Posttraumatic Epilepsy Epidemiology

Posttraumatic Epilepsy Epidemiology

In general, the incidence of Posttraumatic Epilepsy varies with the time period after injury and population age range under study, as well as the spectrum of severity of the inciting injuries, and has been reported to be anywhere from 4 to 53% 1).

Generally posttraumatic epilepsy accounts for less than 10% of epilepsy 2).


In a cohort study, the incidence of self-reported PTE after TBI was found to be 2.8% and was independently associated with unfavorable outcomes 3).


In a large cohort of post-concussion patients Wennberg et al. found no increased incidence of epilepsy. For at least the first 5-10 years post-injury, concussion/mTBI should not be considered a significant risk factor for epilepsy. In patients with epilepsy and a past history of concussion, the epilepsy should not be presumed to be post-traumatic 4).


The Vietnam Head Injury Study (VHIS) is a prospective, longitudinal follow-up of 1,221 Vietnam War veterans with mostly penetrating head injuries (PHIs). The high prevalence (45%-53%) of posttraumatic epilepsy (PTE) in this unique cohort makes it valuable for study.

A standardized multidisciplinary neurologic, cognitive, behavioral, and brain imaging evaluation was conducted on 199 VHIS veterans plus uninjured controls, some 30 to 35 years after injury, as part of phase 3 of this study.

The prevalence of seizures (87 patients, 43.7%) was similar to that found during phase 2 evaluations 20 years earlier, but 11 of 87 (12.6%) reported very late onset of PTE after phase 2 (more than 14 years after injury). Those patients were not different from patients with earlier-onset PTE in any of the measures studied. Within the phase 3 cohort, the most common seizure type last experienced was complex partial seizures (31.0%), with increasing frequency after injury. Of subjects with PTE, 88% were receiving anticonvulsants. Left parietal lobe lesions and retained ferric metal fragments were associated with PTE in a logistic regression model. Total brain volume loss predicted seizure frequency.

Patients with PHI carry a high risk of PTE decades after their injury, and so require long-term medical follow-up. Lesion location, lesion size, and lesion type were predictors of PTE 5).


A study was undertaken to determine the risk of developing posttraumatic epilepsy (PTE) within 3 years after discharge among a population-based sample of older adolescents and adults hospitalized with traumatic brain injury (TBI) in South Carolina. It also identifies characteristics related to development of PTE within this population.

A stratified random sample of persons aged 15 and older with TBI was selected from the South Carolina nonfederal hospital discharge dataset for four consecutive years. Medical records of recruits were reviewed, and they participated in up to three yearly follow-up telephone interviews.

The cumulative incidence of PTE in the first 3 years after discharge, after adjusting for loss to follow-up, was 4.4 per 100 persons over 3 years for hospitalized mild TBI, 7.6 for moderate, and 13.6 for severe. Those with severe TBI, posttraumatic seizures prior to discharge, and a history of depression were most at risk for PTE. This higher risk group also included persons with three or more chronic medical conditions at discharge.

These results raise the possibility that although some of the characteristics related to development of PTE are nonmodifiable, other factors, such as depression, might be altered with intervention 6).


Using Taiwan’s National Health Insurance Research Database of reimbursement claims, Yeh et al. conducted a retrospective cohort study of 19 336 TBI patients and 540 322 non-TBI participants aged ≥15 years as reference group. Data on newly developed epilepsy after TBI with 5-8 years’ follow-up during 2000 to 2008 were collected. HRs and 95% CIs for the risk of epilepsy associated with TBI were analysed with multivariate Cox proportional hazards regressions.

Results: Compared with the non-TBI cohort, the adjusted HRs of developing epilepsy among TBI patients with skull fracture, severe or mild brain injury were 10.6 (95% CI 7.14 to 15.8), 5.05 (95% CI 4.40 to 5.79) and 3.02 (95% CI 2.42 to 3.77), respectively. During follow-up, men exhibited higher risks of post-TBI epilepsy. Patients who had mixed types of cerebral haemorrhage were at the highest risk of epilepsy compared with the non-TBI cohort (HR 7.83, 95% CI 4.69 to 13.0). The risk of post-TBI epilepsy was highest within the first year after TBI (HR 38.2, 95% CI 21.7 to 67.0).

Conclusions: The risk of epilepsy after TBI varied by patient gender, age, latent interval and complexity of TBI. Integrated care for early identification and treatment of post-trauma epilepsy were crucial for TBI patients 7)


Christensen et al. aimed to assess the risk of epilepsy up to 10 years or longer after traumatic brain injury, taking into account sex, age, severity, and family history.

Methods: We identified 1 605 216 people born in Denmark (1977-2002) from the Civil Registration System. We obtained information on traumatic brain injury and epilepsy from the National Hospital Register and estimated relative risks (RR) with Poisson analyses.

Findings: Risk of epilepsy was increased after a mild brain injury (RR 2.22, 95% CI 2.07-2.38), severe brain injury (7.40, 6.16-8.89), and skull fracture (2.17, 1.73-2.71). The risk was increased more than 10 years after mild brain injury (1.51, 1.24-1.85), severe brain injury (4.29, 2.04-9.00), and skull fracture (2.06, 1.37-3.11). RR increased with age at mild and severe injury and was especially high among people older than 15 years of age with mild (3.51, 2.90-4.26) and severe (12.24, 8.52-17.57) injury. The risk was slightly higher in women (2.49, 2.25-2.76) than in men (2.01, 1.83-2.22). Patients with a family history of epilepsy had a notably high risk of epilepsy after mild (5.75, 4.56-7.27) and severe brain injury (10.09, 4.20-24.26) 8).


A total of 647 individuals (>/=16 y) with any of the following abnormal computed tomography (CT) scan findings: extent of midline shift and/or cisternal compression or presence of any focal pathology (eg, punctate, subarachnoid, or intraventricular hemorrhage; cortical or subcortical contusion; extra-axial lesions) during the first 7 days postinjury or best Glasgow Coma Scale (GCS) score of </=10 during the first 24 hours post-TBI. Subjects were enrolled from August 1993 through September 1997 and followed for up to 24 months, until death or their first late posttraumatic seizures.

Main outcome measures: Cumulative probability, relative risk, and survival analyses were used to stratify risks for development of late postttraumatic seizures on the basis of demographic factors, etiology of injury, initial GCS, early posttraumatic seizures, time post-TBI, types of intracerebral lesion by CT scan, and number and types of intracranial procedures.

Results: Sixty-six individuals had a late posttraumatic seizures; 337 had no late posttraumatic seizures during full 24-month follow-up; 167 had no late posttraumatic seizures during time followed (<24 mo); and 54 were placed on anticonvulsants without a late posttraumatic seizures, whereas 23 died before their first late posttraumatic seizures. The highest cumulative probability for late posttraumatic seizures included biparietal contusions (66%), dural penetration with bone and metal fragments (62.5%), multiple intracranial operations (36.5%), multiple subcortical contusions (33.4%), subdural hematoma with evacuation (27.8%), midline shift greater than 5mm (25.8%), or multiple or bilateral cortical contusions (25%). Initial GCS score was associated with the following cumulative probabilities for development of late posttraumatic seizures at 24 months: GCS score of 3 to 8, 16.8%; GCS score of 9 to 12, 24.3%; and GCS score of 13 to 15, 8.0%.

Conclusions: Stratification by CT scan findings and neurosurgical procedures performed were the most useful findings in defining individuals at highest risk for late posttraumatic seizures 9).


A cohort of 2747 patients with head injuries was followed for 28,176 person-years to determine the magnitude and duration of the risk of posttraumatic seizures. Injuries were classified as severe (brain contusion, intracerebral or intracranial hematoma, or 24 hours of eight unconsciousness of amnesia), moderate (skull fracture or 30 minutes to 24 hours of unconsciousness or amnesia), and mild (briefer unconsciousness or amnesia). The risk of posttraumatic seizures after severe injury was 7.1% within 1 year and 11.5% in 5 years, after moderate injury the risk was 0.7 and 1.6%, and after mild injury the risk was 0.1 and 0.6%. The incidence of seizures after mild head injuries was not significantly greater than in the general population 10)


The true incidence of PTE in children is still uncertain because most research has been based primarily on adults.

see Posttraumatic epilepsy in children.


1)

Frey LC. Epidemiology of posttraumatic epilepsy: a critical review. Epilepsia. 2003;44(s10):11-7. doi: 10.1046/j.1528-1157.44.s10.4.x. PMID: 14511389.
2)

Christensen J. The Epidemiology of Posttraumatic Epilepsy. Semin Neurol. 2015 Jun;35(3):218-22. doi: 10.1055/s-0035-1552923. Epub 2015 Jun 10. PMID: 26060901.
3)

Burke J, Gugger J, Ding K, Kim JA, Foreman B, Yue JK, Puccio AM, Yuh EL, Sun X, Rabinowitz M, Vassar MJ, Taylor SR, Winkler EA, Deng H, McCrea M, Stein MB, Robertson CS, Levin HS, Dikmen S, Temkin NR, Barber J, Giacino JT, Mukherjee P, Wang KKW, Okonkwo DO, Markowitz AJ, Jain S, Lowenstein D, Manley GT, Diaz-Arrastia R; TRACK-TBI Investigators, Badjatia N, Duhaime AC, Feeser VR, Gaudette E, Gopinath S, Keene CD, Korley FK, Madden C, Merchant R, Schnyer D, Zafonte R. Association of Posttraumatic Epilepsy With 1-Year Outcomes After Traumatic Brain Injury. JAMA Netw Open. 2021 Dec 1;4(12):e2140191. doi: 10.1001/jamanetworkopen.2021.40191. PMID: 34964854.
4)

Wennberg R, Hiploylee C, Tai P, Tator CH. Is Concussion a Risk Factor for Epilepsy? Can J Neurol Sci. 2018 May;45(3):275-282. doi: 10.1017/cjn.2017.300. Epub 2018 Mar 20. PMID: 29557322.
5)

Raymont V, Salazar AM, Lipsky R, Goldman D, Tasick G, Grafman J. Correlates of posttraumatic epilepsy 35 years following combat brain injury. Neurology. 2010 Jul 20;75(3):224-9. doi: 10.1212/WNL.0b013e3181e8e6d0. PMID: 20644150; PMCID: PMC2906177.
6)

Ferguson PL, Smith GM, Wannamaker BB, Thurman DJ, Pickelsimer EE, Selassie AW. A population-based study of risk of epilepsy after hospitalization for traumatic brain injury. Epilepsia. 2010 May;51(5):891-8. doi: 10.1111/j.1528-1167.2009.02384.x. Epub 2009 Oct 20. PMID: 19845734.
7)

Yeh CC, Chen TL, Hu CJ, Chiu WT, Liao CC. Risk of epilepsy after traumatic brain injury: a retrospective population-based cohort study. J Neurol Neurosurg Psychiatry. 2013 Apr;84(4):441-5. doi: 10.1136/jnnp-2012-302547. Epub 2012 Oct 31. PMID: 23117492.
8)

Christensen J, Pedersen MG, Pedersen CB, Sidenius P, Olsen J, Vestergaard M. Long-term risk of epilepsy after traumatic brain injury in children and young adults: a population-based cohort study. Lancet. 2009 Mar 28;373(9669):1105-10. doi: 10.1016/S0140-6736(09)60214-2. Epub 2009 Feb 21. PMID: 19233461.
9)

Englander J, Bushnik T, Duong TT, Cifu DX, Zafonte R, Wright J, Hughes R, Bergman W. Analyzing risk factors for late posttraumatic seizures: a prospective, multicenter investigation. Arch Phys Med Rehabil. 2003 Mar;84(3):365-73. doi: 10.1053/apmr.2003.50022. PMID: 12638104.
10)

Annegers JF, Grabow JD, Groover RV, Laws ER Jr, Elveback LR, Kurland LT. Seizures after head trauma: a population study. Neurology. 1980 Jul;30(7 Pt 1):683-9. doi: 10.1212/wnl.30.7.683. PMID: 7190235.

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)

Xu FF, Chen JH, Leung GK, Hao SY, Xu L, Hou ZG, Mao X, Shi GZ, Li JS, Liu BY. Quantitative computer tomography analysis of post-operative subdural fluid volume predicts recurrence of chronic subdural haematoma. Brain Inj. 2014;28(8):1121-6. doi: 10.3109/02699052.2014.910702. Epub 2014 May 6. PubMed PMID: 24801643.
18)

Pripp AH, Stanišić M. The Correlation between Pro- and Anti-Inflammatory Cytokines in Chronic Subdural Hematoma Patients Assessed with Factor Analysis. PLoS One. 2014 Feb 27;9(2):e90149. doi: 10.1371/journal.pone.0090149. eCollection 2014. PubMed PMID: 24587250.
19)

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