma Epidemiology.

Spontaneous Interhemispheric Subdural Hematoma.

Traumatic Interhemispheric Subdural Hematoma.

Acute Interhemispheric Subdural Hematoma.

Chronic Interhemispheric Subdural Hematoma

Its natural history is still quite unknown in terms of potential origin and course.

They usually occur in patients with bleeding disorders and are associated with trauma in 83% of cases 2).

Other causes include history of birth trauma, forceps delivery, child abuse with shaking, hemodialysis, anticoagulation and aneurysmal bleeding 3).

Fruin et al. 4) suggested that an occipital blow in the sagittal plane lead to an interhemispheric ASDH because of the anatomic orientation of the veins in the interhemispheric fissure, which tend to course antero-medially from the cortex to the midline sinuses. Before the CT era, it was difficult to detect an interhemispheric ASDH. Though removal of the blood has proved to be an option in the management of these patients, there is danger due to the close proximity of the superior sagittal sinus and bridging veins. Some of these hematomas migrate superiorly (to a more favorable position) with time, as they liquefy. It is also conceivable that if a patient with an interhemispheric ASDH is relatively asymptomatic, initial conservative management might be followed by migration of the clot to a position over the convexity where removal is considerably less dangerous. Thus there is no consensus on the ideal management of these rare hematomas, conservative treatment may be followed in those who are neurologically stable or have concurrent risk factors, while surgical treatment should be reserved for those who have pronounced symptoms or neurological deficits 5).

The hyperdense hematoma can best be visualized on the coronal and sagittal views. This is in contrast with typical subdural hematomas, which can be best appreciated on the axial views. Thus, it is important to image all three main views of the brain looking out for interhemispheric hematoma 6).

Interhemispheric Subdural Hematoma Treatment.

Interhemispheric Subdural Hematoma Case Series.

Interhemispheric Subdural Hematoma Case Reports.


1)

Aring CD, Evans JP. Aberrant location of subdural hematoma. Arch Neurol Psychiatry. 1940;44:1296–306.
2)

Houtteville JP, Toumi K, Theron J, Derlon JM, Benazza A, Hubert P. Interhemispheric subdural haematomas: seven cases and review of the literature. Br J Neurosurg. 1988;2:357–67. doi: 10.3109/02688698809001007.
3)

Ishikawa E, Sugimoto K, Yanaka K, Ayuzawa S, Iguchi M, Moritake T, Kobayashi E, Nose T. Interhemispheric subdural hematoma caused by a ruptured internal carotid artery aneurysm: case report. Surg Neurol. 2000;54:82–6. doi: 10.1016/S0090-3019(00)00262-7.
4)

Fruin AH, Juhl GL, Taylon C. Interhemispheric subdural hematoma. Case report. J Neurosurg. 1984;60:1300–2. doi: 10.3171/jns.1984.60.6.1300.
5)

Kawoosa NN, Bhat AR, Rashid B. Interhemispheric acute subdural hematomas. Iran Red Crescent Med J. 2011 Apr;13(4):289-90. Epub 2011 Apr 1. PubMed PMID: 22737484; PubMed Central PMCID: PMC3371964.

Chronic subdural hematoma recurrence

Chronic subdural hematoma recurrence

In 2 large cohorts of US patients, approximately 5% to 10% of patients who underwent surgery for nontraumatic SDH were required to undergo repeated operation within 30 to 90 days. These results may inform the design of future prospective studies and trials and help practitioners calibrate their index of suspicion to ensure that patients are referred for timely surgical care 1).

Recurrence rates after chronic subdural hematoma (CSDH) evacuation with any of actual techniques twist drill craniostomy (TDC), burr hole craniostomy, craniotomy range from 5% to 30%. 2).

Oslo grading system.

Hyperdense hematoma components were the strongest prognostic factor of recurrence after surgery. Awareness of these findings allows for individual risk assessment and might prompt clinicians to tailor treatment measures 3).


In the series of Santos et al. it was possible to demonstrate an age-related protective factor, analyzed as a continuous variable, regarding the recurrence of the chronic subdural hematoma (CSDH), with a lower rate of recurrence the higher the age.

The results indicate that, among possible factors associated with recurrence, only age presented a protective factor with statistical significance. The fact that no significant difference between the patients submitted to trepanning or craniotomy was found favors the preferential use of burr-hole surgery as a procedure of choice due to its fast and less complex execution 4).


In the series of Han et al. independent risk factors for recurrence were as follows: age > 75 years (HR 1.72, 95% CI 1.03-2.88; p = 0.039), obesity (body mass index ≥ 25.0 kg/m2), and a bilateral operation 5).


Chon et al. shown that postoperative midline shifting (≥5 mm), diabetes mellitus, preoperative seizure, preoperative width of hematoma (≥20 mm), and anticoagulant therapy were independent predictors of the recurrence of chronic subdural hematoma.

According to internal architecture of hematoma, the rate of recurrence was significantly lower in the homogeneous and the trabecular type than the laminar and separated type 6).


The recurrence rate of chronic subdural hematoma cSDH seems to be related to the excessive neoangiogenesis in the parietal membrane, which is mediated via vascular endothelial growth factor (VEGF). This is found to be elevated in the hematoma fluid and is dependent on eicosanoid/prostaglandin and thromboxane synthesis via cyclooxygenase-2 (COX-2).

see Chronic subdural hematoma and anticoagulant therapy.

Antiplatelet therapy significantly influences the recurrence of CSDH 7).

Timing of Low-Dose Aspirin Discontinuation for chronic subdural hematoma.

Pneumocephalus

Remaining pneumocephalus is seen as an approved factor of recurrence 8) 9).

Septation

Jack et al.found a 12% reoperation rate. CSDH septation (seen on computed tomogram scan) was found to be an independent risk factor for recurrence requiring reoperation (p=0.04). Larger post-operative subdural haematoma volume was also significantly associated with requiring a second drainage procedure (p<0.001). Independent risk factors of larger post-operative haematoma volume included septations within a CSDH (p<0.01), increased pre-operative haematoma volume (p<0.01), and a greater amount of parenchymal atrophy (p=0.04). A simple scoring system for quantifying recurrence risk was created and validated based on patient age (< or ≥80 years), haematoma volume (< or ≥160cc), and presence of septations within the subdural collection (yes or no).

Septations within CSDHs are associated with larger post-operative residual haematoma collections requiring repeat drainage. When septations are clearly visible within a CSDH, craniotomy might be more suitable as a primary procedure as it allows greater access to a septated subdural collection. The proposed scoring system combining haematoma volume, age, and presence of septations might be useful in identifying patients at higher risk for recurrence 10).

Membranectomy

Opening the internal hematoma membrane does not alter the rate of patients requiring revision surgery and the number of patients showing a marked residual hematoma six weeks after evacuation of a CSDH 11).

In the study of Lee et al, an extended surgical approach with partial membranectomy has no advantages regarding the rate of reoperation and the outcome. As initial treatment, burr-hole drainage with irrigation of the hematoma cavity and closed-system drainage is recommended. Extended craniotomy with membranectomy is now reserved for instances of acute rebleeding with solid hematoma 12).

Diabetes

Surgeons should consider informing patients with diabetes mellitus that this comorbidity is associated with an increased likelihood of recurrence

13) 14) 15).


Balser et al. report 11% recurrence, which included individuals who recurred as late as 3 years after initial diagnosis 16).

Close imaging follow-up is important for CSDH patients for recurrence prediction. Using quantitative CT volumetric analysis, strong evidence was provided that changes in the residual fluid volume during the ‘self-resolution’ period can be used as significantly radiological predictors of recurrence 17).

A structural equation model showed a significant association between increased antiinflammatory activity in hematoma fluid samples and a lower risk of recurrence, but this relationship was not statistically significant in venous blood samples. Moreover, these findings indicate that anti-inflammatory activities in the hematoma may play a role in the risk of a recurrence of CSDH 18).

Irrigation with artificial cerebrospinal fluid (ACF) decreased the rate of CSDH recurrence 19).

Little is known about the best type of drainage system and its relationship with recurrence. In a study, Takroni et al. compared the use of two drainage systems on the recurrence rate of CSDH. They retrospectively analyzed the charts of 180 CSDH patients treated with bedside twist drill craniostomy (TDC) and subdural drain insertion. Patients were divided into two groups: Group A (n=123) received our traditional drain (pediatric size nasogastric tube (NGT), while group B (n=49) had the external ventricular drain (EVD). Various demographic and radiological data were collected. Our main outcome was recurrence, defined as symptomatic re-accumulation of hematoma on the previously operated side within 3 months. Results 212 cases of subdural hematoma were treated in 172 patients. Majority of patients were male (78%) and had a history of previous head trauma (73%). 17 cases had recurrence, 11 in the NGT group drain and 6 in the EVD group. The use of antiplatelet or anticoagulation agents was associated with recurrence (P= 0.038 and 0.05, respectively). There was no difference between both groups in terms of recurrence [OR=1.42, 95% CI:0.49 to 4.08, P=0.573].

Chronic subdural hematoma is a common disease with a high rate of recurrence. Although using a drain postoperatively has shown to improve the incidence of recurrence, little remains known about the best type of drain to use. The analysis showed no difference in the recurrent rate between using the pediatric size NGT and the EVD catheter post TDC 20).

There is no definite operative procedure for patients with intractable chronic subdural hematoma (CSDH).

Most recurrent hematomas are managed successfully with burr hole craniostomies with postoperative closed-system drainage. Refractory hematomas may be managed with a variety of techniques, including craniotomy or subdural-peritoneal shunt placement 21).

Although many studies have reported risk factors or treatments in efforts to prevent recurrence, those have focused on single recurrence, and little cumulative data is available to analyze refractory CSDH.

Matsumoto et al. defined refractory CSDH as ≥2 recurrences, then analyzed and compared clinical factors between patients with single recurrence and those with refractory CSDH in a cohort study, to clarify whether patients with refractory CSDH experience different or more risk factors than patients with single recurrence, and whether burr-hole irrigation with closed-system drainage reduces refractory CSDH.

Seventy-five patients had at least one recurrence, with single recurrence in 62 patients and ≥2 recurrences in 13 patients. In comparing clinical characteristics, patients with refractory CSDH were significantly younger (P=0.04) and showed shorter interval to first recurrence (P<0.001). Organized CSDH was also significantly associated with refractory CSDH (P=0.02). Multivariate logistic regression analysis identified first recurrence interval <1 month (OR 6.66, P<0.001) and age <71 years (OR 4.16, P<0.001) as independent risk factors for refractory CSDH. On the other hand, burr-hole irrigation with closed-system drainage did not reduce refractory CSDH.

When patients with risk factors for refractory CSDH experience recurrence, alternative surgical procedures may be considered as the second surgery, because burr-hole irrigation with closed-system drainage did not reduce refractory CSDH 22).

Implantation of a reservoir 23) 24) 25).

Subdural-peritoneal shunt 26).

Embolization of the MMA is effective for refractory CSDH or CSDH patients with a risk of recurrence, and is considered an effective therapeutic method to stop hematoma enlargement and promote resolution 27) 28) 29) 30) 31) 32).

A pilot study indicated that perioperative middle meningeal artery (MMA) embolization could be offered as the least invasive and most effectual means of treatment for resistant patients of CSDHs with 1 or more recurrences 33).

Chihara et al. have treated three cases of CSDH with MMA embolization to date, but there was a postoperative recurrence in one patient, which required a craniotomy for hematoma removal and capsulectomy. MMA embolization blocks the blood supply from the dura to the hematoma outer membrane in order to prevent recurrences of refractory CSDH. Histopathologic examination of the outer membrane of the hematoma excised during craniotomy showed foreign-body giant cells and neovascular proliferation associated with embolization. Because part of the hematoma was organized in this case, the CSDH did not resolve when the MMA was occluded, and the development of new collateral pathways in the hematoma outer membrane probably contributed to the recurrence. Therefore, in CSDH with some organized hematoma, MMA embolization may not be effective. Magnetic resonance imaging (MRI) should be performed in these patients before embolization 34).

see Chronic subdural hematoma recurrence case series.

Chronic subdural hematoma recurrence case reports.


1)

Knopman J, Link TW, Navi BB, Murthy SB, Merkler AE, Kamel H. Rates of Repeated Operation for Isolated Subdural Hematoma Among Older Adults. JAMA Netw Open. 2018 Oct 5;1(6):e183737. doi: 10.1001/jamanetworkopen.2018.3737. PubMed PMID: 30646255.
2)

Escosa Baé M, Wessling H, Salca HC, de Las Heras Echeverría P. Use of twist-drill craniostomy with drain in evacuation of chronic subdural hematomas: independent predictors of recurrence. Acta Neurochir (Wien). 2011 May;153(5):1097-103. doi: 10.1007/s00701-010-0903-3. Epub 2010 Dec 31. PubMed PMID: 21193935.
3)

Miah IP, Tank Y, Rosendaal FR, Peul WC, Dammers R, Lingsma HF, den Hertog HM, Jellema K, van der Gaag NA; Dutch Chronic Subdural Hematoma Research Group. Radiological prognostic factors of chronic subdural hematoma recurrence: a systematic review and meta-analysis. Neuroradiology. 2020 Oct 22. doi: 10.1007/s00234-020-02558-x. Epub ahead of print. Erratum in: Neuroradiology. 2020 Nov 5;: PMID: 33094383.
4)

Santos RGD, Xander PAW, Rodrigues LHDS, Costa GHFD, Veiga JCE, Aguiar GB. Analysis of predisposing factors for chronic subdural hematoma recurrence. Rev Assoc Med Bras (1992). 2019 Jul 22;65(6):834-838. doi: 10.1590/1806-9282.65.6.834. PubMed PMID: 31340313.
5)

Han MH, Ryu JI, Kim CH, Kim JM, Cheong JH, Yi HJ. Predictive factors for recurrence and clinical outcomes in patients with chronic subdural hematoma. J Neurosurg. 2017 Nov;127(5):1117-1125. doi: 10.3171/2016.8.JNS16867. Epub 2016 Dec 16. PubMed PMID: 27982768.
6)

Chon KH, Lee JM, Koh EJ, Choi HY. Independent predictors for recurrence of chronic subdural hematoma. Acta Neurochir (Wien). 2012 Sep;154(9):1541-8. doi: 10.1007/s00701-012-1399-9. Epub 2012 Jun 1. PubMed PMID: 22653496.
7)

Wada M, Yamakami I, Higuchi Y, Tanaka M, Suda S, Ono J, Saeki N. Influence of antiplatelet therapy on postoperative recurrence of chronic subdural hematoma: a multicenter retrospective study in 719 patients. Clin Neurol Neurosurg. 2014 May;120:49-54. doi: 10.1016/j.clineuro.2014.02.007. Epub 2014 Feb 24. PubMed PMID: 24731576.
8)

Mori K, Maeda M (2001) Surgical treatment of chronic subdural hematoma in 500 consecutive cases: clinical characteristics, surgical outcome, complications, and recurrence rate. Neurol Med Chir (Tokyo) 41:371–381
9)

Stanišić M, Hald J, Rasmussen IA, Pripp AH, Ivanović J, Kolstad F, Sundseth J, Züchner M, Lindegaard KF (2013) Volume and densities of chronic subdural haematoma obtained from CT imaging as predictors of postoperative recurrence: a prospective study of 107 operated patients. Acta Neurochir 155:323–333
10)

Jack A, O’Kelly C, McDougall C, Max Findlay J. Predicting Recurrence after Chronic Subdural Haematoma Drainage. Can J Neurol Sci. 2015 Jan 5:1-6. [Epub ahead of print] PubMed PMID: 25557536.
11)

Unterhofer C, Freyschlag CF, Thomé C, Ortler M. Opening the Internal Hematoma Membrane does not Alter the Recurrence Rate of Chronic Subdural Hematomas – A Prospective Randomized Trial. World Neurosurg. 2016 May 2. pii: S1878-8750(16)30210-8. doi: 10.1016/j.wneu.2016.04.081. [Epub ahead of print] PubMed PMID: 27150644.
12)

Lee JY, Ebel H, Ernestus RI, Klug N. Various surgical treatments of chronic subdural hematoma and outcome in 172 patients: is membranectomy necessary? Surg Neurol. 2004 Jun;61(6):523-7; discussion 527-8. PubMed PMID: 15165784.
13)

Matsumoto K, Akagi K, Abekura M, Ryujin H, Ohkawa M, Iwasa N, Akiyama C. Recurrence factors for chronic subdural hematomas after burr-hole craniostomy and closed system drainage. Neurol Res. 1999 Apr;21(3):277-80. PubMed PMID: 10319336.
14)

Yamamoto H, Hirashima Y, Hamada H, Hayashi N, Origasa H, Endo S. Independent predictors of recurrence of chronic subdural hematoma: results of multivariate analysis performed using a logistic regression model. J Neurosurg. 2003 Jun;98(6):1217-21. PubMed PMID: 12816267.
15)

Pang CH, Lee SE, Kim CH, Kim JE, Kang HS, Park CK, Paek SH, Kim CH, Jahng TA, Kim JW, Kim YH, Kim DG, Chung CK, Jung HW, Yoo H. Acute intracranial bleeding and recurrence after bur hole craniostomy for chronic subdural hematoma. J Neurosurg. 2015 Jul;123(1):65-74. doi: 10.3171/2014.12.JNS141189. Epub 2015 Feb 13. PubMed PMID: 25679282.
16)

Balser D, Rodgers SD, Johnson B, Shi C, Tabak E, Samadani U. Evolving management of symptomatic chronic subdural hematoma: experience of a single institution and review of the literature. Neurol Res. 2013 Apr;35(3):233-42. doi: 10.1179/1743132813Y.0000000166. Review. PubMed PMID: 23485050.
17)

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