Lenticulostriate artery aneurysm

Lenticulostriate artery aneurysm

Charcot-Bouchard aneurysms are minute aneurysms (microaneurysms) in the brain that occur in small penetrating blood vessels with a diameter that is less than 300 micrometers. The most common vessels involved are the lenticulostriate branches (LSA) of the middle cerebral artery (MCA). LSAs originate from the MCA just before its bifurcation, and they can vary between 2 to 12 in number (average 8.1). Most branches arise medially (99.2%), close to the internal carotid artery. They supply the basal ganglia, and more specifically, the putamen and caudate, followed by the thalamus, pons, and cerebellum.

Charcot-Bouchard aneurysms are named after the French physician Jean-Martin Charcot and his student Charles Joseph Bouchard. In the 19th century, Bouchard discovered these aneurysms during his research under Charcot. Cole and Yates strengthened Charcot and Bouchard’s work by demonstrating that aneurysms truly exist using microangiographic techniques in the 1960s. However, it has been a topic of lively debate if it is, in fact, the rupture of these aneurysms that are responsible for the intracerebral bleeds.

Individuals with chronic systemic hypertension are at high risk of developing atrophy of the outer muscular layer. With the loss of integrity of the vessel wall, microaneurysms develop in LSA, which are at high risk of rupture. Bleeding of aneurysms into the deep structures of the brain parenchyma is also referred to as intraparenchymal hemorrhage or, more broadly, as intracerebral hemorrhage. Clinically the deficits that present can point towards the location of the bleed. The first-line diagnostic modality for these patients is a non-contrast computed tomography (CT) of the head to visualize the bleed. Depending on the severity and location of the hemorrhage, the treatment options vary from observation to neurosurgical intervention 1)

Aneurysms of lenticulostriate artery (LSA) perforators are uncommon. There are few data on their natural history, and opinions differ on the treatment strategies.

Aneurysms of the lenticulostriate artery (LSA) are rare lesions that are categorized into either proximal (at the junction of the middle cerebral artery trunk) or distal (within the basal ganglia).

Vargas et al, report a case series and summarize the most recent literature with current treatment recommendations, and propose an anatomical classification for these entities.

A retrospective review of all patients who were diagnosed with an LSA aneurysm on cerebral angiogram was performed. An extensive online literature search was performed to identify other studies reporting on the diagnosis and management of ruptured and unruptured lenticulostriate aneurysms.

48 cases were identified in the literature and reviewed: 27 patients were treated surgically; five cases were treated with endovascular therapy; two cases underwent gamma knife radiosurgery; and 13 cases were managed conservatively.

They classified these aneurysms into three types: type 1 describes aneurysms arising from the middle cerebral artery next to a perforating LSA; type 2 is an LSA aneurysm from which the perforating artery or arteries arise-the type 2A subtype is one in which the aneurysm neck incorporates the origin of the perforating arteries and the type 2B describes perforating arteries arising from the dome of the aneurysm; and type 3 describes a fusiform aneurysm beyond the first loop or turn of an LSA.

LSA aneurysms are rare entities that present several treatment challenges 2).


These lesions have been reported against the background of a diverse array of pathologies including hypertensionvascular malformations, moyamoya disease, substance abuse, systemic lupus erythematosusventricular neurocytoma, and Sneddon syndrome; however, most cases are idiopathic.

The ruptured aneurysm has a high risk of re-bleeding with a consequent marked decreased risk of patient survival and functional independence, for proximal LSA aneurysm, neurosurgery has been the mainstay of treatment, but its efficacy remains controversial.

Development of devices and improved operator experience have rendered endovascular coiling an alternative and acceptable option for such patients 3).

Using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, a literature search was conducted in the PubMed, Cochrane, EBSCOhost, Scopus, Web of Science, and ProQuest search engines to identify reported studies of LSA aneurysms until July 1, 2020. A descriptive analysis was performed.

Results: A total of 71 studies with 112 cases of LSA aneurysms were included. Patient age ranged from 2 months to 83 years (median, 44.5 years). Male and female patients were affected similarly (49% and 51%, respectively). The most common presentation was aneurysmal rupture (78%), and headache was the most frequently reported symptom (36%). Overall, 48% of the patients had undergone underwent surgical treatment, 30% conservative management, 21% endovascular treatment, and 1% radiosurgery. Four patients died, all of whom had presented with aneurysmal rupture.

Hinojosa-Gonzalez et al. summarized the reported cases of LSA aneurysms, with their clinical presentation, management, and outcomes, for physicians who may be confronted with this diagnosis. Future studies that use available classification systems and include as much detail as possible should be encouraged to fully elucidate the optimal management strategy for these patients 4).

An 81-year-old woman developed consciousness disturbance. Computed tomography revealed hemorrhage in the right caudate nucleus and lateral ventricles. Three-dimensional computed tomographic angiography demonstrated only an aneurysm at the basilar artery. On angiography, on the sixth day, an aneurysm at the right lenticulostriate artery was demonstrated. Then, the aneurysm disappeared on three-dimensional computed tomographic angiography on the 15th day. Subsequent radiological examinations revealed no vascular anomaly in the right lenticulostriate artery.

An aneurysm at this location can show dynamic changes based on radiological findings. Close radiological observation is necessary 5).

Patients with moyamoya disease and LSA aneurysm rupture admitted to Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medicine School from October 2012 to March 2015 were analyzed retrospectively. They were followed up for 1 year. The modified Rankin Scale (mRS) was used to evaluate the outcomes, and 0-2 was defined as good outcome. The demographic characteristics, image anatomical features, treatment schemes, and outcomes of the patients were summarized. The Pubmed database was used to retrieve other similar studies, which combined with this group of cases for analysis. Results A total of 10 patients were enrolled, 2 males and 8 females, aged 29-72 years, with an average of 43. 6 years. All cases were intracranial hemorrhage, including 3 cases of cerebral hemorrhage, 6 cases of ventricular hemorrhage, and 1 case of subarachnoid hemorrhage. At the time of admission, 7 patients had disturbance of consciousness, and 3 patients underwent emergency extraventricular drainage. Among them, 5 patients received endovascular embolization, 4 had good outcome, 1 had mild neurological deficit (mRS score 3); 2 received surgical treatment, all had good outcome; 3 received conservative treatment, all had re-bleeding, 2 died, and 1 had severe disability (mRS score 4). Fourteen eligible articles were included, and a total of 18 patients were included in the analysis: surgical treatment in 7 cases, endovascular treatment in 6 cases, and conservative treatment in 5 cases (self-healing in 1 case). According to the data of this group of patients and literature reports, the good outcome rate of the patients with early interventional embolization or craniotomy clipping treatment was significantly higher than that of conservative treatment (70. 6%vs. 22. 2%; P = 0. 038). Conclusion There is a certain risk of conservative treatment of Moyamoya disease complicated with LSA aneurysm rupture and requires active treatment. Interventional embolization of the parent artery or surgically clipping of aneurysm can effectively improve the clinical outcome of such patients. Interventional embolization of the parent artery and aneurysm can be selected simultaneously if the condition of the parent artery is allowed. Surgery can be selected when the condition of parent artery is poor and the aneurysm is located in the superficial part 6).

A case report of a child with a ruptured distal lenticulostriate artery aneurysm that required careful decision-making and preparation before microsurgical excision. MR angiography was performed in the planning phase and neuronavigation was used during surgery. The surgery was a success, with the patient suffering minimal postoperative focal deficit, which later turned out to be transient 7).


A 42-year-old woman presented with a sudden onset of dysarthria and right hemiparesis. Putaminal hemorrhage from a ruptured aneurysm in the left LSA was detected. Angiographically, moyamoya vessels were revealed. The aneurysm in the left LSA was saccular type and seemed to be related to Moyamoya disease. As the aneurysm was successfully approached with a microcatheter, coil embolization without parent artery occlusion was performed. Rebleeding from the embolized aneurysm in the LSA did not occur. This is the first report of a ruptured LSA aneurysm embolized using coils through a flow-guiding microcatheter without parent artery occlusion in a case of Moyamoya disease 8).


One case of ruptured LSA aneurysm is related to Moyamoya disease (MMD). Surgical treatment of this aneurysm is challenging because of its deep location and complex neural structures around the LSA. They report one case treated with endovascular Onyx embolization, successfully and review the LSA aneurysm associated with MMD 9)


A 49-year-old man who presented with a hemorrhage in the basal ganglia. An angiogram revealed a distal LSA aneurysm in the setting of moyamoya disease. The patient’s aneurysm was successfully embolized by the use of Onyx 18. In this report, we present the first case of onyx embolization of a LSA aneurysm and review all the previous cases that were managed with endovascular techniques.

Conclusion: Treatment of these lesions with either surgery or endovascular therapy is challenging and requires specialized expertise. Given the risks of surgery, we believe that LSA aneurysms are best treated by endovascular means, especially in the setting of moyamoya disease 10).


1)

Gupta K, M Das J. Charcot-Bouchard Aneurysm. 2023 Jul 17. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan–. PMID: 31971704.
2)

Vargas J, Walsh K, Turner R, Chaudry I, Turk A, Spiotta A. Lenticulostriate aneurysms: a case series and review of the literature. J Neurointerv Surg. 2014 Feb 26. doi: 10.1136/neurintsurg-2013-010969. [Epub ahead of print] PubMed PMID: 24574545.
3)

Ma N, Tomancok B, Jiang P, Yang XJ, Ojar D, Jia W. Endovascular Coiling for a Ruptured Proximal Lenticulostriate Artery Aneurysm. Chin Med J (Engl). 2016 May;129(5):606-8. doi: 10.4103/0366-6999.176985. PubMed PMID: 26904998.
4)

Hinojosa-Gonzalez DE, Ferrigno AS, Martinez HR, Farias JS, Caro-Osorio E, Figueroa-Sanchez JA. Aneurysms of the Lenticulostriate Artery: A Systematic Review. World Neurosurg. 2021 Jan;145:471-479.e10. doi: 10.1016/j.wneu.2020.08.160. Epub 2020 Sep 2. PMID: 32889194.
5)

Nomura M, Baba E, Shirokane K, Tsuchiya A. Aneurysm of lenticulostriate artery in a patient presenting with hemorrhage in the caudate nucleus and lateral ventricle-delayed appearance and spontaneous resolution. Surg Neurol Int. 2018 Sep 21;9:192. doi: 10.4103/sni.sni_126_18. PMID: 30294496; PMCID: PMC6169348.
7)

Kheyreddin A, Semenov D, Abramyan A. Microsurgical excision of a ruptured distal lenticulostriate aneurysm in a child. BMJ Case Rep. 2023 Sep 25;16(9):e256627. doi: 10.1136/bcr-2023-256627. PMID: 37748812.
8)

Ando M, Maki Y, Hojo M, Hatano T. Ruptured saccular aneurysm of the lenticulostriate artery embolized without parent artery occlusion in a case of moyamoya disease. Neuroradiol J. 2022 May 12:19714009221101307. doi: 10.1177/19714009221101307. Epub ahead of print. PMID: 35545931.
9)

Byeon Y, Kim HB, You SH, Yang K. A Ruptured lenticulostriate artery aneurysm in moyamoya disease treated with Onyx embolization. J Cerebrovasc Endovasc Neurosurg. 2021 Oct 26. doi: 10.7461/jcen.2021.E2021.06.011. Epub ahead of print. PMID: 34696549.
10)

Chalouhi N, Tjoumakaris S, Gonzalez LF, Dumont AS, Shah Q, Gordon D, Rosenwasser R, Jabbour P. Onyx embolization of a ruptured lenticulostriate artery aneurysm in a patient with moyamoya disease. World Neurosurg. 2013 Sep-Oct;80(3-4):436.e7-10. doi: 10.1016/j.wneu.2012.03.030. Epub 2012 Apr 3. PMID: 22484074.

Woven EndoBridge (WEB)

Woven EndoBridge (WEB)

The WEB device is made of a fine mesh composed of nitinol, a biocompatible metal alloy. It is designed to be delivered through a catheter and deployed within the aneurysm sac.
The Woven EndoBridge device is a treatment option for bifurcation wide-neck intracranial aneurysm. While this device has had good results, there remains a subset that fail this treatment.

For the treatment of both ruptured and unruptured aneurysms. The WEB has received the CE mark and to date has been used to treat a wide variety of more than 1,400 aneurysms in Europe, Latin America and New Zealand. The WEB is not available for sale or use in the United States.

The WEB is a self-expanding, oblate, braided nitinol mesh.

The device is composed of an inner and outer braid held together by proximal, middle, and distal radiopaque markers, creating 2 compartments: 1 distal and 1 proximal. Depending on the device diame- ter, the inner and outer braids are 108 wires or 144 wires. Therefore, blood flow into a WEB-embolized aneurysm initially encounters 2 layers of wires comprising 216 or 288 wires, with the largest interwire distance ranging from 106 to 181 􏰅m, respectively, depending on the device size. The WEB implant is deployed—or retrieved before de- tachment—in a manner similar to that in endovascular coil systems, through microcatheters with an internal diameter 􏰆0.027 inch. For devices with a diameter of 􏰇7 mm, microcatheters with an internal diameter of 0.027 inch are used; and for devices with a diameter 􏰁7 mm, microcatheters with an internal diameter 0.032 inch are used. The detachment system is electrothermal and instantaneous. 2).


In a study, there was no difference in the early clinical course between those treated with WEB embolization, coil embolization, or neurosurgical clipping. Since WEB embolization is a valuable treatment alternative to coiling, it seems not justified to exclude this procedure from upcoming clinical SAH trials, yet the clinical long-term outcome, aneurysm occlusion, and retreatment rates have to be analyzed in further studies 3).

WEB Intrasaccular Therapy Study (WEB-IT)


The WEB Clinical Assessment of Intrasaccular Aneurysm Therapy (WEBCAST) trial is a prospective European trial evaluating the safety and efficacy of WEB in wide necked aneurysm of the bifurcation.

The WEB Occlusion Scale (WOS) 4), a Raymond-inspired scale, is up to now the most frequently used for WEB angiographic evaluation, but it may not be optimal for this device. Indeed, the new concept of intrasaccular flow-disruption introduces new analytical issues, such as proximal recess appearance, residual filling of the WEB, and device compression 5).

see Bicêtre Occlusion Scale Score

Larger aneurysms are at risk for incomplete occlusion status post WEB treatment. Larger, ruptured aneurysms with minimal difference in aneurysm and WEB diameter that fail to occlude immediately post-treatment are more likely to present as residual aneurysms at short-term follow-up 6).


It does not immediately secure the aneurysm in most subarachnoid hemorrhage cases. Second, it may not be suitable for embolization of wide-neck aneurysms with an unfavorable aspect ratio. To overcome these limitations, Zanaty et al., used the WEB device in conjunction with stenting and/or coiling.

They presented a technical note with an illustrated case-series, and provide a detailed step-by-step description on how the WEB device can be used in adjunct to coiling and/or stenting to achieve successful angiographic results. Accurate sizing of the WEB device before deployment is critical. Larger case-series are required to further assess the safety and success of these combined techniques 7).

Zhang et al. searched the PubMedOvid MEDLINE, and EMBASE databases between December 1, 2012 and June 30, 2018.

Studies that included five or more patients undergoing WEB for Wide necked intracranial aneurysms, reported an angiographic or clinical outcome and risk factors, and were published after December 1, 2012 were eligible.

Major outcomes included initial or short-term complete and adequate occlusion. Secondary outcomes included treatment failure, recanalizationmortalitymorbidity, and complication (e.g., thromboembolism or intraoperative rupture) rates. A random-effect model was used to pool the data. To assess risk factors for short-term angiographic outcomes and the most common complications, they conducted subgroup analyses and obtained odds ratios with 95% confidence intervals.

They included 36 studies (1759 patients with 1749 aneurysms). The initial complete and adequate occlusion rates were 35% and 77%, respectively. After a mean follow-up of 9.34 months, the short-term complete and adequate occlusion rates were 53% and 80%, respectively. Thromboembolism and recanalization were the most common complications (both 9%), followed by mortality (7%), morbidity (6%), failure (5%) and intraoperative rupture (3%). The following factors were related to higher short-term obliteration rates: unruptured status, in the anterior circulation, a medium neck (4-9.9 mm), newer-generation WEB and treatment without additional devices. Ruptured status, anterior circulation, preoperative antiplatelet therapy and newer-generation WEB were not significantly related to withto thromboembolism.

WEB has a satisfactory safety profile and shows promising efficacy in treating wide-neck intracranial aneurysms. They preliminarily identified several risk factors for short-term angiographic outcomes 8).

A 68-year-old male patient with known hypertensioncoronary artery disease, and Benign Prostatic Hyperplasia was admitted after a ruptured aneurysm of 4.5 mm in the right middle cerebral artery M1 segment and subarachnoid hemorrhage were detected in the emergency room imaging after syncope at home. WEB device was placed into the aneurysm in the patient who was planned for endovascular treatment. After 3 days of the procedureneurologic examination showed regression. In the brain computed tomography imaging, it was observed that there was an intraparenchymal hematoma of 4,5 cm in the right temporoparietal region, and the aneurysm, which had been treated with endovascular WEB, was ruptured. The aneurysm was clipped in the patient for whom emergency surgical treatment was planned.

As a conclusion, re-bleeding can be seen after aneurysm treatment with the Web device. If it is planned to re-close the aneurysm treated with the web device with a surgical clip, the pressure created by the device against the vessel can be reduced with the additional clip 9).

A case of a shallow basilar tip aneurysm treated with the WEB device that required stabilization with Y-stent through radial access 10).
 

1) 

Ding YH, Lewis DA, Kadirvel R, Dai D, Kallmes DF. The Woven EndoBridge: a new aneurysm occlusion device. AJNR Am J Neuroradiol. 2011 Mar;32(3):607-11. doi: 10.3174/ajnr.A2399. Epub 2011 Feb 17. PubMed PMID: 21330397.
2) 

Pierot L, Liebig T, Sychra V, Kadziolka K, Dorn F, Strasilla C, Kabbasch C, Klisch J. Intrasaccular flow-disruption treatment of intracranial aneurysms: preliminary results of a multicenter clinical study. AJNR Am J Neuroradiol. 2012 Aug;33(7):1232-8. doi: 10.3174/ajnr.A3191. Epub 2012 Jun 7. PubMed PMID: 22678844.
3) 

Sauvigny T, Nawka MT, Schweingruber N, Mader MM, Regelsberger J, Schmidt NO, Westphal M, Czorlich P. Early clinical course after aneurysmal subarachnoid hemorrhage: comparison of patients treated with Woven EndoBridge, microsurgical clipping, or endovascular coiling. Acta Neurochir (Wien). 2019 Jul 6. doi: 10.1007/s00701-019-03992-4. [Epub ahead of print] PubMed PMID: 31280480.
4) 

Fiorella D, Arthur A, Byrne J, Pierot L, Molyneux A, Duckwiler G, Mccarthy T, Strother C (2014) Interobserver variability in the assessment of aneurysm occlusion with the WEB aneurysm embolization system. J Neurointerv Surg:1-6. doi:10.1136/neurintsurg2014-011251
5) 

Cognard C, Januel AC (2015) Remnants and recurrences after the use of the WEB intrasaccular device in large-neck bifurcation aneurysms. Neurosurgery 76(5):522–530. doi:10.1227 /NEU.0000000000000669
6) 

Fortunel A, Javed K, Holland R, Ahmad S, Haranhalli N, Altschul D. Impact of aneurysm diameter, angulation, and device sizing on complete occlusion rates using the woven endobridge (WEB) device: Single center United States experience. Interv Neuroradiol. 2022 Mar 7:15910199221084804. doi: 10.1177/15910199221084804. Epub ahead of print. PMID: 35253525.
7) 

Zanaty M, Roa JA, Dandapat S, Samaniego EA, Jabbour P, Hasan D. Diverse Use of the WEB Device: A Technical Note on WEB Stenting and WEB Coiling of Complex Aneurysms. World Neurosurg. 2019 Jul 10. pii: S1878-8750(19)31933-3. doi: 10.1016/j.wneu.2019.07.027. [Epub ahead of print] PubMed PMID: 31301439.
8) 

Zhang SM, Liu LX, Ren PW, Xie XD, Miao J. Effectiveness, safety and risk factors of Woven EndoBridge device in the treatment of wide-neck intracranial aneurysms : systematic review and meta-analysis. World Neurosurg. 2019 Aug 13. pii: S1878-8750(19)32175-8. doi: 10.1016/j.wneu.2019.08.023. [Epub ahead of print] PubMed PMID: 31419591.
9) 

Sahin MC, Oncu F, Karaaslan B. Clipping of a Rebleeding Ruptured Aneurysm After Woven EndoBridge Treatment. Turk Neurosurg. 2023;33(5):916-918. doi: 10.5137/1019-5149.JTN.41381-22.2. PMID: 37715605.
10) 

Nordmann NJ, Weber MW, Dayoub H. Woven Endobridge (WEB) augmented by Y-stent in a shallow basilar tip aneurysm. J Cerebrovasc Endovasc Neurosurg. 2022 Feb 17. doi: 10.7461/jcen.2022.E2021.08.006. Epub ahead of print. PMID: 3517207

Aneurysm clipping and Test

Aneurysm clipping



Aneurysm clipping is a neurosurgical procedure performed to treat cerebral or intracranial aneurysms.

The purpose of intracranial aneurysm clipping is to prevent the aneurysm from rupturing by sealing it off from normal blood circulation. Here is an overview of the procedure:

Preoperative Evaluation: Before the surgery, a patient’s medical history and imaging studies, such as CT scans, MRI scans, or angiography, are thoroughly reviewed to determine the size, location, and characteristics of the aneurysm.

Anesthesia: The patient is placed under general anesthesia, rendering them unconscious and pain-free throughout the procedure.

Access to the Aneurysm: A neurosurgeon typically performs the surgery. They make an incision in the scalp to create a small opening in the skull, called a craniotomy, to access the brain and the aneurysm.

Clipping the Aneurysm: Once access is achieved, the surgeon carefully locates the aneurysm. A tiny metal clip is placed across the base of the aneurysm, effectively sealing it off from the surrounding blood vessels. This prevents blood from flowing into the aneurysm, reducing the risk of rupture.

Closure: After successfully clipping the aneurysm, the surgeon closes the incision in the scalp and may use surgical materials such as sutures, screws, or plates to secure the bone flap in place. The wound is then closed with stitches or staples.

Recovery: The patient is closely monitored in the intensive care unit (ICU) for a period to ensure stable vital signs and neurological function. Recovery times vary but can be several days to weeks depending on the complexity of the surgery and the patient’s overall health.

Intracranial aneurysm clipping is a highly effective treatment for preventing aneurysm rupture. However, it is a complex procedure with potential risks, including infection, bleeding, and damage to nearby structures in the brain. The choice of treatment, whether clipping or endovascular coiling (a less invasive procedure), depends on the specific characteristics of the aneurysm and the patient’s overall health.


Evolution in the surgical treatment of intracranial aneurysms is driven by the need to refine and innovate. From an early application of the Hunterian carotid ligation to modern-day sophisticated aneurysm clip designs, progress was made through dedication and technical maturation of the cerebrovascular neurosurgeons to overcome challenges in their practices. The global expansion of endovascular services has challenged the existence of aneurysm surgery, changing the complexity of aneurysm case mix and volume that are presently referred for surgical repair. Concepts of how to best treat intracranial aneurysms have evolved over generations, and will continue to do so with further technological innovations. As with the evolution of any type of surgery, innovations frequently arise from the criticism of currently available techniques 1).


Intracranial aneurysm surgery by clipping requires meticulous technique and is usually performed through open approaches. Endoscopic endonasal clipping of intracranial aneurysms may use the same techniques through an alternative corridor.

Clipping is an important technique for intracranial aneurysm surgery. Although clip mechanisms and features have been refined, little attention has been paid to clip appliers. Clip closure is traditionally achieved by opening the grip of the clip applier. Sato et al.. reconsidered this motion and identified an important drawback, namely that the standard applier holding power decreased at the moment of clip release, which could lead to unstable clip application develop a forceps to address this clip applier design flaw.The new clip applier has a non–cross-type fulcrum that is closed at the time of clip release, with an action similar to that of a bipolar forceps or scissors. Thus, a surgeon can steadily apply the clip from various angles. They successfully used the clip applier to treat 103 aneurysms. Although training was required to ensure smooth applier use, no difficulties associated with applier use were noted. This clip applier can improve clipping surgery safety because it offers additional stability during clip release. 2).

see Surgical clipping versus endovascular coiling for intracranial aneurysm.


Intracranial Aneurysm treatment with surgery remains the recommended form of treatment in high-grade SAH patients with intracerebral space occupying hematomas, where the surgical decompression of the mass effect may be warranted, and along with it the clipping of the bleeding aneurysm.

In the US, a number of training programs include endovascular exposure to residents during their training, assuming the endovascular suite as a regular OR room.

The training of surgeons in both techniques seems promising and the right way to go, regardless of whether a dually trained neurosurgeon will end up opting for the use of one technique over the other. The important is that we guarantee the ability to deliver our patients the best possible care by providing them with a choice that is not born out of a turf war but based on evidence both on a general, but similarly important, local one 3).

Three-dimensional printing in vascular neurosurgery is trending and is useful for the visualization of intracranial aneurysms for both neurosurgeons and trainees. The 3D models gives the surgeon time to practice beforehand and plan the surgery accordingly. The aim of the study of Ozgıray et al. was to examine the effect of preoperative planning with 3D printing models of aneurysms in terms of surgical time and patient outcomes.

Forty patients were prospectively enrolled in this study and divided into two groups: Groups I and II. In group I, only the angiograms were studied before surgery. Solid 3D modeling was performed only for group II before the operation and was studied accordingly. All surgeries were performed by the same senior vascular neurosurgeon. Demographic data, surgical data, both preoperative and postoperative modified Rankin Scale scores (mRS), and Glasgow Outcome Scores (GOS) were evaluated.

The average time of surgery was shorter in Group II, and the difference was statistically significant between the two groups (p < 0.001). However, no major differences were found for the GOS, hospitalization time, or mRS.

This study is the first prospective study of the utility of 3D aneurysm models. They show that 3D models are useful in surgery preparation. In the near future, these models will be used widely to educate trainees and pre-plan surgical options for senior surgeons 4).

The guidelines relevant to the anesthesiologists in the day-to-day perioperative management of patients with ruptured intracranial aneurysm given by various societies are:

Diringer MN, Bleck TP, Claude Hemphill J, 3rd, Menon D, Shutter L, Vespa P, et al. Critical care management of patients following aneurysmal subarachnoid hemorrhage: Recommendations from the Neurocritical Care Society’s Multidisciplinary Consensus Conference. Neurocrit Care. 2011;15:211–40.

Bederson JB, Connolly ES, Jr, Batjer HH, Dacey RG, Dion JE, Diringer MN, et al. Guidelines for the management of aneurysmal subarachnoid hemorrhage: A statement for healthcare professionals from a special writing group of the Stroke Council, American Heart Association. Stroke. 2009;40:994–1025.

Steiner T, Juvela S, Unterberg A, Jung C, Forsting M, Rinkel G, et al. European Stroke Organization guidelines for the management of intracranial aneurysms and subarachnoid haemorrhage. Cerebrovasc Dis. 2013;35:93–112.


Both intravenous and inhalational anesthetic technique may be used for maintenance keeping in mind the objectives of stable intraoperative hemodynamics, early smooth recovery and effect on special monitoring techniques. Cerebral perfusion increases with isoflurane when compared with propofol without increase in ICP in aSAH.

Hypocapnia is not essential in good grade patients as it can reduce ICP and increase transmural pressure within aneurysmal sac predisposing it to rupture. In poor grade patients, hyperventilation however is beneficial to reduce ICP and provide lax brain.

Brain laxity is crucial to obtain good surgical access to the aneurysm without causing IOAR or compromising underlying brain from excessive retractor pressure. This is important as early surgery risks a tense/full brain and dissection without adequate exposure can result in IOAR. Both 20% mannitol and 3% hypertonic saline are suitable osmotic agents for intraoperative brain relaxation in the dose of 2-4 ml/kg. Head end elevation, avoiding jugular venous compression, avoiding high concentration of inhalational agents and nitrous-oxide and mild hyperventilation are other measures to achieve a lax brain. If full brain persists, additional measures like moderate hyperventilation, switching to intravenous anesthetic maintenance and release of cerebrospinal fluid might be helpful. 5).

Pterional approach via standard frontotemporal craniotomy and interhemispheric approach via bifrontal craniotomy is the gold standard for clipping of cerebral aneurysms in the anterior circulationEndovascular treatment is now widely used, but subsets of aneurysms are still indicated for surgical clipping. Modern technological advances allow less invasive clipping techniques such as the keyhole approach. Mori and Watanabe discussed the surgical indications, preoperative simulation, surgical techniques, and pros and cons of keyhole (supraorbital) clipping. Selection of standard craniotomy or keyhole craniotomy should be uncontroversial, but keyhole clipping requires definite surgical indications based on the characteristics of the target aneurysm for safe clipping 6).

To enhance visual confirmation of regional anatomy, endoscopy was introduced.

see Endoscopic endonasal approach for intracranial aneurysm

A challenge is to ensure noninclusion of normal vessel/perforators within the clip and perform complete aneurysmal isolation. This is done with either intraoperative microvascular Doppler sonography (IMD) or Indocyanine green videoangiography (ICG-VA) as they are simple and safe. Anesthesiologists administer ICG and also help perform IMD. ICG-VA appropriately assessed vessel patency and aneurysm obliteration in 93.5% of 109 aneurysms clipped 7) However, ICG can cause transient oxygen desaturation 8). IMD use confirms aneurysm isolation and patency of parent vessel and branching arteries. Hui et al. observed that clip repositioning was required based on IMD findings in 24% of aneurysms clipped in 91 patients and concluded that IMD could reduce the rate of residual aneurysm and unanticipated vessel stenosis 9).

The complete clipping of a cerebral aneurysm usually warrants its sustained occlusion, while clip remnants may have far-reaching consequences. The aim of this study is to identify the risk factors for clip remnants requiring retreatment and/or exhibiting growth. METHODS All consecutive patients with primary aneurysm clipping performed at University Hospital of Essen between January 1, 2003, and December 31, 2013, were eligible for this study. Aneurysm occlusion was judged on obligatory postoperative digital subtraction angiography and the need for repeated vascular control. The identified clip remnants were correlated with various demographic and clinical characteristics of the patients, aneurysm features, and surgery-related aspects. RESULTS Of 616 primarily clipped aneurysms, postoperative angiography revealed 112 aneurysms (18%) with clip remnants requiring further control (n = 91) or direct retreatment (n = 21). Seven remnants exhibited growth during follow-up, whereas 2 cases were associated with aneurysmal bleeding. Therefore, a total of 28 aneurysms (4.5%) were retreated as clip remnants (range 1 day to 67 months after clipping). In the multivariate analysis, the need for retreatment of clip remnant was correlated with the aneurysm’s initial size (> 12 mm; OR 3.22; p = 0.035) and location (anterior cerebral artery > internal carotid artery > posterior circulation > middle cerebral artery; OR 1.85; p = 0.003). Younger age with a cutoff at 45 years (OR 33.31; p = 0.004) was the only independent predictor for remnant growth. CONCLUSIONS The size and location of the aneurysm are the main risk factors for clip remnants requiring retreatment. Because of the risk for growth, younger individuals (< 45 years old) with clip remnants require a long-term (> 5 years) vascular follow-up. Clinical trial registration no: DRKS00008749 (Deutsches Register Klinischer Studien) 10).

Total index hospitalization costs for clipping are lower than for coiling. Costs of clipping and coiling are driven by different clinical variables. The cost of coils and devices is the predominant contributor to the higher total costs of coiling 11).


1)

Lai LT, O’Neill AH. History, Evolution and Continuing Innovations of Intracranial Aneurysm Surgery. World Neurosurg. 2017 Feb 9. pii: S1878-8750(17)30166-3. doi: 10.1016/j.wneu.2017.02.006. [Epub ahead of print] Review. PubMed PMID: 28189863.
2)

Sato A, Koyama JI, Hanaoka Y, Hongo K. A Reverse-Action Clip Applier for Aneurysm Surgery. Neurosurgery. 2015 Mar 12. [Epub ahead of print] PubMed PMID: 25774701.
3)

Santiago BM, Cunha E Sá M. How do we maintain competence in aneurysm surgery. Acta Neurochir (Wien). 2015 Jan;157(1):9-11. doi: 10.1007/s00701-014-2265-8. Epub 2014 Nov 14. PubMed PMID: 25391972.
4)

Ozgıray E, Husemoglu B, Cınar C, Bolat E, Akınturk N, Bıceroglu H, Kızmazoglu C. The Effect of Preoperative Three Dimensional Modeling and Simulation on Outcome of Intracranial Aneursym Surgery. J Korean Neurosurg Soc. 2023 Sep 15. doi: 10.3340/jkns.2023.0035. Epub ahead of print. PMID: 37709549.
5)

Sriganesh K, Venkataramaiah S. Concerns and challenges during anesthetic management of aneurysmal subarachnoid hemorrhage. Saudi J Anaesth. 2015 Jul-Sep;9(3):306-13. doi: 10.4103/1658-354X.154733. Review. PubMed PMID: 26240552; PubMed Central PMCID: PMC4478826.
6)

Mori K, Watanabe S. Keyhole Approach in Cerebral Aneurysm Surgeries. Adv Tech Stand Neurosurg. 2022;44:265-275. doi: 10.1007/978-3-030-87649-4_15. PMID: 35107685.
7)

Özgiray E, Aktüre E, Patel N, Baggott C, Bozkurt M, Niemann D, et al. How reliable and accurate is indocyanine green video angiography in the evaluation of aneurysm obliteration? Clin Neurol Neurosurg. 2013;115:870–8.
8)

Sriganesh K, Vinay B, Bhadrinarayan V. Indocyanine green dye administration can cause oxygen desaturation. J Clin Monit Comput. 2013;27:371.
9)

Hui PJ, Yan YH, Zhang SM, Wang Z, Yu ZQ, Zhou YX, et al. Intraoperative microvascular Doppler monitoring in intracranial aneurysm surgery. Chin Med J (Engl) 2013;126:2424–9.
10)

Jabbarli R, Pierscianek D, Wrede K, Dammann P, Schlamann M, Forsting M, Müller O, Sure U. Aneurysm remnant after clipping: the risks and consequences. J Neurosurg. 2016 Feb 12:1-7. [Epub ahead of print] PubMed PMID: 26871206.
11)

Duan Y, Blackham K, Nelson J, Selman W, Bambakidis N. Analysis of short-term total hospital costs and current primary cost drivers of coiling versus clipping for unruptured intracranial aneurysms. J Neurointerv Surg. 2014 Jun 2. pii: neurintsurg-2014-011249. doi: 10.1136/neurintsurg-2014-011249. [Epub ahead of print] PubMed PMID: 24891453.
  1. What is the primary purpose of intracranial aneurysm clipping? a) To reduce blood pressure b) To remove the aneurysm entirely c) To prevent the aneurysm from rupturing by sealing it off d) To increase blood flow to the aneurysm
  2. What is the first step in the intracranial aneurysm clipping procedure? a) Clipping the aneurysm b) Closing the incision c) Anesthesia d) Accessing the aneurysm
  3. Which type of anesthesia is typically used during intracranial aneurysm clipping? a) Local anesthesia b) Regional anesthesia c) General anesthesia d) Spinal anesthesia
  4. What is the purpose of a craniotomy in intracranial aneurysm clipping? a) To access the brain and the aneurysm b) To close the incision in the scalp c) To perform angiography d) To remove the aneurysm
  5. How is the aneurysm sealed off during clipping? a) By removing the aneurysm entirely b) By injecting a special sealing material c) By placing a tiny metal clip across its base d) By cauterizing it with heat
  6. After successfully clipping the aneurysm, what is the next step in the procedure? a) Performing additional imaging studies b) Closing the incision in the scalp c) Administering postoperative antibiotics d) Checking the patient’s blood pressure
  7. What is one potential risk associated with intracranial aneurysm clipping? a) Loss of vision b) Heart attack c) Joint pain d) Infection
  8. Which factor determines whether intracranial aneurysm clipping or endovascular coiling is the preferred treatment? a) The patient’s preference b) The surgeon’s preference c) The characteristics of the aneurysm and the patient’s overall health d) The availability of equipment
  9. How has technology impacted the surgical treatment of intracranial aneurysms? a) It has made clipping obsolete b) It has made clipping the only available treatment option c) It has led to the development of more advanced clip designs d) It has eliminated the need for preoperative evaluation
  10. What is the role of three-dimensional printing in vascular neurosurgery? a) To create models of the surgical team b) To visualize intracranial aneurysms for surgical planning c) To replace the need for anesthesia d) To monitor patient vital signs during surgery

Answers:

  1. c) To prevent the aneurysm from rupturing by sealing it off from normal blood circulation.
  2. c) Anesthesia
  3. c) General anesthesia
  4. a) To access the brain and the aneurysm
  5. c) By placing a tiny metal clip across its base
  6. b) Closing the incision in the scalp
  7. d) Infection
  8. c) The characteristics of the aneurysm and the patient’s overall health
  9. c) It has led to the development of more advanced clip designs
  10. b) To visualize intracranial aneurysms for surgical planning

Test your knowledge about external lumbar cerebrospinal fluid drainage for cerebral vasospasm prevention


What is the primary purpose of external lumbar CSF drainage in the context of cerebral vasospasm prevention?
a) To directly remove blood from the brain's blood vessels.
b) To increase intracranial pressure.
c) To monitor CSF characteristics.
d) To administer calcium channel blockers.

Why is lowering intracranial pressure through CSF drainage beneficial in preventing cerebral vasospasm?
a) It reduces the risk of infection.
b) It prevents CSF leakage.
c) It decreases pressure on blood vessels in the brain.
d) It increases blood flow to the brain.

In addition to pressure reduction, what other information can be obtained from CSF analysis during lumbar drainage?
a) Hemoglobin levels.
b) Platelet count.
c) Red blood cell count and protein concentration.
d) Electrolyte levels.

How might external lumbar CSF drainage be used to administer medications in the context of cerebral vasospasm prevention?
a) Medications cannot be administered through CSF drainage.
b) Medications are injected directly into blood vessels.
c) Medications are infused into the CSF through the drainage system.
d) Medications are administered orally.

What is therapeutic volume expansion in the context of external lumbar CSF drainage?
a) The removal of CSF without replacement.
b) The replacement of CSF with blood.
c) The simultaneous removal of CSF and replacement with other fluids.
d) The use of external lumbar CSF drainage for diagnostic purposes only.

What are some potential risks associated with external lumbar CSF drainage?
a) Heart attack and stroke.
b) Infection, bleeding, and CSF leak.
c) Allergic reactions to medications.
d) Loss of consciousness.

What did the LUMAS trial find regarding the benefit of lumbar drainage in preventing cerebral vasospasm?
a) It confirmed the significant benefit of lumbar drainage.
b) It found no benefit of lumbar drainage.
c) It suggested that lumbar drainage might be beneficial in certain cases.
d) It recruited severely affected patients only.

What was the primary outcome measure in the EARLYDRAIN trial, and what did it find?
a) The primary outcome was CSF pressure reduction, which was not achieved.
b) The primary outcome was angiographic vasospasm, which was reduced.
c) The primary outcome was the modified Rankin Scale (mRS) score at 6 months, which showed improved outcomes with lumbar drainage.
d) The primary outcome was shunt-dependent hydrocephalus (SDHC) prevention, which was not affected by lumbar drainage.

According to the meta-analysis, which type of drainage (lumbar drainage or external ventricular drainage) had a better outcome in aneurysmal SAH patients?
a) Both had similar outcomes.
b) Lumbar drainage had a better outcome.
c) External ventricular drainage had a better outcome.
d) The meta-analysis did not provide a conclusion regarding outcomes.

What is the overall conclusion regarding the effectiveness of continuous CSF drainage for aneurysmal SAH patients, according to the meta-analysis?
a) Continuous CSF drainage is not effective in preventing vasospasm.
b) Lumbar drainage is the most effective method for preventing vasospasm.
c) Continuous CSF drainage is an effective treatment for aneurysmal SAH patients.
d) Further research is needed to determine the effectiveness of continuous CSF drainage.

Answers

Intracranial Aneurysm treatment

Intracranial Aneurysm treatment

Volovici et al. reviewed and analyzed studies investigating devices and procedures used in intracranial aneurysm (IA) treatment for methods and completeness of reporting and to compare the results of studies with positive, uncertain, and negative conclusions.

EmbaseMEDLINEWeb of Science, and The Cochrane Central Register of Clinical Trials were searched for studies on IA treatment published between January 1, 1995, and October 1, 2022. Grey literature was retrieved from Google Scholar.

All studies making any kind of claims of safety, effectiveness, or durability in the field of IA treatment were included.

Data extraction and synthesis: Using a predefined data dictionary and analysis plan, variables ranging from patient and aneurysm characteristics to the results of treatment were extracted, as were details pertaining to study methods and completeness of reporting. Extraction was performed by 10 independent reviewers. A blinded academic neuro-linguist without involvement in IA research evaluated the conclusion of each study as either positive, uncertain, or negative. The study followed Preferring Reporting Items for Systematic Reviews and Meta-Analyses guidelines.

Main outcomes and measures: The incidence of domain-specific outcomes between studies with positive, uncertain, or hostile conclusions regarding safety, effectiveness, or durability were compared. The number of studies that provided a definition of safety, effectiveness, or durability and the incidence of incomplete reporting of domain-specific outcomes were evaluated.

Overall, 12 954 studies were screened, and 1356 studies were included, comprising a total of 410 993 treated patients. There was no difference in the proportion of patients with poor outcomes or in-hospital mortality between studies claiming a technique was safe, uncertain, or not safe. Similarly, there was no difference in the proportion of IAs completely occluded at the last follow-up between studies claiming a technique was effective, uncertain, or ineffective. Less than 2% of studies provided any definition of safety, effectiveness, or durability, and only 1 of the 1356 studies provided a threshold under which the technique would be considered unsafe. Incomplete reporting was found in 546 reports (40%).

Conclusions and Relevance: In this systematic review and meta-analysis of IA treatment literature, studies claiming safety, effectiveness, or durability of IA treatment had methodological flaws and incomplete reporting of relevant outcomes supporting these claims 1).


see Ruptured intracranial aneurysm treatment.


The treatment of intracranial aneurysm aims for the complete elimination of the aneurysm from the circulation with neuroendovascular treatment or surgery.

The efficacy of intracranial aneurysm treatment (long-term success or effectiveness of the treatment) is measured by evidence of the aneurysm obliteration (failure to be demonstrated by conventional or noninvasive angiography), without evidence of aneurysm recanalization (any blood flow into the aneurysm) or aneurysm recurrence (reappearance).


Intracranial Aneurysms (IA) can be treated with microsurgery or by endovascular treatments (EVT). EVT has taken an increasingly important part in IA management; the ability of neurosurgical teams to perform such surgery as well as the quality of their training is being questioned.

The decision-making process and patient selection for ruptured aneurysms treatment has evolved more as an art than as a science, which is a consequence of the collaborative efforts occurring between all subspecialties involved, the availability of both techniques on a 24–48-h window of treatment, the anatomical factors of the aneurysm neck and sac, as well as local expertise and morbidity factors involved with both options of treatment.

Management of these patients depends upon a number of factors including aneurysmal, patient, institutional, and operator factors. The ultimate goal of treating patients with IAs is complete and permanent occlusion of the aneurysm sac in order to eliminate future hemorrhagic risk, while preserving or restoring the patient’s neurological function. The most common treatment approaches include microsurgical clipping and endovascular coiling, and multiple studies have compared these two techniques. To date, three large prospective, randomized studies have been done: a study from Finland, International Subarachnoid Aneurysm Trial (ISAT), and the Barrow Ruptured Aneurysm Trial (BRAT). Despite differences in methodology, the results were similar: in patients undergoing coiling, although rates of rebleeding and retreatment are higher, the overall rate of poor outcomes at 12 months was significantly lower. As minimally invasive procedures and devices continue to be refined, endovascular strategies are likely to increase in popularity. However, as long-term outcome studies become available, it is increasingly apparent that they are complementary treatment strategies, with patient selection of critical importance 2).

Although each of these trials was not methodologically flawless, the combined results from all three suggest that endovascular treatment of ruptured aneurysms suitable for this treatment strategy results in quicker recovery and better functional outcomes at one year at the expenses of lower rates of complete aneurysm obliteration frequently requiring retreatment 3).

The treatment of intracranial aneurysms is best performed at high volume centers that utilize a multidisciplinary, team-based approach 4).

In a trained team, the multidisciplinary approach appears to be a valuable strategy in the management of intracranial aneurysms, to achieve good functional outcomes 5).

Given the similar clinical results of both modalities, the patient should be advised on the necessity of repeated follow-ups and of possible technical failure and eventually repeated procedure which is more likely if an endovascular procedure is chosen 6).

European Stroke Organization Guidelines for the Management of Intracranial Aneurysms and Subarachnoid Haemorrhage – February 2013

http://www.karger.com/Article/FullText/346087


1)

Volovici V, Verploegh IS, Satoer D, Vrancken Peeters NJMC, Sadigh Y, Vergouwen MDI, Schouten JW, Bruggeman G, Pisica D, Yildirim G, Cozar A, Muller F, Zidaru AM, Gori K, Tzourmpaki N, Schnell E, Thioub M, Kicielinski K, van Doormaal PJ, Velinov N, Boutarbouch M, Lawton MT, Lanzino G, Amin-Hanjani S, Dammers R, Meling TR. Outcomes Associated With Intracranial Aneurysm Treatments Reported as Safe, Effective, or Durable: A Systematic Review and Meta-Analysis. JAMA Netw Open. 2023 Sep 5;6(9):e2331798. doi: 10.1001/jamanetworkopen.2023.31798. PMID: 37656458.
2)

Liu A, Huang J. Treatment of Intracranial Aneurysms: Clipping Versus Coiling. Curr Cardiol Rep. 2015 Sep;17(9):628. doi: 10.1007/s11886-015-0628-2. PubMed PMID: 26238743.
3)

Sorenson T, Lanzino G. Trials and tribulations: an evidence-based approach to aneurysm treatment. J Neurosurg Sci. 2015 Oct 16. [Epub ahead of print] PubMed PMID: 26474147.
4)

Shivashankar R, Miller TR, Jindal G, Simard JM, Aldrich EF, Gandhi D. Treatment of cerebraPIIneurysms-surgical clipping or endovascular coiling: the guiding principles. Semin Neurol. 2013 Nov;33(5):476-87. doi: 10.1055/s-0033-1364217. Epub 2014 Feb 6. PubMed PMID: 24504611.
5)

Aboukais R, Zairi F, Thines L, Aguettaz P, Leclerc X, Lejeune JP. Multidisciplinary management of intracranial aneurysms: The experience of Lille university hospital center. Neurochirurgie. 2014 Sep 19. pii: S0028-3770(14)00121-0. doi: 10.1016/j.neuchi.2014.06.010. [Epub ahead of print] PubMed PMID: 25245925.
6)

Beneš V, Štekláčová A, Bradáč O. Repeated Aneurysm Intervention. Adv Tech Stand Neurosurg. 2022;44:277-296. doi: 10.1007/978-3-030-87649-4_16. PMID: 35107686.

Carotid artery stenting (CAS)

Carotid artery stenting (CAS)



Common carotid artery stenting is a medical procedure performed to treat carotid artery stenosis, which is the narrowing of the carotid arteries that supply blood to the brain. It is a less invasive alternative to carotid endarterectomy, a surgical procedure used for the same purpose.

During common carotid artery stenting, a thin, flexible tube called a catheter is inserted into an artery, usually in the groin, and guided up to the site of the carotid artery stenosis. Using X-ray guidance, the catheter is advanced to the affected area. Once in position, a small, expandable mesh tube called a stent is placed at the site of the stenosis. The stent is then expanded, pushing against the walls of the artery, and helps to keep the artery open.

The stent acts as a scaffold, improving blood flow through the carotid artery and reducing the risk of stroke. Some stents are designed with a filter or a protective device to capture any debris that may break loose during the procedure, preventing it from reaching the brain.

Common carotid artery stenting is typically performed under local anesthesia, meaning the patient is awake but the area being treated is numbed. It is often considered for patients who are at high risk for complications from carotid endarterectomy, such as those with previous neck surgery, radiation therapy, or significant medical comorbidities.

Like any medical procedure, common carotid artery stenting carries some risks, including the potential for blood vessel injury, stroke, infection, or allergic reactions to contrast dye used during the procedure. However, it is generally considered safe and effective when performed by experienced medical professionals.

Carotid artery stenting is indicated for the treatment of carotid artery stenosis, which is the narrowing of the carotid arteries that supply blood to the brain. The procedure may be recommended in certain situations, depending on the severity of the stenosis and the patient’s overall health. The main indications for carotid artery stenting include:

Symptomatic Carotid Artery Stenosis: Carotid artery stenting is commonly recommended for patients who have experienced symptoms related to carotid artery stenosis, such as a transient ischemic attack (TIA) or a minor stroke. These symptoms may include temporary vision loss, weakness or numbness on one side of the body, difficulty speaking, or dizziness. In such cases, carotid artery stenting aims to reduce the risk of future stroke by improving blood flow through the carotid arteries.

Asymptomatic Carotid Artery Stenosis: Carotid artery stenting may also be considered in certain cases of asymptomatic carotid artery stenosis, particularly when the stenosis is severe (greater than 70% narrowing). The decision to proceed with stenting in asymptomatic cases is often based on factors such as the patient’s age, overall health, life expectancy, and the presence of other risk factors for stroke.

High-Risk Candidates for Carotid Endarterectomy (CEA): Carotid artery stenting is sometimes recommended for patients who are at high risk for complications from carotid endarterectomy, which is a surgical procedure used to treat carotid artery stenosis. High-risk factors may include previous neck surgery, radiation therapy to the neck, severe heart or lung disease, or advanced age. Carotid artery stenting is considered a less invasive alternative for these patients.

It is important to note that the decision to undergo carotid artery stenting should be made on an individual basis, taking into consideration the patient’s specific medical condition, overall health, and the expertise of the healthcare team. A thorough evaluation by a vascular specialist or a neurologist is typically conducted to determine the most appropriate treatment approach for each patient.


Carotid artery angioplasty and stenting (CAS) has experienced an astonishing rate of development, becoming a viable alternative to carotid endarterectomy (CEA) in the management of carotid artery stenosis. Many trials have attempted to compare both treatment modalities and establish indications for each, depending on clinical and anatomic features.

Eller et al. review the historical evolution of carotid stenting; its main technical aspects, indications, and contraindications; as well as the most important clinical trials comparing CAS and CEA 1).

Primary carotid stenting, performed using self-expanding stents alone without deliberate use of embolic protection devices and balloon angioplasty, has been shown to be effective and faster, cheaper, and potentially safer than conventional techniques.

see also Bilateral carotid artery stenting.

Carotid artery stenting (CAS) is a neuroendovascular treatment where a stent is deployed within the lumen of the carotid artery to prevent a stroke by treating carotid artery stenosis.

It has emerged as an alternative to carotid endarterectomy. In randomised trials comparing stenting with endarterectomy for symptomatic carotid artery stenosis, stenting was associated with a higher risk of procedure-related stroke, particularly in elderly patients, but with lower risks of myocardial infarction, cranial nerve palsy, and access site haematoma 2) 3) 4) 5).

A systematic review showed that the increase in procedure-related risk was driven by non-disabling stroke, with no evidence for a difference in rates of major or disabling stroke or death between the treatments 6).

A study investigated the effect of residual stenosis after carotid artery stenting (CAS) on periprocedural and long-term outcomes.

Patients treated with CAS for symptomatic or asymptomatic carotid arterial stenosis were consecutively enrolled. Residual stenosis was estimated from post-procedure angiography findings. The effects of residual stenosis on 30-day periprocedural outcome and times to restenosis and clinical outcome were analyzed using logistic regression models and Wei-Lin-Weissfeld models, respectively.

A total of 412 patients (age, 64.7 ± 17.0 years; male, 82.0%) were enrolled. The median baseline stenosis was 80% (interquartile range [IQR], 70-90%), which improved to 10% (0-30%) for residual stenosis. Residual stenosis was significantly associated with periprocedural outcome (adjusted odds ratio, 0.983; 95% confidence interval [CI], 0.965-0.999, P = 0.01) after adjustment for baseline stenosis, age, hypertension, symptomaticity, and statin use. Over the 5-year observation period, residual stenosis did not increase the global hazard for restenosis and clinical outcome (adjusted hazard ratio, 1.011; 95% CI, 0.997-1.025. In the event-specific model, residual stenosis increased the hazard for restenosis (adjusted hazard ratio, 1.041; 1.012-1.072) but not for clinical outcome (adjusted hazard ratio, 1.011; 0.997-1.025).

Residual stenosis after carotid artery stenting may be useful to predict periprocedural outcome and restenosis 7).

Endovascular revascularization of a stenotic lesion requires appropriate stent positioning. In particular, stenting of the common carotid artery (CCA) ostium makes it difficult to avoid proptosis into the aorta. Furthermore, the guiding catheter may become unstable during the stenting because of its position under the aortic arch. To resolve these problems, Terakado et al. performed antegrade stenting for a patient with a symptomatic stenotic left CCA ostium that was treated by lifting a balloon-guiding catheter with a gooseneck snare. A patient was a 74-year-old man who presented to the hospital with main complaints of right hemiparesis and motor aphasia. A left cerebral infarction due to severe stenotic left CCA ostium was diagnosed. A CT perfusion study showed decreased cerebral blood flow in the left hemisphere. Stenting of the stenotic left CCA ostium was performed using an antegrade approach. A balloon-guiding catheter positioned under the aortic arch was inflated and lifted from the right brachiocephalic artery using a gooseneck snare. The guiding catheter was stabilized during stenting. This method is highly effective for stenting CCA ostium 8)


A 68-year-old man was admitted. Neurological examination revealed severe left-sided motor weakness. Magnetic resonance imaging showed no cerebral infarction, but magnetic resonance angiography revealed complete occlusion of the right internal carotid artery. Systemic intravenous injection of recombinant tissue plasminogen activator was performed within 4h after the onset. But, magnetic resonance angiography still revealed complete occlusion. Revascularization of the right cervical internal carotid artery was performed via endovascular surgery. The occluded artery was successfully recanalized using the Penumbra System® and stent placement at the origin of the internal carotid artery. Immediately after surgery, dual antiplatelet therapy (aspirin and clopidogrel) was initiated, and then cilostazol was added on the following day. Carotid ultrasonography and three-dimensional computed tomographic angiography at 14days revealed no further obstruction to flow.

When trying to perform emergency carotid artery stenting within 24h after intravenous recombinant tissue plasminogen activator administration, several issues require attention, such as the decisions regarding the type of stent and embolic protection device, the selection of antiplatelet therapy and the methods of preventing hyperperfusion syndrome.

Emergency carotid artery stenting for the acute internal carotid artery occlusion may be considered a safe procedure in preventing early stroke recurrence in selected patients 9).


1)

Eller JL, Snyder KV, Siddiqui AH, Levy EI, Hopkins LN. Endovascular treatment of carotid stenosis. Neurosurg Clin N Am. 2014 Jul;25(3):565-82. doi: 10.1016/j.nec.2014.04.012. Epub 2014 Jun 2. PubMed PMID: 24994091.
2)

Mas JL, Chatellier G, Beyssen B, et al. Endarterectomy versus stenting in patients with symptomatic severe carotid stenosis. N Engl J Med 2006; 355: 1660–71.
3)

The SPACE Collaborative Group. 30 day results from the SPACE trial of stent-protected angioplasty versus carotid endarterectomy in symptomatic patients: a randomised non-inferiority trial. Lancet 2006; 368: 1239–47.
4)

International Carotid Stenting Study investigators. Carotid artery stenting compared with endarterectomy in patients with symptomatic carotid stenosis (International Carotid Stenting Study): an interim analysis of a randomised controlled trial. Lancet 2010; 375: 985–97.
5)

Brott TG, Hobson RW, Howard G, et al. Stenting versus endarterectomy for treatment of carotid-artery stenosis. N Engl J Med 2010; 363: 11–23.
6)

Bonati LH, Lyrer P, Ederle J, Featherstone R, Brown MM. Percutaneous transluminal balloon angioplasty and stenting for carotid artery stenosis. Cochrane Database Syst Rev 2012; 9: CD000515.
7)

Kang J, Hong JH, Kim BJ, Bae HJ, Kwon OK, Oh CW, Jung C, Lee JS, Han MK. Residual stenosis after carotid artery stenting: Effect on periprocedural and long-term outcomes. PLoS One. 2019 Sep 9;14(9):e0216592. doi: 10.1371/journal.pone.0216592. eCollection 2019. PubMed PMID: 31498785.
8)

Terakado T, Matumaru Y, Ishikawa E. Stenting of the Common Carotid Artery Ostium: Balloon Catheter Lifting-Up Technique With a Gooseneck Snare. Vasc Endovascular Surg. 2023 May 22:15385744231178179. doi: 10.1177/15385744231178179. Epub ahead of print. PMID: 37212169.
9)

Inoue A, Kohno K, Fukumoto S, Ozaki S, Ninomiya S, Tomita H, Kamogawa K, Okamoto K, Ichikawa H, Onoue S, Miyazaki H, Okuda B, Iwata S. Importance of perioperative management for emergency carotid artery stenting within 24h after intravenous thrombolysis for acute ischemic stroke: Case report. Int J Surg Case Rep. 2016 Jul 27;26:108-112. doi: 10.1016/j.ijscr.2016.07.027. [Epub ahead of print] PubMed PMID: 27478968.

Intracranial hemorrhage from Dengue

Intracranial hemorrhage from Dengue



Dengue fever is a viral infection caused by the dengue virus, which is primarily transmitted by the Aedes mosquito. The virus belongs to the Flaviviridae family and has four different serotypes: DEN-1, DEN-2, DEN-3, and DEN-4. Dengue is prevalent in tropical and subtropical regions, particularly in urban and semi-urban areas.



Symptoms of dengue fever typically appear within 4 to 7 days after a person is bitten by an infected mosquito. They can range from mild to severe and may include high fever, severe headache, joint and muscle pain, rash, nausea, vomiting, and in some cases, bleeding manifestations.

Severe forms of dengue, known as dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS), can cause life-threatening complications such as severe bleeding, organ damage, and circulatory failure.


A rare but possibly dangerous consequence of dengue illness is intracranial hemorrhage (ICH). Currently, the pathogenesis of ICH is unknown.

There is no specific antiviral treatment for dengue fever, and management mainly involves supportive care to relieve symptoms and prevent complications. Rest, hydration, and over-the-counter pain relievers such as acetaminophen can help alleviate fever and pain. It is important to avoid medications like aspirin, ibuprofen, and naproxen, as they can increase the risk of bleeding.

Studies have reported the use of emergency surgery while monitoring thrombocytopenia in the therapy of dengue ICH 1).

Prevention is crucial in controlling the spread of dengue. Measures include eliminating mosquito breeding sites by emptying standing water containers, using insect repellents, wearing protective clothing, and using mosquito nets or screens. In some high-risk areas, mosquito control programs may be implemented to reduce the mosquito population.

If you suspect you have dengue fever or are in an area with a dengue outbreak, it is advisable to seek medical attention for diagnosis and appropriate management.


Bangladesh reported the highest number of annual deaths (n = 281) related to dengue virus infection in 2022 since the virus reappeared in the country in 2000. Earlier studies showed that >92% of the annual cases occurred between the months of August and September. The 2022 outbreak is characterized by late onset of dengue cases with unusually higher deaths in colder months, that is, October-December. Haider et al. present possible hypotheses and explanations for this late resurgence of dengue cases. First, in 2022, the rainfall started late in the season. Compared to the monthly average rainfall for September and October between 2003 and 2021, there was 137 mm of additional monthly rainfall recorded in September and October 2022. Furthermore, the year 2022 was relatively warmer with a 0.71°C increased temperature than the mean annual temperature of the past 20 yr. Second, a new dengue virus serotype, DENV-4, had recently reintroduced/reappeared in 2022 and become the dominant serotype in the country for a large naïve population. Third, the post-pandemic return of normalcy after 2 yr of nonpharmaceutical social measures facilitates extra mosquito breeding habitats, especially in construction sites. Community engagement and regular monitoring and destruction of Aedes mosquitoes’ habitats should be prioritized to control dengue virus outbreaks in Bangladesh 2).

A 65-year-old man who presented with dengue fever symptoms and developed altered consciousness and focal neurological deficits. The findings of the tests showed thrombocytopenia, increased AST and ALT, positive anti-dengue IgG, and subdural hematoma on brain imaging. The urgent operations were completed satisfactorily.

Dengue-related intracerebral haemorrhage is still a complicated condition. Thrombocytopenia and leukopenia are the first symptoms that point to dengue. Some risk factors, such as thrombocytopenia and increased AST and ALT, have been identified as bleeding factors in dengue fever. For a possible intracerebral haemorrhage, radiological imaging should be performed. In an emergency neurosurgery setting, thrombocyte administration could be used to monitor thrombocytopenia.

Subdural hematoma is a possible dengue fever complication. If the patient’s symptoms with thrombocytopenia and elevated liver enzymes indicate the possibility of intracranial haemorrhage, immediate radiological imaging should be performed 3)


A 65-year-old male patient was admitted with high-grade febrile illness and diagnosed with dengue. The patient had no focal neurology and was managed adequately following the primary survey on admission but, then, developed severe thrombocytopenia and eventually the critical phase of dengue illness. On the 5th admission day, the patient collapsed. Glasgow Coma Score was 3/15 with bilaterally dilated, fixed pupils. Immediate computed tomography head revealed a large left SDH with a significant midline shift. SDH was emergently evacuated with two units of platelets transfused peroperatively and two additional units postoperatively. Thrombocytopenia resolved within 48 h, and interval scanning showed gradual resolution of SDH. The patient was discharged 18 days later. Five months later, on follow-up, the patient is well with mild left-sided weakness and an Extended Glasgow Outcome Score of 7.

Isolated SDH is a rare but life-threatening hemorrhagic complication of DHF. Even in the critical phase of illness, with severe thrombocytopenia, surgical evacuation should be considered if the SDH is present in isolation, within an accessible area, and can be operated on immediately 4).


A 48-year-old Indian woman presented with fever and body aches followed by acute onset of paraplegia with bladder and bowel dysfunction and loss of sensations below the level of the umbilicus. She had severe thrombocytopenia and positive dengue serology. Magnetic resonance imaging of the spine showed compression of the spinal cord due to intradural hematoma at the D7-D8 vertebral level. The patient received symptomatic treatment for dengue fever and steroids. Emergency D7-D8 laminectomy with excision of the clot and dural repair was done after stabilizing the platelet count with multiple platelet transfusions. The constitutional symptoms responded well to the treatment. There was good improvement in sensory symptoms but negligible improvement in paraplegia with a change in muscle power from grade 0/5 to grade 1/5 in the postoperative period. The patient was discharged from the hospital in a stable condition, but paraplegia showed little improvement during follow-up of 1 year.

Spontaneous spinal cord hemorrhage can present as acute paraplegia in dengue fever. Failure to recognize this complication can delay initiating appropriate treatment with permanent loss of neurologic function 5).


A 18-year-old Pakistani male, presented with fever, colicky abdominal pain, vomiting, diarrhea, dark-colored urine, and oliguria.

Diagnoses: Dengue rapid NS-1 test came back positive. Along with myoglobinuria both serum creatine phosphokinase and creatine levels were abnormal. Hence, the patient was diagnosed with rhabdomyolysis-induced acute kidney injury. On physical examination, his right arm was painful and tender with restricted movement at the elbow. A Doppler ultrasound of the arm revealed thickening of the skin and underlying muscles, as well as edematous abnormalities affecting the entire right upper limb, both of which are indications of compartment syndrome.

Interventions and outcome: The management included rehydration, administration of dextrose and bicarbonate (bicarbonate infusion) prepared by adding 150 mEq sodium bicarbonate in 850 mL dextrose 5%, pain killers, along with platelet, and packed red cell transfusions. Additionally, right upper limb was kept elevated at 90° for 30 minutes every 2 hours to reduce edema and crept bandages were applied. The patient was discharged after 11 days and the follow-up was uneventful.

Lesson: Physicians should be aware that rhabdomyolysis-induced acute kidney damage and limb compartment syndrome are also possible DF consequences, and they should be on the lookout for any indications pointing to these complications in DF. A prompt diagnosis can prevent further complications and fatality 6).


Four patients referred for neurosurgical intervention as sequelae to dengue coagulopathy. Among them, three had intracranial bleeds and one had spinal cord hematoma along with intracranial hemorrhages. This small series includes the youngest reported case of dengue coagulopathy with intracranial bleed and only the second case of spontaneous intraspinal hematoma sequelae to dengue hemorrhagic fever. The situations where patients contract dengue in a setting of neurosurgical intervention are grave. The margin of safety in the presence of dengue coagulopathy is narrow. The surgeon has to outweigh benefit against risk of surgery in each individual. A subdural and intramedullary spinal cord hematoma, which was summarized in the article “Burden of Dengue related neurosurgical emergencies during an epidemic- A tertiary care experience 7)


A report of quadriparesis in dengue fever due to hematomyelia 8).


The first report of intradural spinal hematoma secondary to dengue was reported by Kaur et al 9).


A patient with dengue fever with symptoms suggestive of acute flaccid paralysis, and on subsequent investigation he was diagnosed as a case of hypokalaemic quadriparesis. Clinicians in the endemic area should be aware of such association of acute pure motor reversible quadriparesis with dengue fever 10).


Dengue infection causing acute hypokalemic quadriparesis 11).



1)

Siahaan AMP, Tandean S, Nainggolan BWM, Tarigan J, Sitanggang JS. A Critical Analysis of Intracranial Hemorrhage (ICH) as a Fatal Complication of Dengue Fever. J Korean Neurosurg Soc. 2023 Jan 16. doi: 10.3340/jkns.2022.0205. Epub ahead of print. PMID: 36642946.
2)

Haider N, Hasan MN, Khalil I, Tonge D, Hegde S, Chowdhury MAB, Rahman M, Hossain Khan M, Ansumana R, Zumla A, Uddin MJ. The 2022 dengue outbreak in Bangladesh: hypotheses for the late resurgence of cases and fatalities. J Med Entomol. 2023 May 18:tjad057. doi: 10.1093/jme/tjad057. Epub ahead of print. PMID: 37202843.
3)

Siahaan AMP, Tandean S, Saragih EB, Nainggolan BWM. Spontaneous acute subdural hematoma in dengue fever: Case report and review of the literature. Int J Surg Case Rep. 2022 Sep;98:107512. doi: 10.1016/j.ijscr.2022.107512. Epub 2022 Aug 13. PMID: 35985111; PMCID: PMC9411658.
4)

Ashraf M, Hussain SS, Farooq M, Fatima L, Majeed N, Ashraf N. Isolated subdural hematoma due to dengue hemorrhagic fever: Surgical intervention and review of the literature. Surg Neurol Int. 2022 Jun 10;13:244. doi: 10.25259/SNI_334_2022. PMID: 35855175; PMCID: PMC9282807.
5)

Kaushik RM, Kumar R, Kaushik M, Saini M, Kaushik R. Spontaneous spinal intradural hemorrhage in dengue fever: a case report. J Med Case Rep. 2022 May 30;16(1):213. doi: 10.1186/s13256-022-03451-2. PMID: 35644613; PMCID: PMC9150361.
6)

Arif A, Abdul Razzaque MR, Kogut LM, Tebha SS, Shahid F, Essar MY. Expanded dengue syndrome presented with rhabdomyolysis, compartment syndrome, and acute kidney injury: A case report. Medicine (Baltimore). 2022 Feb 18;101(7):e28865. doi: 10.1097/MD.0000000000028865. PMID: 35363190; PMCID: PMC9281986.
7)

Kutty RK, Sreemathyamma SB, Sivanandapanicker JL, Mundhe V, Chhabra K, Peethambaran A. Burden of Dengue-related Neurosurgical Emergencies during an Epidemic: A Tertiary Care Experience. Asian J Neurosurg. 2019 Jan-Mar;14(1):211-218. doi: 10.4103/ajns.AJNS_318_17. PMID: 30937037; PMCID: PMC6417330.
8)

Kumar MS, Srinanthini KR, Gopal S. A report of quadriparesis in dengue fever due to hematomyelia. Neurol India. 2019 Mar-Apr;67(2):530-531. doi: 10.4103/0028-3886.258054. PMID: 31085871.
9)

Kaur J, Virk JS, Paul BS, Saggar K. Dengue fever presenting as cauda equina syndrome. BMJ Case Rep. 2017 Jul 24;2017:bcr2017221251. doi: 10.1136/bcr-2017-221251. PMID: 28739570; PMCID: PMC5624003.
10)

Gupta DK, Vaish AK, Arya RK, Chaudhary SC. Hypokalaemic quadriparesis: an unusual manifestation of dengue fever. BMJ Case Rep. 2011 Jun 17;2011:bcr1220103673. doi: 10.1136/bcr.12.2010.3673. PMID: 22692495; PMCID: PMC3118907.
11)

Gulati S. Dengue infection causing acute hypokalemic quadriparesis. Neurol India. 2011 Jan-Feb;59(1):143. doi: 10.4103/0028-3886.76887. PMID: 21339693.

Aneurysmal subarachnoid hemorrhage outcome

Aneurysmal subarachnoid hemorrhage outcome

Several studies have investigated the changes in CSF metabolomics that occur after aSAH. These studies have identified alterations in various metabolites and metabolic pathways, including those involved in energy metabolism, amino acid metabolism, and lipid metabolism.

One study found that levels of lactate, a marker of anaerobic metabolism, were significantly increased in the CSF of aSAH patients compared to controls. This suggests that there is a shift towards anaerobic metabolism in the brain following aSAH, possibly due to decreased oxygen delivery and increased metabolic demand.

Other studies have reported alterations in amino acid metabolism, particularly involving glutamate and gamma-aminobutyric acid (GABA). Glutamate is an excitatory neurotransmitter that can lead to neuronal damage when present in excess, while GABA is an inhibitory neurotransmitter that can protect against excitotoxicity. Studies have shown that CSF levels of glutamate are increased and GABA levels are decreased in aSAH patients, which may contribute to the pathophysiology of the disease.

Alterations in lipid metabolism have also been reported in aSAH patients, with decreased levels of sphingomyelins and phosphatidylcholines in the CSF. These lipids play important roles in cellular membrane structure and function, and their depletion may contribute to neuronal damage and inflammation.

Overall, the findings of metabolomics studies suggest that aSAH leads to widespread metabolic alterations in the brain, involving multiple metabolic pathways. These alterations may contribute to the pathophysiology of the disease and represent potential targets for therapeutic intervention.


There is increasing evidence suggesting that biomarkers can give insight into the aneurysmal subarachnoid hemorrhage pathogenesis and can serve as an outcome predictor 1)

NFE2L2 SNP, rs10183914, is significantly associated with aneurysmal subarachnoid hemorrhage outcome. This is consistent with a clinically relevant pathophysiological role for oxidative and inflammatory brain injury due to blood and its breakdown products in aSAH. Furthermore, the findings support NRF2 as a potential therapeutic target following aSAH and other forms of intracranial hemorrhage 2)


In a study by Hammer et al. from the Paracelsus Medical University, complications like pneumonia (β = 5.11; 95% CI = 1.75-8.46; p = 0.0031), sepsis (β = 9.54; 95% CI = 3.27-15.82; p = 0.0031), hydrocephalus (β = 4.63; 95% CI = 1.82-7.45; p = 0.0014), and delayed cerebral ischemia (DCI) (β = 3.38; 95% CI = 0.19-6.56; p = 0.038) were critical factors depending on the LOS in intensive care as well as decompressive craniectomy (β = 5.02; 95% CI = 1.35-8.70; p = 0.0077). All analyzed comorbidities such as hypertensiondiabeteshypothyroidismcholesterolemia, and smoking history had no significant impact on the LOS in intensive care. LOS in intensive care (OR = 1.09; 95% CI = 1.03-1.15; p = 0.0023), as well as World Federation of Neurosurgical Societies grading for subarachnoid hemorrhage (OR = 3.72; 95% CI = 2.23-6.21; p < 0.0001) and age (OR = 1.06; 95% CI = 1.02-1.10; p = 0.0061), were significant factors that had an impact on the outcome after 1 year. Complications in intensive care but not comorbidities are associated with higher LOS in intensive care. LOS in intensive care is a modest but significant predictor of outcomes after subarachnoid hemorrhage 3).


Aneurysmal subarachnoid hemorrhage (aSAH) occurs in about 5% of all strokes and has still a mortality of 50% and a significant morbidity in survivors 4).

The second cause of disability after the initial hemorrhage is cerebral vasospasm and the delayed cerebral ischemia which occurs in 50–70% of patients 5).

These two pathological entities seem to have different pathophysiological etiologies and cannot be detected by the same techniques. Vasospasms of the vessels of the circle of Willis can be detected by transcranial Doppler ultrasonography (TCD), whereas microcirculation disturbances can be detected by perfusion imaging techniques. Digital subtraction angiography (DSA) remains until now the gold standard of imaging vasospasms, but it is invasive, and it is proven to be associated with the risk of mild neurological deficit as well as ischemic insults 6).


As angiographic vasospasm is strongly associated with delayed cerebral ischemia (DCI) and clinical outcome, clinical trials in the last few decades focused on prevention of these angiographic spasms. Despite all efforts, no new pharmacological agents have shown to improve patient outcome. As such, it has become clear that our understanding of the pathophysiology of SAH is incomplete and we need to reevaluate our concepts on the complex pathophysiological process following SAH. Angiographic vasospasm is probably important.

The case fatality in aneurysmal subarachnoid hemorrhage (aSAH) is 50% due to the initial hemorrhage or subsequent complications like aneurysm rebleeding or delayed cerebral ischemia (DCI).


One factor that might influence the initial brain damage or subsequent complications is the use of antiplatelet medication before the initial hemorrhage.

Improvements in multidisciciplinary neurocritical care and advancements in medical and surgical treatment have contributed to a decline in the case fatality rate of aneurysmal subarachnoid hemorrhage 7).

A greater proportion of patients, therefore, are surviving their initial hemorrhagic event but remain at increased risk of a number of complications.

see Aneurysmal subarachnoid hemorrhage complications.

The case fatality after aneurysmal haemorrhage is 50%; one in eight patients with subarachnoid haemorrhage dies outside hospital. Rebleeding is the most imminent danger; a first aim is therefore occlusion of the aneurysm 8).

Prothrombotic states of early brain injury (EBI) and delayed cerebral ischemia (DCI) after aSAH determine morbidity and mortality.

The outcome depends on their condition on arrival at the hospital. However, a small number of patients recover from an initially poor condition.

Associated with intracerebral hematoma (ICH) typically has a poor outcome. SAH with ICH tends to have a worse prognosis than SAH alone.


It has a high socioeconomic impact as it tends to affect younger patients. The NCEPOD study looking into management of aSAH has recommended that neurovascular units in the United Kingdom should aim to secure cerebral aneurysms within 48 h and that delays because of weekend admissions can increase the mortality and morbidity attributed to aSAH.

A study provides important data showing excess in-Hospital mortality of patients with SAH on weekend admissions served by the United Kingdom’s National Health Service.; However, there were no effects of weekend admission on long-term outcomes 9).

Prediction models

Clinical prediction models were developed with individual patient data from 10 936 patients and validated with data from 3355 patients after development of the model. In the validation cohort, a core model including patient age, premorbid hypertension, and neurological grade on admission to predict risk of functional outcome had good discrimination, with an area under the receiver operator characteristics curve (AUC) of 0.80 (95% confidence interval 0.78 to 0.82). When the core model was extended to a “neuroimaging model,” with inclusion of clot volume, aneurysm size, and location, the AUC improved to 0.81 (0.79 to 0.84). A full model that extended the neuroimaging model by including treatment modality had AUC of 0.81 (0.79 to 0.83). Discrimination was lower for a similar set of models to predict risk of mortality (AUC for full model 0.76, 0.69 to 0.82). All models showed satisfactory calibration in the validation cohort.

The prediction models reliably estimate the outcome of patients who were managed in various settings for ruptured intracranial aneurysms that caused subarachnoid haemorrhage. The predictor items are readily derived at hospital admission. The web based SAHIT prognostic calculator (http://sahitscore.com) and the related app could be adjunctive tools to support management of patients 10).

National Institute of Health Stroke Scale

Barthel Index

Extended Glasgow Outcome Scale.

Modified Rankin Scale


Systematic reviews for clinical prognostic factors and clinical prediction tools in aneurysmal subarachnoid hemorrhage (aSAH) face a number of methodological challenges. These include within and between study patient heterogeneity, regional variations in treatment protocols, patient referral biases, and differences in treatment, and prognosis viewpoints across different cultures 11).

It is critical to determine the neural basis for executive deficits in aSAH, in order to better understand and improve patient outcomes.


In a tertiary care center in India, despite recent advances in the treatment of patients with aSAH, the morbidity and mortality rates have failed to improve significantly in unselected patients and natural cohorts. This may be attributed to the natural history of aSAH, and calls for new strategies to diagnose and treat such patients before the catastrophe 12).

In the series of Nieuwkamp et al., despite an increase in the mean age of patients with SAH, case-fatality rates have decreased by 17% between 1973 and 2002 and show potentially important regional differences. This decrease coincides with the introduction of improved management strategies 13).

The case fatality after aneurysmal haemorrhage is 50%; one in eight patients with subarachnoid haemorrhage dies outside hospital.

Mortality is 10% within first few days

30-day mortality rate was 46% in one series, and in others over half the patients died within 2 weeks of their SAH.

overall mortality is 45% (range: 32—67%)

causes of mortality

neurogenic stunned myocardium

about 8% die from progressive deterioration from the initial hemorrhage

of those reaching neurosurgical care, vasospasm kills 7%, and causes severe deficit in another 7%.

about 30% of survivors have moderate to severe disability.

about 66 % of those who hove successful aneurysm clipping never return to the same quality of life as before the SAH.

With the limitation of an explorative cohort study the results indicate that routine transcranial doppler (TCD) studies do not improve the overall outcome of patients after aSAH 14).

Quantitative imaging indicators of ventricular hemorrhage (standard deviation of third ventricular hemorrhage density, minimum density of fourth ventricular hemorrhage, and left ventricular sphericity) are helpful to predict the poor prognosis of patients with aSAH with ventricular hemorrhage. The dimensional fusion model has greater value in predicting the poor prognosis of patients 15)

Quantitative estimation of the hemorrhage volume associated with aneurysm rupture is a tool of assessing prognosis.

A prospective cohort of 206 patients consecutively admitted with the diagnosis of aneurysmal subarachnoid hemorrhage to Hospital 12 de Octubre were included in the study. Subarachnoid, intraventricular, intracerebral, and total bleeding volumes were calculated using analytic software. For assessing factors related to prognosis, univariate and multivariate analysis (logistic regression) were performed. The relative importance of factors in determining prognosis was established by calculating their proportion of explained variation. Maximum Youden index was calculated to determine the optimal cut point for subarachnoid and total bleeding volume.

Variables independently related to prognosis were clinical grade at admission, age, and the different bleeding volumes. The proportion of variance explained is higher for subarachnoid bleeding. The optimal cut point related to poor prognosis is a volume of 20 mL both for subarachnoid and total bleeding.

Volumetric measurement of subarachnoid or total bleeding volume are both independent prognostic factors in patients with aneurysmal subarachnoid hemorrhage. A volume of more than 20 mL of blood in the initial noncontrast computed tomography is related to a clear increase in poor outcome risk 16).

Acute lung injury or acute respiratory distress syndrome (ALI/ARDS) is a common complication after aneurysmal subarachnoid hemorrhage (aSAH), and is associated with worse neurologic outcomes and longer hospitalization. However, the effect of ALI/ARDS in SAH has not been well elucidated. The purpose of this study was to determine the incidence of ALI/ARDS in a cohort of patients with SAH and to determine the risk factors for ALI/ARDS and their impact on patient prognosis. We performed a retrospective analysis of 167 consecutive patients with aSAH enrolled. ALI/ARDS patients were rigorously adjudicated using North American-European Consensus Conference definition. Regression analyses were used to test the risk factors for ALI/ARDS in patients with SAH. A total of 167 patients fulfilled the inclusion criteria, and 27% patients (45 of 167) developed ALI. Among all 45 ALI patients, 33 (20%, 33 of 167) patients met criteria for ARDS. On multivariate analysis, elderly patients, lower glasgow coma scale (GCS), higher Hunt-Hess grade, higher simplified acute physiology score (SAPS) II score, pre-existing pneumonia, gastric aspiration, hypoxemia, and tachypnea were the strongest risk factor for ALI/ARDS. Patients with ALI/ARDS showed worse clinical outcomes measured at 30 days. Development of ALI/ARDS was associated with a statistically significant increasing the odds of tracheostomy and hospital complications, and increasing duration of mechanical ventilation, intensive care unit (ICU) length and hospitalization stay. Development of ALI/ARDS is a severe complication of SAH and is associated with a poor clinical outcome, and further studies should focus on both prevention and management strategies specific to SAH-associated ALI/ARDS 17).

Higher early IL6 serum levels after aSAH are associated with poor outcome at discharge. In addition, involvement of leukemia inhibitory factor (LIF) in the early inflammatory reaction after aSAH has been demonstrated 18).

The APOΕε4 polymorphism was analysed in 147 patients with aSAH. Allele and genotype frequencies were compared to those found in a gender- and area-matched control group of healthy individuals (n = 211). Early cerebral vasospasm (CVS) was identified and treated according to neurointensive care unit (NICU) guidelines. Neurological deficit(s) at admittance and at 1-year follow-up visit was recorded. Neurological outcome was assessed by the National Institute of Health Stroke ScaleBarthel Index and the Extended Glasgow Outcome Scale.

APOEε4 and non-APOEε4 allele frequencies were similar in aSAH patients and healthy individuals. The presence of APOEε4 was not associated with the development of early CVS. We could not find an influence of the APOE polymorphism on 1-year neurological outcome between groups. Subgroup analyses of patients treated with surgical clipping vs endovascular coiling did not reveal any associations.

For Csajbok et al. APOEε4 polymorphism has no major influence on risk of aSAH, the occurrence of CVS or long-term neurological outcome after aSAH 19).


For Cheng et al., Apolipoprotein E (APOEε4) may induce cerebral perfusion impairment in the early phase, contributing to early brain injury (EBI) following aneurysmal subarachnoid hemorrhage (aSAH), and assessment of APOE genotypes could serve as a useful tool in the prognostic evaluation and therapeutic management of aSAH 20).

Iatrogenic coagulopathy caused by Direct oral anticoagulants or vitamin K antagonists was not associated with more severe radiological or clinical subarachnoid hemorrhage or worse clinical outcomes in hospitalized SAH patients 21).

Brain edema in aneurysmal subarachnoid hemorrhage


Myosteatosis was found to be associated with poor physical condition directly after the onset of aSAH. Skeletal muscle atrophy and myosteatosis were however irrelevant to outcome in the Western-European aSAH patient. Future studies are needed to validate these finding 22).

A low PbtO2 value is associated with a worse prognosis, and an increase in the PbtO2 value in response to treatment is a marker of a good outcome 23).

The inverse correlation between mean arterial pressure and mean transit time (MTT) in early perfusion computed tomography, increasing with the severity of aSAH, suggests an increasing disturbance of cerebral autoregulation with the severity of early brain injury. The results emphasize the importance of maintaining physiological blood pressure values in the early phase of aSAH and preventing hypotension, especially in patients with poor-grade aSAH 24)


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Liang JJ, Zhang ZQ, Zhang QR, Li CY, Zheng LJ, Lu GM. [Predictive performance for prognosis of aneurysmal subarachnoid hemorrhage with ventricular hemorrhage by imaging combined with clinical and laboratory quantitative index model]. Zhonghua Yi Xue Za Zhi. 2023 Mar 21;103(11):842-849. Chinese. doi: 10.3760/cma.j.cn112137-20221101-02280. PMID: 36925118.
16)

Lagares A, Jiménez-Roldán L, Gomez PA, Munarriz PM, Castaño-León AM, Cepeda S, Alén JF. Prognostic Value of the Amount of Bleeding After Aneurysmal Subarachnoid Hemorrhage: A Quantitative Volumetric Study. Neurosurgery. 2015 Dec;77(6):898-907. doi: 10.1227/NEU.0000000000000927. PubMed PMID: 26308629.
17)

Wu J, Gao W, Zhang H. Development of acute lung injury or acute respiratory distress syndrome after subarachnoid hemorrhage, predictive factors, and impact on prognosis. Acta Neurol Belg. 2023 Mar 15. doi: 10.1007/s13760-023-02207-z. Epub ahead of print. PMID: 36922484.
18)

Höllig A, Remmel D, Stoffel-Wagner B, Schubert GA, Coburn M, Clusmann H. Association of early inflammatory parameters after subarachnoid hemorrhage with functional outcome: A prospective cohort study. Clin Neurol Neurosurg. 2015 Aug 28;138:177-183. doi: 10.1016/j.clineuro.2015.08.030. [Epub ahead of print] PubMed PMID: 26355810.
19)

Csajbok LZ, Nylén K, Öst M, Blennow K, Zetterberg H, Nellgård P, Nellgård B. Apolipoprotein E polymorphism in aneurysmal subarachnoid haemorrhage in West Sweden. Acta Neurol Scand. 2015 Sep 16. doi: 10.1111/ane.12487. [Epub ahead of print] PubMed PMID: 26374096.
20)

Cheng C, Jiang L, Yang Y, Wu H, Huang Z, Sun X. Effect of APOE Gene Polymorphism on Early Cerebral Perfusion After Aneurysmal Subarachnoid Hemorrhage. Transl Stroke Res. 2015 Sep 14. [Epub ahead of print] PubMed PMID: 26370543.
21)

Veldeman M, Rossmann T, Weiss M, Conzen-Dilger C, Korja M, Hoellig A, Virta JJ, Satopää J, Luostarinen T, Clusmann H, Niemelä M, Raj R. Aneurysmal Subarachnoid Hemorrhage in Hospitalized Patients on Anticoagulants-A Two Center Matched Case-Control Study. J Clin Med. 2023 Feb 13;12(4):1476. doi: 10.3390/jcm12041476. PMID: 36836011; PMCID: PMC9958876.
22)

Shen Y, Levolger S, Zaid Al-Kaylani AHA, Uyttenboogaart M, van Donkelaar CE, Van Dijk JMC, Viddeleer AR, Bokkers RPH. Skeletal muscle atrophy and myosteatosis are not related to long-term aneurysmal subarachnoid hemorrhage outcome. PLoS One. 2022 Mar 4;17(3):e0264616. doi: 10.1371/journal.pone.0264616. PMID: 35245308.
23)

Gouvea Bogossian E, Battaglini D, Fratino S, Minini A, Gianni G, Fiore M, Robba C, Taccone FS. The Role of Brain Tissue Oxygenation Monitoring in the Management of Subarachnoid Hemorrhage: A Scoping Review. Neurocrit Care. 2023 Feb 17. doi: 10.1007/s12028-023-01680-x. Epub ahead of print. PMID: 36802011.
24)

Hofmann BB, Donaldson DM, Fischer I, Karadag C, Neyazi M, Piedade GS, Abusabha Y, Muhammad S, Rubbert C, Hänggi D, Beseoglu K. Blood Pressure Affects the Early CT Perfusion Imaging in Patients with aSAH Reflecting Early Disturbed Autoregulation. Neurocrit Care. 2023 Feb 17. doi: 10.1007/s12028-023-01683-8. Epub ahead of print. PMID: 36802010.

Basal ganglia hemorrhage surgery

Basal ganglia hemorrhage surgery

The main surgical techniques for spontaneous basal ganglia hemorrhage include stereotactic aspirationendoscopic aspiration, and craniotomy. However, credible evidence is still needed to validate the effect of these techniques.

Outcome analysis was stratified using hematoma volume, ICH score, preoperative GCS score, and decompressive craniectomy (DC).

Results: The mean hematoma volume was 70.8 mL, and 68 patients (26.9%) underwent DC. The mean postoperative ICP was 28.8 ± 6.7 mmHg for patients without DC, and only 17.5 ± 8.6 mmHg for patients with DC. Twenty-five patients (9.9%) died within 30 days of the operation, and 88 patients (34.8%, GOS ≥ 4) had good outcome 3 months after surgery. ICH volume > 50 mL, preoperative GCS score ≤ 8, and ICH score ≥ 3 are risk factors for unfavorable outcomes.

Conclusions: DC can be used for patients with low preoperative GCS score, and it effectively reduces ICP and 30-day mortality. Hematoma volume, preoperative GCS score, and ICH score are of predictive value for surgical outcome of large basal ganglia hemorrhage 1).

A total of 61 patients with hypertensive basal ganglia hemorrhage were recruited at the Binzhou Medical University Hospital, between October 2019 and January 2021, and their clinical information was retrospectively analyzed. Based on the surgical approach used, patients were assigned into either laser navigation or small bone window groups depending on the surgical approach. Then, they compared the operation times, intraoperative blood loss, clinic stay, Glasgow Outcome Scale (GOS) rating at 30 days, Barthel index (BI) rating at 6 months, postoperative pneumonia incidences, and intracranial contamination complications between groups. Intraoperative blood lossoperation time, and sanatorium were significantly low in the laser navigation group, relative to the small bone window group. At the same time, there were no significant differences between the groups with regard to postoperative hematoma volume, lung contamination, cerebrospinal fluid (CSF) leak, and intracranial contamination, as well as the 6-month BI and 30-day GOS rating. There were no deaths in either group. Compared with traditional small bone window surgery, laser-guided puncture, and drainage is a low-cost, accurate, and safe method for the treatment of basal ganglia hemorrhage, which is suitable for promotion in developing countries and economically underdeveloped areas 2)

Postoperative hemorrhage is a severe complication, and it’s relative to neurosurgical techniques.

The favorable outcome group was slightly younger (p-value 0.050*). Also, the volume and extension of hematoma into the ventricular system, hydrocephalic dilatation, and midline shift greater than 5 mm had a significantly worse outcome with a statistically significant difference.

The early surgical management with the removal of the hematoma led to a dramatic reduction of ICP and improved the prognosis. Patients with signs of brain herniation, a midline shift > 5 mm, hydrocephalic dilatation, ventricular hemorrhage, and a depressed level of consciousness have a poor prognosis 3)


1)

Li Q, Yang CH, Xu JG, Li H, You C. Surgical treatment for large spontaneous basal ganglia hemorrhage: retrospective analysis of 253 cases. Br J Neurosurg. 2013 Oct;27(5):617-21. doi: 10.3109/02688697.2013.765938. Epub 2013 Feb 14. PMID: 23406426.
2)

Yuan Z, Wei Q, Chen Z, Xing H, Zhang T, Li Z. Laser navigation combined with XperCT technology-assisted puncture of basal ganglia intracerebral hemorrhage. Neurosurg Rev. 2023 May 5;46(1):104. doi: 10.1007/s10143-023-02015-2. PMID: 37145343.
3)

khallaf, M., Abdelrahman, M. Surgical management for large hypertensive basal ganglionic hemorrhage: single center experience. Egypt J Neurosurg 34, 19 (2019). https://doi.org/10.1186/s41984-019-0044-9

Superior sagittal sinus dural arteriovenous fistula

Superior sagittal sinus dural arteriovenous fistula

intracranial dural arteriovenous fistula (dAVF) involving the superior sagittal sinus (SSS) is relatively rare, and its clinical course is usually aggressive. Its concomitance with a tumor has rarely been reported.


Supratentorial dural arteriovenous fistula DVAs mostly drained in the superior sagittal sinus (80%), while all of infratentorial/combined DVAs drained in deep ependymal veins of the 4th ventricle. All the supratentorial dAVFs drained into the superior sagittal sinus, while the infratentorial/combined dAVFs mostly drained in the jugular bulb, Vein of Rosenthal, or transverse-sigmoid sinuses (75%) 1).


Gigliotti et al. reported the first case of a superior sagittal sinus DAVF occurring after surgical resection of a parasagittal meningioma 2).

A case of SSS dAVF due to meningioma invasion, which was treated with sinus reconstruction and endovascular embolization. A 75-year-old man who had undergone tumor resection for parasagittal meningioma 4 years prior presented with intra-ventricular hemorrhage. Computed tomography angiography and magnetic resonance imaging revealed recurrent tumor invasion into the SSS causing occlusion. Cerebral angiography revealed multiple shunts along the occluded segment of the SSS, diffuse deep venous congestion, and cortical reflux. Borden type 3 SSS dAVF was diagnosed. We first performed direct tumor resection, followed by stenting for the occluded SSS and partial embolization of the shunts. After a 6-month interval, transvenous occlusion of the SSS was performed along the stent, resulting in complete obliteration of the dAVF. Sinus reconstruction therapy was effective in the immediate improvement of venous hypertension, obtaining the access route to the fistulas, and eradicating the shunts 3)


A 78-year-old man presented after trauma with basal and cortical subarachnoid hemorrhage (SAH). Computed tomography revealed a parietal bone fracture overlying the superior sagittal sinus (SSS). Catheter angiography performed within 24 hours of the injury demonstrated an SSS dAVF supplied by the middle meningeal artery, adjacent to the fracture.

Lessons: The authors present the case of an acute traumatic dAVF adjacent to a calvarial fracture. In this case, the authors proprose that the underlying pathogenesis is suggestive of direct vessel injury rather than the pathway commonly associated with this pathology 4)


Spontaneous closure of a superior sagittal sinus dural arteriovenous fistula after treatment of subarachnoid hemorrhage and secondary hydrocephalus 5).


A 61-year-old male with a history of meningioma previously managed with subtotal resection and stereotactic radiosurgery presented with progressive right-sided vision loss and bilateral papilledema. Initial imaging suggested possible sinus occlusion. Catheter angiogram revealed a Borden-Shucart grade III DAVF of the superior sagittal sinus and elevated venous pressures and the patient subsequently underwent endovascular transarterial intervention twice. We report on the first case of a superior sagittal sinus DAVF occurring after surgical resection of a parasagittal meningioma 6).


sagittal sinus dural arteriovenous fistula manifesting as dysphonia secondary to vocal cord paresis. The patient presented with a 6-week history of hoarseness. Imaging studies demonstrated findings suggestive of a dural arteriovenous fistula affecting the superior sagittal sinus. Direct laryngoscopy demonstrated paresis of the right vocal fold. We hypothesized that pressure on the vagus nerve from a dilated and arterialized internal jugular vein within the jugular foramen was responsible for the cranial neuropathy. The patient’s dysphonia resolved with embolization of the fistula, and repeat laryngoscopy showed resolution of the vocal fold paresis 7).


Beer-Furlan A, Joshi KC, Dasenbrock HH, Chen M. Endovascular management of complex superior sagittal sinus dural arteriovenous fistula. Neurosurg Focus. 2019 Apr 1;46(Suppl_2):V11. doi: 10.3171/2019.2.FocusVid.18687. PMID: 30939439.


Song W, Sun H, Liu J, Liu L, Liu J. Spontaneous Resolution of Venous Aneurysms After Transarterial Embolization of a Variant Superior Sagittal Sinus Dural Arteriovenous Fistula: Case Report and Literature Review. Neurologist. 2017 Sep;22(5):186-195. doi: 10.1097/NRL.0000000000000137. Review. PubMed PMID: 28859024.


A DAVF of the SSS in a patient who presented uniquely with increasing dizziness and disequilibrium who was treated with a single modality, endovascular embolization with ethyl vinyl alcohol co-polymer (Onyx, EV3, Irvine, CA). The patient underwent staged embolization in 2 sessions with no complications. An angiographic cure was achieved and the patient’s symptoms were ameliorated. Single modality therapy with endovascular embolization of a SSS DAVF can be achieved. Careful attention to technique during embolization with Onyx is required, but complete obliteration is possible without the need for adjunctive surgical resection 8)


A 61-year-old man who had been treated with anticoagulation for a known SSS thrombosis presented with a sudden onset of headache. CT scan revealed an intraventricular hemorrhage and cerebral angiography revealed DAVFs involving the SSS which had severe venous congestion and sinus occlusion. We treated this case with a staged endovascular approach which consisted of stent placement for the occluded sinus and transarterial intravenous embolization resulting in complete eradication of DAVFs. Recanalization of an occluded sinus by stent placement can reduce venous congestion and transarterial intravenous embolization can obliterate dural arteriovenous shunts. This staged strategy is feasible and should be considered a first option of treatment, especially for DAVFs which presented with intracranial hemorrhage and aggressive venous hypertension 9)


A case report and review of the literature of 16 dural arteriovenous fistulas (DAVFs) involving the superior sagittal sinus region are presented. In the case, magnetic resonance angiography detected the DAVF with multiple arterial feeding vessels from both external carotid arteries. The patient was successfully treated endovascularly, with complete occlusion of arterial feeders and a total resolution of symptoms 10).


1)

Agosti E, De Maria L, Panciani PP, Serioli S, Mardighian D, Fontanella MM, Lanzino G. Developmental venous anomaly associated with dural arteriovenous fistula: Etiopathogenesis and hemorrhagic risk. Front Surg. 2023 Mar 21;10:1141857. doi: 10.3389/fsurg.2023.1141857. PMID: 37025268; PMCID: PMC10071040.
2) , 6)

Gigliotti MJ, Patel N, Simon S. Superior sagittal sinus dural arteriovenous fistula caused by treatment of meningioma masquerades as sinus thrombosis. J Cerebrovasc Endovasc Neurosurg. 2021 Sep;23(3):260-265. doi: 10.7461/jcen.2021.E2021.01.002. Epub 2021 Aug 25. PMID: 34428863; PMCID: PMC8497717.
3)

Shima S, Sato S, Kushi K, Okada Y, Niimi Y. Sinus reconstruction therapy for superior sagittal sinus dural arteriovenous fistula caused by parasagittal meningioma invasion: a case report. Neuroradiol J. 2023 May 4:19714009231173103. doi: 10.1177/19714009231173103. Epub ahead of print. PMID: 37142419.
4)

Pryce ML, Chung KHC, Zeineddine HA, Dawes BH. Acute traumatic dural arteriovenous fistula of the superior sagittal sinus: illustrative case. J Neurosurg Case Lessons. 2023 Apr 10;5(15):CASE2392. doi: 10.3171/CASE2392. PMID: 37039291.
5)

Endo H, Ishizuka T, Murahashi T, Oka K, Nakamura H. Spontaneous closure of a superior sagittal sinus dural arteriovenous fistula after treatment of subarachnoid hemorrhage and secondary hydrocephalus. Neurol Sci. 2023 Mar 30. doi: 10.1007/s10072-023-06786-w. Epub ahead of print. PMID: 36995470.
7)

Rinaldo L, Ekbom DC, Lanzino G. Sagittal sinus dural arteriovenous fistula manifesting as unilateral vocal fold paresis. Clin Neurol Neurosurg. 2021 Aug 2;208:106856. doi: 10.1016/j.clineuro.2021.106856. Epub ahead of print. PMID: 34365240.
8)

Chong BW, Demaerschalk BM. Unusual Presentation of a Dural Arteriovenous Fistula of the Superior Sagittal Sinus and Single Modality Therapy with Onyx. Radiol Case Rep. 2015 Nov 6;3(1):158. doi: 10.2484/rcr.v3i1.158. PMID: 27303511; PMCID: PMC4896129.
9)

Ohara N, Toyota S, Kobayashi M, Wakayama A. Superior sagittal sinus dural arteriovenous fistulas treated by stent placement for an occluded sinus and transarterial embolization. A case report. Interv Neuroradiol. 2012 Sep;18(3):333-40. doi: 10.1177/159101991201800314. Epub 2012 Sep 10. PMID: 22958774; PMCID: PMC3442309.
10)

Kurl S, Saari T, Vanninen R, Hernesniemi J. Dural arteriovenous fistulas of superior sagittal sinus: case report and review of literature. Surg Neurol. 1996 Mar;45(3):250-5. doi: 10.1016/0090-3019(95)00361-4. PMID: 8638222.