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With great interest, we read the article of Venkatraman et al.[1] published in the Journal of NeuroInterventional Surgery recently. They presented a comprehensive picture depicting the effect of intra-arterial vasodilators (IADs) on the vasospasm following aneurysmal subarachnoid hemorrhage. But we were concerned with several questions weakening the reliability and generalization of the meta-analysis.
Firstly , though the detailed including criteria and searching strategy were provided in their meta-analysis, at least two eligible studies2,3 were missed which conformed to their including criteria and unfulfilled the excluding criteria. Two cohort studies of Morgan [2] and Mortimer [3] reported the effects of IADs on vasospasm with documentation of interested events, which should be included in Venkatraman’s analysis. Whether addition of these two studies could change the overall effect of IADs was unclear, but including any eligible study was in accordance with PRISMA principle.
Secondly, owing to the large number of included studies, the heterogeneity was substantial. Venkatraman et al.[1] conducted subgroup and sensitivity analyses, in which the heterogeneity remained significant (most values of I2 greater than 50%). It was rationale to turn to regression analyses in order to find and solve the heterogeneity.
Besides, this article included studies combining IADs with balloon angioplasty, which might overestimate effectiveness of IADs. IADs w...
With great interest, we read the article of Venkatraman et al.[1] published in the Journal of NeuroInterventional Surgery recently. They presented a comprehensive picture depicting the effect of intra-arterial vasodilators (IADs) on the vasospasm following aneurysmal subarachnoid hemorrhage. But we were concerned with several questions weakening the reliability and generalization of the meta-analysis.
Firstly , though the detailed including criteria and searching strategy were provided in their meta-analysis, at least two eligible studies2,3 were missed which conformed to their including criteria and unfulfilled the excluding criteria. Two cohort studies of Morgan [2] and Mortimer [3] reported the effects of IADs on vasospasm with documentation of interested events, which should be included in Venkatraman’s analysis. Whether addition of these two studies could change the overall effect of IADs was unclear, but including any eligible study was in accordance with PRISMA principle.
Secondly, owing to the large number of included studies, the heterogeneity was substantial. Venkatraman et al.[1] conducted subgroup and sensitivity analyses, in which the heterogeneity remained significant (most values of I2 greater than 50%). It was rationale to turn to regression analyses in order to find and solve the heterogeneity.
Besides, this article included studies combining IADs with balloon angioplasty, which might overestimate effectiveness of IADs. IADs worked in coordination with balloon angioplasty, for balloon angioplasty dilated proximal vessel assisting IADs to expand distal vessels. We could not exclude the possibility partial effect on the outcomes was attributable to balloon angioplasty. Similarly, it was reasonable to ascribe many complications to the balloon angioplasty, like vessel perforation.
In all, we would like to congratulate Venkatraman for the great work of meta-analyzing the impact of IADs on the treatment of vasospasm following subarachnoid hemorrhage.
References
1. Venkatraman A, Khawaja AM, Gupta S, et al. Intra-arterial vasodilators for vasospasm following aneurysmal subarachnoid hemorrhage: a meta-analysis. J Neurointerv Surg. 2017.
2. Morgan M, Halcrow S, Sorby W, Grinnell V. Outcome of aneurysmal subarachnoid haemorrhage following the introduction of papaverine angioplasty. J Clin Neurosci. 1996;3(2):139-142.
3. Mortimer AM, Steinfort B, Faulder K, et al. The detrimental clinical impact of severe angiographic vasospasm may be diminished by maximal medical therapy and intensive endovascular treatment. Journal of Neurointerventional Surgery. 2015;7(12):881-887.
We would like to thank Dr. Shotar and colleagues for their interest in our article. As highlighted by Dr. Shotar, delayed enhancing lesions (DEL) after coil embolization of aneurysm are suspected as a result of foreign body reaction 1-5. We agree with their opinion that the catheter coating of the inner wall of guiding catheter and/or the outer wall of microcatheter may be the source of foreign body. However, according to our experiences and analysis, it is our opinion that the coating material of the inner wall of microcatheter may also be the source.
Dr Shotar suggests that the distribution of the MR lesions in the territory of the parent artery (i.e.: ICA) in our series suggests the guiding catheter as the culprit. However, in all our cases 6, the aneurysms were located at the distal ICA (Ophthalmic artery, IC-anterior choroidal artery, superior hypophyseal artery). Thus, we believe that the distribution of the DELs on MR is not in conflict with our claim that the inner wall of the microcatheter is the source. Foreign body fragments from the microcatheter probably migrated into the aneurysmal sac during multiple coil introduction attempts under unusual friction and were swept downstream. Our benchtop analyses also support this finding.
Regarding Dr Shotar’s suggestion that "the patient treated with the microcatheter that showed coating fragments at the location of the friction on bench tests did not have DELs", this microcatheter was withdrawn imme...
We would like to thank Dr. Shotar and colleagues for their interest in our article. As highlighted by Dr. Shotar, delayed enhancing lesions (DEL) after coil embolization of aneurysm are suspected as a result of foreign body reaction 1-5. We agree with their opinion that the catheter coating of the inner wall of guiding catheter and/or the outer wall of microcatheter may be the source of foreign body. However, according to our experiences and analysis, it is our opinion that the coating material of the inner wall of microcatheter may also be the source.
Dr Shotar suggests that the distribution of the MR lesions in the territory of the parent artery (i.e.: ICA) in our series suggests the guiding catheter as the culprit. However, in all our cases 6, the aneurysms were located at the distal ICA (Ophthalmic artery, IC-anterior choroidal artery, superior hypophyseal artery). Thus, we believe that the distribution of the DELs on MR is not in conflict with our claim that the inner wall of the microcatheter is the source. Foreign body fragments from the microcatheter probably migrated into the aneurysmal sac during multiple coil introduction attempts under unusual friction and were swept downstream. Our benchtop analyses also support this finding.
Regarding Dr Shotar’s suggestion that "the patient treated with the microcatheter that showed coating fragments at the location of the friction on bench tests did not have DELs", this microcatheter was withdrawn immediately after detection of unusual friction without additional coil introduction attempts. We believe that ‘immediate withdrawl’ was essential in preventing distal migration of foreign body materials.
We agree with Dr Shotar’s analyses on the recent increase in the literature on such complications. Further investigation is necessary for identification of its causes. In the meanwhile, based on our series and the experiences of others, we believe that both the inner and outer walls of the micro and/or guiding catheters may be the source 1 6. Our main interest was to identify the cause and elucidate the signs during the procedure –unusual friction development- at which such phenomenon occurs so that clinical complications may be prevented.
1. Shotar E, Law-Ye B, Baronnet-Chauvet F, et al. Non-ischemic cerebral enhancing lesions secondary to endovascular aneurysm therapy: nickel allergy or foreign body reaction? Case series and review of the literature. Neuroradiology 2016 doi: 10.1007/s00234-016-1699-5 [published Online First: 2016/05/25]
2. Shapiro M, Ollenschleger MD, Baccin C, et al. Foreign Body Emboli following Cerebrovascular Interventions: Clinical, Radiographic, and Histopathologic Features. AJNR American journal of neuroradiology 2015;36(11):2121-6. doi: 10.3174/ajnr.A4415 [published Online First: 2015/08/22]
3. Cruz J, Marotta T, O'Kelly C, et al. Enhancing Brain Lesions after Endovascular Treatment of Aneurysms. American Journal of Neuroradiology 2014
4. Skolarus LE, Gemmete JJ, Braley T, et al. Abnormal white matter changes after cerebral aneurysm treatment with polyglycolic-polylactic acid coils. World neurosurgery 2010;74(6):640-4. doi: 10.1016/j.wneu.2010.03.026 [published Online First: 2011/04/16]
5. Fealey ME, Edwards WD, Giannini C, et al. Complications of endovascular polymers associated with vascular introducer sheaths and metallic coils in 3 patients, with literature review. The American journal of surgical pathology 2008;32(9):1310-16.
6. Oh SW, Shin NY, Lee HJ, et al. Delayed enhancing lesions after coil embolization of aneurysms: clinical experience and benchtop analyses. Journal of neurointerventional surgery 2017 doi: 10.1136/neurintsurg-2016-012833 [published Online First: 2017/01/08]
We read with great interest the article by McTaggart et al. on the new embolectomy technique called Continuous Aspiration Prior To Intracranial Vascular Embolectomy (CAPTIVE).(1) The paper adds information on the supporting evidence that a combined approach of stentretriever and aspiration-catheter utilization may be the optimal path in achieving higher rates of complete reperfusion in patients with large vessel occlusions.(2, 3) While the idea of starting aspiration with the intermediate catheter prior to and during the stentretriever placement is intriguing, attention has to be paid on the effect of prolonged aspiration on collateral flow, as reported in a recent JNIS publication.(4) Additionally, the ‘continuous’ part of the title may be misleading, as the authors state that they advance the aspiration-catheter towards the face of the clot until the drip rate has stopped. As seen in Fig 1E of the CAPTIVE publication, the tip of the aspiration-catheter becomes clogged with clot as ‘a portion is held captive within the distal aspiration catheter.’ This probably results in vacuum within the aspiration-catheter and non-existent aspiration in the vicinity of the aspiration-catheter tip during immobilization of the stentretriever/clot/aspiration-catheter unit. At last, the authors describe thoroughly a ‘De-CAPTIVE shear’ on Fig 2 but neglect to acknowledge that the same danger of clot-shearing applies to the moments of stentretriever/clot/aspiration-cath...
We read with great interest the article by McTaggart et al. on the new embolectomy technique called Continuous Aspiration Prior To Intracranial Vascular Embolectomy (CAPTIVE).(1) The paper adds information on the supporting evidence that a combined approach of stentretriever and aspiration-catheter utilization may be the optimal path in achieving higher rates of complete reperfusion in patients with large vessel occlusions.(2, 3) While the idea of starting aspiration with the intermediate catheter prior to and during the stentretriever placement is intriguing, attention has to be paid on the effect of prolonged aspiration on collateral flow, as reported in a recent JNIS publication.(4) Additionally, the ‘continuous’ part of the title may be misleading, as the authors state that they advance the aspiration-catheter towards the face of the clot until the drip rate has stopped. As seen in Fig 1E of the CAPTIVE publication, the tip of the aspiration-catheter becomes clogged with clot as ‘a portion is held captive within the distal aspiration catheter.’ This probably results in vacuum within the aspiration-catheter and non-existent aspiration in the vicinity of the aspiration-catheter tip during immobilization of the stentretriever/clot/aspiration-catheter unit. At last, the authors describe thoroughly a ‘De-CAPTIVE shear’ on Fig 2 but neglect to acknowledge that the same danger of clot-shearing applies to the moments of stentretriever/clot/aspiration-catheter unit retraction within the tip of the guide catheter/sheath. This exact case is depicted in our example ( http://onestopinstroke.eu/wp-content/uploads/Fig1-1.jpg ) during embolectomy of a mid-basilar occlusion (A). B shows recanalization of the occlusion after one maneuver but without proximal aspiration on the guide catheter there is clot-shearing at the catheter tip seen on the early images of the series (C), with dislocation of the clot towards the basilar artery during the angiogram (D and E). Control-angiogram shows re-occlusion of the basilar artery (F) which could be recanalized with another maneuver (G), but resulted in an incomplete reperfusion of the downstream territory. This danger can be reduced by applying aspiration on the guide catheter during retraction of the unit, while preserving vacuum within the aspiration catheter either with pump-aspiration or with the use of a vacuum-lock syringe. In our experience, the addition of proximal aspiration to a primarily combined approach (stentretriever plus aspiration-catheter) results in high rates of mTICI3 reperfusion.(3)
1. McTaggart RA, Tung EL, Yaghi S, Cutting SM, Hemendinger M, Gale HI, et al. Continuous aspiration prior to intracranial vascular embolectomy (CAPTIVE): a technique which improves outcomes. Journal of neurointerventional surgery. 2016. Epub 2016/12/18.
2. Massari F, Henninger N, Lozano JD, Patel A, Kuhn AL, Howk M, et al. ARTS (Aspiration-Retriever Technique for Stroke): Initial clinical experience. Interventional neuroradiology : journal of peritherapeutic neuroradiology, surgical procedures and related neurosciences. 2016;22(3):325-32. Epub 2016/02/26.
3. Maus V, Behme D, Kabbasch C, Borggrefe J, Tsogkas I, Nikoubashman O, et al. Maximizing First-Pass Complete Reperfusion with SAVE. Clinical neuroradiology. 2017. Epub 2017/02/15.
4. Lally F, Soorani M, Woo T, Nayak S, Jadun C, Yang Y, et al. In vitro experiments of cerebral blood flow during aspiration thrombectomy: potential effects on cerebral perfusion pressure and collateral flow. Journal of neurointerventional surgery. 2016;8(9):969-72. Epub 2015/09/01.
With great interest we read the recent paper by Martinez-Galdámez et al. regarding the periprocedural outcomes and early safety after placement of a Pipeline Embolization Device with Shield Technology (PEDshield) (1). Evaluation of new endovascular devices, such as PEDshield, is of the utmost importance to give future users a chance to objectively review possible benefits for their clinical practice.
In the study of Martinez-Galdámez et al. 76% of the target aneurysms were small (< 10 mm). It is known that small aneurysms are associated with a lower probability of thromboembolisms and ischemic stroke after flow diverter treatment than large and giant aneurysms (2,3). The size of the treated aneurysms, and not the PEDshield, might therefore explain the lack of thromboembolic complications reported in the study of Martinez-Galdámez et al. Selection bias might thus have led to the conclusion that the early safety of the PEDshield device is warranted.
Furthermore, it is hard to understand why only 21 out of 50 patients (42%) underwent platelet reactivity testing, especially since the primary outcome measure focused on identifying thromboembolic complications in the territory supplied by the treated artery. To make matters worse: when platelet reactivity tests revealed the presence of hyporesponders, anti-platelet therapy was left unchanged in most cases. If thromboembolic complications do occur in the 6-month and 1-year follow-up of this...
With great interest we read the recent paper by Martinez-Galdámez et al. regarding the periprocedural outcomes and early safety after placement of a Pipeline Embolization Device with Shield Technology (PEDshield) (1). Evaluation of new endovascular devices, such as PEDshield, is of the utmost importance to give future users a chance to objectively review possible benefits for their clinical practice.
In the study of Martinez-Galdámez et al. 76% of the target aneurysms were small (< 10 mm). It is known that small aneurysms are associated with a lower probability of thromboembolisms and ischemic stroke after flow diverter treatment than large and giant aneurysms (2,3). The size of the treated aneurysms, and not the PEDshield, might therefore explain the lack of thromboembolic complications reported in the study of Martinez-Galdámez et al. Selection bias might thus have led to the conclusion that the early safety of the PEDshield device is warranted.
Furthermore, it is hard to understand why only 21 out of 50 patients (42%) underwent platelet reactivity testing, especially since the primary outcome measure focused on identifying thromboembolic complications in the territory supplied by the treated artery. To make matters worse: when platelet reactivity tests revealed the presence of hyporesponders, anti-platelet therapy was left unchanged in most cases. If thromboembolic complications do occur in the 6-month and 1-year follow-up of this cohort, it will make interpretation of the primary outcome measure more difficult as it will be impossible to rule out ineffective anti-platelet therapy.
References
1) Martinez-Galdámez M, Lamin SM, Lagios KG, et al. Periprocedural outcomes and early safety with the use of Pipeline Flex Embolization Device with Shield Technology for unruptured intracranial aneurysms: preliminary results from a prospective clinical study. J Neurointervent Surg 2017;0:1-6.
2) Heller RS, Dandamundi V, Lanfranchi M, et al. Effect of antiplatelet therapy on thromboembolism after flow diversion with the Pipeline Embolization Device. J Neurosurg 2013;119:1603-10.
3) Brinjikji W, Murad MH, Lanzino G, et al. Endovascular treatment of intracranial aneurysms with flow diverters. A meta-analysis. Stroke 2013;44:442-7.
We have read with great interest the article describing the CAPTIVE technique for endovascular acute ischemic treatment by McTaggart et al.1. Firstly, we would like to commend the great clarity they used to describe the combination of distal aspiration and stent retriever to perform mechanical thrombectomy. Notably, they illustrated the rationale for aspiration prior to stent deployment as well as the removal of both distal aspiration catheter and stent as a single unit to decrease possible clot fragmentation.
We adopt a very similar approach for most of our cases, although we would like to emphasize a slight variant that appears clinically interesting.
In combination with stent retrievers, the balloon guide catheter (BGC) has been shown to improve the effectiveness of mechanical thrombectomy2, 3. In our experience, we typically use the CAPTIVE technique in association with a BGC which presents several potential advantages.
Firstly, in cases of tortuous anatomy it provides excellent support for navigating the distal aspiration catheter. In addition, the balloon can be temporarily inflated at this stage to provide an anchoring effect in order to avoid potential push back of the guiding catheter4.
Secondly, McTaggart et al. reported 5% embolization to new territory with the CAPTIVE technique; an equivalent rate to previous reports on distal aspiration with no stent retriever5. In an in vitro study, Chueh et al.6 demonstrated a significant decrease o...
We have read with great interest the article describing the CAPTIVE technique for endovascular acute ischemic treatment by McTaggart et al.1. Firstly, we would like to commend the great clarity they used to describe the combination of distal aspiration and stent retriever to perform mechanical thrombectomy. Notably, they illustrated the rationale for aspiration prior to stent deployment as well as the removal of both distal aspiration catheter and stent as a single unit to decrease possible clot fragmentation.
We adopt a very similar approach for most of our cases, although we would like to emphasize a slight variant that appears clinically interesting.
In combination with stent retrievers, the balloon guide catheter (BGC) has been shown to improve the effectiveness of mechanical thrombectomy2, 3. In our experience, we typically use the CAPTIVE technique in association with a BGC which presents several potential advantages.
Firstly, in cases of tortuous anatomy it provides excellent support for navigating the distal aspiration catheter. In addition, the balloon can be temporarily inflated at this stage to provide an anchoring effect in order to avoid potential push back of the guiding catheter4.
Secondly, McTaggart et al. reported 5% embolization to new territory with the CAPTIVE technique; an equivalent rate to previous reports on distal aspiration with no stent retriever5. In an in vitro study, Chueh et al.6 demonstrated a significant decrease of distal emboli when a BGC is combined with a stent retriever. They also showed an increased risk of distal embolization when using the direct aspiration technique (ADAPT). Since the CAPTIVE technique has evolved from the ADAPT technique, so similarly, once the clot is engaged inside the aspiration catheter the flow reversal stops. By promoting flow arrest, the addition of a BGC could potentially decrease the rate of embolization in new territory, particularly in cases of either long clots incompletely covered by the stent or soft elastic clots, as suggested in vitro6.
Finally, the large lumen of the BGC is likely to avoid any shearing of the embolus during withdrawal of the distal aspiration catheter inside the guiding catheter. A similar potential hazard was importantly illustrated by McTaggart et al. in cases of inadvertent advance of the distal aspiration catheter over the clot-stent complex during removal of the stent.
The use of a BGC in addition to the CAPTIVE technique could however pose certain limitations. Firstly, navigating a 9F catheter is clearly more challenging than a 6F catheter, particularly in cases of tortuous anatomy; although often an exchange manoeuver over a stiff wire allows an appropriate positioning of the BGC in the targeted vessel. The aspiration from the BGC is here limited due to the triaxial approach, hower the additional effect of blockage of the flow could also support the aspiration force of the distal catheter.
Also, in cases of M1 occlusion inflating the balloon may limit collateral flow to the ischemic area. Considering this, and as described by McTaggart et al., our strategy is to turn on distal aspiration prior to deployment of the stent retriever but only prior to removal of the stent the BGC is inflated and proximal aspiration is turned on.
To conclude we would like to thank McTaggart et al. for sharing their experience. In accordance with other recently published studies7 their work emphasize the need to reach high rates of TICI3 recanalization to maximize the likelihood of good clinical outcomes for our patients.
1. McTaggart RA, Tung EL, Yaghi S, et al. Continuous aspiration prior to intracranial vascular embolectomy (CAPTIVE): a technique which improves outcomes. Journal of NeuroInterventional Surgery; 2016:neurintsurg-2016-012838-012836
2. Velasco A, Buerke B, Stracke CP, et al. Comparison of a Balloon Guide Catheter and a Non–Balloon Guide Catheter for Mechanical Thrombectomy. Radiology; 2016:169-176
3. Nguyen TN, Malisch T, Castonguay AC, et al. Balloon Guide Catheter Improves Revascularization and Clinical Outcomes With the Solitaire Device: Analysis of the North American Solitaire Acute Stroke Registry. Stroke; 2013:141-145
4. Matsumoto H, Nishiyama H, Tetsuo Y, et al. Initial clinical experience using the two-stage aspiration technique (TSAT) with proximal flow arrest by a balloon guiding catheter for acute ischemic stroke of the anterior circulation. Journal of NeuroInterventional Surgery: British Medical Journal Publishing Group; 2016:neurintsurg-2016-012787-012786
5. Kowoll A, Weber A, Mpotsaris A, et al. Direct aspiration first pass technique for the treatment of acute ischemic stroke: initial experience at a European stroke center. Journal of NeuroInterventional Surgery; 2016:230-234
6. Chueh J-Y, Puri AS, Wakhloo AK, et al. Risk of distal embolization with stent retriever thrombectomy and ADAPT. Journal of NeuroInterventional Surgery; 2016:197-202
7. Dargazanli C, Consoli A, Barral M, et al. Impact of Modified TICI 3 versus Modified TICI 2b Reperfusion Score to Predict Good Outcome following Endovascular Therapy. American Journal of Neuroradiology: American Society of Neuroradiology; 2017:90-96
Giragani S et al. (published online 25 January 2017) described a remarkable case of recurrent transient ischemic attacks (TIA) due to carotid free floating thrombus. They successfully used stentriever with distal filter protection in retrieving the thrombus.
Here we share a similar case of TIA with right common carotid artery (CCA) floating thrombus that was effectively managed with distal filter protection and aspiration. A 48-year-male with recurrent ischemic symptoms detected to have right CCA long segment floating thrombus (approximately 4.5 cm) extending upto right proximal external carotid artery.* Under general anaesthesia through right femoral route long sheath guiding catheter (Neuron Max 6F088; Penumbra, Inc. Alameda, USA) was placed in right proximal CCA. After parking the filter device (Spider FX 6mm; eV3, Plymouth, Minnesota, USA) at distal cervical segment, thrombus was aspirated using penumbra system (5MAX ACE, 132 cm; Penumbra, Inc. Alameda, USA).* Final check angiography showed 80 % reduction in clot burden .*
Placing the filter protection device in the distal cervical segment does not protect thrombus migration to ECA, although it primarily prevent intracranial shower. In our index case thrombus fragment migrated to ECA, although it did not cause any neurological deficit. These cases highlight a novel technique to treat free floating thrombus.
With interest, I read this article and the authors' claim that their technique has not been previously described. A cursory search using PubMed would have shown that we described this approach almost 30 years ago:
Treatment of dural sinus thrombosis with local urokinase infusion. Case report. Scott JA, Pascuzzi RM, Hall PV, Becker GJ. J Neurosurg. 1988 Feb;68(2):284-7.
We appreciate the letter in response to our study and would like to offer the following. First and
foremost, it is obvious the authors of the letter feel that this study is an indictment of chiropractic care or spinal manipulation. To the neurosurgical and neurointerventional community, it should be clear that this study downplays any potential causality between chiropractic care and extracranial vessel dissection, as the study...
We appreciate the letter in response to our study and would like to offer the following. First and
foremost, it is obvious the authors of the letter feel that this study is an indictment of chiropractic care or spinal manipulation. To the neurosurgical and neurointerventional community, it should be clear that this study downplays any potential causality between chiropractic care and extracranial vessel dissection, as the study was not powered to analyze this with any significant statistical models. At no point is a causal link suggested and, in fact, we acknowledge the following in our discussion: The relationship between dissections and chiropractic manipulation remains controversial because of limited population studies and potentially confounding factors, such as underlying connective-tissue disorders and symptoms overlapping those of musculoskeletal disorders. The authors should be aware that the purpose of the study was to analyze our experience with dissections that required intervention and to discuss the safety/efficacy of our various endovascular modalities. It remains unclear why the authors feel that an analysis of rates of homocysteinaemia, yoga, and defecation are relevant to a technical article detailing catheter-based therapies for severe carotid or vertebral artery dissection.
Several other points warrant a response. The authors state that our study confirms that cervical artery dissection is a very rare condition, only identifying 116 cases from 20 years of records. This is a gross misinterpretation of the data. Again, this study only included cases of intervention. While cervical artery dissection can still generally be considered rare, the vast majority of dissections can be treated medically - therefore, the 116 cases only represent a minority of cervical dissections that have presented to our institution, and at no point does the study confirm that the pathology in general is a very rare condition. This misinterpretation is evident later in the authors letter, where they claim that the numbers provided in the study highlight how extremely rare VAD is in connection with chiropractic care. The study does not, in fact, highlight this at all because, once again, these are only cases that required endovascular intervention. One could, however, conclude that it is extremely rare that VAD in the setting of chiropractic care requires intervention.
The authors are absolutely correct in stating that the study did not report the timeline of events related to chiropractic treatment. Again, this was not a study powered to investigate potential causality between chiropractic care and cervical dissection - despite attempts to be as complete as possible, the study is inherently limited by its retrospective analysis. Furthermore, the authors suggest that it is merely protopathic bias or coincidence that patients who present with symptoms of acute onset neck/head pain have dissections after chiropractic care, given these symptoms can be attributable to dissections, themselves. The problem with this argument is that there are a myriad of other medical conditions in our field (i.e. subarachnoid hemorrhage) that present with the same symptoms - if protopathic bias were in play, one could conceivably make the same associations with dissection and other disease processes with similar presentations, yet this has not been shown. Additionally, and perhaps more concerning, if the authors truly believe that these symptoms suggest dissection was already present at the time of manipulation, why has the chiropractic community not recommended referring the patient to the nearest emergency department instead of proceeding with cervical manipulation?
Another point that remains unclear is why the authors feel it is more valuable to investigate the traumatic and iatrogenic VAD cases from a public health perspective. We would argue that there is little to no question about mechanism of injury when cervical or skull base fractures result in arterial dissection or when catheter-based angiography results in intimal injury (a well-known risk of angiography that is always disclosed to patients) - to suggest that this is relevant from a public health perspective is as logical as to suggest that patients either should not drive cars or undergo indicated invasive procedures. The larger question of whether or not cervical spinal manipulation carries with it the risk of arterial dissection (or worsening of pre-existing dissection) is, however, very relevant to the public health arena, and should be investigated with the proper studies - patients undergoing spinal manipulation certainly deserve an answer to this question for the purposes of informed consent. To reiterate, however, this study did not have the goal of answering this question in the least. What we aim to contribute to the literature with this study is a long-term comprehensive experience with catheter-based intervention for medically refractory dissection, a pathology that carries with it potentially life-threatening natural history if untreated.
Sincerely,
Karam Moon, MD
Bradley Gross. MD
Felipe C. Albuquerque, MD
We would like to raise some issues regarding the Moon et al article
"Stroke prevention by endovascular treatment of carotid and vertebral
artery dissections", recently published in Neurointerventional Surgery.1
We commend the authors for conducting research in the important area of
cervical artery dissection. Their study confirms that cervical artery
dissection is a very rare condition, with the...
We would like to raise some issues regarding the Moon et al article
"Stroke prevention by endovascular treatment of carotid and vertebral
artery dissections", recently published in Neurointerventional Surgery.1
We commend the authors for conducting research in the important area of
cervical artery dissection. Their study confirms that cervical artery
dissection is a very rare condition, with their study only identifying 116
cases from neurosurgery dept. records over 20 years.
Of Vertebral Artery Dissections (VAD) the authors reported that n=2
had received chiropractic care (i.e. 9%) prior to the VAD, which is an
extremely small number, over a 20 year period, especially in comparison to
39% who had trauma (which wasn't defined). The specifics of the
chiropractic care are unreported. Chiropractic care often does not
actually include spinal manipulation2, which is the specific treatment
potentially assumed to lead to VAD, therefore there is no way to exclude
obvious protopathic bias in place of the suggestion of causation.3 The
largest category of purported causes of VAD was spontaneous onset n=10
cases (44%), with iatrogenic cases (which also wasn't defined) being noted
as n=4 cases (17%). From these figures, another conclusion of this study
could be that iatrogenesis is twice as likely to cause VAD stroke than
even speciously assuming chiropractic care was the cause. It has been
concluded that chiropractic care is not causative for VAD. 2, 4-6 Church
et al in a systematic review conclude; "There is no convincing evidence to
support a causal link, and unfounded belief in causation may have dire
consequences." 7 An example of such dire consequences is found in Foreman
it al's case report where the assumption the patient's condition was a VAD
caused by prior chiropractic care delayed making an accurate diagnosis and
lead to a horrendous outcome.8
The authors also identified 93 cases of carotid artery dissection (CAD),
where n=57 (61%) were described as spontaneous onset, n=27 (29%) as
traumatic (again also not defined), and n=4 (4.3%) as after chiropractic
manipulation. The possible mechanisms for chiropractic spinal manipulative
therapy (SMT) causing CAD is tenuous, without even a biomechanically
plausible mechanism as the internal carotid artery is not subject to
appreciable strains during manipulation.9 Given the fact that no study has
found that CAD is associated with spinal manipulation the association
mentioned in Moon et al is also specious.
The total number of cases in their study (CAD and VAD) which may have been
preceded by chiropractic care was n=6, five percent of the 116 cases. This
compared to the 67/116 of total population, the authors reported that were
spontaneous (over 60%), which highlights how extremely rare VAD is in
connection with chiropractic care. From a public health perspective, it
would have been more valuable to investigate the traumatic (n=36), or
iatrogenic (n=13) VAD cases, which occurred at a frequently eight times
greater than chiropractic care.10-13
The author's write: "Not surprisingly, our patients with VAD were more
susceptible than those with CAD to traumatic dissection, undoubtedly
because of their anatomy and the widely accepted pathophysiology of
dissection." There is no reference for this and to our knowledge there is
no widely accepted pathophysiology of dissection that points to trauma and
VAD as opposed to CAD.10
According to Wolsko et al, five percent of the US population consult a
chiropractor every week, and many seek chiropractic treatment for neck
pain or headache.14 These symptoms are the most common presentation of
VAD or CAD, which infers the dissections may have occurred prior to any
chiropractic treatment15, 16 thus the association is likely protopathic
bias (Horwitz et al) This theory has been reported in previous studies.6,
7 Thus, studies that suggest a causal link of VAD with chiropractic care
remain speculative at best.
To us the most significant limitations of the Moon et al paper
related to the under-emphasis on pathogenesis of CAD stroke and associated
risk factors. For example, the authors neglected to assess the importance
of the myriad of risk factors that have been previously reported in the
literature. These include: body mass, smoking, hypertension,
hyperlipidemia, history of homocysteinaemia, migraine, recent
infection/fever, NSAID use, genetic blood vessel or connective tissue
disorders, cardiac abnormalities (such as patent foramen ovale), excessive
alcohol consumption, and recent physical or potential traumatic
activities.17, 18 These are all significant, well-established risk factors
in increasing the risk of stroke, and probably much more significant than
chiropractic SMT.
For example, other studies have also reported trivial mechanical factors
(hyperextension or rotation of the neck, including practicing yoga,
"beauty palour" visits, painting a ceiling, coughing, sneezing, vomiting
and the act of resuscitation), as trivial triggers for VAD. In addition,
several sports (trampolining, soccer, archery, etc), post motor vehicle
accident, conducting an orchestra and even defecation, have been reported
as potential trigger factors for stroke.11, 19-22
In addition, the paper had further weaknesses relating to theories
that chiropractic care may have been associated with VAD. For example, the
paper did not report the timeline of events related to the chiropractic
treatment. This includes the time from onset of presenting symptoms (eg
neck pain &/or headache) to presentation for treatment. The timeline
discussion should also include any other previous treatment(s), the
interval between onset of stroke symptoms to time of treatment, and post
treatment events. These factors are critical in any discussion of a
treatment being associated with, or causative to an adverse event.
There have been many examples of where a VAD occurred in time periods of
several weeks after chiropractic treatment, but still CMT is suggested as
causing the VAD. 15 Many recent studies have now repudiated this theory.
In addition, chiropractic care is also blamed as the cause of cases of
VAD when the practitioner was not even a chiropractor, in some cases a
medical practitioner (orthopaedist), physiotherapist, or an untrained
layman such as a barber.23 Such misattribution of stroke and
"chiropractic" has been found in the literature in the past and
inappropriately uses the term "chiropractic" as a synonym for spinal
manipulation.15, 24, 25
Furthermore, the quality of reporting with respect to CAD remains
problematic as a recent review found no single case report fulfilled all
Bradford-Hill causality criteria and under-report factors that would yield
valuable data concerning the specific profile of SMT procedures. For
example, data on type of manipulation (manual, mechanical-assisted),
technique (Diversified, Gonstead, etc) and anatomical location of SMT
application (C2-3 spinal segment) would generate important data regarding
the safety of various SMT procedures.
1. Moon K, Albuquerque FC, Cole T, Gross BA, McDougall CG. Stroke
prevention by endovascular treatment of carotid and vertebral artery
dissections. Journal of neurointerventional surgery. 2016
2. Kosloff TM, Elton D, Tao J, Bannister WM. Chiropractic care and the
risk of vertebrobasilar stroke: Results of a case-control study in u.S.
Commercial and medicare advantage populations. Chiropractic & manual
therapies. 2015;23:19
3. Feinstein AR, Horwitz RI. Choosing cases and controls: The clinical
epidemiology of "clinical investigation". Journal of Clinical
Investigation. 1988;81:1-5
4. Tuchin P. Chiropractic and stroke: Association or causation?
International journal of clinical practice. 2013;67:825-833
5. Wynd S, Westaway M, Vohra S, Kawchuk G. The quality of reports on
cervical arterial dissection following cervical spinal manipulation. PloS
one. 2013;8:e59170
6. Cassidy JD, Boyle E, Cote P, He Y, Hogg-Johnson S, Silver FL, et al.
Risk of vertebrobasilar stroke and chiropractic care: Results of a
population-based case-control and case-crossover study. Spine.
2008;33:S176-183
7. Church EW, Sieg EP, Zalatimo O, Hussain NS, Glantz M, Harbaugh RE.
Systematic review and meta-analysis of chiropractic care and cervical
artery dissection: No evidence for causation. Cureus. 2016;8:e498
8. Foreman SM, Stahl MJ, Schultz GD. Paraplegia in a chiropractic patient
secondary to atraumatic dural arteriovenous fistula with perimedullary
hypertension: Case report. Chiropractic & manual therapies. 2013;21:23
-23
9. Herzog W, Tang C, Leonard T. Internal carotid artery strains during
high-speed, low-amplitude spinal manipulations of the neck. Journal of
manipulative and physiological therapeutics. 2015;38:664-671
10. Debette S, Leys D. Cervical-artery dissections: Predisposing factors,
diagnosis, and outcome. Lancet neurology. 2009;8:668-678
11. Dittrich R, Rohsbach D, Heidbreder A, Heuschmann P, Nassenstein I,
Bachmann R, et al. Mild mechanical traumas are possible risk factors for
cervical artery dissection. Cerebrovascular diseases (Basel, Switzerland).
2007;23:275-281
12. Schievink WI, Roiter V. Epidemiology of cervical artery dissection.
Frontiers of neurology and neuroscience. 2005;20:12-15
13. Chandra A, Suliman A, Angle N. Spontaneous dissection of the carotid
and vertebral arteries: The 10-year ucsd experience. Annals of vascular
surgery. 2007;21:178-185
14. Wolsko PM, Eisenberg DM, Davis RB, Kessler R, Phillips RS. Patterns
and perceptions of care for treatment of back and neck pain: Results of a
national survey. Spine. 2003;28:292-297; discussion 298
15. Tuchin P. A replication of the study 'adverse effects of spinal
manipulation: A systematic review'. Chiropractic & manual therapies.
2012;20:30
16. Biller J, Sacco RL, Albuquerque FC, Demaerschalk BM, Fayad P, Long PH,
et al. Cervical arterial dissections and association with cervical
manipulative therapy: A statement for healthcare professionals from the
american heart association/american stroke association. Stroke; a journal
of cerebral circulation. 2014;45:3155-3174
17. Yaghi S, Maalouf N, Keyrouz SG. Cervical artery dissection: Risk
factors, treatment, and outcome; a 5-year experience from a tertiary care
center. The International journal of neuroscience. 2012;122:40-44
18. Micheli S, Paciaroni M, Corea F, Agnelli G, Zampolini M, Caso V.
Cervical artery dissection: Emerging risk factors. The open neurology
journal. 2010;4:50-55
19. Engelter ST, Grond-Ginsbach C, Metso TM, Metso AJ, Kloss M, Debette S,
et al. Cervical artery dissection: Trauma and other potential mechanical
trigger events. Neurology. 2013;80:1950-1957
20. Lleva P, Ahluwalia BS, Marks S, Sahni R, Tenner M, Risucci DA, et al.
Traumatic and spontaneous carotid and vertebral artery dissection in a
level 1 trauma center. Journal of clinical neuroscience : official journal
of the Neurosurgical Society of Australasia. 2012;19:1112-1114
21. Rubinstein S, Cote P. Mild mechanical traumas are possible risk
factors for cervical artery dissection. Cerebrovascular diseases (Basel,
Switzerland). 2007;24:319
22. Nyberg J, Olsson T, Malm J. Carotid and vertebral artery dissection a
common cause of stroke among younger persons. Minor trauma a precipitating
factor in more than fifty percent according to a retrospective study.
Lakartidningen. 2007;104:24-28
23. Melikyan G, Kamran S, Akhtar N, Deleu D, Miyares FR. Cortex-sparing
infarction in triple cervical artery dissection following chiropractic
neck manipulation. Qatar medical journal. 2015;2015:16
24. Wenban AB. Inappropriate use of the title chiropractor: Reason for
concern? Clinical neurology and neurosurgery. 2008;110:425-426
25. Terrett AG. Misuse of the literature by medical authors in discussing
spinal manipulative therapy injury. Journal of manipulative and
physiological therapeutics. 1995;18:203-210
We read with interest the article entitled: “Delayed enhancing lesions after coil embolization of aneurysms: clinical experience and benchtop analyses” by Oh et al [1]. This interesting case series deals with a recently described complication of intracranial endovascular procedures [2–8]: delayed enhancing lesions (DELs), also known as NICE (non-ischemic cerebral enhancing) lesions [8]. This rare complication consists in delayed appearance of cortical leptomeningeal enhancement associated with vasogenic subcortical edema [8]. The authors describe 3 more cases, in addition to the 19 previously reported [8]. We congratulate the authors for their efforts to understand the mechanism of this rare complication by performing benchtop tests.
Numerous hypotheses have been proposed to explain this complication.
First, an allergic reaction to nickel has been suggested [4,7]. In a series we recently published in Neuroradiology [8], we did not find any allergic reaction to the devices used for the embolization of the patients who presented NICE lesions. The fact that, in the series of Oh et al [1], none of the three patients had an allergic background, seems to confirm the absence of any relationship between these lesions and allergy.
The second hypothesis is a reaction to foreign bodies (catheter coating) released during the embolization. We do believe that, according to our experience [8] and to the data of the literature [2,3,5,6], these lesions are more likely to...
We read with interest the article entitled: “Delayed enhancing lesions after coil embolization of aneurysms: clinical experience and benchtop analyses” by Oh et al [1]. This interesting case series deals with a recently described complication of intracranial endovascular procedures [2–8]: delayed enhancing lesions (DELs), also known as NICE (non-ischemic cerebral enhancing) lesions [8]. This rare complication consists in delayed appearance of cortical leptomeningeal enhancement associated with vasogenic subcortical edema [8]. The authors describe 3 more cases, in addition to the 19 previously reported [8]. We congratulate the authors for their efforts to understand the mechanism of this rare complication by performing benchtop tests.
Numerous hypotheses have been proposed to explain this complication.
First, an allergic reaction to nickel has been suggested [4,7]. In a series we recently published in Neuroradiology [8], we did not find any allergic reaction to the devices used for the embolization of the patients who presented NICE lesions. The fact that, in the series of Oh et al [1], none of the three patients had an allergic background, seems to confirm the absence of any relationship between these lesions and allergy.
The second hypothesis is a reaction to foreign bodies (catheter coating) released during the embolization. We do believe that, according to our experience [8] and to the data of the literature [2,3,5,6], these lesions are more likely to be related to fragments migration of the inner wall’s coating of the guiding catheter and/or of the outer wall of the microcatheters, rather than from the inner wall of the microcatheters. Indeed, as in our experience [8], in all the patients of the series published by Oh et al [1], the lesions were located in the territory of the endovascular treatment (i.e.: in the territory of the parent artery in which the guiding catheter was positioned). If the coating fragments have come from the inner lumen of the microcatheters, as claimed by the authors, the emboli would have only occur distally to the microcatheter’s tip (i.e. in the aneurysm’s sac). This hypothesis does not explain the distribution of the lesions observed on MRI. Additionally, as underlined by the authors, the patient treated with the microcatheter that showed coating fragments at the location of the friction on bench tests did not have DEL.
Shapiro et al [5] reported three cases of delayed NICE lesions after endovascular aneurysm treatment with pathological examination of the lesions. Foreign bodies were found and identified as being identical in stain appearance to polyvinylpolypyrrolidone (PVP) catheter coating.
What seems very surprising for us, is the recent increasing of these complications reported in the literature. Indeed, brain aneurysms treated by embolizations have been followed by MRI for many years but this complication has only been recently described. Three hypotheses may be advanced. First, the neurointerventional community only recently became aware of this complication first published in the cardiology and pathology literature [3]. Second, the emergence of this complication may be related to increased use of triaxial catheter access in endovascular aneurysm treatments, that may favor mechanical stress on the inner lumen coating of the guiding catheters. Finally, the emergence of this complication may be related to a recent modification of coating technology, which has yet to be identified.
References:
1 Oh SW, Shin NY, Lee H-J, et al. Delayed enhancing lesions after coil embolization of aneurysms: clinical experience and benchtop analyses. J Neurointerventional Surg Published Online First: 6 January 2017. doi:10.1136/neurintsurg-2016-012833
2 Cruz JP, Marotta T, O’Kelly C, et al. Enhancing brain lesions after endovascular treatment of aneurysms. AJNR Am J Neuroradiol 2014;35:1954–8. doi:10.3174/ajnr.A3976
3 Fealey ME, Edwards WD, Giannini C, et al. Complications of endovascular polymers associated with vascular introducer sheaths and metallic coils in 3 patients, with literature review. Am J Surg Pathol 2008;32:1310–6. doi:10.1097/PAS.0b013e318165582a
4 Lobotesis K, Mahady K, Ganesalingam J, et al. Coiling-associated delayed cerebral hypersensitivity: Is nickel the link? Neurology 2015;84:97–9. doi:10.1212/WNL.0000000000001106
5 Shapiro M, Ollenschleger MD, Baccin C, et al. Foreign Body Emboli following Cerebrovascular Interventions: Clinical, Radiographic, and Histopathologic Features. AJNR Am J Neuroradiol Published Online First: 20 August 2015. doi:10.3174/ajnr.A4415
6 Skolarus LE, Gemmete JJ, Braley T, et al. Abnormal white matter changes after cerebral aneurysm treatment with polyglycolic-polylactic acid coils. World Neurosurg 2010;74:640–4. doi:10.1016/j.wneu.2010.03.026
7 Ulus S, Yakupoğlu A, Kararslan E, et al. Reversible intracranial parenchymal changes in MRI after MCA aneurysm treatment with stent-assisted coiling technique; possible nickel allergy. Neuroradiology 2012;54:897–9. doi:10.1007/s00234-012-1048-2
8 Shotar E, Law-Ye B, Baronnet-Chauvet F, et al. Non-ischemic cerebral enhancing lesions secondary to endovascular aneurysm therapy: nickel allergy or foreign body reaction? Case series and review of the literature. Neuroradiology Published Online First: 23 May 2016. doi:10.1007/s00234-016-1699-5
With great interest, we read the article of Venkatraman et al.[1] published in the Journal of NeuroInterventional Surgery recently. They presented a comprehensive picture depicting the effect of intra-arterial vasodilators (IADs) on the vasospasm following aneurysmal subarachnoid hemorrhage. But we were concerned with several questions weakening the reliability and generalization of the meta-analysis.
Show MoreFirstly , though the detailed including criteria and searching strategy were provided in their meta-analysis, at least two eligible studies2,3 were missed which conformed to their including criteria and unfulfilled the excluding criteria. Two cohort studies of Morgan [2] and Mortimer [3] reported the effects of IADs on vasospasm with documentation of interested events, which should be included in Venkatraman’s analysis. Whether addition of these two studies could change the overall effect of IADs was unclear, but including any eligible study was in accordance with PRISMA principle.
Secondly, owing to the large number of included studies, the heterogeneity was substantial. Venkatraman et al.[1] conducted subgroup and sensitivity analyses, in which the heterogeneity remained significant (most values of I2 greater than 50%). It was rationale to turn to regression analyses in order to find and solve the heterogeneity.
Besides, this article included studies combining IADs with balloon angioplasty, which might overestimate effectiveness of IADs. IADs w...
We would like to thank Dr. Shotar and colleagues for their interest in our article. As highlighted by Dr. Shotar, delayed enhancing lesions (DEL) after coil embolization of aneurysm are suspected as a result of foreign body reaction 1-5. We agree with their opinion that the catheter coating of the inner wall of guiding catheter and/or the outer wall of microcatheter may be the source of foreign body. However, according to our experiences and analysis, it is our opinion that the coating material of the inner wall of microcatheter may also be the source.
Show MoreDr Shotar suggests that the distribution of the MR lesions in the territory of the parent artery (i.e.: ICA) in our series suggests the guiding catheter as the culprit. However, in all our cases 6, the aneurysms were located at the distal ICA (Ophthalmic artery, IC-anterior choroidal artery, superior hypophyseal artery). Thus, we believe that the distribution of the DELs on MR is not in conflict with our claim that the inner wall of the microcatheter is the source. Foreign body fragments from the microcatheter probably migrated into the aneurysmal sac during multiple coil introduction attempts under unusual friction and were swept downstream. Our benchtop analyses also support this finding.
Regarding Dr Shotar’s suggestion that "the patient treated with the microcatheter that showed coating fragments at the location of the friction on bench tests did not have DELs", this microcatheter was withdrawn imme...
To the Editor:
We read with great interest the article by McTaggart et al. on the new embolectomy technique called Continuous Aspiration Prior To Intracranial Vascular Embolectomy (CAPTIVE).(1) The paper adds information on the supporting evidence that a combined approach of stentretriever and aspiration-catheter utilization may be the optimal path in achieving higher rates of complete reperfusion in patients with large vessel occlusions.(2, 3) While the idea of starting aspiration with the intermediate catheter prior to and during the stentretriever placement is intriguing, attention has to be paid on the effect of prolonged aspiration on collateral flow, as reported in a recent JNIS publication.(4) Additionally, the ‘continuous’ part of the title may be misleading, as the authors state that they advance the aspiration-catheter towards the face of the clot until the drip rate has stopped. As seen in Fig 1E of the CAPTIVE publication, the tip of the aspiration-catheter becomes clogged with clot as ‘a portion is held captive within the distal aspiration catheter.’ This probably results in vacuum within the aspiration-catheter and non-existent aspiration in the vicinity of the aspiration-catheter tip during immobilization of the stentretriever/clot/aspiration-catheter unit. At last, the authors describe thoroughly a ‘De-CAPTIVE shear’ on Fig 2 but neglect to acknowledge that the same danger of clot-shearing applies to the moments of stentretriever/clot/aspiration-cath...
Show MoreTo the editor,
With great interest we read the recent paper by Martinez-Galdámez et al. regarding the periprocedural outcomes and early safety after placement of a Pipeline Embolization Device with Shield Technology (PEDshield) (1). Evaluation of new endovascular devices, such as PEDshield, is of the utmost importance to give future users a chance to objectively review possible benefits for their clinical practice.
In the study of Martinez-Galdámez et al. 76% of the target aneurysms were small (< 10 mm). It is known that small aneurysms are associated with a lower probability of thromboembolisms and ischemic stroke after flow diverter treatment than large and giant aneurysms (2,3). The size of the treated aneurysms, and not the PEDshield, might therefore explain the lack of thromboembolic complications reported in the study of Martinez-Galdámez et al. Selection bias might thus have led to the conclusion that the early safety of the PEDshield device is warranted.
Furthermore, it is hard to understand why only 21 out of 50 patients (42%) underwent platelet reactivity testing, especially since the primary outcome measure focused on identifying thromboembolic complications in the territory supplied by the treated artery. To make matters worse: when platelet reactivity tests revealed the presence of hyporesponders, anti-platelet therapy was left unchanged in most cases. If thromboembolic complications do occur in the 6-month and 1-year follow-up of this...
Show MoreWe have read with great interest the article describing the CAPTIVE technique for endovascular acute ischemic treatment by McTaggart et al.1. Firstly, we would like to commend the great clarity they used to describe the combination of distal aspiration and stent retriever to perform mechanical thrombectomy. Notably, they illustrated the rationale for aspiration prior to stent deployment as well as the removal of both distal aspiration catheter and stent as a single unit to decrease possible clot fragmentation.
We adopt a very similar approach for most of our cases, although we would like to emphasize a slight variant that appears clinically interesting.
In combination with stent retrievers, the balloon guide catheter (BGC) has been shown to improve the effectiveness of mechanical thrombectomy2, 3. In our experience, we typically use the CAPTIVE technique in association with a BGC which presents several potential advantages.
Show MoreFirstly, in cases of tortuous anatomy it provides excellent support for navigating the distal aspiration catheter. In addition, the balloon can be temporarily inflated at this stage to provide an anchoring effect in order to avoid potential push back of the guiding catheter4.
Secondly, McTaggart et al. reported 5% embolization to new territory with the CAPTIVE technique; an equivalent rate to previous reports on distal aspiration with no stent retriever5. In an in vitro study, Chueh et al.6 demonstrated a significant decrease o...
To the editor,
Giragani S et al. (published online 25 January 2017) described a remarkable case of recurrent transient ischemic attacks (TIA) due to carotid free floating thrombus. They successfully used stentriever with distal filter protection in retrieving the thrombus.
Here we share a similar case of TIA with right common carotid artery (CCA) floating thrombus that was effectively managed with distal filter protection and aspiration. A 48-year-male with recurrent ischemic symptoms detected to have right CCA long segment floating thrombus (approximately 4.5 cm) extending upto right proximal external carotid artery.* Under general anaesthesia through right femoral route long sheath guiding catheter (Neuron Max 6F088; Penumbra, Inc. Alameda, USA) was placed in right proximal CCA. After parking the filter device (Spider FX 6mm; eV3, Plymouth, Minnesota, USA) at distal cervical segment, thrombus was aspirated using penumbra system (5MAX ACE, 132 cm; Penumbra, Inc. Alameda, USA).* Final check angiography showed 80 % reduction in clot burden .*
Placing the filter protection device in the distal cervical segment does not protect thrombus migration to ECA, although it primarily prevent intracranial shower. In our index case thrombus fragment migrated to ECA, although it did not cause any neurological deficit. These cases highlight a novel technique to treat free floating thrombus.
*Representative image available.
With interest, I read this article and the authors' claim that their technique has not been previously described. A cursory search using PubMed would have shown that we described this approach almost 30 years ago:
Treatment of dural sinus thrombosis with local urokinase infusion. Case report. Scott JA, Pascuzzi RM, Hall PV, Becker GJ. J Neurosurg. 1988 Feb;68(2):284-7.
We appreciate the letter in response to our study and would like to offer the following. First and foremost, it is obvious the authors of the letter feel that this study is an indictment of chiropractic care or spinal manipulation. To the neurosurgical and neurointerventional community, it should be clear that this study downplays any potential causality between chiropractic care and extracranial vessel dissection, as the study...
To the editor,
We would like to raise some issues regarding the Moon et al article "Stroke prevention by endovascular treatment of carotid and vertebral artery dissections", recently published in Neurointerventional Surgery.1 We commend the authors for conducting research in the important area of cervical artery dissection. Their study confirms that cervical artery dissection is a very rare condition, with the...
We read with interest the article entitled: “Delayed enhancing lesions after coil embolization of aneurysms: clinical experience and benchtop analyses” by Oh et al [1]. This interesting case series deals with a recently described complication of intracranial endovascular procedures [2–8]: delayed enhancing lesions (DELs), also known as NICE (non-ischemic cerebral enhancing) lesions [8]. This rare complication consists in delayed appearance of cortical leptomeningeal enhancement associated with vasogenic subcortical edema [8]. The authors describe 3 more cases, in addition to the 19 previously reported [8]. We congratulate the authors for their efforts to understand the mechanism of this rare complication by performing benchtop tests.
Show MoreNumerous hypotheses have been proposed to explain this complication.
First, an allergic reaction to nickel has been suggested [4,7]. In a series we recently published in Neuroradiology [8], we did not find any allergic reaction to the devices used for the embolization of the patients who presented NICE lesions. The fact that, in the series of Oh et al [1], none of the three patients had an allergic background, seems to confirm the absence of any relationship between these lesions and allergy.
The second hypothesis is a reaction to foreign bodies (catheter coating) released during the embolization. We do believe that, according to our experience [8] and to the data of the literature [2,3,5,6], these lesions are more likely to...
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