Microvascular decompression for trigeminal neuralgia

Microvascular decompression for trigeminal neuralgia


Microvascular decompression is a first-line neurosurgical approach for classical trigeminal neuralgia with neurovascular conflict, but can show clinical relapse despite proper decompression. Second-line destructive techniques like radiofrequency thermocoagulation have become reluctantly used due to their potential for irreversible side effects. Subcutaneous peripheral nerve field stimulation (sPNFS) is a minimally invasive neuromodulatory technique which has been shown to be effective for chronic localised pain conditions.

The most frequently used surgical management of trigeminal neuralgia is Microvascular decompression (MVD), followed closely by stereotactic radiosurgery (SRS). Percutaneous stereotactic rhizotomy (PSR) , despite being the most cost-effective, is by far the least utilized treatment modality 1).

Microvascular decompression (MVD) via lateral suboccipital approach is the standard surgical intervention for trigeminal neuralgia treatment.

Teflon™ and Ivalon® are two materials used in MVD for TN. It is an effective treatment with long-term symptom relief and recurrence rates of 1-5% each year. Ivalon® has been used less than Teflon™ though is associated with similar success rates and similar complication rates 2)

Although microvascular decompression (MVD) is the most effective long-term operative treatment for TN, its use in older patient populations has been debated due to its invasive nature.

see Microvascular decompression for trigeminal neuralgia and multiple sclerosis

see Awake Microvascular Decompression for Trigeminal Neuralgia.

see also Endoscope assisted microvascular decompression for trigeminal neuralgia.


Compared with the standard microscope-assisted techniques, the 3D exoscopic endoscope-assisted MVD offers an improved visualisation without compromising the field of view within and outside the surgical field 3).

97 patients with primary trigeminal neuralgia (PTN) underwent fully endoscopic microvascular decompression (MVD) via keyhole approach in Capital Medical University Affiliated Beijing Shijitan Hospital from December 2014 to February 2019 was collected. During fully endoscopic MVD in PTN via keyhole approach, performer use natural clearance without grinding except developed rock bone crest or excessive retraction of the brain tissue, visually and panoramically observe and evaluate the CPA area, accurately identify the responsible vessels, to avoid the omission of responsible vessels or insufficient decompression. And the use of preplaced technology, bridging technology and submersible technology, ensure the efficacy of surgery and reduce the surgical side injuries. Barrow Neurological Institute Pain Intensity Score was used to evaluate the efficacy and identify the recurrence. The surgical efficacy was analyzed. The offending vessels were identified under endoscope in 96 cases. Among them, arterial compression was found in 77 cases, venous compression in 6 cases, and both arterial and venous compression in 13 cases. About the pain outcomes, 87 cases had immediate and complete relief of pain, 5 cases had almost relief of pain, 4 cases had partial relief of pain, and still needed medication control, but the dose was lower than that before operation, and 1 case had no obvious relief of pain. About complications, there were 4 cases of temporary facial numbness, 1 case of temporary hearing loss, both of them recovered after symptomatic treatment. There was no cerebral infarction or hemorrhage, intracranial or incision infection. All cases were followed up for 3.0-38.0 months with a median period of(22.4±2.2) months. During the follow-up periods, postoperative recurrence occurred in 3 cases. Fully endoscopic MVD for PTN through keyhole approach, provides panoramic view to avoid omission of offending vessels and reduce complications, seemed to be a safe and effective surgical method 4).

Using preferred reporting items for systematic reviews and meta-analyses (PRISMA) guidelines, PubMedCochrane Library, and Scopus were queried for primary studies examining pain outcomes after MVD for TN published between 1988 and March 2018. Potential biases were assessed for included studies. Pain freedom (ie, Barrow Neurological Institute score of 1) at last follow-up was the primary outcome measure. Variables associated with pain freedom on preliminary analysis underwent formal meta-analysis. Odds ratios (OR) and 95% confidence intervals (CI) were calculated for possible predictors.

Outcome data were analyzed for 3897 patients from 46 studies (7 prospective, 39 retrospective). Overall, 76.0% of patients achieved pain freedom after MVD with a mean follow-up of 1.7 ± 1.3 (standard deviation) yr. Predictors of pain freedom on meta-analysis using random effects models included (1) disease duration ≤5 yr (OR = 2.06, 95% CI = 1.08-3.95); (2) arterial compression over venous or other (OR = 3.35, 95% CI = 1.91-5.88); (3) superior cerebellar artery involvement (OR = 2.02, 95% CI = 1.02-4.03), and (4) type 1 Burchiel classification (OR = 2.49, 95% CI = 1.32-4.67).

Approximately three-quarters of patients with drug-resistant TN achieve pain freedom after MVD. Shorter disease duration, arterial compression, and type 1 Burchiel classification may predict a more favorable outcome. These results may improve patient selection and provider expectations 5).

Microvascular decompression for trigeminal neuralgia technique.

Microvascular decompression for trigeminal neuralgia outcome.

Microvascular decompression for trigeminal neuralgia complications

Microvascular decompression for trigeminal neuralgia case series.


1)

Sivakanthan S, Van Gompel JJ, Alikhani P, van Loveren H, Chen R, Agazzi S. Surgical management of trigeminal neuralgia: use and cost-effectiveness from an analysis of the medicare claims database. Neurosurgery. 2014 Sep;75(3):220-6. doi: 10.1227/NEU.0000000000000430. PubMed PMID: 24871139.
2)

Pressman E, Jha RT, Zavadskiy G, Kumar JI, van Loveren H, van Gompel JJ, Agazzi S. Teflon™ or Ivalon®: a scoping review of implants used in microvascular decompression for trigeminal neuralgia. Neurosurg Rev. 2019 Nov 30. doi: 10.1007/s10143-019-01187-0. [Epub ahead of print] Review. PubMed PMID: 31786660.
3)

Li Ching Ng A, Di Ieva A. How I do it: 3D exoscopic endoscope-assisted microvascular decompression. Acta Neurochir (Wien). 2019 May 29. doi: 10.1007/s00701-019-03954-w. [Epub ahead of print] PubMed PMID: 31144166.
4)

Peng WC, Guan F, Hu ZQ, Huang H, Dai B, Zhu GT, Mao BB, Xiao ZY, Zhang BL, Liang X. [Efficacy analysis of fully endoscopic microvascular decompression in primary trigeminal neuralgia via keyhole approach]. Zhonghua Yi Xue Za Zhi. 2021 Mar 30;101(12):856-860. Chinese. doi: 10.3760/cma.j.cn112137-20200630-02002. PMID: 33789367.
5)

Holste K, Chan AY, Rolston JD, Englot DJ. Pain Outcomes Following Microvascular Decompression for Drug-Resistant Trigeminal Neuralgia: A Systematic Review and Meta-Analysis. Neurosurgery. 2020 Feb 1;86(2):182-190. doi: 10.1093/neuros/nyz075. PubMed PMID: 30892607.

Mesial temporal lobe epilepsy

Mesial temporal lobe epilepsy

Temporal lobe epilepsy (TLE) is a chronic neurological condition characterized by recurrent seizures (epilepsy) which originate in the temporal lobe of the brain with progressive neurological disabilities, including cognitive deficitanxiety and depression.

The seizures involve sensory changes, for example smelling an unusual odour that is not there, and disturbance of memory.

Mesial temporal lobe epilepsy with hippocampal sclerosis (mTLE-HS) is the most common type of focal epilepsy.

see Temporal lobe epilepsy etiology.

In order to understand the pathophysiology of temporal lobe epilepsy (TLE), and thus to develop new pharmacological treatments, in vivo animal models that present features similar to those seen in TLE patients have been developed during the last four decades. Some of these models are based on the systemic administration of chemoconvulsants to induce an initial precipitating injury (status epilepticus) that is followed by the appearance of recurrent seizures originating from limbic structures.

Kainic acid and pilocarpine models, have been widely employed in basic epilepsy research. Their behavioral, electroencephalographic and neuropathologic features and response of these models to antiepileptic drugs and the impact they might have in developing new treatments are explained in the work of Lévesque et al. 1).


The transition to the ictal stage is accompanied by increasing global synchronization and a more ordered spectral content of the signals, indicated by lower spectral entropy. The interictal connectivity imbalance (lower ipsilateral connectivity) is sustained during the seizure, irrespective of any appreciable imbalance in the spectral entropy of the mesial recordings 2).

Recurrent seizures (epilepsy) which originate in the temporal lobe of the brain with progressive neurological disabilities, including cognitive deficitanxiety and depression.

The seizures involve sensory changes, for example smelling an unusual odour that is not there, and disturbance of memory.

Olfactory function was significantly impaired in patients with MTLE compared with healthy controls in all domains, namely threshold, discrimination, and identification. In addition, the olfactory bulb volume was smaller in patients with olfactory dysfunction 3).

Earlier tachycardia for seizures originating from the right versus left hemisphere in a patient with bilateral mesial temporal lobe epilepsy 4).


A strong association of this ailment has been established with psychiatric comorbidities, primarily mood and anxiety disorders. The side of epileptogenic may contribute to depressive and anxiety symptoms; thus, in a study, Radaelli et al. performed a systematic review to evaluate the prevalence of depression in TLE in surgical patients. The literature search was performed using PubMed/MedlineWeb of Science, and PsycNet to gather data from inception until January 2019. The search strategy was related to TLE, depressive disorder, and anxiety. After reading full texts, 14 articles meeting the inclusion criteria were screened. The main method utilized for psychiatric diagnosis was Diagnostic and Statistical Manual of Structured Clinical Interview for DSM Disorders. However, most studies failed to perform the neuropsychological evaluation. For those with lateralization of epilepsy, focus mostly occurred in the left hemisphere. For individual depressive diagnosis, 9 studies were evaluated, and 5 for anxiety. Therefore, from the data analyzed in both situations, no diagnosis was representative in preoperative and postoperative cases. In order to estimate the efficacy of surgery in the psychiatry episodes and its relation to seizure control, the risk of depression and anxiety symptoms in epileptic patients need to be determined before surgical procedures. Rigorous preoperative and postoperative evaluation is essential for psychiatry conditions in patients with refractory epilepsy candidates for surgery 5).

pilot study demonstrates that seizures in mesial temporal and temporal-plus epilepsies (i.e., temporoperisylvian) can be detected reliably in the anterior thalamic nucleus (ATN). Further studies are needed to validate these findings 6).

Fractional anisotropy asymmetry (FAA) values can be potentially used to identify the seizures of origin of TLE and to help understand the relationship between fiber tracts with the side of seizure origin of TLE 7).

The area of predominant perifocal 18F positron emission tomography hypometabolism and reduced [11C]flumazenil (11C-FMZ) -binding on PET scans is currently considered to contain the epileptogenic zone and corresponds anatomically to the area localizing epileptogenicity in patients with temporal lobe epilepsy (TLE).

Mesial temporal lobe epilepsy differential diagnosis.

Drug resistant epilepsy is a major clinical challenge affecting about 30% of temporal lobe epilepsy (TLE) patients.

The reasons for failure of surgical treatment for mesial temporal lobe epilepsy (MTLE) associated with hippocampal sclerosis (HS) remain unclear.

Mesial temporal lobe epilepsy treatment.

Temporal lobe epilepsy (TLE) is considered to be the most common form of epilepsy, and it has been seen that most patients are refractory to antiepileptic drugs.

After surgery for intractable mesiotemporal lobe epilepsy (mTLE) seizures recur in 30-40%. One predictor for seizure recurrence is the distribution of seizure onset and interictal epileptiform discharges (IED).

Preoperative bilateral ictal foci are a negative predictor for seizure outcome. Contrarily, IED exceeding the affected temporal lobe in the ipsilateral hemisphere or even bilateral IED had favorable seizure outcome if seizure onset is strictly limited to the affected temporal lobe. Reoperation for seizure persistence constitutes a promising therapeutic option 8).


The extent of pre-surgical perifocal PET abnormalities, the extent of their resection, and the extent of non-resected abnormalities were not useful predictors of individual freedom from seizures in patients with TLE 9).

see Mesial temporal lobe epilepsy case series.


1)

Lévesque M, Avoli M, Bernard C. Animal Models of temporal Lobe Epilepsy Following Systemic Chemoconvulsant Administration. J Neurosci Methods. 2015 Mar 10. pii: S0165-0270(15)00091-6. doi: 10.1016/j.jneumeth.2015.03.009. [Epub ahead of print] PubMed PMID: 25769270.
2)

Vega-Zelaya L, Pastor J, de Sola RG, Ortega GJ. Disrupted Ipsilateral Network Connectivity in Temporal Lobe Epilepsy. PLoS One. 2015 Oct 21;10(10):e0140859. doi: 10.1371/journal.pone.0140859. eCollection 2015. PubMed PMID: 26489091.
3)

Türk BG, Metin B, Tekeli H, Sayman ÖA, Kızılkılıç O, Uzan M, Özkara Ç. Evaluation of olfactory and gustatory changes in patients with mesial temporal lobe epilepsy. Seizure. 2020 Jan 7;75:110-114. doi: 10.1016/j.seizure.2020.01.001. [Epub ahead of print] PubMed PMID: 31945715.
4)

Yanai K, Shimada S, Kunii N, Takasago M, Takabatake K, Saito N. Earlier tachycardia for seizures originating from the right versus left hemisphere in a patient with bilateral mesial temporal lobe epilepsy [published online ahead of print, 2020 Jun 25]. Clin Neurophysiol. 2020;131(9):2168-2170. doi:10.1016/j.clinph.2020.06.011
5)

Radaelli G, Majolo F, Leal-Conceição E, de Souza Santos F, Escobar V, Zanirati GG, Portuguez MW, Scorza FA, da Costa JC. Left Hemisphere Lateralization of Epileptic Focus Can Be More Frequent in Temporal Lobe Epilepsy Surgical Patients with No Consensus Associated with Depression Lateralization. Dev Neurosci. 2021 Mar 31:1-8. doi: 10.1159/000513537. Epub ahead of print. PMID: 33789300.
6)

Pizarro D, Ilyas A, Toth E, Romeo A, Riley KO, Esteller R, Vlachos I, Pati S. Automated detection of mesial temporal and temporoperisylvian seizures in the anterior thalamic nucleus. Epilepsy Res. 2018 Jul 23;146:17-20. doi: 10.1016/j.eplepsyres.2018.07.014. [Epub ahead of print] PubMed PMID: 30055392.
7)

Li H, Xue Z, Dulay MF Jr, Verma A, Karmonik C, Grossman RG, Wong ST. Fractional anisotropy asymmetry and the side of seizure origin for partial onset-temporal lobe epilepsy. Comput Med Imaging Graph. 2014 Jul 2. pii: S0895-6111(14)00102-5. doi: 10.1016/j.compmedimag.2014.06.009. [Epub ahead of print] PubMed PMID: 25037096.
8)

Schmeiser B, Zentner J, Steinhoff BJ, Brandt A, Schulze-Bonhage A, Kogias E, Hammen T. The role of presurgical EEG parameters and of reoperation for seizure outcome in temporal lobe epilepsy. Seizure. 2017 Sep 6;51:174-179. doi: 10.1016/j.seizure.2017.08.015. [Epub ahead of print] PubMed PMID: 28888215.
9)

Stanišić M, Coello C, Ivanović J, Egge A, Danfors T, Hald J, Heminghyt E, Mikkelsen MM, Krossnes BK, Pripp AH, Larsson PG. Seizure outcomes in relation to the extent of resection of the perifocal fluorodeoxyglucose and flumazenil PET abnormalities in anteromedial temporal lobectomy. Acta Neurochir (Wien). 2015 Sep 8. [Epub ahead of print] PubMed PMID: 26350516.

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.
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