Published online before print September 13, 2007, doi: 10.1161/STROKEAHA.107.500116
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(Stroke. 2007;38:e141.)
© 2007 American Heart Association, Inc.
Letters to the Editor |
Response to Letter by Arnold et al
Department of Neurology, Helsinki University Central Hospital, Helsinki, Finland
Helsinki Medical Imaging Center, Helsinki University Central Hospital, Helsinki, Finland
Department of Neurology, Helsinki University Central Hospital, Helsinki, Finland
Response:
We thank Dr Arnold et al for their interest in our recent article.1 In their Letter,2 Arnold et al suggest that (1) the present data are not sufficient to conclude the safety of anticoagulation in intracranial artery dissection (IAD) patients presenting without subarachnoidal hemorrhage (SAH), and a routine lumbar puncture (LP) is necessary to exclude CT or MRI negative SAH, and (2) a filiform stenosis is not a reliable marker of dissection and more strict diagnostic criteria, ie, pathognomonic signs only, should be used for reliable diagnosis of IAD.
Apparently, Arnold and his coauthors themselves2 use anticoagulation treatment in (some) IAD patients after routinely performing a LP to exclude SAH, as some patients may have a normal CT but blood in cerebrospinal fluid. In contrast to their view, our point is that a LP is unnecessary if the initial CT or MRI is negative for SAH and there is no clinical suspicion of acute SAH. We have not seen any reports on the frequency of clinically and CT negative but LP positive SAHs in IAD patients. However, we can assume that some of our patients with negative brain scans for SAH may have had minor SAHs, but still none showed deterioration despite anticoagulation. Furthermore, one should keep in mind that LP immediately followed by anticoagulation may increase the risk of epidural hemorrhage, but anticoagulation alone did not lead to a single clinically overt SAH in our fairly large patient population.
The development of versatile and precise imaging methodology, especially high-field MRI accomplished within the correct time frame, has improved cervicocephalic artery dissection (CCAD) diagnostics revealing a number of pathognomonic radiological findings, ie, intramural hematoma, double lumen, intimal flap, and pseudoaneurysm at a nonbifurcation site. Although presence of intramural hematoma along the dissection site is considered to be a highly specific sign, it is not "sine qua non" because it may be absent or invisible especially if MRI is done within the first symptomatic days, which is common diagnostic practice, or if raw data are no longer available for reanalysis and, furthermore, false positivity may occur. We1 have found the filiform stenosis sign to be a reliable marker, and many others have used this sign in dissection diagnostics,3,4 including Arnold et al.5 We emphasize that a long filiform stenosis in a nonatherosclerotic artery or an occlusion recanalized into a long filiform stenosis in a nonatherosclerotic artery are in the absence of vasculitis widely accepted CCAD criteria that are applied by the Cervical Artery Dissection and Ischemic Stroke Patients (CADISP) workgroup (http://www.chazard.org/cadisp/). If the diagnostic criteria suggested by Arnold et al2 were used, this would lead to an obvious underdiagnosing and overselection bias in many of the CCAD studies.
Arnold et al2 make a point about extracranial dissections extending intracranially (ie, combined dissections) that display nonspecific but typical radiological findings. They ask whether these arteries displayed the above-mentioned specific signs intracranially. We ascertained inclusion of correct patients by carefully reviewing all clinical data by experienced stroke neurologists and radiological data by experienced neuroradiologists and excluded patients who did not fulfill preset diagnostic criteria.1 There were altogether 3 combined dissection patients, all having definite CCADs extracranially, for whom the radiological diagnosis for the intracranial segment was based on probable signs (ie, rat tail–shaped or flame-like occlusion). Thus, we do not think that these observations jeopardize our conclusions.
A major handicap in the field of CCAD has been the lack of large-sized multicenter studies carried out with reliable and standardized criteria leading to sound conclusions. Such collaborations now exist (http://www.chazard.org/cadisp/ and http://www.dissection.co.uk/). These ongoing studies will certainly shed more light on a number of issues concerning CCADs in the near future with high level of certainty satisfying most of us. We urge all scientists to join the existing networks because it is prime time for putting efforts together to improve knowledge and develop evidence-based treatment(s) for CCAD.
Acknowledgments
Disclosures
None.
References
1. Metso TM, Metso AJ, Helenius J, Haapaniemi E, Salonen O, Porras M, Hernesniemi J, Kaste M, Tatlisumak T. Prognosis and safety of anticoagulation in intracranial artery dissections in adults. Stroke. 2007; 38: 1837–1842.
2. Arnold M, Bousser MG, Baumgartner RW. Prognosis and safety of anticoagulation in intracranial artery dissections in adults. Stroke. 2007; 38: e140.
3. Pezzini A, Del Zotto E, Archetti S, Negrini R, Bani P, Albertini A, Grassi M, Assanelli D, Gasparotti R, Vignolo LA, Magoni M, Padovani A. Plasma homocysteine concentration, c677t MTHFR genotype, and 844INS68BP CBS genotype in young adults with spontaneous cervical artery dissection and atherothrombotic stroke. Stroke. 2002; 33: 664–669.
4. Grau AJ, Brandt T, Buggle F, Orberk E, Mytilineos J, Werle E, Conradt C, Krause M, Winter R, Hacke W. Association of cervical artery dissection with recent infection. Arch Neurol. 1999; 56: 851–856.
5. Arnold M, Bousser MG, Fahrni G, Fischer U, Georgiadis D, Gandjour J, Benninger D, Sturzenegger M, Mattle HP, Baumgartner RW. Vertebral artery dissection: presenting findings and predictors of outcome. Stroke. 2006; 37: 2499–2503.
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