| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Stroke. 1995;26:235-239.)
© 1995 American Heart Association, Inc.
Articles |
From the Service de Neurologie, Hôpital Saint-Antoine, 184 rue du faubourg Saint-Antoine, Paris (V.B., P.-J.T., P.A., M.-G.B.), and the Unité de Neurologie C2, Hôpital de Versailles, 177 rue de Versailles, Le Chesnay (J.D'A.-C.), France.
Correspondence to Pr M.-G. Bousser, Service de Neurologie, Hôpital Saint-Antoine, 184 rue du faubourg Saint-Antoine, 75571 Paris, cedex 12, France.
| Abstract |
|---|
|
|
|---|
Methods We studied 80 consecutive patients (29 retrospectively, 51 prospectively) with angiographically diagnosed extracranial internal carotid artery dissection and, during a 6-month follow-up, recorded the time elapsed between the onset of the first symptoms and the onset of any ischemic event (transient ischemic attack or stroke). We compared patients with and without ischemic events, with and without completed stroke, and, among patients who had local signs at onset, those with and without subsequent ischemic events.
Results Cerebral or retinal infarction occurred in 42 patients.
It was inaugural in 9 patients. In the 33 others, the time interval
between the first symptoms (local signs and/or transient ischemic
attacks) and the onset of stroke ranged from a few minutes to 31 days;
it was
7 days in 82% of the patients. No significant difference in
the baseline characteristics of the patients or in the angiographic
pattern of dissection was found based on the presence or absence of
ischemic signs or of completed stroke.
Conclusions In carotid artery dissections, completed stroke usually occurs in the first few days after the onset of the first symptoms, whether local or ischemic, but it can occur as much as 1 month later. This suggests that any potential preventive treatment should be initiated as early as possible after the onset of the first symptoms but might also be worth initiating even 1 month later.
Key Words: carotid arteries cerebral ischemia, transient dissection
| Introduction |
|---|
|
|
|---|
| Subjects and Methods |
|---|
|
|
|---|
Traumatic and spontaneous dissections were grouped together because of the well-known difficulty in determining whether a dissection is spontaneous or secondary to a minor or trivial trauma and because their clinical presentation does not significantly differ.1 5 7 In the present study, dissections were classified as traumatic when occurring after an obvious head or neck trauma, during sport activities involving the neck, or after unusual neck movements. Dissections were otherwise classified as spontaneous.
No uniform treatment was applied in the first (retrospective) part of the study, but heparin was systematically used as soon as the diagnosis was established in the prospective part of the study whether or not ischemic signs were present.
We recorded the baseline characteristics of the patients, including age, sex, history of hypertension, present or past use of oral contraceptives, history of migraine, and the angiographic pattern of the dissection. We recorded all ischemic events that occurred in the 6 months after the dissection.
We first compared patients with and without ischemic events
(transient or permanent); second, those with and without completed
stroke (cerebral or retinal infarction); and third, patients with local
signs at onset with or without subsequent ischemic events. These groups
were compared using the
2 test for
proportion.
| Results |
|---|
|
|
|---|
Ischemic Events
Ischemic events occurred in 66 patients (82.5%). These events
were more frequently observed in the early (27/29) than in the late
(42/53) part of the study. They were purely transient in 24 subjects
(36.5%), but a completed stroke occurred in 42 subjects (63.5%).
Baseline characteristics of the patients and angiographic patterns of
dissections according to the presence or absence of ischemic events, or
of completed stroke, are shown in Tables 1
and 2
. There were no significant differences
between these groups.
|
|
Inaugural Symptoms
Inaugural symptoms were local in 53 patients (isolated head or
neck pain in 31, painful Horner's syndrome in 15, tinnitus in 7 [with
pain in 3]) and ischemic in 27 (completed stroke in 9, transient
ischemic attack [TIA] in 18) (Fig 1
). Among the 53
patients with local symptoms, 39 (73.5%) later had ischemic events
(TIAs in 23, completed stroke in 16). Characteristics of the patients
and the dissection according to the presence or absence of ischemic
events are shown in Table 3
. There was no difference
between these two groups.
|
|
Time Course of Symptoms
No apparent difference was found in the time course of symptoms
between the retrospective and the prospective part of the study.
Results concerning the two parts of the study were therefore grouped
(Fig 1
).
Nine patients had a completed stroke at onset; 1 patient with a bilateral extracranial ICA dissection and suffering from Ehlers-Danlos syndrome experienced recurrent strokes that occurred 52, 68, and 81 days, respectively, after the first completed stroke.
Eighteen patients had TIAs as presenting symptoms (10 amaurosis fugax, 8 cerebral TIAs). Eight of them experienced a single TIA, 6 had two TIAs, and 4 had three TIAs. The time interval between the first and last TIA ranged from 2 hours to 27 days (6±9 days). Ten patients with TIA as an inaugural symptom later had a completed stroke that occurred from 6 hours to 31 days after the first TIA (mean, 5.7±9 days). Among the 53 patients with local symptoms at onset of ICA dissection, 23 later had TIAs, which occurred from a few minutes to 66 days (10.5±13.5 days) after onset, and 16 had a completed stroke occurring from 2 hours to 16 days after the onset of local symptoms. Among the 23 TIA patients, 11 had recurrent TIAs, with the time interval between the first and last TIA being 2 hours to 45 days (8±13.1 days) and the number of TIAs ranging from one to six. Seven of the 23 patients who presented with local signs followed by TIAs had a completed stroke that occurred from a few minutes to 10 days (mean, 3.8±3.8 days) after the first TIA and from 1 hour to 31 days (9.2±10 days) after the onset of local symptoms. In this group of 53 patients with local symptoms at onset, 14 had no ischemic sign (2 in the retrospective part of the study, 12 in the prospective): 11 had isolated painful Horner's syndrome, 1 had Horner's syndrome with tinnitus, and 2 had isolated head and cervical pain.12
Among the 42 patients who had a completed stroke (Fig 1
), this was
preceded by other symptoms in 33: purely local signs in 16 and TIAs in
7. The time interval between the inaugural symptom and the onset of
stroke is represented in Fig 2
: it ranged
from a few minutes to 31 days, with the majority of strokes (82%)
occurring in the first 7 days.
|
The time course of symptoms in the 16 patients with traumatic ICA dissection was as follows: the time elapsed between the trauma and the first symptom ranged from 0 to 15 days (2.3±4 days), and the time between the trauma and TIA and/or completed stroke (n=14) ranged from 0 to 31 days (4.8±8.4 days).
| Discussion |
|---|
|
|
|---|
The overall frequency of ischemic events (TIAs and completed
strokes) was 82.5%, which is in accordance with the 50% to 95% rates
seen in other series (Table 4
). However, the frequency
in our series is possibly overestimated because, in the early years,
the diagnosis was suspected mainly in the presence of ischemic events,
and noninvasive screening was not available. Ischemic signs were thus
more frequent in the early part (93%) of the study than in the late
part (77%). This difference in the frequency of ischemic events will
be important to consider when planning future therapeutic trials, but
it should not interfere with the time course of ischemic signs.
|
All but 7 of our patients received some form of antithrombotic treatment (heparin in 58 and aspirin in 15), which might have altered the course of the disease. The present study is thus not a study of the natural history of extracranial ICA dissection, which would have been ethically difficult to justify given the frequency of ischemic signs and the documented importance of thromboembolism in their pathogenesis.1 7 9 The present study is not a therapeutic trial either, and no firm conclusion can be drawn about the efficacy of treatments. It can only be said that heparin did not prevent all infarcts since, among the 5 patients who experienced stroke more than 2 weeks after the onset of the first symptoms, 4 were treated with heparin when these strokes occurred. The time course of symptoms as recorded in this study is thus mostly that of patients receiving antithrombotic treatment in the form of heparin or aspirin.
Forty-two patients experienced a completed stroke. Of these patients,
33 had previous symptoms, local and/or TIAs, that preceded the onset of
stroke by a few minutes to 31 days (Figs 1
and 2
). Most strokes (82%)
occurred in the first week after the first symptoms appeared, which is
in agreement with previous reports1 2 3 4 5 6 7 8 9 10 and implies that
any potential preventive treatment should be started as early as
possible. It is, however, important to note that five strokes occurred
as late as 3 or 4 weeks after onset of the first symptoms. The longest
interval was 31 days, regardless of the pattern of inaugural symptoms,
local signs, or TIAs and whether the dissection was considered
traumatic or spontaneous. This late occurrence suggests that it might
be worth initiating treatment even as much as 1 month after the onset
of symptoms. Stroke recurrence was observed in only one case, a patient
with Ehlers-Danlos syndrome who had bilateral ICA dissections and
experienced three recurrent strokes from 52 to 81 days after the
initial stroke. Such recurrences would support prolonged treatment, at
least in patients with underlying arterial disease.13
Ischemic events have been reported years after traumatic dissections in
retrospective series5 and weeks after spontaneous
vertebral artery dissections,14 but such late strokes are
extremely rare. This issue was not addressed in the present study,
in which follow-up was limited to the first 6 months.
TIAs occurred in 41 patients: as inaugural symptoms in 18 and following local signs in 23. Most occurred in the first few days, but in contrast to completed strokes, they were often recurrent (50%), and in 2 patients they recurred after the first month (45 and 66 days). The mechanism of these late TIAs might be hemodynamic, since both patients had a persisting carotid occlusion. Such patients with TIAs occurring up to 5 months later were also reported by Fisher3 in his series of 26 patients. Despite these late TIAs, no completed strokes occurred in Fisher's patients or in our 2 patients.
Given the prognostic importance of ischemic strokes in ICA dissections, we compared some of the characteristics of the patients and of the dissections in patients with or without ischemic events. No difference could be found as far as age, sex, presence of hypertension, use of oral contraceptives, history of migraine, or angiographic pattern of the dissection (stenosis, aneurysm, or occlusion) were concerned. We were thus unable to identify clinical or angiographic features predictive of stroke associated with ICA dissection. These negative results, however, should be interpreted cautiously because of the small numbers of patients in each group and the absence of other similar studies. Large prospective studies are needed to clarify this important issue.
In conclusion, the risk of ischemic stroke in ICA dissection remains unpredictable. Stroke usually occurs in the first few days but can occur up to 1 month later. This suggests that any potential preventive treatment should be initiated as early as possible after the onset of the first symptoms and might be worth initiating even as much as 1 month later.
| Footnotes |
|---|
Received June 27, 1994; revision received November 18, 1994; accepted November 19, 1994.
| References |
|---|
|
|
|---|
2. Fisher CM, Ojemann RG, Robertson GH. Spontaneous dissection of cervicocerebral arteries. Can J Neurol Sci. 1978;5:9-19. [Medline] [Order article via Infotrieve]
3. Fisher CM. The headache and pain of spontaneous carotid artery dissection. Headache. 1982;22:60-65. [Medline] [Order article via Infotrieve]
4. Mokri B, Sundt TM, Houser OW, Piepgras DG. Spontaneous dissection of the cervical internal carotid artery. Ann Neurol. 1986;19:126-138. [Medline] [Order article via Infotrieve]
5. Mokri B. Traumatic and spontaneous extracranial internal carotid artery dissections. J Neurol. 1990;237:356-361. [Medline] [Order article via Infotrieve]
6.
Schievink WI, Mokri B, O'Fallon M. Recurrent spontaneous
cervical-artery dissection. N Engl J Med. 1994;330:393-397.
7. Anson J, Crowell RM. Cervicocranial arterial dissection. Neurosurgery. 1991;29:89-96. [Medline] [Order article via Infotrieve]
8.
Biller J, Hingtgen WL, Adams HP, Smoker WRK, Godersky JC,
Toffol GJ. Cervicocephalic arterial dissections: a ten year experience.
Arch Neurol. 1986;43:1234-1238.
9.
Bogousslavsky J, Despland PA, Regli F. Spontaneous carotid
dissection with acute stroke. Arch Neurol. 1987;44:137-140.
10.
Ehrenfeld WK, Wylie EJ. Spontaneous dissection of the internal
carotid artery. Arch Surg. 1976;111:1294-1301.
11. Biousse V, D'Anglejan-Chatillon J, Massiou H, Bousser MG. Head pain in nontraumatic artery dissection: a series of 65 patients. Cephalalgia. 1994;14:33-36. [Medline] [Order article via Infotrieve]
12. Biousse V, Woimant F, Amarenco P, Touboul PJ, Bousser MG. Pain as the only manifestation of extracranial internal carotid artery dissection. Cephalalgia. 1992;12:314-317. [Medline] [Order article via Infotrieve]
13. Schievink WI, Michels VV, Piepgras DG. Neurovascular manifestations of heritable connective tissue disorders: a review. Stroke. 1994;25:889-902. [Abstract]
14. Caplan LR, Baquis G, Pessin MS, D'Alton J, Adelman LS, DeWitt LD, Ho K, Izukawa D, Kwan ES. Dissection of the intracranial vertebral artery. Neurology. 1988;38:838-877.
This article has been cited by other articles:
![]() |
N. R Chopra, D. A Jones, N. Gadi, and F. Huwez Sudden onset of pain in the eye and blurring of vision BMJ, January 21, 2009; 338(jan21_2): a3111 - a3111. [Full Text] |
||||
![]() |
R Menon, S Kerry, J W Norris, and H S Markus Treatment of cervical artery dissection: a systematic review and meta-analysis J. Neurol. Neurosurg. Psychiatry, October 1, 2008; 79(10): 1122 - 1127. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. H. Rodallec, V. Marteau, S. Gerber, L. Desmottes, and M. Zins Craniocervical Arterial Dissection: Spectrum of Imaging Findings and Differential Diagnosis1 RadioGraphics, October 1, 2008; 28(6): 1711 - 1728. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. T. Engelter, T. Brandt, S. Debette, V. Caso, C. Lichy, A. Pezzini, S. Abboud, A. Bersano, R. Dittrich, C. Grond-Ginsbach, et al. Antiplatelets Versus Anticoagulation in Cervical Artery Dissection Stroke, September 1, 2007; 38(9): 2605 - 2611. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. H. Benninger, J. Gandjour, D. Georgiadis, E. Stockli, M. Arnold, and R. W. Baumgartner BENIGN LONG-TERM OUTCOME OF CONSERVATIVELY TREATED CERVICAL ANEURYSMS DUE TO CAROTID DISSECTION Neurology, July 31, 2007; 69(5): 486 - 487. [Full Text] [PDF] |
||||
![]() |
M Arnold, R Cumurciuc, C Stapf, P Favrole, K Berthet, and M-G Bousser Pain as the only symptom of cervical artery dissection J. Neurol. Neurosurg. Psychiatry, September 1, 2006; 77(9): 1021 - 1024. [Abstract] [Full Text] [PDF] |
||||
![]() |
O. Lanczik, K. Szabo, O. Lecei, J. Binder, S. Thiel, A. Gass, and M. Hennerici Central respiratory dysfunction following vertebral artery dissection Neurology, March 28, 2006; 66(6): 944 - 944. [Full Text] [PDF] |
||||
![]() |
M. Tola, M. Yurdakul, and T. Cumhur B-Flow Imaging in Low Cervical Internal Carotid Artery Dissection J. Ultrasound Med., November 1, 2005; 24(11): 1497 - 1502. [Abstract] [Full Text] [PDF] |
||||
![]() |
Y. Kadkhodayan, D. T. Jeck, C. J. Moran, C. P. Derdeyn, and D. T. Cross III Angioplasty and Stenting in Carotid Dissection with or without Associated Pseudoaneurysm AJNR Am. J. Neuroradiol., October 1, 2005; 26(9): 2328 - 2335. [Abstract] [Full Text] [PDF] |
||||
![]() |
Y. Yakushiji, M. Yasaka, T. Takada, and K. Minematsu Serial Transoral Carotid Ultrasonographic Findings in Extracranial Internal Carotid Artery Dissection J. Ultrasound Med., June 1, 2005; 24(6): 877 - 880. [Full Text] [PDF] |
||||
![]() |
A. L. Adkins, G. B. Zelenock, P. J. Bendick, and C. J. Shanley Duplex Ultrasound Recognition of Spontaneous Carotid Dissection: A Case Report and Review of the Literature Vascular and Endovascular Surgery, September 1, 2004; 38(5): 455 - 460. [Abstract] [PDF] |
||||
![]() |
L. L. Thomsen, E. Ostergaard, J. Olesen, and M. B. Russell Evidence for a separate type of migraine with aura: Sporadic hemiplegic migraine Neurology, February 25, 2003; 60(4): 595 - 601. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. Kremer, M. Mosso, D. Georgiadis, E. Stockli, D. Benninger, M. Arnold, and R.W. Baumgartner Carotid dissection with permanent and transient occlusion or severe stenosis: Long-term outcome Neurology, January 28, 2003; 60(2): 271 - 275. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Arnold, K. Nedeltchev, M. Sturzenegger, G. Schroth, T. J. Loher, F. Stepper, L. Remonda, C. Bassetti, and H. P. Mattle Thrombolysis in Patients With Acute Stroke Caused by Cervical Artery Dissection: Analysis of 9 Patients and Review of the Literature Arch Neurol, April 1, 2002; 59(4): 549 - 553. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. Milhaud, G. R. de Freitas, G. van Melle, and J. Bogousslavsky Occlusion Due to Carotid Artery Dissection: A More Severe Disease Than Previously Suggested Arch Neurol, April 1, 2002; 59(4): 557 - 561. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. W. Baumgartner, M. Arnold, I. Baumgartner, M. Mosso, F. Gonner, A. Studer, G. Schroth, B. Schuknecht, and M. Sturzenegger Carotid dissection with and without ischemic events: Local symptoms and cerebral artery findings Neurology, September 11, 2001; 57(5): 827 - 832. [Abstract] [Full Text] [PDF] |
||||
![]() |
W. I. Schievink Spontaneous Dissection of the Carotid and Vertebral Arteries N. Engl. J. Med., March 22, 2001; 344(12): 898 - 906. [Full Text] [PDF] |
||||
![]() |
M. A. Duncan, N. Dowd, D. Rawluk, and A. J. Cunningham Traumatic bilateral internal carotid artery dissection following airbag deployment in a patient with fibromuscular dysplasia Br. J. Anaesth., September 1, 2000; 85(3): 476 - 478. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. Djouhri, B. Guillon, L. Brunereau, C. Levy, V. Bousson, V. Biousse, L. Arrive, and J. M. Tubiana MR Angiography for the Long-Term Follow-Up of Dissecting Aneurysms of the Extracranial Internal Carotid Artery Am. J. Roentgenol., April 1, 2000; 174(4): 1137 - 1140. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. J. Cloft, M. E. Jensen, D. F. Kallmes, and J. E. Dion Arterial Dissections Complicating Cerebral Angiography and Cerebrovascular Interventions AJNR Am. J. Neuroradiol., March 1, 2000; 21(3): 541 - 545. [Abstract] [Full Text] |
||||
![]() |
J. A. Bounds, C. Lucas, D. Deplanque, T. Moulin, L. Tatu, D. Chavot, C. Lucas, T. Moulin, D. Deplanque, L. Tatu, et al. Carotid Dissection: Pathophysiology of Stroke and Treatment Implications • Response Stroke, May 1, 1999; 30(5): 1149 - 1150. [Full Text] [PDF] |
||||
![]() |
P J MARTIN and P R D HUMPHREY Disabling stroke arising five months after internal carotid artery dissection J. Neurol. Neurosurg. Psychiatry, July 1, 1998; 65(1): 136 - 137. [Full Text] |
||||
![]() |
V. Biousse, M. Schaison, P.-J. Touboul, J. D'Anglejan-Chatillon, and M.-G. Bousser Ischemic Optic Neuropathy Associated With Internal Carotid Artery Dissection Arch Neurol, May 1, 1998; 55(5): 715 - 719. [Abstract] [Full Text] [PDF] |
||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
Stroke Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1995 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |