Local symptoms and recanalization in spontaneous carotid artery dissection.
- [Show abstract] [Hide abstract]
ABSTRACT: Spontaneous bilateral internal carotid artery dissection has frequently been described in the literature as a cause of stroke. In more than half of the patients with internal carotid artery dissection, recanalization occurs early after the event and is unusual later than 6 months after onset of the dissection. We describe a patient with ischemic stroke due to left internal carotid artery occlusion in the extracranial segment. The patient was treated with anticoagulants and early vessel recanalization did not occur. Ten months later, he developed contralateral internal carotid occlusion in the intracranial tract, which was followed by early complete recanalization. Anticoagulation therapy was continued and, 16 months after the initial event, the left internal carotid artery unexpectedly also reopened.Journal of Clinical Ultrasound 01/2011; 39(1):48-53. · 0.80 Impact Factor
- [Show abstract] [Hide abstract]
ABSTRACT: Background: Intra- and extracranial internal carotid artery dissections (ICD) are two different pathological conditions. Extracranial dissection is considered to be among the most frequent causes of stroke in the young and the segment generally reopens in 2 out of 3 cases, completely or partially, within 6 months. Intracranial ICD (IICD) is considered a rare occurrence in stroke and, accordingly, there are few systematic published data. However, it is a clinically significant condition that may cause severely disabling ischemic stroke or subarachnoid hemorrhage. In the past, sole availability of invasive imaging methods for its detection may have induced an underreporting. The aim of the study was to analyze ultrasound findings, timing and predictors of recanalization in patients with IICD. Methods: IICD acute patients admitted to our Stroke Unit were submitted to carotid sonographic seriated monitoring, daily for the 1st week after symptom onset, at day 14, at month 1 and every 3 months thereafter up to a follow-up of 4 years. Contrast carotid ultrasound was performed in patients with persistent occlusion after month 1. Results: Fourteen acute patients with IICD were enrolled. Extracranial internal carotid patency was observed in 8 patients at first ultrasound scans; all of these showed complete intracranial recanalization within the 1st week and oral anticoagulants were withdrawn after 6 months. Conversely, in 6 patients retrograde extracranial internal carotid thrombosis was immediately observed, since the first ultrasound scans. In 4 of these the occlusion persisted after 4 years while 2 of them had only a partial recanalization, with evidence at contrast ultrasound of still late remodeling processes in the extracranial thrombus up to 2 years after the first observation; for this reason, in these 2 patients anticoagulation was not discontinued, while in the 4 patients with persistent, stable, occlusion, therapy was suspended 1 year after the diagnosis. Conclusions: Identification of the site of dissection - i.e. extra- versus intracranial - is fundamental in clinical studies for outcome and prognosis evaluation. Carotid ultrasound strict surveillance is important to monitor eventual recanalization in patients with ICD, even in a late phase. Retrograde internal carotid thrombosis seems to be correlated with persistent occlusion and partial recanalization. Remodeling of thrombotic material in the internal carotid artery may, however, continue for up to 2 years. In these cases, contrast ultrasound evidence of thrombus morphological changes may support the decision to continue anticoagulation.Cerebrovascular Diseases 05/2013; 35(5):476-482. · 3.70 Impact Factor
- [Show abstract] [Hide abstract]
ABSTRACT: Cervical artery dissection (CeAD) is a frequent cause of stroke among young patients. It is unclear how many CeADs occur asymptomatically or cause subtle and unspecific clinical symptoms. We hypothesize that CeAD remains often unrecognized. Accordingly, the incidence of CeAD might be higher and the stroke risk lower than generally assumed. Lack of CeAD-indicating clinical symptoms is regarded as the main cause of missed diagnoses. We further hypothesize that underrepresentation of asymptomatic and oligosymptomatic patients in CeAD studies may have biased the association between ischemia and local symptoms in CeAD patients as well as the associations of CeAD with risk factors or co-morbidities. We finally hypothesize that symptomatic CeAD may be preceded by an initial asymptomatic phase. According to this final hypothesis, the time of onset of CeAD should be considered uncertain. The issue of unrecognized CeAD is relevant, as it may affect the associations between CeAD and putative risk factors. Furthermore, the existence of clinically silent CeADs may explain why recurrent and familial CeAD have been rarely observed.Medical Hypotheses 04/2013; · 1.15 Impact Factor
Antti J. Metso, Tiina M. Metso and Turgut Tatlisumak
Local Symptoms and Recanalization in Spontaneous Carotid Artery Dissection
Copyright © 2009 American Heart Association. All rights reserved. Print ISSN: 0039-2499. Online
Stroke is published by the American Heart Association. 7272 Greenville Avenue, Dallas, TX 72514
2009, 40:e629: originally published online September 17, 2009
located on the World Wide Web at:
The online version of this article, along with updated information and services, is
Reprints: Information about reprints can be found online at
Fax:Kluwer Health, 351 West Camden Street, Baltimore, MD 21202-2436. Phone: 410-528-4050.
Permissions: Permissions & Rights Desk, Lippincott Williams & Wilkins, a division of Wolters
Subscriptions: Information about subscribing to Stroke is online at
by guest on October 14, 2011http://stroke.ahajournals.org/Downloaded from
Letters to the Editor
Stroke welcomes Letters to the Editor and will publish them, if suitable, as space permits. They should not exceed 750 words (including references)
and may be subject to editing or abridgment. Please submit letters in duplicate, typed double-spaced. Include a fax number for the corresponding author and
a completed copyright transfer agreement form (available online at http://stroke.ahajournals.org and http://submit-stroke.ahajournals.org).
Local Symptoms and Recanalization in
Spontaneous Carotid Artery Dissection
To the Editor:
We congratulate Nedeltchev and coworkers for their merito-
rious report1on recanalization of spontaneous internal carotid
artery dissection. The strengths of this work are a fairly large
patient population compared with most previous reports and the
repeated ultrasound examinations of the vasculature at 1, 3, 6,
and 12 months. Recanalization always occurred within 6 months,
but not later. We, having similar experience, currently repeat
vascular imaging only at 6 months.
Nedeltchev et al discuss that they did not detect any beneficial
effect of complete recanalization and refer to 2 articles that do not
directly support their view; of these, one is a small study on 60
cervical artery dissection patients treated with anticoagulants2and
the second3is a review in Spanish that discusses the merits of
thrombolysis in acute ischemic stroke. In patients with carotid artery
dissection, ischemic stroke may occur either by artery-to-artery
embolism or by hemodynamic mechanisms. The risk for embolism
is substantially reduced with timely anticoagulation, and prevention
of hemodynamic infarction may not require complete recanaliza-
tion, but modest recanalization may establish enough blood flow.
Although most of their patients may have had late recanalization,
still it would be interesting to see if different levels of recanalization
correlated with clinical outcome. We recently showed that patients
in whom complete recanalization occurred within 6 months from
symptom onset returned to work more often.4
Nedeltchev et al state in their “Results” that presentation with
local symptoms and signs only increased the likelihood of
recanalization. Local symptoms included headache, neck pain,
pulsatile tinnitus, Horner syndrome, and cranial nerve palsy, all
ipsilateral to the spontaneous internal carotid artery dissection.
They suggest that an outward-expanding hematoma could ex-
plain the association of local symptoms and the tendency to
recanalize, whereas inward expansion of the artery wall would
cause less local symptoms and a tendency not to recanalize. This
interpretation about the location of the hematoma versus recan-
alization is logical but speculative and requires confirmation by
imaging data. Their series and others indicate that initial stenosis
compared with initial occlusion. Emphasizing the presence of local
symptoms and signs may lead to false conclusions about their
prognostic significance. Patients who sustain less severe strokes,
or no brain ischemia at all, are more likely to spontaneously
report these minor symptoms and most of them, indeed, arrive to
medical attention particularly with those complaints. On the
other hand, local symptoms such as pain and tinnitus experienced
by patients with more severe strokes are more likely to be
overlooked and underestimated or cannot be reported at all due to
barriers such as aphasia, inattention, or depressed consciousness.
In the “Results,” the authors write that there were 79 patients
who presented with local symptoms only that were associated
with a high rate of complete recanalization. However, several
typographic errors in Table 3 obscure this finding, and the patient
numbers used for statistical analysis may be erroneous. Surpris-
ingly, migraine was found in 30 patients, a figure much lower
than expected. On the other hand, we fully agree with the authors
on the use of Rankin 0 to 1 as a favorable outcome.5A patient
with a Rankin score of 2 will be independent in daily life but will
not return to his or her work. Patients with carotid artery
dissection are mostly young to middle-aged adults and working
ability after carotid artery dissection is critical for most of them.
Regarding the risks and benefits of anticoagulation and anti-
platelet therapies6and for many other unanswered questions in
the carotid artery dissection field, multicenter collaborations with
large numbers of patients such as the Cervical Artery Dissection
in Ischemic Stroke Patients (CADISP) network7are needed
instead of overinterpreting results from small patient series.
Antti J. Metso, MD, PhD
Tiina M. Metso, MD
Turgut Tatlisumak, MD, PhD
Department of Neurology
Helsinki University Central Hospital
1. Nedeltchev N, Bickel S, Arnold M, Sarikaya H, Georgiadis D, Stur-
zenegger M, Mattle HP, Baumgartner RW. Recanalization of spontaneous
carotid artery dissection. Stroke. 2009;40:499–504.
2. Desfontaines P, Despland PA. Dissection of the internal carotid artery:
aetiology, symptomatology, clinical and neurosonological follow-up, and
treatment in 60 consecutive cases. Acta Neurol Belg. 1995;95:226–234.
therapeutic option at our disposal [in Spanish]. Rev Neurol. 2007;45:42–52.
4. Metso TM, Metso AJ, Salonen O, Haapaniemi E, Putaala J, Artto V, Helenius
J, Kaste M, Tatlisumak T. Adult cervicocerebral artery dissection: a single-
center study of 301 Finnish patients. Eur J Neurol. 2009;16:656–661.
5. Putaala J, Metso AJ, Metso TM, Konkola N, Kraemer Y, Haapaniemi E,
Kaste M, Tatlisumak T. Analysis of 1008 consecutive patients aged 15 to
49 with first-ever ischemic stroke. The Helsinki Young Stroke Registry.
6. Engelter ST, Brandt T, Debette S, Caso V, Lichy C, Pezzini A, Abboud S,
Bersano A, Dittrich R, Grond-Ginsbach C, Hausser I, Kloss M, Grau AJ,
Tatlisumak T, Leys D, Lyrer PA. Antiplatelets versus anticoagulation in
cervical artery dissection. Stroke. 2007;38:2605–2611.
7. Debette S, Metso TM, Pezzini A, Engelter ST, Leys D, Lyrer P, Metso AJ,
V, Bersano A, Grau A, Altintas A, Amouyel P, Tatlisumak T, Dallongeville J,
Grond-Ginsbach C; on behalf of the CADISP-group. CADISP-genetics: an
international project searching for genetic risk factors of cervical artery dis-
sections. Int J Stroke. 2009;3:224–230.
KEY WORDS: carotid artery?dissection?embolism?stroke in young adults
© 2009 American Heart Association, Inc.
Stroke is available at http://stroke.ahajournals.org DOI: 10.1161/STROKEAHA.109.552463
by guest on October 14, 2011http://stroke.ahajournals.org/ Downloaded from