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
We would like to thank our colleagues for reading our publication and
for the thorough review of the paper. We greatly look forward to reading
their own experience and believe that it will add substantially to the
literature on this new and interesting device.
At the outset we would like to make it clear that we stand by our
initial comment in saying that we believe the combination of a MED and
other devices,...
We would like to thank our colleagues for reading our publication and
for the thorough review of the paper. We greatly look forward to reading
their own experience and believe that it will add substantially to the
literature on this new and interesting device.
At the outset we would like to make it clear that we stand by our
initial comment in saying that we believe the combination of a MED and
other devices, in particular intra-luminal FDS may have excellent and
extremely rapid results. To that end we are currently in the process of
collating our cases of this nature in preparation to submit for
publication but we have seen extremely rapid aneurysm exclusion.
The use of adjunctive devices in some instances was not planned. In
one case, which was discussed in the original article, after deployment of
the MED it was noted that the residual flow into the aneurysm had been
inadvertently redirected into an aneurysm bleb. We do not believe this
was due to a sizing issue but rather an effect that can occur from the
position of the petals which can in our experience be relatively difficult
to determine even after deployment of the MED. We did not feel this was a
safe situation to leave the aneurysm and therefore treated the bleb with
coils. A similar situation was encountered with the basilar tip aneurysm.
In both scenarios we felt uncomfortable leaving parts of the aneurysm
unprotected. The use of FDS was to treat the aneurysm neck in certain
cases e.g. the patients represented in Fig. 8 and 9. However, in another
case the use of the FDS was not to treat the aneurysm with MED's but an
adjacent blister like aneurysm (Fig. 10). Furthermore, in patient 9, again
there were multiple aneurysms on the right with only one suitable for
treatment with MED and therefore the placement of the FDS subsequently
served as an additional treatment strategy for the other smaller aneurysms
as well as the aneurysm that contained the MED. This patient represented
one of our first patients in whom we used the MED and hence our
understanding of its pro's and con's was not fully developed.
Our reasoning for the deployment of MED and FDS was covered in the discussion section of our publication. However, in our literature search for our upcoming paper we have come across evidence which we believe supports our initial assertion of the effectiveness of MED+FDS. Jing et al [1] recently published their work on the heamodynamic effect of flow diverters in combination with coils in large and giant aneurysms. The FDS used in this study was the Tubridge FDS. Their computational fluid dynamics (CFD) study showed that the combination of coils and FDS resulted in significantly decreased intra-aneurysmal flow velocity, wall shear stress and increase in low wall shear area with a decrease of 54%, 66% and increase of 1001% respectively. Damiano et al [2] recently showed that the principle action of FDS, in the early stages of treatment, are flow redirection away from the aneurysm with 2 overlapping FDS compounding the effect but no significant increased effect seen with the addition of a third FDS. In this study the role of coils was to disturb aneurysmal flow, reduce intra-aneurysmal flow velocity and WSS and disturb aneurysmal flow patterns when the coil packing density exceeds 11%. Below this level the coils may have a scaffolding effect for intra-aneurysmal thrombus but do not appear to have a significant heamodynamic effect. It is likely that the MED has a heamodynamic effect greater than 11% coil packing density, although we are unaware of any studies that have looked at this. Therefore, the combination of MED and FDS is likely similar to that of FDS and coils with high packing density, a strategy which has shown a higher occlusion rate and lower rate of retreatment in a recent study by Lin et al. [3].
Whilst it is indeed true that the MED was not used as the sole device
in many of our aneurysms our primary aim when using this device was to
determine its effectiveness in a 'real-world' setting. As the device is
designed to adopt a spherical shape, and if it was only used in spherical
aneurysms, it would only be suitable for use in approximately 1/3 of
unruptured aneurysms according to the study of You et al [4]. This
problem was covered in the discussion. We chose to use the MED in non-
spherical aneurysms because we believed that the flow disruption caused by
the device inside the aneurysm would nevertheless promote thrombosis.
Furthermore, in the first publication regarding the MED, by Turk et al[5],
1/3 of the aneurysms were not 'spherical'. For example, patient 1 in the
series of Turk et al. had an aneurysm with dimensions 12.1 x 7.24 x 5.47mm
and yet at 1 month follow-up occlusion was reported as 95%. In addition
this group also used a 'sequential' filling of an ACOM aneurysm that is
represented in Fig. 3 and 4 in their publication. This was a strategy that
we have used that takes advantage of the flow disrupting effect but not
really of the shape the MED adopts.
The use of adjunctive devices such as the pCONus may or may not
hamper the deployment of the device but as of yet there is no evidence to
suggest a conclusion. The assertion that the pCONus somehow interfered
with the deployment of the MED appears to be nothing more than conjecture.
Our standard procedure is to mechanically detach the pCONus as the last
step in any procedure involving it. As such we may reposition it in
during the coiling or MED deployment procedure and hence we may reposition
it to allow maximum neck protection and minimum 'hampering' with any intra
-saccular devices be they coils or MED's.
We agree with the authors that the follow-up period is short and we
hope to publish subsequent studies in the future with longer-term follow-
up. However, the follow-up period in the original Turk et al. [5] paper
was also short with 1 month angiographic follow-up available for 5/9
aneurysms and no occlusion seen in 2 of the 5 with early follow-up. Our
publication was not meant to be a study with long term follow-up, rather
our initial experience and insights that we believed may be useful to our
colleagues should they wish to use the MED. We are therefore slightly
confused as to why short-term follow-up is a problem in our paper but not
in the paper of Turk et al.
With regards to sizing, this is perhaps also a matter of debate. It
is important to recall that very recently the sizing recommendations of
the WEB were altered based on clinical experience and observation. As
discussed earlier the problem with sizing relates to the spherical shape
of the MED. In our cases that are said to be undersized the MED was
actually sized to fit the most 'spherical' part of the aneurysms. By
oversizing the MED one cannot predict how the leaflets will position
themselves and then one cannot predict the effect on flow created by the
device. This was described for one of our cases (Fig. 5c) despite using
our sizing technique and this inability to accurately predict the position
of the leaflets has been one of our main observations.
As suggested by the authors coils would be an alternative, and in
fact would be an excellent alternative in all of these cases, although the
additional uses of stents, neck bridging devices etc. may still be needed.
The issue of cost is of course important however, with the current cost of
the device relative to coils, the use of 2 MED's is approximately the
equivalent cost to 40coils - and very few aneurysms would require this
many coils. In fact very few aneurysms require 20 coils and therefore, the
issue reverts to the speed and security of any occlusion obtained. This
then reverts back to our original supposition that the combination of
intra-saccular and intra-luminal flow diversion. We believe that a rapid
and durable aneurysm exclusion can be achieved through a single intra-
luminal flow diverter and in all likelihood only one or two MED's.
In conclusion we thank the authors for their comments and look
forward to reading their publication in the coming months. We hope they
will also enjoy our second publication dedicated to the use of intra-
luminal and intra-saccular flow diversion.
Funding Statement
This research received no specific grant from any funding agency in the
public, commercial or not-for-profit sectors
Conflict of interest
MAP, PB and RMM serve as proctors and consultants for phenox GmbH, with
moderate financial compensation.
HH is a co-founder and shareholder of phenox GmbH.
The other authors have no potential conflict of interest.
References:
1 Jing L, Zhong J, Liu J, et al. Hemodynamic Effect of Flow Diverter and
Coils in Treatment of Large and Giant Intracranial Aneurysms. World
Neurosurg 2016;89:199-207. doi:10.1016/j.wneu.2016.01.079
2 Damiano RJ, Ma D, Xiang J, et al. Finite Element Modeling of
Endovascular Intervention Enables Hemodynamic Prediction of Complex
Treatment Strategies for Coiling and Flow Diversion. J Biomech
2015;48:3332-40. doi:10.1016/j.jbiomech.2015.06.018
3 Lin N, Brouillard AM, Krishna C, et al. Use of coils in conjunction
with the pipeline embolization device for treatment of intracranial
aneurysms. Neurosurgery 2015;76:142-9. doi:10.1227/NEU.0000000000000579
4 You S-H, Kong D-S, Kim J-S, et al. Characteristic features of
unruptured intracranial aneurysms: predictive risk factors for aneurysm
rupture. J Neurol Neurosurg Psychiatry 2010;81:479-84.
doi:10.1136/jnnp.2008.169573
5 Turk AS, Maia O, Ferreira CC, et al. Periprocedural safety of aneurysm
embolization with the Medina Coil System: the early human experience. J
Neurointerventional Surg 2016;8:168-72. doi:10.1136/neurintsurg-2014-
011585
Conflict of Interest:
MAP, PB and RMM serve as proctors and consultants for phenox GmbH, with moderate financial compensation.
HH is a co-founder and shareholder of phenox GmbH.
The other authors have no potential conflict of interest.
We read with great interest the article of Haussen et al. 1 outlining the problem of identifying patients with minor stroke symptoms (low NIHSS) despite proximal vessel occlusion who should undergo thrombectomy. Intension-to-treat analysis showed significantly higher reduction of stroke severity in the primary thrombectomy group compared to the medical group. But more interestingly, per-protocol analysis revealed a high propo...
We read with great interest the article of Haussen et al. 1 outlining the problem of identifying patients with minor stroke symptoms (low NIHSS) despite proximal vessel occlusion who should undergo thrombectomy. Intension-to-treat analysis showed significantly higher reduction of stroke severity in the primary thrombectomy group compared to the medical group. But more interestingly, per-protocol analysis revealed a high proportion of rescue thrombectomies due to neurological deterioration with a clearly time-dependent effect on outcome after the procedure in the medical group. In our opinion, the problem is multidimensional. In proximal vessel occlusion, intravenous thrombolysis combined with thrombectomy is superior to thrombolysis alone. Current guidelines strongly recommend thrombectomy in these patients and not to stop after intravenous thrombolysis 2. Therefore, it is critical to identify ischemic stroke due to proximal vessel occlusion. High stroke severity measured by the NIHSS has been used as a clinical surrogate to detect major vessel occlusion. Fischer et al. reported an NIHSS threshold of 12 to have a positive predictive value of 91% for central occlusion 3. But this approach can be misleading as the NIHSS represents the amount of ischemic tissue, which is influenced by residual blood supply beyond the occlusion, especially by collateral circulation. Good collaterals can lead to a low NIHSS score in stroke with proximal vessel occlusion. Maas et al. showed that higher NIHSS cutoffs to predict major vessel occlusion missed more proximal occlusions, concluding that there was no NIHSS threshold to identify the majority of clinically important occlusive lesions. An NIHSS threshold of 10, for example had only 48% sensitivity 4. Minor stroke severity resulting in a low NIHSS is not uncommon in proximal vessel occlusion. One group identified 23% of patients with NIHSS <8 in a retrospective database search 5. In another population, approx. 90% of patients presenting with an NIHSS <=10 were found to have major vessel occlusion 4. In our opinion, current data indicate that all stroke patients admitted within the therapeutic time window should undergo vascular imaging. Another question is how to treat these patients. Until a few years ago intravenous thrombolysis was given only to patients with a "significant" neurological deficit, commonly defined as an NIHSS of 4 or higher. Today we know that low NIHSS stroke, even without proximal vessel occlusion, has unfavourable long-term outcome and that intravenous thrombolysis seems to be beneficial in this setting 6 with low risk of intracrcanial bleeding 7. In clinical practice, we today concentrate on individual deficits and try to individualize the treatment decision. In patients with central occlusion and NIHSS 2-7, the natural course is also rather unfavourable. Even in this low NIHSS stratum higher stroke severity was significantly associated with discharge into a facility and gait problems 5. The current study adds important knowledge for decision making in this situation as 41% of the medical group deteriorated a few hours after admission, which was likely caused by failure of the collateral system. Those who were "lucky" to suffer fast breakdown of collateral supply had better functional outcome after rescue thrombectomy than those with later failure. For future treatment algorithms, it will be essential to know more about the dynamics of collateral circulation and to develop a strategy to predict their failure. Currently, it is very difficult to make individual treatment decisions in this subset of patients as the thrombectomy procedure itself has a risk of recurrent stroke, vasospasm and subarchnoid hemorrhage 8.
References
1. Haussen DC, Bouslama M, Grossberg JA, et al. Too good to
intervene? Thrombectomy for large vessel occlusion strokes with minimal
symptoms: an intention-to-treat analysis. J Neurointerv Surg Published
Online First: 2 Sep 2016. doi: 10.1136/neurintsurg-2016-012633.
2. Powers WJ, Derdeyn CP, Biller J, et al. 2015 AHA/ASA Focused Update of
the 2013 Guidelines for the Early Management of Patients With Acute
Ischemic Stroke Regarding Endovascular Treatment: A Guideline for
Healthcare Professionals From the American Heart Association/American
Stroke Association. Stroke 2015;46:3020-3035.
3. Fischer U, Arnold M, Nedeltchev K, et al. NIHSS score and
arteriographic findings in acute ischemic stroke. Stroke 2005;36:2121-
2125.
4. Maas MB, Furie KL, Lev MH, et al. National Institutes of Health Stroke
Scale score is poorly predictive of proximal occlusion in acute cerebral
ischemia. Stroke 2009;40:2988-2993.
5. Mokin M, Masud MW, Dumont TM, et al. Outcomes in patients with acute
ischemic stroke from proximal intracranial vessel occlusion and NIHSS
score below 8. J Neurointerv Surg 2014;6:413-417.
6. Greisenegger S, Seyfang L, Kiechl S, et al. Thrombolysis in Patients
With Mild Stroke. Stroke 2014;45:765-769.
7. Strbian D, Piironen K, Meretoja A, et al. Intravenous Thrombolysis for
Acute Ischemic Stroke Patients Presenting with Mild Symptoms. Int J Stroke
2013;8:293-299.
8. Emprechtinger R, Piso B, Ringleb PA. Thrombectomy for ischemic stroke:
meta-analyses of recurrent strokes, vasospasms, and subarachnoid
hemorrhages. Journal of Neurology Published Online First: 20 Jun 2016.
doi: 10.1007/s00415-016-8205-1
Thank you for your technical considerations regarding stent in stent placement without hooking the first stent.
Use of 3 D Roadmap may be helpful. Moreover, following passage of the microwire, reconstructions of a second flat panel angioCT with the microwire in place clearly outlines the relationship between the microwire and the struts of the first stent, especially if reconstructions perpendicular to the orientati...
Thank you for your technical considerations regarding stent in stent placement without hooking the first stent.
Use of 3 D Roadmap may be helpful. Moreover, following passage of the microwire, reconstructions of a second flat panel angioCT with the microwire in place clearly outlines the relationship between the microwire and the struts of the first stent, especially if reconstructions perpendicular to the orientation of the first stent are performed. This may avoid the passage of the stent with a DAC (Distal Access Catheter) which may demage or displace the first stent, especially at it's proximal end.
Using this technique, even passage through a deformed and fragmented stent can be performed, and the location of the microwire within the central axis of the first stent can be confirmed before introduction of the second stent or flow diverter.
Mordasini P, Al-Senani F, Gralla J, Do D, Schroth G: The use of flat Panel angioCT (DynaCT) for Navigation through a deformed and fractured carotid stent. Neuroradiology 52; 2010:629-632.
Prof. Gerhard Schroth Neurologist and Radiologist gerhard.schroth@insel.ch University of Bern Senior Consultant of the Institute for Diagnostic and Interventional Neuroradiology
Dear Editor,
We read with great interest the original article by Boned S. et al. (1)
which demonstrates that CT perfusion (CTP) may overestimate the final
infarct core, especially in the early time window. Interestingly, the
authors introduce the "ghost infarct core" concept in ischemic stroke,
referring to that particular condition where the final infarct core at
follow up imaging may be smaller than the one observed on...
Dear Editor,
We read with great interest the original article by Boned S. et al. (1)
which demonstrates that CT perfusion (CTP) may overestimate the final
infarct core, especially in the early time window. Interestingly, the
authors introduce the "ghost infarct core" concept in ischemic stroke,
referring to that particular condition where the final infarct core at
follow up imaging may be smaller than the one observed on admission CTP.
We think that some considerations on this topic might be useful.
The "ischemic core" and "penumbra" theoretical concepts are now fully
accepted as they identify respectively the tissue which is already dead
(core), whilst the so-called "penumbra" is the ischemic but still living
brain tissue which is no longer functional and will therefore die, unless
blood flow is rapidly restored. With current advances in endovascular
treatment, the identification by imaging techniques of both core and
penumbra is constantly changing. However, the possibility to identify them
with CTP through blood flow measurements is unfortunately affected by
conceptual and technical pitfalls.
First of all, a single time point perfusional measurement, such as
cerebral blood volume (CBV) or other related parameters, may not be a
reliable indicator of whether that tissue will live if left alone or,
conversely, survive if reperfused (2). It is known that any attempt to
determine the tissue vitality or its necrosis with hemodynamic perfusion
can only be represented from a single snapshot in time, but this
assumption is however misleading. Conversely, core and ischemic penumbra
concepts are both "time" and "intensity" dependent (3). For example, the
tissue with a CBV of less than 2 mL/100 g/min may survive for 10 minutes,
but probably not for 3 hours. Cell death following ischemic stroke is a
dynamic process depending on numerous variables (collateral vessels,
metabolic state, depolarization, apoptosis, etc) which are not yet fully
understood (4). This condition makes a single time perfusion study easily
prone to errors and, therefore, it may be expected that this method will
provide an unreliable estimate extension of the final infarct core.
There are also few technical limitations inherent to the imaging
technique: the calculation methods (either deconvolution or non-
deconvolution based), the choice of the arterial input function (AIF), the
lack of standardization in post-processing between vendors and
laboratories and, lastly, the poor signal-to-noise ratio (SNR) of CTP
derived images which makes them too "noisy" (5). Accordingly, we are of
the opinion that CTP cannot compete with the sensitivity (which is nearly
100%) (6) of the diffusion weighted imaging (DWI) technique in detecting
the ischemic core. Indeed, DWI is able to identify the tissue that is
irreparably damaged, as it shows the cytotoxic edema due to metabolic
impairment and irreversible energetic failure of the cell. Although it may
be argued that DWI abnormalities might sometimes reverse, this is however
rather unusual (7). The uncertainty of measurements based on CTP may also
limit the number of patients for whom the decision on whether to proceed
with endovascular treatment based on core infarct size could be justified
or not.
The "small core-occlusion paradigm" (8) through good quality non-enhanced
CT and CT angiography (also called "CT-based paradigm") might represent
instead a simple, alternative and pragmatic approach for selecting those
patients eligible for endovascular treatment, without the risk of
incurring in CTP-based over- or under-estimated measurements of the core.
Thus, every effort to define the ischemic core in a reliable manner would
be vain due to the inability in exceeding the intrinsic limit of
hemodynamic measurement carried out "at a single time" with perfusion
imaging.
References
1) Boned S, Padroni M, Rubiera M, Tomasello A, Coscojuela P, Romero
N, Muchada M, Rodriguez-Luna D, Flores A, Rodr?guez N, Juega J, Pagola J,
Alvarez-Sabin J, Molina CA, Rib? M. Admission CT perfusion may
overestimate initial infarct core: the ghost infarct core concept. J
Neurointerv Surg. 2016 Aug 26. pii: neurintsurg-2016-012494. doi:
10.1136/neurintsurg-2016-012494. [Epub ahead of print]
2) Lev MH. Acute stroke imaging: what is sufficient for triage to
endovascular therapies? AJNR Am J Neuroradiol. 2012;33(5):790-2.
3) Davis S, Donnan GA. Time is Penumbra: imaging, selection and
outcome. The Johann jacob wepfer award 2014. Cerebrovasc Dis.
2014;38(1):59-72.
4) Sheth SA, Liebeskind DS. Collaterals in endovascular therapy for
stroke. Curr Opin Neurol. 2015;28(1):10-5.
5) Gonzalez RG. Low signal, high noise and large uncertainty make CT
perfusion unsuitable for acute ischemic stroke patient selection for
endovascular therapy. J Neurointerv Surg. 2012;4(4):242-5.
6) Schellinger PD, Bryan RN, Caplan LR et al. Evidence-based
guideline: The role of diffusion and perfusion MRI for the diagnosis of
acute ischemic stroke: report of the Therapeutics and Technology
Assessment Subcommittee of the American Academy of Neurology. Neurology
2010; 75:177-185.
7) Campbell BC, Purushotham A, Christensen S, Desmond PM, Nagakane Y,
Parsons MW, Lansberg MG, Mlynash M, Straka M, De Silva DA, Olivot JM,
Bammer R, Albers GW, Donnan GA, Davis SM; EPITHET-DEFUSE Investigators.
The infarct core is well represented by the acute diffusion lesion:
sustained reversal is infrequent. J Cereb Blood Flow Metab. 2012;32(1):50-
6.
8) Demchuk AM, Menon B, Goyal M. Imaging-based selection in acute
ischemic stroke trials - a quest for imaging sweet spots. Ann N Y Acad
Sci. 2012;1268:63-71.
1. Department of Interventional Neuroradiology. Pitie-Salpetriere Hospital.
APHP. Paris France.
2. Paris VI University Pierre et Marie Curie. Paris. France
* Corresponding author
We read with great interest the case series entitled: "The Medina
Embolic Device: early clinical experience from a single center" by Aguilar
Perez M et al, recently published online in JNIS. 1 We would like to
congratulate the authors for this interesting feedback from their
preliminary experience, the largest published to date, with a new device
that combines the design of a detachable coil and the one of a
intrasaccular flow disrupter device: the Medina Embolization Device (MED)
(Medtronic, Irvine, CA). 2
However, we would like to make some comments and raise some disagreements
with the Methods used in this retrospective case series.
First, in the Abstract, the authors state that their objective was "To
report (their) initial experience with the Medina Embolic Device (MED) in
unruptured intracranial aneurysms either as sole treatment or in
conjunction with additional devices". However, only 2/15 patients (13%)
were treated by means of MED alone or MED with filing coils. Although we
agree with the authors that the use of adjunctive devices such as balloon
remodeling, support devices such as pCONus (Phenox, Bochum, Germany) or
PulseRider (Codman Neurovascular, Raynham, MA) or even filing coils
deployed in the MED's mesh, may not, by themselves, dramatically affect
the angiographic outcome and the occlusion rate, we would like to stress
the fact that additional flow diverter stent (FDS) deployed during the
same session or after early follow-up, prevents from any conclusion about
the angiographic outcome with the MED. Indeed, FDS (p64, Phenox) were
deployed in 47% (7/15) of the cases in this series either during the
procedure or after early follow-up. Since, FDSs are not adjunctive tools
but therapeutic tools by themselves, they may have a dramatic influence on
the angiographic outcome. Additionally, one may wonder why using MED for
loose intra-saccular packing in large paraclinoid aneurysms treated by FDS
(like in Patients # 9 and 14). The use of regular coils would be easier,
sufficient for aneurysm occlusion and more cost-effective.
Second, we would like to underline the fact that the use of a support
device like the pCONus (20% [3/15] of the cases in this series), with
flares deployed inside the aneurysm, may hamper the satisfactory
deployment of the MED's petals, especially at the neck. This may lead to
an incomplete sealing of the neck and finally to inadequate occlusion of
the aneurysm, as shown in the Figure 7 of the article.
Third, the delay for the angiographic follow-up is very short
(average: 2.2 months). We believe that it is impossible to evaluate the
effect of an endosaccular device with such a short-term follow-up,
especially if patients are under dual anti-platelet therapy (in at least
13/15 patients in this series). As observed with other endovascular flow
disruption devices such as the WEB (Sequent Medical, Aliso Viejo, CA) or
LUNA (NFocus/Covidien, Irvine, CA), the mechanism that leads to aneurysm
occlusion is a gradual thrombosis triggered by the flow disruption effect.
3 Consequently, the occlusion of the aneurysm's sac obtained with MED may
be delayed and cannot be evaluated with an as short delay as the one
provided in this article.
Finally, we have some concerns about the choice of the aneurysms
treated by MED in this series and about the sizing. Indeed, the MED is a
spherical device that may be suitable mostly for spherical or ovoid
aneurysm, especially with wide neck. Probably a conical shape (patient #
6) or an irregular giant aneurysm as presented in Figure 12, are a priori
not suitable for the MED.
We also tried to find the aneurysms' size as well as necks' size in the
article, in vain. For instance, on Figure 8, the aneurysm's largest
diameter is obviously over 10 mm. However, the largest diameter available
to date in MED in 9 mm. Additionally, why the authors chose to undersize
the MED in spherical aneurysms ("In spherical saccular aneurysms with a
fundus diameter of 9 mm or less, the size of the first framing MED was
purposely undersized by about 1 mm"). We do believe that one should at
least use the same size as the aneurysms' maximum diameter for the first
MED Framer or even oversize by 1 mm. The rational of our strategy is that
it allows for a satisfactory application of the petals along the
aneurysm's wall, and across the neck, which is of tremendous importance to
obtain a neck sealing and subsequently a flow disruption effect. In the
Figures 5, 6 and 8, the MED is obviously undersized, which lead to
incomplete covering of the neck by the petals and thus to residual filing
of the sac and the bleb. In our early monocenter experience, presented at
the ABC-WIN 2016 congress 4 and under consideration for publication in
another journal, using a proper sizing strategy, we obtained an 83% (10/12
cases) occlusion rate at angiographic follow-up (average delay: 5.2
months).
Owing to the above-mentioned drawbacks in the Methods of this case
series, we think that the only conclusion that can be drawn from this
article is that the MED can be safely deployed in an intracranial aneurysm
in a human been. Other considerations on the effectiveness in terms of
angiographic outcome cannot be supported by the data presented in this
series.
References
1. Aguilar Perez M, Bhogal P, Martinez Moreno R, et al. The Medina Embolic
Device: early clinical experience from a single center. J Neurointerv Surg
2016.
2. Turk AS, Maia O, Ferreira CC, et al. Periprocedural safety of aneurysm
embolization with the Medina Coil System: the early human experience. J
Neurointerv Surg 2015.
3. Asnafi S, Rouchaud A, Pierot L, Brinjikji W, Murad MH, Kallmes DF.
Efficacy and Safety of the Woven EndoBridge (WEB) Device for the Treatment
of Intracranial Aneurysms: A Systematic Review and Meta-Analysis. AJNR Am
J Neuroradiol 2016.
4. Sourour N, Di Maria F, Vande Perre S, Gabrieli J, Chiras J, Clarencon
F. Medina devices in the treatment of wide neck intracranial aneurysms:
single-center preliminary experience. ABC-WIN annual congress, 2016.
Conflict of Interest:
F. Clarencon is consultant for Medtronic and Codman Neurovascular
NA Sourour is consultant Medtronic , MicroVention and investor for Medina
Dear Editor,
we read with great interest the paper by Durst at al. [1], aimed to define
the anatomy of cerebral dural sinus system in the generalized population,
evaluating the prevalence of sinus venous stenosis and hypoplasia. This
condition is considered of pathogenetic relevance in idiopathic
intracranial hypertension (IIH) [2-4] and has been also associated to
chronic and, mostly, to refractory headaches [5-7].
We a...
Dear Editor,
we read with great interest the paper by Durst at al. [1], aimed to define
the anatomy of cerebral dural sinus system in the generalized population,
evaluating the prevalence of sinus venous stenosis and hypoplasia. This
condition is considered of pathogenetic relevance in idiopathic
intracranial hypertension (IIH) [2-4] and has been also associated to
chronic and, mostly, to refractory headaches [5-7].
We appreciate the Authors' efforts in reconstructing the venous system
anatomy by using as source the CT Angiography (CTA) of a large sample of
selected patients. However, we would point that their sample cannot be
easily considered representative of the "generalized population" and that
study results might be appreciably overestimated.
The study has been performed on a large series of cases selected among
patients that, on the basis of their own clinical presentation, underwent
a CTA. At the Author's institution, a CTA was routinely performed in "all
suspected strokes, many trauma patients, and anyone suspected of having a
vascular disorder". In order to make their sample representative of the
general population, out of 600 screened examinations, 245 have been
excluded for technical reasons or because of clinic presentations or
pathologic findings that could "conceivably alter venous outflow".
However, according to the exclusion criteria list, posterior fossa lesions
were excluded, but anterior focal ischemia and head trauma - both
conditions usually running with at least a mild brain edema and consequent
raised intracranial pressure (ICP) - were presumably included. There is
evidence that raised ICP is associated with focal or diffuse narrowing of
sinus venous tree [8].
Moreover, a number of other clinical presentations that could prompt
neurovascular investigations but might result from a cerebral venous
outflow derangement despite a negative CTA, are not listed within the
exclusion criteria. These include: responsive chronic migraine [9-10]
(only refractory chronic headaches were excluded but there is evidence of
> 50% sinus stenosis prevalence in chronic migraine); acute vertigo
(often comorbid with episodic or chronic migraine); cough, exertional and
sexual activity-associated headaches [11], and idiopathic stabbing
headache [12]. Finally, Transient global amnesia may result from a
deranged cerebral venous outflow with jugular valve incompetence [13].
Based on the above considerations, we believe that the design of this
otherwise excellent study implies a not negligible overestimation of the
prevalence of sinus stenosis and hypoplasia in the general population. The
true prevalence of sinus stenosis in healthy subjects remains unknown.
1. Durst CR, Ornan DA, Reardon MA, et al.. Prevalence of dural venous
sinus stenosis and hypoplasia in a generalized population. J Neurointerv
Surg. 2016. [Epub ahead of print]. doi: 10.1136/neurintsurg-2015-012147
2.Farb RI, Vanek I, Scott JN, et al. Idiopathic intracranial
hypertension: the prevalence and morphology of sinovenous stenosis.
Neurology. 2003 May 13; 60(9):1418-24.
3. De Simone R, Ranieri A, Montella S, et al. The role of dural sinus
stenosis in idiopathic intracranial hypertension pathogenesis: the self-
limiting venous collapse feedback-loop model. Panminerva Med. 2014 Sep;
56(3):201-9
4. Puffer RC, Mustafa W, Lanzino G. Venous sinus stenting for
idiopathic intracranial hypertension: a review of the literature. J
Neurointerv Surg. 2013;5(5):483-486
5. Bono F, Salvino D, Tallarico T, et al. Abnormal pressure waves in
headache sufferers with bilateral transverse sinus stenosis. Cephalalgia
2010; 30: 1419-1425
6. De Simone R, Ranieri A, Montella S, et al. Sinus venous stenosis-
associated idiopathic intracranial hypertension without papilledema as a
powerful risk factor for progression and refractoriness of headache. Curr
Pain Headache Rep. 2012 Jun;16(3):261-9.
7. De Simone R, Ranieri A, Montella S, et al. Intracranial pressure
in unresponsive chronic migraine. J Neurol. 2014 Jul;261(7):1365-73.
8. Rohr A, Bindeballe J, Riedel C, et al. The entire dural sinus tree
is compressed in patients with idiopathic intracranial hypertension: a
longitudinal, volumetric magnetic resonance imaging study. Neuroradiology.
2012 Jan;54(1):25-33
9. Bono F, Cristiano D, Mastrandrea C, et al. The upper limit of
normal CSF opening pressure is related to bilateral transverse sinus
stenosis in headache sufferers. Cephalalgia 2010; 30: 145-151.
10. Fofi L, Giugni E, Vadal? R, et al. Cerebral transverse sinus
morphology as detected by MR venography in patients with chronic migraine.
Headache. 2012 Sep;52(8):1254-61.
11. Donnet A, Valade D, Houdart E. Primary cough headache, primary
exertional headache, and primary headache associated with sexual activity:
a clinical and radiological study. Neuroradiology 2013; 55:297-305
12. Montella S, Ranieri A, Marchese M, De Simone R. Primary stabbing
headache: a new dural sinus stenosis-associated primary headache? Neurol
Sci. 2013 May;34 Suppl 1:S157-9.
13. Chung CP, Hsu HY, Chao AC, et al. Transient global amnesia:
cerebral venous outflow impairment-insight from the abnormal flow patterns
of the internal jugular vein. Ultrasound Med Biol. 2007 Nov;33(11):1727-
35. Epub 2007 Jul 16.
Letter by Parthasarathy et al. regarding article, "Unwanted
detachment of the Solitaire device during mechanical thrombectomy in acute
ischemic stroke ".
Letter by Parthasarathy et al. regarding article, "Unwanted
detachment of the Solitaire device during mechanical thrombectomy in acute
ischemic stroke ".
Department of Neurointerventional surgery, Institute of Neuroscience,
Medanta, the Medicity, Gurgaon, India.
Title word count: 14
Word Count: Abstract: 157; Manuscript count excluding references: 554
References: 4
Key words:Stentriever, mechanical thrombectomy, detachment, stent
based retrieval
Corresponding Author
Dr Vipul Gupta MD,
Additional Director and Head, Neurointerventional Surgery,
Medanta Institute of Neurosciences
Medanta - the Medicity,
Gurgaon 122001
Tel: 00919810542372
drvipulgupta25@gmail.com
Abstract:
Stent detachment is a dreaded device complication in the setting of
acute stroke management and may result in poor outcome. The principal
objective in the event of stent detachment is to establish flow in the
occluded territory. Techniques including balloon angioplasty, local
infusion of antiplatelet or thrombolytic agent and suction have been
described with variable success in achieving meaningful reperfusion. Stent
retrieval can potentially restore flow to the occluded territory and
negate the need for administering dual antiplatelet. We read with interest
the article by Castano et al (2016) on unwanted detachment of the
Solitaire device during mechanical thrombectomy in acute ischemic
stroke.Stents with type 'A' detachment were retrievable; whereas, attempts
at retrieving stents with type B detachment were invariably unsuccessful.
Therefore, a rescue strategy, 'stent based retrieval',may prove to be
useful when snare retrieval fails. Stent based retrieval could be
considered in both type A and type B detachments when snare retrieval is
unsuccessful.
Letter to the Editor
We read with great interest the article by Casta?o et al (2016) on
unwanted detachment of the Solitaire device(Medtronic/Covidien/ev3,
Dublin, Ireland) during mechanical thrombectomy in acute ischemic stroke.1
Stent detachment in their series was invariably associated with a poor
outcome, higher rates of symptomatic intracranial hemorrhage and higher
mortality.
They had classified stent detachment as either type A or type B based
on if the separation occurred before or after the proximal radiopaque
stent marker. They attempted stent retrieval with an Amplatz GooseNeck
snare (Medtronic/Covidien/ev3, Dublin, Ireland) in all irrespective of the
type of detachment.A rescue strategy in case of failure of snare retrieval
was not described.Stents were retrievable with 'type A' detachments;
however, attempts to retrieve stents with 'type B' detachmentwere
invariably unsuccessful. The likely explanation is that with type B
detachment the 'stent legs' either open or stay together making a
'spearhead' that digs into the wall of the artery making snare retrieval
not possible.
The primary aim in such a situation is to re-establish flow in the
occluded territory. A number of techniques including balloon angioplasty,
local infusion of antiplatelet/ thrombolytic agent, and suction have been
described with variable success in achieving meaningful reperfusion.(2,3)
Furthermore, leaving a stent in situ necessitates administration of dual
antiplateletto a patient in whom the infarct core can increase either due
to delayed occlusion or failure to recanalise. Therefore, an attempt to
restore flow by retrieving the detached stent is likely to be crucial to
achieving a good outcome. Castano et al (2016) were able to achieve
meaningful reperfusion in 50% of patients; however, the outcomes were poor
despite device retrieval.(1) This further reiterates the importance of
time and the need to establish perfusion early. Therefore, a second
strategy may be beneficial when snare retrieval fails.
Snare retrieval may not be successful in type A detachments and not likely
to be the appropriate strategy in type B stent detachments. Therefore, an
alternate strategy, 'Solitaire stentectomy' may prove to be effective
under these circumstances. (4) 'Stent based retrieval' using a Solitaire
device can be performed as a '4 step' process in a patient with stent
detachment. Step 1: Partial deployment of an appropriately sized solitaire
device proximal to the detached stent [the distal end of microcatheter is
positioned proximal to the proximal radiopaque marker/ proximal legs
(struts) of the detached stent and then the stent is partly unsheathed to
allow for its expansion]. Step 2: Engaging the proximal end of the
detached stent by the distal end of the second stent by advancing the
microcatheter and the stent together. Step 3: re-sheathing the device in
an attempt to capture the proximal legs/ struts of the detached stent.
Step 4: retrieval of microcatheter, device and detached stent. This
strategy may be useful in both type A and type B detachments when snare
retrieval fails.
Clearly, stent detachment is a dreaded device complication for the
neurointerventionist in the setting of acute stroke management and may
result in poor outcome. Development of methods and techniques is crucial
to dealing with stent detachments in a timely and effective manner. "Stent
based retrieval" can be a useful alternate technique when snare retrieval
fails and may be employed as the primary technique in type B detachments.
References:
1. Castano C, Dorado L, Remollo S, et al. Unwanted detachment of the
Solitaire device during mechanical thrombectomy in acute ischemic stroke.
J Neurointerv Surg. 2016 Jan 27. [Epub ahead of print]
2. Kim ST, Jin SC, Jeong HW, et al. Unexpected detachment of
solitaire stents during
mechanical thrombectomy. J Korean Neurosurg Soc 2014;56:463-8.
3. Yub Lee S, Won Youn S, Kyun Kim H, et al. Inadvertent detachment
of a retrievable intracranial stent: review of manufacturer and user
facility device experience. Neuroradiol J 2015;28:172-6.
4. Chapot R, Stracke P, Nordmeyer H, Heddier M. Stentectomy:
Retrieval of stents after stent assisted coiling. Interventional
Neuroradiology 2015; 21(1S):160
We read with great interest the article by Fargen et al(1), which
reports the Journal of Neurointerventional Surgery (JNIS) experience in
social media. The journal recently implemented a three-pronged social
media strategy, along with the hiring of dedicated social media staffing,
to enhance their online viewership. Since implementing this marketing
approach, JNIS has had significantly more website accessions to their pe...
We read with great interest the article by Fargen et al(1), which
reports the Journal of Neurointerventional Surgery (JNIS) experience in
social media. The journal recently implemented a three-pronged social
media strategy, along with the hiring of dedicated social media staffing,
to enhance their online viewership. Since implementing this marketing
approach, JNIS has had significantly more website accessions to their peer
reviewed articles, and gained more insight into their Twitter analytics.
The information presented provide a road-map to guide social media
marketing strategies for journals in neurosurgery, neurology, and
radiology.
While not studied in this manuscript directly, the authors discuss
the potential for social media metrics to predict subsequent article
citations. In Toronto, our group studied the association between social
media metrics and traditional indices of scientific impact among
neurosurgical journals as well as departments.(2) We found that
neurosurgical journals and departments with active social media presences
had significantly higher H-indices as well as overall citation counts. As
a journal not limited purely to neurosurgery, JNIS was outside the scope
of our study; however, a repeat analysis with JNIS' social media metrics
included did not alter our findings. Of particular note, our data did not
meet the criteria for parametric analysis because of many outliers.
Interestingly, JNIS' primary outcome data, the number of clicks per
article, showed similar distributional skew (Figure 3, in Fargen et al.).
The authors made significant efforts to identify associated covariates,
identifying the day of the week of tweet posting as a significant
predictor. With significant outlying data however, there may certainly be
other unidentified covariates which may influence social media
dissemination. The complexity of established and emerging social media
analytics requires careful conceptualization for future studies.
In conclusion, we commend the authors' efforts to advance JNIS's
social media presence. This is another study that contradicts
Circulation's randomized trial results which failed to show any benefits
for social media on readership numbers and article downloads.(3) Without a
doubt, there are many unanswered questions for the use of social media in
neurosurgery and neurointerventional surgery. Are there independent
predictors for citations in all specialties, or this is specialty/audience
dependent effect? While difficult to assess given the relative anonymity
online, it would be interesting to note the demographics of clicks and
followers, whether they be faculty, residents, local or international
fellows, etc.. We look forward to future analyses from the JNIS team, and
the wider medical community.
Naif M Alotaibi, Daipayan Guha, Andres M Lozano (Division of
Neurosurgery, Department of Surgery, University of Toronto, Toronto,
Ontario, Canada)
References
1. Fargen KM, Ducruet AF, Hyer M, Hirsch JA, Tarr RW. Expanding the
social media presence of the Journal of Neurointerventional Surgery:
editor's report. J Neurointerv Surg. Feb 29 2016.
2. Alotaibi NM, Guha D, Fallah A, et al. Social Media Metrics and
Bibliometric Profiles of Neurosurgical Departments and Journals: Is There
a Relationship? World Neurosurg. Feb 5 2016.
3. Fox CS, Bonaca MA, Ryan JJ, Massaro JM, Barry K, Loscalzo J. A
randomized trial of social media from Circulation. Circulation. Jan 6
2015;131(1):28-33.
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...
We would like to thank our colleagues for reading our publication and for the thorough review of the paper. We greatly look forward to reading their own experience and believe that it will add substantially to the literature on this new and interesting device.
At the outset we would like to make it clear that we stand by our initial comment in saying that we believe the combination of a MED and other devices,...
We read with great interest the article of Haussen et al. 1 outlining the problem of identifying patients with minor stroke symptoms (low NIHSS) despite proximal vessel occlusion who should undergo thrombectomy. Intension-to-treat analysis showed significantly higher reduction of stroke severity in the primary thrombectomy group compared to the medical group. But more interestingly, per-protocol analysis revealed a high propo...
Thank you for your technical considerations regarding stent in stent placement without hooking the first stent.
Use of 3 D Roadmap may be helpful. Moreover, following passage of the microwire, reconstructions of a second flat panel angioCT with the microwire in place clearly outlines the relationship between the microwire and the struts of the first stent, especially if reconstructions perpendicular to the orientati...
Dear Editor, We read with great interest the original article by Boned S. et al. (1) which demonstrates that CT perfusion (CTP) may overestimate the final infarct core, especially in the early time window. Interestingly, the authors introduce the "ghost infarct core" concept in ischemic stroke, referring to that particular condition where the final infarct core at follow up imaging may be smaller than the one observed on...
Frederic Clarencon, MD, PhD 1, 2, Nader-Antoine Sourour, MD 1 *
1. Department of Interventional Neuroradiology. Pitie-Salpetriere Hospital.
APHP. Paris France. 2. Paris VI University Pierre et Marie Curie. Paris. France
* Corresponding author
We read with great interest the case series entitled: "The Medina Embolic Device: early clinical experience from a single center" by Aguilar Per...
Dear Editor, we read with great interest the paper by Durst at al. [1], aimed to define the anatomy of cerebral dural sinus system in the generalized population, evaluating the prevalence of sinus venous stenosis and hypoplasia. This condition is considered of pathogenetic relevance in idiopathic intracranial hypertension (IIH) [2-4] and has been also associated to chronic and, mostly, to refractory headaches [5-7]. We a...
Letter by Parthasarathy et al. regarding article, "Unwanted detachment of the Solitaire device during mechanical thrombectomy in acute ischemic stroke ".
Rajsrinivas Parthasarathy MRCP (UK) Neurology, Vipul Gupta MD, Gaurav Goel MD DM
Department of Neurointerventional surgery, Institute of Neuroscience, Medanta, the Medicity, Gurgaon, India.
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We read with great interest the article by Fargen et al(1), which reports the Journal of Neurointerventional Surgery (JNIS) experience in social media. The journal recently implemented a three-pronged social media strategy, along with the hiring of dedicated social media staffing, to enhance their online viewership. Since implementing this marketing approach, JNIS has had significantly more website accessions to their pe...
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