Vascular

3D Exoscope for Vascular neurosurgery

3D Exoscope for Vascular neurosurgery

3D Exoscope for Intracranial aneurysm clipping

In aneurysm clipping, three-dimensional exoscopes are noninferior to operating microscopes in terms of surgery duration, safety, and outcomes, based on limited series. Progressive experience enables the surgeon to perform significantly more device adjustments within the same amount of surgical time 1)

Visualization and Maneuverability Features of a Robotic Arm Three-Dimensional Exoscope and Operating Microscope for Clipping an Unruptured Intracranial Aneurysm: Video Comparison and Technical Evaluation 2).

A case of a 11-year-old male with Alagille syndrome, pancytopenia, and peripheral pulmonary stenosis found to have a 12 × 13 × 7 mm distal left M1 aneurysm arising from the inferior M1/M2 junction. The patient was neurologically intact without evidence of rupture. In order to prevent catastrophic rupture, the decision was made to treat the lesion. Due to the patients underlying medical conditions including baseline coagulopathy, surgical management was felt to be superior to an endovascular reconstruction, which would require long-term antiplatelet therapy. Thus the patient underwent a left-sided pterional craniotomy with exoscopic 3D ICG-VA. As demonstrated in Video 1, ICG-VA was performed before definitive clip placement in order to understand flow dynamics with particular emphasis on understanding the middle cerebral artery outflow. Postoperatively, the patient remained at his neurologic baseline and subsequent imaging demonstrated complete obliteration of the aneurysm without any neck remnant. The patient continues to follow and remains asymptomatic and neurologically intact without radiographic evidence of residual or recurrence 3)

Cerebral revascularization

3D Exoscope for cerebral revascularization.

Case reports

The Kinevo 900 exoscope was used in 3 patients with cerebral (2) and spinal (1) vascular pathology, we evaluated the image quality, equipment management, ergonomics, educational utility, 3D glasses, we recorded the characteristics of the cases. and we show a review of the experience of other authors.

Results: 3 patients underwent surgery: one occipital cavernoma, one cerebral dural fistula, and 1 spinal dural fistula. Excellent 3D visualization with Zeiss Kinevo 900 exoscope (Carl Zeiss, Germany), surgical comfort, and educational utility is shown. There were no complications.

The experience and that of other authors suggests that the 3D exoscope shows excellent visualization, better ergonomics, and an innovative educational experience. Vascular microsurgery can be performed safely and effectively 4).

1)

Rossmann T, Veldeman M, Nurminen V, Huhtakangas J, Niemelä M, Lehecka M. 3D Exoscopes are Noninferior to Operating Microscopes in Aneurysm Surgery: Comparative Single-Surgeon Series of 52 Consecutive Cases. World Neurosurg. 2023 Feb;170:e200-e213. doi: 10.1016/j.wneu.2022.10.106. Epub 2022 Nov 9. PMID: 36334715.
2)

Haeren R, Hafez A, Lehecka M. Visualization and Maneuverability Features of a Robotic Arm Three-Dimensional Exoscope and Operating Microscope for Clipping an Unruptured Intracranial Aneurysm: Video Comparison and Technical Evaluation. Oper Neurosurg (Hagerstown). 2022 Jan 1;22(1):28-34. doi: 10.1227/ONS.0000000000000060. Erratum in: Oper Neurosurg (Hagerstown). 2022 Aug 1;23(2):e157. PMID: 34982902.
3)

Wali AR, Kang KM, Rennert R, Santiago-Dieppa D, Khalessi AA, Levy M. First-in-Human Clinical Experience Using High-Definition Exoscope with Intraoperative Indocyanine Green for Clip Reconstruction of Unruptured Large Pediatric Aneurysm. World Neurosurg. 2021 Jul;151:52. doi: 10.1016/j.wneu.2021.04.019. Epub 2021 Apr 17. PMID: 33872836.
4)

Acha JL, Contreras L, Lopez K, Azurin M, Cueva M, Bellido A, Contreras S, Santos O. Neurovascular microsurgical experience through 3D exoscopy. Case report and literature review. World Neurosurg. 2023 Mar 3:S1878-8750(23)00270-X. doi: 10.1016/j.wneu.2023.02.120. Epub ahead of print. PMID: 36871654.

Stroke guidelines

Stroke guidelines

There are multiple stroke guidelines globally. To synthesize these and summarize what existing stroke guidelines recommend about the management of people with stroke, the World Stroke Organization (WSO) Guideline committee, under the auspices of the WSO, reviewed available guidelines. They identified areas of strong agreement across guidelines, and their global coverage.

To systematically review the literature to identify stroke guidelines (excluding primary stroke prevention and subarachnoid hemorrhage) since 1st January 2011, evaluate quality (AGREE II), tabulate strong recommendations, and judge applicability according to stroke care available (minimal, essential, advanced).

Searches identified 15400 titles, 911 texts were retrieved, 203 publications scrutinized by the three subgroups (acute, secondary prevention, rehabilitation), and recommendations extracted from most recent version of relevant guidelines. For acute treatment, there were more guidelines about ischemic stroke than intracerebral hemorrhage; recommendations addressed pre-hospital, emergency, and acute hospital care. Strong recommendations were made for reperfusion therapies for acute ischemic stroke. For secondary prevention, strong recommendations included establishing aetiological diagnosis, management of hypertension, weight, diabetes, lipids, lifestyle modification; and for ischemic stroke: management of atrial fibrillation, valvular heart disease, left ventricular and atrial thrombi, patent foramen ovale, atherosclerotic extracranial large vessel disease, intracranial atherosclerotic disease, antithrombotics in non-cardioembolic stroke. For rehabilitation there were strong recommendations for organized stroke unit care, multidisciplinary rehabilitation, task specific training, fitness training, and specific interventions for post-stroke impairments.Most recommendations were from high income countries, and most did not consider comorbidity, resource implications and implementation. Patient and public involvement was limited.

The review identified a number of areas of stroke care in there was strong consensus. However there was extensive repetition and redundancy in guideline recommendations. Future guidelines groups should consider closer collaboration to improve efficiency, include more people with lived experience in the development process, consider comorbidity, and advise on implementation 1).

American Heart Association Guidelines for the Early Management of Patients With Acute Ischemic Stroke

American Heart Association Guidelines for the Early Management of Patients With Acute Ischemic Stroke.

European Stroke Organisation Guidelines

https://eso-stroke.org/guidelines/eso-guideline-directory/

The fifth edition of the National Clinical Guideline for Stroke 2016

https://www.strokeaudit.org/Guideline/Full-Guideline.aspx

Stroke Foundation – Australia

https://strokefoundation.org.au/what-we-do/for-health-professionals/clinical-guidelines

1)

Mead GE, Sposato LA, Silva GS, Yperzeele L, Wu S, Kutlubaev MA, Cheyne J, Wahab K, Urrutia VC, Sharma VK, Sylaja PN, Hill K, Steiner T, Liebeskind DS, Rabinstein AA. Systematic review and synthesis of global stroke guidelines for the World Stroke Organization. Int J Stroke. 2023 Feb 1:17474930231156753. doi: 10.1177/17474930231156753. Epub ahead of print. PMID: 36725717.

Intracranial Aneurysm (IA)

Intracranial Aneurysm (IA)

Natural history

see Intracranial Aneurysm Natural history

History

see Intracranial Aneurysm History.

Epidemiology

see Intracranial Aneurysm Epidemiology.

Classification

see Intracranial Aneurysm classification.

Pathogenesis

see Intracranial aneurysm pathogenesis.

Computational fluid dynamics

see Computational fluid dynamics for intracranial aneurysm

Risk Factors

Intracranial aneurysm risk factors.

Clinical features

The clinical presentation is varied, ranging from asymptomatic lesions to those presenting with major rupture

see Ruptured intracranial aneurysm.

Diagnosis

Intracranial Aneurysm Diagnosis.

Complications

see Intracranial aneurysm complications.

Treatment

see Intracranial Aneurysm treatment.

Systematic Review and Meta-Analysis

Intracranial aneurysm Systematic Review and Meta-Analysis.

Case series

see Intracranial aneurysm case series.

Books

see Intracranial Aneurysm Books.

Preoperative Embolization for Brain Arteriovenous Malformation

Preoperative Embolization for Brain Arteriovenous Malformation

Latest Pubmed Related Articles

Systematic Review and Meta-analysis

Preoperative embolization has traditionally been regarded as a safe and effective adjunct to cerebral arteriovenous malformation surgery. However, there is currently no high-level evidence to ascertain this presumption.

Sattari et al. from the Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Tehran School of Medicine, Tehran University of Medical Science, Tehran, Iran. compared the outcomes of microsurgery (MS) vs microsurgery with preoperative embolization (E + MS) in patients with cerebral arteriovenous malformation through a systematic review.

They searched MEDLINE, PubMed, and Embase. The primary outcome was cerebral arteriovenous malformation obliteration. Secondary outcomes were intraoperative bleeding (mL), complications, worsened modified Rankin Scale (mRS), and mortality. The pooled proportions of outcomes were calculated through the logit transformation method. The odds ratio (OR) of categorical data and the mean difference of continuous data were estimated through the Mantel-Haenszel and the inverse variance methods, respectively.

Thirty-two studies met the eligibility criteria. One thousand eight hundred twenty-eight patients were treated by microsurgery alone, and 1088 were treated by microsurgery with preoperative embolization, respectively. The meta-analysis revealed no significant difference in AVM obliteration (94.1% vs 95.6%, OR = 1.15 [0.63-2.11], P = .65), mortality (1.7% vs 2%, OR = 0.88 [0.30-2.58], P = .82), procedural complications (18.2% vs 27.2%, OR = 0.47 [0.19-1.17], P = .10), worsened mRS (21.2% vs 18.5%, OR = 1.08 [0.33-3.54], P = .9), and intraoperative blood loss (mean difference = 182.89 [-87.76, 453.55], P = .19).

The meta-analysis showed no significant difference in AVM obliteration, mortality, complications, worse mRS, and intraoperative blood loss between MS and E + MS groups. For AVMs where MS alone has acceptable results, it is reasonable to bypass unnecessary preoperative embolization given the higher postoperative complication risk 1).

In a meta-analysis, preoperative embolization appears to have substantially reduced the lesional volume with active AV shunting before AVM resection. Anecdotally, preoperative embolization facilitates safe and efficient resection; however, differences in outcomes were not significant. The decision to pursue preoperative embolization remains a nuanced decision based on individual lesion anatomy and treatment team experience 2).

Brosnan et al. performed a systematic review of randomized trials and cohort studies evaluating preoperative embolization of bAVMs published between 01 January 2000 and 31 March 2021 and appraise its role in clinical practice. A MEDLINE search was performed, and articles reporting on outcomes following preoperative embolization, as an adjunct to microsurgery, were eligible for inclusion. PRISMA reporting and Cochrane Handbook guidelines were followed. The primary outcome measure was the risk of complications associated with preoperative embolization. The study was registered with PROSPERO (CRD42021244231). Of the 1661 citations, 8 studies with 588 patients met predefined inclusion criteria. No studies specifically compared outcomes of surgical excision of bAVMs between those with and without preoperative embolization. Spetzler Martin (SM) grading was available in 301 cases. 123 of 298 (41⋅28%) patients presented with hemorrhage. Complications related to embolization occurred in 175/588 patients (29.4%, 95% CI 19.6-40.2). Permanent neurological deficits occurred in 36/541 (6%, 95% CI 3.9-8.5) and mortality in 6/588 (0.41%, 95% CI 0-1.4). This is the first systematic review evaluating the preoperative embolization of bAVMs. Existing studies assessing this intervention are of poor quality. Associated complication rates are significant. Based on published literature, there is currently insufficient evidence to recommend the preoperative embolization of AVMs. Further studies are required to ascertain if there are benefits of this procedure and if so, in which cases 3).

Case series

A study included patients with brain AVM who underwent embolization at our hospital between April 2011 and May 2021. Risk factors for peri- and postoperative complications were analyzed.

During the study period, 36 AVMs were treated during 58 embolization sessions. The goal of the embolization was preoperative in 24 (67%), pre-radiosurgical in 9 (25%), and palliative in 3 (8%) cases. The overall complication rate was 43% (25 of 58) per session and 36% (13 of 36) per patient. Ischemic and hemorrhagic complications were observed in 14 (24%) and 14 (24%) cases, respectively. n-Butyl cyanoacrylate (n-BCA) embolization was detected as the significant risk for postoperative hemorrhage in the univariate (79% vs. 36%, P = 0.012; Fisher exact test) and the multivariable analysis (odds ratio 4.90, 95% confidence interval 1.08-22.2, P = 0.039). The number of embolized feeder in a single session also tended to be higher in a hemorrhagic complication group (median 3.5 vs. 2.0, P = 0.11; Mann-Whitney U-test).

The risk of embolization in multimodality treatment for complex brain AVM was substantial. n-BCA embolization may carry a higher risk of postoperative hemorrhage. An accumulation of cases is awaited to investigate the effectiveness of minimal target embolization in the future 4).

A total of 11 patients who underwent 12 preoperative SPE procedures were included for analysis. Five AVMs were ruptured (45%), and the median nidus volume was 3.0 cm3 (range: 1.3-42.9 cm3). The Spetzler-Martin grade was I-II in seven patients (64%) and III-IV in four patients (36%). The degree of nidal obliteration was less than 25% in two procedures (17%), 25-50% in one procedure (8%), 50-75% in eight procedures (67%), and greater than 75% in one procedure (8%). The rates of post-embolization AVM hemorrhage and mortality were 8% and 0%, respectively. The postoperative angiographic obliteration rate was 100%, and the modified Rankin Scale score improved or stable in 91% of patients (median follow-up duration 2 months).

Preoperative AVM SPE affords a reasonable risk-to-benefit profile for appropriately selected patients 5)

Embolization of intracranial arteriovenous malformations (AVMs) is generally a preoperative adjunctive procedure in the USA.

Preoperative embolization may also be a contributing factor with the potential for recurrence of unresected but embolized portions of an AVM. Follow-up angiography at 1 to 3 years appears to be warranted 6).

A total of 107 patients were treated for cAVMs during the study period. Of those patients, 41 underwent cAVM embolizations with Onyx in 82 procedures.

Results: After the embolization, the cAVM diameter was reduced from 3.71 +/- 1.55 cm to 3.06 +/- 1.89 cm (P < .05). Median volume reduction was 75%. Complete occlusion with embolization alone was achieved in 4 (10%) cAVMs. The recurrence rate for completely occluded cAVMs was 50% (2 patients). A total of 71% of the 41 patients treated with Onyx underwent surgery, and 15% underwent radiosurgery. There were 9% who have not yet received definitive treatment of their residual cAVMs. A new permanent neurologic deficit occurred in 5 patients (6.1% per procedure or 12.2% per patient).

A considerable risk for a permanent neurologic deficit remains for cAVM embolization with Onyx. The risk has to be carefully weighted against the benefit of volume reduction in the treatment of cAVMs 7).

1)

Sattari SA, Shahbandi A, Yang W, Feghali J, Xu R, Huang J. Microsurgery versus Microsurgery With Preoperative Embolization for Brain Arteriovenous Malformation Treatment: A Systematic Review and Meta-analysis. Neurosurgery. 2023 Jan 1;92(1):27-41. doi: 10.1227/neu.0000000000002171. Epub 2022 Oct 26. PMID: 36519858.
2)

Park MT, Essibayi MA, Srinivasan VM, Catapano JS, Graffeo CS, Lawton MT. Surgical management outcomes of intracranial arteriovenous malformations after preoperative embolization: a systematic review and meta-analysis. Neurosurg Rev. 2022 Dec;45(6):3499-3510. doi: 10.1007/s10143-022-01860-x. Epub 2022 Sep 27. PMID: 36168072.
3)

Brosnan C, Amoo M, Javadpour M. Preoperative embolisation of brain arteriovenous malformations: a systematic review and meta-analysis. Neurosurg Rev. 2022 Jun;45(3):2051-2063. doi: 10.1007/s10143-022-01766-8. Epub 2022 Mar 9. PMID: 35260972; PMCID: PMC9160113.
4)

Koizumi S, Shojima M, Shinya Y, Ishikawa O, Hasegawa H, Miyawaki S, Nakatomi H, Saito N. Risk Factors of Brain Arteriovenous Malformation Embolization as Adjunctive Therapy: Single-Center 10-Year Experience. World Neurosurg. 2022 Sep 18:S1878-8750(22)01346-8. doi: 10.1016/j.wneu.2022.09.069. Epub ahead of print. PMID: 36130658.
5)

Conger JR, Ding D, Raper DM, Starke RM, Durst CR, Liu KC, Jensen ME, Evans AJ. Preoperative Embolization of Cerebral Arteriovenous Malformations with Silk Suture and Particles: Technical Considerations and Outcomes. J Cerebrovasc Endovasc Neurosurg. 2016 Jun;18(2):90-99. doi: 10.7461/jcen.2016.18.2.90. Epub 2016 Jun 30. PMID: 27790398; PMCID: PMC5081503.
6)

Ivanov AA, Alaraj A, Charbel FT, Aletich V, Amin-Hanjani S. Recurrence of Cerebral Arteriovenous Malformations Following Resection in Adults: Does Preoperative Embolization Increases the Risk? Neurosurgery. 2016 Apr;78(4):562-71. doi: 10.1227/NEU.0000000000001191. PubMed PMID: 26702837.
7)

Hauck EF, Welch BG, White JA, Purdy PD, Pride LG, Samson D. Preoperative embolization of cerebral arteriovenous malformations with onyx. AJNR Am J Neuroradiol. 2009 Mar;30(3):492-5. doi: 10.3174/ajnr.A1376. Epub 2008 Dec 26. PMID: 19112062; PMCID: PMC7051448.

Cervical Sympathetic Nerve Block for cerebral vasospasm

Cervical Sympathetic Nerve Block for cerebral vasospasm

Sympathetic perivascular nerve fibers originate from the superior cervical ganglion (SCG) to innervate the cerebral vasculature, with activation resulting in vasoconstriction. Sympathetic pathways are thought to be a significant contributor to cerebral vasospasm 1).

A simple treatment such as a cervical sympathetic nerve block may be an effective therapy but is not routinely performed as cerebral vasospasm treatment/DCI. cervical sympathetic nerve block consists of injecting local anesthetic at the level of the cervical sympathetic trunk, which temporarily blocks the innervation of the cerebral arteries to cause arterial vasodilatation. cervical sympathetic nerve block is a local, minimally invasive, low cost and safe technique that can be performed at the bedside and may offer significant advantages as a complementary treatment in combination with more conventional neurointerventional surgery interventions. Bombardieri et al. reviewed the literature that describes cervical sympathetic nerve block for vasospasm/DCI prevention or treatment in humans after aSAH. The studies outlined in this review show promising results for a cervical sympathetic nerve block as a treatment for vasospasm/DCI. Further research is required to standardize the technique, explore how to integrate a cervical sympathetic nerve block with conventional neurointerventional surgery treatments of vasospasm and DCI, and study its long-term effect on neurological outcomes 2).

SCG was surgically identified in 15 swine and were electrically stimulated to achieve sympathetic activation. CT perfusion scans were performed to assess for changes in cerebral blood flow (CBF), cerebral blood volume (CBV), mean transit time (MTT), and time-to-maximum (TMax). Syngo. via software was used to determine regions of interest and quantify perfusion measures.

Results: SCG stimulation resulted in 20-30% reduction in mean ipsilateral CBF compared to its contralateral unaffected side (p < 0.001). Similar results of hypoperfusion were seen with CBV, MTT and TMax with SCG stimulation. Prior injection of lidocaine to SCG inhibited the effects of SCG stimulation and restored perfusion comparable to baseline (p > 0.05).

Conclusion: In swine, SCG stimulation resulted in significant cerebral perfusion deficit, and this was inhibited by prior local anesthetic injection into the SCG. Inhibiting sympathetic activation by targeting the SCG may be an effective treatment for sympathetic-mediated cerebral hypoperfusion 3).

Hu et al. investigated the therapeutic effects of SGB in a rat model of subarachnoid hemorrhage (SAH) complicated by delayed CVS and explore the underlying mechanisms. The SAH model was established by the double injection of autologous arterial blood into the cisterna magna. They simulated SGB by transection of the cervical sympathetic trunk (TCST), and measured changes in the diameter, perimeter, and cross-sectional area of the basilar artery (BA) and middle cerebral artery (MCA) to evaluate its vasodilatory effect. To investigate the underlying mechanisms, we determined the expression level of vasoactive molecules endothelin-1 (ET-1) and calcitonin gene-related peptide (CGRP) in the plasma, and apoptotic modulators Bcl-2 and Bax in the hippocampus. We found a significant increase in the diameter, perimeter, and cross-sectional area of the BA and right MCA in SAH rats subjected to TCST. Application of SGB significantly reduced the expression of ET-1 while increasing that of CGRP in SAH rats. We also found a significant increase in the expression of Bcl-2 and a decrease in the expression of Bax in the hippocampus of SAH rats subjected to TCST, when compared to untreated SAH rats. The mechanism of action of SGB is likely mediated through alterations in the ratio of ET-1 and CGRP, and Bax and Bcl-2. These results suggest that SGB can alleviate the severity of delayed CVS by inducing dilation of intracerebral blood vessels, and promoting anti-apoptotic signaling. Our findings provide evidence supporting the use of SGB as an effective and well-tolerated approach to the treatment of CVS in various clinical settings 4)

After successful modeling of cervical sympathetic block, 18 healthy male white rabbits were randomly divided into three groups (n=6), ie, sham operation group (Group A), SAH group (Group B) and SAH with cervical sympathetic block group (Group C). Models of delayed CVS were established by puncturing cisterna magna twice with an injection of autologous arterial blood in Groups B and C. A sham injection of blood through cisterna magna was made in Group A. 0.5 ml saline was injected each time through a catheter for cervical sympathetic block after the first injection of blood three times a day for 3 d in Group B (bilateral alternating). 0.5 ml of 0.25% bupivacaine was injected each time through a catheter for cervical sympathetic block after the first injection of blood three times a day for 7 d in Group B. 2 ml venous blood and cerebrospinal fluid were obtained before (T1), 30 min (T2) and 7 d (T3) after the first injection of blood, respectively, and conserved in a low temperature refrigerator. Basilar artery value at T1, T2 and T3 was measured via cerebral angiography. The degree of damage to nervous system at T1 and T3 was recorded.

Results: There was no significant difference in diameter of basilar artery at T1 among three groups. The diameters of basilar artery at T2 and T3 of Groups B and C were all smaller than that in Group A, which was smaller than Group C, with a significant difference. There was no significant difference in NO and NOS in plasma and cerebrospinal fluid among three groups. The NO and NOS contents at T2 and T3 of Groups B and C were all lower than Group A; Group C was higher than Group B, with a significant difference. The nerve function at T3 of Groups B and C were all lower than Group A and that of Group C higher than Group B, with a significant difference.

Cervical sympathetic block can relieve cerebral vasospasm after subarachnoid hemorrhage and increase NO content and NOS activity in plasma and cerebrospinal fluid to promote neural functional recovery 5)

1) , 3)

Kim WJ, Dacey M, Samarage HM, Zarrin D, Goel K, Chan C, Qi X, Wang AC, Shivkumar K, Ardell J, Colby GP. Sympathetic nervous system hyperactivity results in potent cerebral hypoperfusion in swine. Auton Neurosci. 2022 Sep;241:102987. doi: 10.1016/j.autneu.2022.102987. Epub 2022 May 6. PMID: 35567916; PMCID: PMC9659432.
2)

Bombardieri AM, Albers GW, Rodriguez S, Pileggi M, Steinberg GK, Heit JJ. Percutaneous cervical sympathetic block to treat cerebral vasospasm and delayed cerebral ischemia: a review of the evidence. J Neurointerv Surg. 2022 Dec 6:jnis-2022-019838. doi: 10.1136/jnis-2022-019838. Epub ahead of print. PMID: 36597947.
4)

Hu N, Wu Y, Chen BZ, Han JF, Zhou MT. Protective effect of stellate ganglion block on delayed cerebral vasospasm in an experimental rat model of subarachnoid hemorrhage. Brain Res. 2014 Oct 17;1585:63-71. doi: 10.1016/j.brainres.2014.08.012. Epub 2014 Aug 13. PMID: 25128600.
5)

Chun-jing H, Shan O, Guo-dong L, Hao-xiong N, Yi-ran L, Ya-ping F. Effect of cervical sympathetic block on cerebral vasospasm after subarachnoid hemorrhage in rabbits. Acta Cir Bras. 2013 Feb;28(2):89-93. doi: 10.1590/s0102-86502013000200001. PMID: 23370920.

Hemorrhagic transformation

Hemorrhagic transformation

Large areas of hemorrhagic transformation within an ischemic infarct may be more indicative of cardiogenic brain embolism (CBE) due to thrombolysis of the clot and reperfusion of infarcted brain with the subsequent hemorrhagic conversion. Hemorrhagic transformation most often occurs within 48 hrs of a CBE stroke, and is more common with larger strokes.

Intraarterial thrombolysis within 6 hours of stroke onset may increase recanalization rates to 37–100% and clinical improvement to 53–94% without a significant increase in the hemorrhagic transformation when compared with intravenous thrombolytic therapy alone.

Risk factors

see also Spontaneous Intracerebral Hemorrhage Risk Factors.

Identifying risk factors and making an early prediction of HT in acute cerebral infarction contributes not only to the selections of therapeutic regimen but also, more importantly, to the improvement of prognosis of acute cerebral infarction.

Decompressive craniectomy for a malignant stroke, after reperfusion, corresponding to an endovascular thrombectomy failure, increases the risk of severe hemorrhagic transformations in a ischemic stroke model in mice. This result support the need of clinical studies to evaluate the added value of DC at the era of endovascular thrombectomy 1).

Prediction

The purpose of a study of Wang et al. was to develop and validate a model to predict a patient’s risk of Hemorrhagic transformation within 30 days of initial ischemic stroke.

They utilized a retrospective multicenter observational cohort study design to develop a Lasso Logistic Regression prediction model with a large, US Electronic Health Record dataset which structured to the Observational Medical Outcomes Partnership (OMOP) Common Data Model (CDM). To examine clinical transportability, the model was externally validated across 10 additional real-world healthcare datasets include EHR records for patients from America, Europe and Asia.

In the database the model was developed, the target population cohort contained 621,178 patients with ischemic stroke, of which 5,624 patients had HT within 30 days following initial ischemic stroke. 612 risk predictors, including the distance a patient travels in an ambulance to get to care for a HT, were identified. An area under the receiver operating characteristic curve (AUC) of 0.75 was achieved in the internal validation of the risk model. External validation was performed across 10 databases totaling 5,515,508 patients with ischemic stroke, of which 86,401 patients had HT within 30 days following initial ischemic stroke. The mean external AUC was 0.71 and ranged between 0.60-0.78.

A HT prognostic predict model was developed with Lasso Logistic Regression based on routinely collected EMR data. This model can identify patients who have a higher risk of HT than the population average with an AUC of 0.78. It shows the OMOP CDM is an appropriate data standard for EMR secondary use in clinical multicenter research for prognostic prediction model development and validation. In the future, combining this model with clinical information systems will assist clinicians to make the right therapy decision for patients with acute ischemic stroke 2).

Outcome

Hemorrhagic transformation (HT) after cerebral infarction is a complex and multifactorial phenomenon in the acute stage of ischemic stroke, and often results in a poor prognosis.

1)

Borha A, Lebrun F, Touzé E, Emery E, Vivien D, Gaberel T. Impact of Decompressive Craniectomy on Hemorrhagic Transformation in Malignant Ischemic Stroke in Mice. Stroke. 2022 Dec 7. doi: 10.1161/STROKEAHA.122.041365. Epub ahead of print. PMID: 36475467.
2)

Wang Q, Reps JM, Kostka KF, Ryan PB, Zou Y, Voss EA, Rijnbeek PR, Chen R, Rao GA, Morgan Stewart H, Williams AE, Williams RD, Van Zandt M, Falconer T, Fernandez-Chas M, Vashisht R, Pfohl SR, Shah NH, Kasthurirathne SN, You SC, Jiang Q, Reich C, Zhou Y. Development and validation of a prognostic model predicting symptomatic hemorrhagic transformation in acute ischemic stroke at scale in the OHDSI network. PLoS One. 2020 Jan 7;15(1):e0226718. doi: 10.1371/journal.pone.0226718. eCollection 2020. PubMed PMID: 31910437.

Mechanical thrombectomy outcome

Mechanical thrombectomy outcome

Clinical trials have shown that mechanical thrombectomy (MT) is associated with improved functional outcomes for patients with acute ischemic stroke presenting with proximal anterior circulation, large vessel occlusion, and salvageable brain tissue 1) 2) 3) 4) 5).

Stroke patients who underwent successful thrombectomy with general anesthesia achieved higher rates of functional independence when procedural ETCO2 exceeded 35 mmHg. Further studies to confirm this effect and investigate optimal ETCO2 parameters should be considered 6)

In a cohort study, more than 1 in 5 patients presenting with an ASPECTS of 2 to 5 achieved 90-day functional independence after MT. A favorable outcome was nearly 5 times more likely for patients with low ASPECTS who had successful recanalization. The association of a low ASPECTS with 90-day outcomes did not differ for patients presenting in the early vs extended MT window 7).

For Gariel et al. the primary outcome was favorable 90-day functional outcome defined as a modified Rankin Scale of ≤2. Secondary outcomes were successful reperfusion following all procedures and after the first-line procedure, number of device passes, and change in National Institutes of Health Stroke Scale score at 24 hours 8).

Early reperfusion after endovascular thrombectomy is associated with an improved outcome in ischemic stroke patients; however, the time dependency in elderly patients remains unclear.

Todo et al. investigated the time-outcome relationships in different age subgroups. Of 2420 patients enrolled in the RESCUE-Japan Registry 2 study, a study based on a prospective registry of stroke patients with acute cerebral large-vessel occlusion at 46 centers, they analyzed the data of 1010 patients with successful reperfusion after endovascular therapy (mTICI of 2b or 3). In 3 age subgroups (< 70, 70 to < 80, and ≥ 80 years), the mRS scores at 90 days were analyzed according to 4 categories of onset-to-reperfusion time (< 180, 180 to < 240, 240 to < 300, and ≥ 300 min). In each age subgroup, the distributions of mRS scores were better with shorter onset-to-reperfusion times. The adjusted common odds ratios for better outcomes per 1-category delay in onset-to-reperfusion time were 0.66 (95% CI 0.55-0.80) in ages < 70 years, 0.66 (95% CI 0.56-0.79) in ages 70 to < 80 years, and 0.83 (95% CI 0.70-0.98) in ages ≥ 80 years. Early reperfusion was associated with better outcomes across all age subgroups. Achieving early successful reperfusion is important even in elderly patients 9).

Mechanical neurothrombectomy achieves a higher likelihood of revascularization than intravenous thrombolysis (IVT), but there remains significant discrepancy between rates of recanalization and rates of favorable outcome. The poor neurological recovery among some stroke patients despite successful recanalization confirms the need for adjuvant therapy, such as pharmacological neuroprotection. Prior clinical trials of neuroprotectant drugs failed perhaps due to inability of the agent to reach the ischemic tissue beyond the occluded artery. A protocol that couples mechanical neurothrombectomy with concurrent delivery of a neuroprotectant overcomes this pitfall. Activated protein C (APC) exerts pleiotropic anti-inflammatory, anti-apoptotic, antithrombotic, cytoprotective, and neuroregenerative effects in stroke and appears a compelling candidate for this novel approach 10).

Embolectomy is the emergency surgical removal of emboli which are blocking blood circulation. It usually involves removal of thrombi (blood clots), and is then referred to as thrombectomy. Embolectomy is an emergency procedure often as the last resort because permanent occlusion of a significant blood flow to an organ leads to necrosis. Other involved therapeutic options are anticoagulation and thrombolysis.

Cervical surgical embolectomy for acute extracranial ICA occlusion resulted in a high complete recanalization rate with an acceptable safety profile. A possible association between severe cardiac illness and huge embolus occluding proximal large artery was suggested 11).

Scores

Javed et al. included all eligible adult acute ischemic stroke (AIS) patients treated with endovascular thrombectomy (EVT) at the Montefiore Medical Center from June 2016 to January 2020. Data was systematically collected via chart review including pre-, intra- and post-procedural variables. The outcome was the Modified Rankin Scale (mRS) at 90 days post-EVT where a poor outcome was defined as mRS 3-6: 3-5 for functional dependency and 6 for death. Model selection methods including stepwise and Lasso were evaluated via cross-validation where the final multivariable logistic regression model was chosen by optimizing the Area Under the Receiver Operating Characteristic Curve (ROC AUC).

They included 224 patients (mean age: 65 years old, male: 55%, 90-day poor outcome: 60%). The final model achieved a median AUC of 0.84, IQR: (0.80, 0.87). A 7-point score, called Bronx Endovascular Thrombectomy (BET) score, was developed with more points indicating higher likelihood of 90-day poor outcome (0 point: ≤21% risk; 1-2: 24%; 3: 61%; 4: 86%; 5: 96%; 6-7: ≥99%). One point was awarded for the following variables: current smoker, diabetic, general anesthesia received, puncture to perfusion time ≥45 minutes, and Thrombolysis in Cerebral Infarction (TICI) score <3. Two points were awarded for a post-EVT National Institute of Health Stroke scale (NIHSS) of ≥10.

Incorporating peri-procedural data they developed the competitive BET score predicting 90-day functional dependency and death, which may help providers, patients and caregivers manage expectations and organize early rehabilitative services 12).

Platelet-to-lymphocyte ratio for mechanical thrombectomy outcome

Platelet-to-lymphocyte ratio for mechanical thrombectomy outcome

1)

Powers WJ, Rabinstein AA, Ackerson T, et al. Guidelines for the early management of patients with acute ischemic stroke: 2019 update to the 2018 guidelines for the early management of acute ischemic stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2019;50(12):e344-e418. doi:10.1161/STR.0000000000000211
2)

Jovin TG, Chamorro A, Cobo E, et al; REVASCAT Trial Investigators. Thrombectomy within 8 hours after symptom onset in ischemic stroke. N Engl J Med. 2015;372(24):2296-2306. doi:10.1056/NEJMoa1503780
3)

Nogueira RG, Jadhav AP, Haussen DC, et al; DAWN Trial Investigators. Thrombectomy 6 to 24 hours after stroke with a mismatch between deficit and infarct. N Engl J Med. 2018;378(1):11-21. doi:10.1056/NEJMoa1706442
4)

Goyal M, Menon BK, van Zwam WH, et al; HERMES collaborators. Endovascular thrombectomy after large-vessel ischaemic stroke: a meta-analysis of individual patient data from five randomised trials. Lancet. 2016;387(10029):1723-1731. doi:10.1016/S0140-6736(16)00163-X
5)

Albers GW, Marks MP, Kemp S, et al; DEFUSE 3 Investigators. Thrombectomy for stroke at 6 to 16 hours with selection by perfusion imaging. N Engl J Med. 2018;378(8):708-718. doi:10.1056/NEJMoa1713973
6)

Parr MS, Salehani A, Ogilvie M, Ethan Tabibian B, Rahm S, Hale AT, Tsemo GB, Aluri A, Kim J, Mathru M, Jones JGA. The effect of procedural end-tidal CO2 on infarct expansion during anterior circulation thrombectomy. Interv Neuroradiol. 2022 Dec 4:15910199221143175. doi: 10.1177/15910199221143175. Epub ahead of print. PMID: 36464668.
7)

Almallouhi E, Al Kasab S, Hubbard Z, Bass EC, Porto G, Alawieh A, Chalhoub R, Jabbour PM, Starke RM, Wolfe SQ, Arthur AS, Samaniego E, Maier I, Howard BM, Rai A, Park MS, Mascitelli J, Psychogios M, De Leacy R, Dumont T, Levitt MR, Polifka A, Osbun J, Crosa R, Kim JT, Casagrande W, Yoshimura S, Matouk C, Kan PT, Williamson RW, Gory B, Mokin M, Fragata I, Zaidat O, Yoo AJ, Spiotta AM; Stroke Thrombectomy and Aneurysm Registry (STAR) Collaborators. Outcomes of Mechanical Thrombectomy for Patients With Stroke Presenting With Low Alberta Stroke Program Early Computed Tomography Score in the Early and Extended Window. JAMA Netw Open. 2021 Dec 1;4(12):e2137708. doi: 10.1001/jamanetworkopen.2021.37708. PMID: 34878550; PMCID: PMC8655598.
8)

Gariel F, Lapergue B, Bourcier R, Berge J, Barreau X, Mazighi M, Kyheng M, Labreuche J, Fahed R, Blanc R, Gory B, Duhamel A, Saleme S, Costalat V, Bracard S, Desal H, Detraz L, Consoli A, Piotin M, Marnat G; ASTER Trial Investigators. Mechanical Thrombectomy Outcomes With or Without Intravenous Thrombolysis. Stroke. 2018 Oct;49(10):2383-2390. doi: 10.1161/STROKEAHA.118.021500. PMID: 30355117.
9)

Todo K, Yoshimura S, Uchida K, Yamagami H, Sakai N, Kishima H, Mochizuki H, Ezura M, Okada Y, Kitagawa K, Kimura K, Sasaki M, Tanahashi N, Toyoda K, Furui E, Matsumaru Y, Minematsu K, Kitano T, Okazaki S, Sasaki T, Sakaguchi M, Takagaki M, Nishida T, Nakamura H, Morimoto T; RESCUE-Japan Registry 2 Investigators. Time-outcome relationship in acute large-vessel occlusion exists across all ages: subanalysis of RESCUE-Japan Registry 2. Sci Rep. 2021 Jun 17;11(1):12782. doi: 10.1038/s41598-021-92100-7. PMID: 34140563.
10)

Amar AP, Griffin JH, Zlokovic BV. Combined neurothrombectomy or thrombolysis with adjunctive delivery of 3K3A-activated protein C in acute ischemic stroke. Front Cell Neurosci. 2015 Sep 2;9:344. doi: 10.3389/fncel.2015.00344. eCollection 2015. Review. PubMed PMID: 26388732.
11)

Kiyofuji S, Inoue T, Tamura A, Saito I. Emergent cervical surgical embolectomy for extracranial internal carotid artery occlusion. Acta Neurochir (Wien). 2015 Sep;157(8):1313-9. doi: 10.1007/s00701-015-2478-5. Epub 2015 Jun 23. PubMed PMID: 26095081.
12)

Javed K, Qin J, Mowery W, Kadaba D, Altschul D, Haranhalli N. Predicting 90-day Functional Dependency and Death after Endovascular Thrombectomy for Stroke: The BET Score. J Stroke Cerebrovasc Dis. 2022 Feb 28;31(5):106342. doi: 10.1016/j.jstrokecerebrovasdis.2022.106342. Epub ahead of print. PMID: 35240423.

Charlson comorbidity index (CCI)

Charlson comorbidity index (CCI)

http://touchcalc.com/calculators/cci_js

https://www.mdcalc.com/charlson-comorbidity-index-cci

The purpose of the study was to assess whether the Charlson Comorbidity Index (CCI) was associated with in-hospital death and short-term functional outcome in elderly patients (age ≥ 70) with intracerebral hemorrhage (ICH).

This was a retrospective cohort of aged ICH patients (≥70 years old) admitted within 24 hours of ICH onset. The CCI was derived using hospital discharge ICD-9 CM codes and patient history obtained from standardized case report forms. Multivariable logistic regression was used to determine the independent effect of the CCI score on clinical outcomes.

In this cohort of 248 aged ICH patients, comorbid conditions were common, with CCI scores ranging from 2 to 12. Logistic regression showed that the CCI score was independently predictive of 1-month functional outcome (OR = 1.642, P < 0.001) and in-hospital death (OR = 1.480, P = 0.003). Neither ICH volume nor the presence of IVH was an independent predictive factor for the 1-month functional outcome or in-hospital mortality (P < 0.05).

Comorbid medical conditions as assessed by the CCI independently influence short-term outcomes in aged ICH patients. The characteristics of the hematoma itself, such as intracerebral hemorrhage volume and the presence of IVH, seem to have a reduced effect on it 1).

Complications in spine trauma patients with Ankylosing spinal disorders may be driven by comorbidity burden rather than operative or injury-related factors. The Charlson Comorbidity Index (CCI) may be a valuable tool for the evaluation of this unique population 2)

Charlson Comorbidity Index (CCI) provides a simple way of predicting recurrence in patients with chronic subdural hematoma and should be incorporated into decision-making processes, when counseling patients 3).

Data show that elderly with a good performance status and few co-morbidity may be treated as younger patients; moreover, age confirms a negative impact on survival while (CCI) ≤ 2 did not correlate with overall survival (OS) 4).

Charlson comorbidity index (CCI), functional status computed by the Karnofsky performance scale (KPS)), tumor characteristics (size, location, isocitrate dehydrogenase mutation, and O-6-methylguanine-DNA methyltransferase promoter methylation status), and treatment parameters (volumetrically quantified extent of resection and adjuvant therapy), evidence that aside established prognostic parameters (age and KPS) for glioblastoma patient outcome, the CCI additionally significantly impacts outcome and may be employed for preoperative patient stratification 5).

Maximal resection and radiochemotherapy treatment completion are associated with longer OS, and age alone should not preclude elderly patients from receiving surgery and adjuvant treatment. However, only a few patients were able to finish the proposed treatments. Poor performance and high comorbidity index status might compromise the benefit of treatment aggressiveness and must be considered in therapeutic decision 6).

Latest articles

References

1)

Zhang T, Chen R, Wen D, Wang X, Ma L. The prognostic value of the Charlson comorbidity index in aged patients with intracerebral hemorrhage. BMC Neurol. 2022 Nov 28;22(1):443. doi: 10.1186/s12883-022-02980-z. PMID: 36443745.
2)

Lakomkin N, Mikula AL, Pinter ZW, Wellings E, Alvi MA, Scheitler KM, Pennington Z, Lee NJ, Freedman BA, Sebastian AS, Fogelson JL, Bydon M, Clarke MJ, Elder BD. Perioperative risk stratification of spine trauma patients with ankylosing spinal disorders: a comparison of 3 quantitative indices. J Neurosurg Spine. 2022 May 27:1-7. doi: 10.3171/2022.4.SPINE211449. Epub ahead of print. PMID: 35623371.
3)

Martinez-Perez R, Tsimpas A, Rayo N, Cepeda S, Lagares A. Role of the patient comorbidity in the recurrence of chronic subdural hematomas. Neurosurg Rev. 2020 Mar 7. doi: 10.1007/s10143-020-01274-7. [Epub ahead of print] PubMed PMID: 32146611.
4)

Balducci M, Fiorentino A, De Bonis P, Chiesa S, Manfrida S, D’Agostino GR, Mantini G, Frascino V, Mattiucci GC, De Bari B, Mangiola A, Miccichè F, Gambacorta MA, Colicchio G, Morganti AG, Anile C, Valentini V. Impact of age and co-morbidities in patients with newly diagnosed glioblastoma: a pooled data analysis of three prospective mono-institutional phase II studies. Med Oncol. 2012 Dec;29(5):3478-83. doi: 10.1007/s12032-012-0263-3. Epub 2012 Jun 7. PubMed PMID: 22674154.
5)

Ening G, Osterheld F, Capper D, Schmieder K, Brenke C. Charlson comorbidity index: an additional prognostic parameter for preoperative glioblastoma patient stratification. J Cancer Res Clin Oncol. 2015 Jan 11. [Epub ahead of print] PubMed PMID: 25577223.
6)

Pereira AF, Carvalho BF, Vaz RM, Linhares PJ. Glioblastoma in the elderly: Therapeutic dilemmas. Surg Neurol Int. 2015 Nov 16;6(Suppl 23):S573-S582. eCollection 2015. PubMed PMID: 26664927.

Moyamoya disease

Moyamoya disease

Moyamoya disease is a chronic, occlusive cerebrovascular disease, characterized by bilateral steno-occlusive changes at the terminal portion of the internal carotid artery and an abnormal vascular network at the base of the brain.

These diagnostic criteria of the moyamoya disease, stated by the Research Committee on Spontaneous Occlusion of the Circle of Willis (moyamoya disease) in Japan, are well established and generally accepted as the definition of this rare entity. On the contrary to the diagnosis of definitive moyamoya disease, there is some confusion in the terminology and understanding of quasi-moyamoya disease; moyamoya disease in association with various disease entities, such as atherosclerosis, autoimmune diseases, Down syndrome, etc. Although the clinical management is not affected by these semantic distinctions, terminological confusion may interfere with the international collaboration of the clinical investigation of these rare conditions 1).

The perforating arteries in the basal ganglia and thalamus markedly dilate and function as an important collateral circulation, called as “moyamoya” vessels. The posterior cerebral artery are also involved in a certain subgroup of patients. Therefore, cerebral hemodynamics is often impaired especially in the frontal lobe, leading to transient ischemic attack (TIa) and cerebral infarction. Furthermore, the dilated, fragile moyamoya vessels often rupture and cause intracranial hemorrhage 2) 3).

Epidemiology

Moyamoya Disease Epidemiology.

Classification

Moyamoya disease classification.

Etiology

Unknown etiology.

A study indicated a higher overall autoimmune disease prevalence in unilateral than in bilateral MMD. Unilateral MMD may be more associated with autoimmune disease than bilateral MMD. Different pathogenetic mechanisms may underlie moyamoya vessel formation in unilateral and bilateral MMD 4).

Risk factors

The p.R4810K mutation in RNF213 gene confers a risk of MMD, but other factors remain largely unknown. Mineharu et al. tested the association of gut microbiota with MMD. Fecal samples were collected from 27 patients with MMD, 7 patients with non-moyamoya intracranial large artery disease (ICAD) and 15 control individuals with other disorders, and 16S rRNA were sequenced. Although there was no difference in alpha diversity or beta diversity between patients with MMD and controls, the cladogram showed Streptococcaceae was enriched in patient samples. The relative abundance analysis demonstrated that 23 species were differentially abundant between patients with MMD and controls. Among them, increased abundance of Ruminococcus gnavus > 0.003 and decreased abundance of Roseburia inulinivorans < 0.002 were associated with higher risks of MMD (odds ratio 9.6, P = 0.0024; odds ratio 11.1, P = 0.0051). Also, Ruminococcus gnavus was more abundant and Roseburia inulinivorans was less abundant in patients with ICAD than controls (P = 0.046, P = 0.012). The relative abundance of Ruminococcus gnavus or Roseburia inulinivorans was not different between the p.R4810K mutant and wildtype. The data demonstrated that gut microbiota was associated with both MMD and ICAD 5).

Histopathological features

The histopathological features of the middle cerebral artery (MCA) and superficial temporal artery (STA) from moyamoya disease (MMD) and their relationships with gender, age, angiography stage were explored. The causes and the clinical significance of vasculopathy of STA were also discussed. The clinical data and specimens of MCA and STA from 30 MMD patients were collected. Twelve samples of MCA and STA from non-MMD patients served as control group. Histopathological examination was then performed by measuring the thickness of intima and media, and statistical analysis was conducted. The MCA and STA specimens from MMD group had apparently thicker intima and thinner media than those from the control group. There was no significant pathological difference between the hemorrhage group and non-hemorrhage group, and between the males and females in MMD patients. Neither the age nor the digital subtraction angiography (DSA) stage was correlated with the thickness of intima in MCA and STA. MMD is a systemic vascular disease involving both intracranial and extracranial vessels. Preoperative external carotid arteriography, especially super-selective arteriography of the STA, benefits the selection of donor vessel 6).

Pathogenesis

Moyamoya Disease Pathogenesis.

Clinical features

see Moyamoya disease clinical features.

Diagnosis

MoyaMoya Disease Diagnosis.

Hemodynamic parameter

Quantification of the severity of vasculopathy and its impact on parenchymal hemodynamics is a necessary prerequisite for informing management decisions and evaluating intervention response in patients with moyamoya.

Computational fluid dynamics (CFD) analysis on eight patients (5 female, 3 male) with MMD treated by EDAS (encephalo-duro-arterio-synangiosis) between 2011 and 2012. All the eight patients presented with haemorrhage, with subsequent 4-12 month follow-up done using Magnetic Resonance Angiography (MRA) to capture auto-remodelling. Karunanithi et al. calculated percentage change in flow rate and pressure drop indicator (ΡDI) across the Left and Right ICA. Pressure drop indicator (PDI) is defined as the difference of pressure reduction within the carotid arteries, measured at post-op and follow up, using patient specific inflow rates. The measured percentage flow change and pressure reduction showed an increase at follow up for improved patients (characterised by angiography according to the method of Matsushima), who did not develop any complications after surgery. The inverse was observed in patients who were clinically classified as no change and retrogressed (according to the method of Matsushima) cases post-operation. This elucidates the findings of a new parameter that may well play a critical role as an assistive clinical decision making tool in MMD 7).

Treatment

see Moyamoya disease treatment.

Outcome

see Moyamoya disease outcome.

Complications

see Stroke in moyamoya disease.

Articles

Artificial intelligence (AI) clustering was used to classify the articles into 5 clusters: (1) pathophysiology (23.5%); (2) clinical background (37.3%); (3) imaging (13.2%); (4) treatment (17.3%); and (5) genetics (8.7%). Many articles in the “clinical background” cluster were published from the 1970s. However, in the “treatment” and “genetics” clusters, the articles were published from the 2010s through 2021. In 2011, it was confirmed that a gene called Ringin protein 213 (RNF213) is a susceptibility gene for moyamoya disease. Since then, tremendous progress in genomic, transcriptomics, and epigenetics (e.g., methylation profiling) has resulted in new concepts for classifying moyamoya disease. The literature survey revealed that the pathogenesis involves aberrations of multiple signaling pathways through genetic mutations and altered gene expression 8).

Case series

see Moyamoya disease case series.

Case reports

Moyamoya disease case reports.

1)

Fujimura M, Tominaga T. Diagnosis of moyamoya disease: international standard and regional differences. Neurol Med Chir (Tokyo). 2015 Mar 15;55(3):189-93. doi: 10.2176/nmc.ra.2014-0307. Epub 2015 Feb 20. PubMed PMID: 25739428.
2)

Suzuki J, Takaku a: Cerebrovascular “moyamoya” disease. disease showing abnormal net-like vessels in base of brain. Arch Neurol 20: 288–299, 1969
3)

Kuroda S, Houkin K: Moyamoya disease: current concepts and future perspectives. Lancet Neurol 7: 1056–1066, 2008
4)

Chen JB, Liu Y, Zhou LX, Sun H, He M, You C. Increased prevalence of autoimmune disease in patients with unilateral compared with bilateral moyamoya disease. J Neurosurg. 2015 Sep 25:1-6. [Epub ahead of print] PubMed PMID: 26406790.
5)

Mineharu Y, Nakamura Y, Sato N, Kamata T, Oichi Y, Fujitani T, Funaki T, Okuno Y, Miyamoto S, Koizumi A, Harada KH. Increased abundance of Ruminococcus gnavus in gut microbiota is associated with moyamoya disease and non-moyamoya intracranial large artery disease. Sci Rep. 2022 Nov 24;12(1):20244. doi: 10.1038/s41598-022-24496-9. PMID: 36424438.
6)

Sun SJ, Zhang JJ, Li ZW, Xiong ZW, Wu XL, Wang S, Shu K, Chen JC. Histopathological features of middle cerebral artery and superficial temporal artery from patients with moyamoya disease and enlightenments on clinical treatment. J Huazhong Univ Sci Technolog Med Sci. 2016 Dec;36(6):871-875. PubMed PMID: 27924520.
7)

Karunanithi K, Han C, Lee CJ, Shi W, Duan L, Qian Y. Identification of a hemodynamic parameter for assessing treatment outcome of EDAS in Moyamoya disease. J Biomech. 2015 Jan 21;48(2):304-9. doi: 10.1016/j.jbiomech.2014.11.029. Epub 2014 Nov 29. PubMed PMID: 25498370.
8)

Kuribara T, Akiyama Y, Mikami T, Komatsu K, Kimura Y, Takahashi Y, Sakashita K, Chiba R, Mikuni N. Macrohistory of Moyamoya Disease Analyzed Using Artificial Intelligence. Cerebrovasc Dis. 2022 Feb 1:1-14. doi: 10.1159/000520099. Epub ahead of print. PMID: 35104814.

Cardiac Complications After Subarachnoid Hemorrhage

Cardiac Complications After Subarachnoid Hemorrhage

Subarachnoid hemorrhage (SAH) is a serious condition, and a myocardial injury or dysfunction could contribute to the outcome.

Acute cardiac complications frequently occur after subarachnoid hemorrhage (SAH). These complications include electrocardiogram (ECG) abnormalities, the release of cardiac biomarkers, and the development of acute stress-induced heart failure resembling Takotsubo cardiomyopathy 1) 2) 3) 4) 5) 6)

non-ST elevation myocardial infarction, ST-elevation myocardial infarction and cardiac arrest, but their clinical relevance is unclear.

Lång et al. assessed the prevalence and prognostic impact of cardiac involvement in a cohort with SAH in a prospective observational multicenter study. They included 192 patients treated for non traumatic subarachnoid hemorrhage. They performed ECG recordings, echocardiogram, and blood sampling within 24 h of admission and on days 3 and 7 and at 90 days. The primary endpoint was the evidence of cardiac involvement at 90 days, and the secondary endpoint was to examine the prevalence of a myocardial injury or dysfunction. The median age was 54.5 (interquartile range [IQR] 48.0-64.0) years, 44.3% were male and the median World Federation of Neurosurgical Societies grading for subarachnoid hemorrhage score was 2 (IQR 1-4). At day 90, 22/125 patients (17.6%) had left ventricular ejection fractions ≤ 50%, and 2/121 patients (1.7%) had evidence of a diastolic dysfunction as defined by mitral peak E-wave velocity by peak e’ velocity (E/e’) > 14. There was no prognostic impact from echocardiographic evidence of cardiac complications on neurological outcomes. The overall prevalence of cardiac dysfunction was modest. They found no demographic or SAH-related factors associated with 90 days cardiac dysfunction 7).

Among patients suffering from cardiac events at the time of aneurysmal subarachnoid hemorrhage, those with myocardial infarction and in particular those with a troponin level greater than 1.0 mcg/L had a 10 times increased risk of death 8).

1)

Zaroff JG, Rordorf GA, Newell JB, Ogilvy CS, Levinson JR. Cardiac outcome in patients with subarachnoid hemorrhage and electrocardiographic abnormalities. Neurosurgery. 1999;44:34–39. doi: 10.1097/00006123-199901000-00013.
2)

Tung P, Kopelnik A, Banki N, et al. Predictors of neurocardiogenic injury after subarachnoid hemorrhage. Stroke. 2004;35:548–551. doi: 10.1161/01.STR.0000114874.96688.54.
3)

Banki N, Kopelnik A, Tung P, et al. Prospective analysis of prevalence, distribution, and rate of recovery of left ventricular systolic dysfunction in patients with subarachnoid hemorrhage. J Neurosurg. 2006;105:15–20. doi: 10.3171/jns.2006.105.1.15.
4)

Lee VH, Connolly HM, Fulgham JR, Manno EM, Brown JRD, Wijdicks EFM. Tako-tsubo cardiomyopathy in aneurysmal subarachnoid hemorrhage: an underappreciated ventricular dysfunction. J Neurosurg. 2006;105:264–270. doi: 10.3171/jns.2006.105.2.264.
5)

Oras J, Grivans C, Bartley A, Rydenhag B, Ricksten SE, Seeman-Lodding H. Elevated high-sensitive troponin T on admission is an indicator of poor long-term outcome in patients with subarachnoid haemorrhage: a prospective observational study. Crit Care (Lond, Engl) 2016;20:11. doi: 10.1186/s13054-015-1181-5.
6)

van der Bilt IA, Hasan D, Vandertop WP, et al. Impact of cardiac complications on outcome after aneurysmal subarachnoid hemorrhage: a meta-analysis. Neurology. 2009;72:635–642. doi: 10.1212/01.wnl.0000342471.07290.07.
7)

Lång M, Jakob SM, Takala R, Lyngbakken MN, Turpeinen A, Omland T, Merz TM, Wiegand J, Grönlund J, Rahi M, Valtonen M, Koivisto T, Røsjø H, Bendel S. The prevalence of cardiac complications and their impact on outcomes in patients with non-traumatic subarachnoid hemorrhage. Sci Rep. 2022 Nov 22;12(1):20109. doi: 10.1038/s41598-022-24675-8. PMID: 36418906.
8)

Ahmadian A, Mizzi A, Banasiak M, Downes K, Camporesi EM, Thompson Sullebarger J, Vasan R, Mangar D, van Loveren HR, Agazzi S. Cardiac manifestations of subarachnoid hemorrhage. Heart Lung Vessel. 2013;5(3):168-78. PubMed PMID: 24364008; PubMed Central PMCID: PMC3848675.