Seizure after aneurysmal subarachnoid hemorrhage

Seizure after aneurysmal subarachnoid hemorrhage

Epilepsy is a common and serious complication of subarachnoid hemorrhage (SAH), giving rise to increased morbidity and mortality. It’s difficult to identify patients at high risk of epilepsy and the application of antiepileptic drugs (AEDs) following SAH is a controversial topic. Therefore, it’s pressingly needed to gain a better understanding of the risk factors, underlying mechanisms, and the optimization of therapeutic strategies for epilepsy after SAH. Neuroinflammation, characterized by microglial activation and the release of inflammatory cytokines has drawn growing attention due to its influence on patients with epilepsy after SAH. In a review, Wang et al. discussed the risk factors for epilepsy after SAH and emphasize the critical role of microglia. Then they discussed how various molecules arising from pathophysiological changes after SAH activates specific receptors such as TLR4NLRP3RAGEP2X7R and initiate the downstream inflammatory pathways. Additionally, they focused on the significant responses implicated in epilepsy including neuronal excitotoxicity, the disruption of the blood-brain barrier (BBB), and the change of immune responses. As the application of AEDs for seizure prophylaxis after SAH remains controversial, the regulation of neuroinflammation targeting the key pathological molecules could be a promising therapeutic method. While neuroinflammation appears to contribute to epilepsy after SAH, more comprehensive experiments on their relationships are needed 1).

Literature has reported seizure rates to be as high as 27% in this population 2).

More recently published studies have found seizure rates to be significantly lower than previously described (1–10%) 3) 4).

Seizure activity has been associated with secondary neurologic injury including reduced cerebral blood flow and intracranial hypertension 5).

see Anticonvulsant in aneurysmal subarachnoid hemorrhage.


1)

Wang J, Liang J, Deng J, Liang X, Wang K, Wang H, Qian D, Long H, Yang K, Qi S. Emerging Role of Microglia-Mediated Neuroinflammation in Epilepsy after Subarachnoid Hemorrhage. Mol Neurobiol. 2021 Jan 26. doi: 10.1007/s12035-021-02288-y. Epub ahead of print. PMID: 33501625.
2)

Lin YJ, Chang WN, Chang HW, Ho JT, Lee TC, Wang HC, Tsai NW, Tsai MH, Lu CH. Risk factors and outcome of seizures after spontaneous aneurysmal subarachnoid hemorrhage. Eur J Neurol. 2008 May;15(5):451-7. doi: 10.1111/j.1468-1331.2008.02096.x. Epub 2008 Mar 5. PubMed PMID: 18325027.
3)

Rosengart AJ, Huo JD, Tolentino J, Novakovic RL, Frank JI, Goldenberg FD, Macdonald RL. Outcome in patients with subarachnoid hemorrhage treated with antiepileptic drugs. J Neurosurg. 2007 Aug;107(2):253-60. PubMed PMID: 17695377.
4)

Chumnanvej S, Dunn IF, Kim DH. Three-day phenytoin prophylaxis is adequate after subarachnoid hemorrhage. Neurosurgery. 2007 Jan;60(1):99-102; discussion 102-3. PubMed PMID: 17228257.
5)

Rhoney DH, Tipps LB, Murry KR, Basham MC, Michael DB, Coplin WM. Anticonvulsant prophylaxis and timing of seizures after aneurysmal subarachnoid hemorrhage. Neurology. 2000 Jul 25;55(2):258-65. PubMed PMID: 10908901.

Osteopontin in subarachnoid hemorrhage

Osteopontin in subarachnoid hemorrhage

Experimental studies reported that osteopontin (OPN), is induced in the brain after subarachnoid hemorrhage (SAH).

OPN may increase MAPK phosphatase-1 that inactivates MAPKs, upstream and downstream of vascular endothelial growth factor A, by binding to L-arginyl-glycyl-L-aspartate-dependent integrin receptors, suggesting a novel mechanism of OPN-induced post-SAH BBB protection 1).


The relationships between osteopontin (OPN) expression and chronic shunt-dependent hydrocephalus (SDHC) have never been investigated. In 166 SAH patients (derivation and validation cohorts, 110 and 56, respectively), plasma OPN levels were serially measured at days 1-3, 4-6, 7-9, and 10-12 after aneurysmal obliteration. The OPN levels and clinical factors were compared between patients with and without subsequent development of chronic SDHC. Plasma OPN levels in the SDHC patients increased from days 1-3 to days 4-6 and remained high thereafter, while those in the non-SDHC patients peaked at days 4-6 and then decreased over time. Plasma OPN levels had no correlation with serum levels of C-reactive protein (CRP), a systemic inflammatory marker. Univariate analyses showed that age, modified Fisher scaleacute hydrocephaluscerebrospinal fluid drainage, and OPN and CRP levels at days 10-12 were significantly different between patients with and without SDHC. Multivariate analyses revealed that higher plasma OPN levels at days 10-12 were an independent factor associated with the development of SDHC, in addition to the more frequent use of cerebrospinal fluid drainage and higher modified Fisher grade at admission. Plasma OPN levels at days 10-12 maintained similar discrimination power in the validation cohort and had good calibration on the Hosmer-Lemeshow goodness-of-fit test. Prolonged higher expression of OPN may contribute to the development of post-SAH SDHC, possibly by excessive repairing effects promoting fibrosis in the subarachnoid space 2).


Abate et al. included 44 patients with the following criteria: (1) age 18 and 80 years, (2) diagnosis of SAH from cerebral aneurysm rupture, (3) insertion of an external ventricular drain. Plasma and CSF were sampled at day 1, 4, and 8. OPN levels, in CSF and plasma, displayed a weak correlation on day 1 and were higher, in CSF, in all time points. Only in poor prognosis patients, OPN levels in CSF significantly increased at day 4 and day 8. Plasma OPN at day 1 and 4 was predictor of poor outcome. In conclusion, plasma and CSF OPN displays a weak correlation, on day 1. The higher levels of OPN found in the CSF compared to plasma, suggest OPN production within the CNS after SAH. Furthermore, plasma OPN, at day 1 and 4, seems to be an independent predictor of poor outcome 3).


The aim of the study was to investigate the relationships between plasma OPN levels and outcome after aneurysmal SAH in a clinical setting. This is a prospective study consisting of 109 aneurysmal SAH patients who underwent aneurysmal obliteration within 48 h of SAH. Plasma OPN concentrations were serially determined at days 1-3, 4-6, 7-9, and 10-12 after onset. Various clinical factors as well as OPN values were compared between patients with 90-day good and poor outcomes. Plasma OPN levels were significantly higher in SAH patients compared with control patients and peaked at days 4-6. Poor-outcome patients had significantly higher plasma OPN levels through all sampling points. Receiver-operating characteristic curves demonstrated that OPN levels at days 10-12 were the most useful predictor of poor outcome at cutoff values of 915.9 pmol/L (sensitivity, 0.694; specificity, 0.845). Multivariate analyses using the significant variables identified by day 3 showed that plasma OPN ≥ 955.1 pmol/L at days 1-3 (odds ratio, 10.336; 95% confidence interval, 2.563-56.077; p < 0.001) was an independent predictor of poor outcome, in addition to increasing age, preoperative World Federation of Neurological Surgeons grades IV-V, and modified Fisher grade 4. Post hoc analyses revealed no correlation between OPN levels and serum levels of C-reactive protein, a non-specific inflammatory parameter, at days 1-3. Acute-phase plasma OPN could be used as a useful prognostic biomarker in SAH 4).


1)

Suzuki H, Hasegawa Y, Kanamaru K, Zhang JH. Mechanisms of osteopontin-induced stabilization of blood-brain barrier disruption after subarachnoid hemorrhage in rats. Stroke. 2010 Aug;41(8):1783-90. doi: 10.1161/STROKEAHA.110.586537. Epub 2010 Jul 8. PMID: 20616319; PMCID: PMC2923856.
2)

Asada R, Nakatsuka Y, Kanamaru H, Kawakita F, Fujimoto M, Miura Y, Shiba M, Yasuda R, Toma N, Suzuki H; pSEED group. Higher Plasma Osteopontin Concentrations Associated with Subsequent Development of Chronic Shunt-Dependent Hydrocephalus After Aneurysmal Subarachnoid Hemorrhage. Transl Stroke Res. 2021 Jan 9. doi: 10.1007/s12975-020-00886-x. Epub ahead of print. PMID: 33423213.
3)

Abate MG, Moretto L, Licari I, Esposito T, Capuano L, Olivieri C, Benech A, Brucoli M, Avanzi GC, Cammarota G, Dianzani U, Clemente N, Panzarasa G, Citerio G, Carfagna F, Cappellano G, Della Corte F, Vaschetto R. Osteopontin in the Cerebrospinal Fluid of Patients with Severe Aneurysmal Subarachnoid Hemorrhage. Cells. 2019 Jul 10;8(7):695. doi: 10.3390/cells8070695. PMID: 31295895; PMCID: PMC6678172.
4)

Nakatsuka Y, Shiba M, Nishikawa H, Terashima M, Kawakita F, Fujimoto M, Suzuki H; pSEED group. Acute-Phase Plasma Osteopontin as an Independent Predictor for Poor Outcome After Aneurysmal Subarachnoid Hemorrhage. Mol Neurobiol. 2018 Jan 20. doi: 10.1007/s12035-018-0893-3. [Epub ahead of print] PubMed PMID: 29353454.

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).

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 20).

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 21).

Implantation of a reservoir 22) 23) 24).

Subdural-peritoneal shunt 25).

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 26) 27) 28) 29) 30) 31).

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 32).

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 33).

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)

Adachi A, Higuchi Y, Fujikawa A, Machida T, Sueyoshi S, Harigaya K, Ono J, Saeki N. Risk factors in chronic subdural hematoma: comparison of irrigation with artificial cerebrospinal fluid and normal saline in a cohort analysis. PLoS One. 2014 Aug 4;9(8):e103703. doi: 10.1371/journal.pone.0103703. eCollection 2014. PubMed PMID: 25089621; PubMed Central PMCID: PMC4121178.
20)

Desai VR, Scranton RA, Britz GW. Management of Recurrent Subdural Hematomas. Neurosurg Clin N Am. 2017 Apr;28(2):279-286. doi: 10.1016/j.nec.2016.11.010. Epub 2017 Jan 4. Review. PubMed PMID: 28325462.
21)

Matsumoto H, Hanayama H, Okada T, Sakurai Y, Minami H, Masuda A, Tominaga S, Miyaji K, Yamaura I, Yoshida Y, Yoshida K. Clinical investigation of refractory chronic subdural hematoma: a comparison of clinical factors between single and repeated recurrences. World Neurosurg. 2017 Aug 24. pii: S1878-8750(17)31402-X. doi: 10.1016/j.wneu.2017.08.101. [Epub ahead of print] PubMed PMID: 28844917.
22)

Sato M, Iwatsuki K, Akiyama C, Masana Y, Yoshimine T, Hayakawa T. [Use of Ommaya CSF reservoir for refractory chronic subdural hematoma]. No Shinkei Geka. 1999 Apr;27(4):323-8. Japanese. PubMed PMID: 10347846.
23)

Sato M, Iwatsuki K, Akiyama C, Kumura E, Yoshimine T. Implantation of a reservoir for refractory chronic subdural hematoma. Neurosurgery. 2001 Jun;48(6):1297-301. PubMed PMID: 11383733.
24)

Laumer R. Implantation of a reservoir for refractory chronic subdural hematoma. Neurosurgery. 2002 Mar;50(3):672. PubMed PMID: 11841742.
25)

Misra M, Salazar JL, Bloom DM. Subdural-peritoneal shunt: treatment for bilateral chronic subdural hematoma. Surg Neurol. 1996 Oct;46(4):378-83. PubMed PMID: 8876720.
26)

Mandai S, Sakurai M, Matsumoto Y. Middle meningeal artery embolization for refractory chronic subdural hematoma. Case report. J Neurosurg. 2000 Oct;93(4):686-8. PubMed PMID: 11014549.
27)

Takahashi K, Muraoka K, Sugiura T, Maeda Y, Mandai S, Gohda Y, Kawauchi M, Matsumoto Y. [Middle meningeal artery embolization for refractory chronic subdural hematoma: 3 case reports]. No Shinkei Geka. 2002 May;30(5):535-9. Japanese. PubMed PMID: 11993178.
28)

Hirai S, Ono J, Odaki M, Serizawa T, Nagano O. Embolization of the Middle Meningeal Artery for Refractory Chronic Subdural Haematoma. Usefulness for Patients under Anticoagulant Therapy. Interv Neuroradiol. 2004 Dec 24;10 Suppl 2:101-4. Epub 2008 May 15. PubMed PMID: 20587257; PubMed Central PMCID: PMC3522210.
29)

Tsukamoto Y, Oishi M, Shinbo J, Fujii Y. Transarterial embolisation for refractory bilateral chronic subdural hematomas in a case with dentatorubral-pallidoluysian atrophy. Acta Neurochir (Wien). 2011 May;153(5):1145-7. doi: 10.1007/s00701-010-0891-3. Epub 2010 Dec 2. PubMed PMID: 21125409.
30)

Mino M, Nishimura S, Hori E, Kohama M, Yonezawa S, Midorikawa H, Kaimori M, Tanaka T, Nishijima M. Efficacy of middle meningeal artery embolization in the treatment of refractory chronic subdural hematoma. Surg Neurol Int. 2010 Dec 13;1:78. doi: 10.4103/2152-7806.73801. PubMed PMID: 21206540; PubMed Central PMCID: PMC3011107.
31)

Hashimoto T, Ohashi T, Watanabe D, Koyama S, Namatame H, Izawa H, Haraoka R, Okada H, Ichimasu N, Akimoto J, Haraoka J. Usefulness of embolization of the middle meningeal artery for refractory chronic subdural hematomas. Surg Neurol Int. 2013 Aug 19;4:104. doi: 10.4103/2152-7806.116679. eCollection 2013. PubMed PMID: 24032079; PubMed Central PMCID: PMC3766342.
32)

Kim E. Embolization Therapy for Refractory Hemorrhage in Patients with Chronic Subdural Hematomas. World Neurosurg. 2017 May;101:520-527. doi: 10.1016/j.wneu.2017.02.070. Epub 2017 Feb 27. PubMed PMID: 28249828.
33)

Chihara H, Imamura H, Ogura T, Adachi H, Imai Y, Sakai N. Recurrence of a Refractory Chronic Subdural Hematoma after Middle Meningeal Artery Embolization That Required Craniotomy. NMC Case Rep J. 2014 May 9;1(1):1-5. doi: 10.2176/nmccrj.2013-0343. eCollection 2014 Oct. PubMed PMID: 28663942; PubMed Central PMCID: PMC5364934.
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