J Neurol (2003) 250 : 11791184 DOI 10.

1007/s00415-003-0174-5

ORIGINAL COMMUNICATION

Rainer Dziewas Carsten Konrad Bianca Drger Stefan Evers Michael Besselmann Peter Ldemann Gregor Kuhlenbumer Florian Stgbauer E. Bernd Ringelstein

Cervical artery dissection clinical features, risk factors, therapy and outcome in 126 patients

s Abstract The highly variable clinical course of cervical artery dissections still poses a major challenge to the treating physician. This study was conducted (1) to de-

Received: 28 January 2003 Received in revised form: 7 May 2003 Accepted: 13 May 2003 Rainer Dziewas, MD () C. Konrad B. Drger S. Evers M. Besselmann P. Ldemann G. Kuhlenbumer F. Stgbauer E. B. Ringelstein Dept. of Neurology University Hospital of Mnster Albert-Schweitzer-Strasse 33 48129 Mnster, Germany Tel.: +49-2518/347-955 Fax: +49-2518/348-181 E-Mail: dziewas@uni-muenster.de G. Kuhlenbumer E. B. Ringelstein Institute of Arteriosclerosis Research University Hospital of Mnster Mnster, Germany

scribe the differences in clinical and angiographic presentation of patients with carotid and vertebral artery dissections (CAD, VAD), (2) to define the circumstances that are related to bilateral arterial dissections, and (3) to determine factors that predict a poor outcome. Retrospectively and by standardised interview, we studied 126 patients with cervical artery dissections. Preceding traumata, vascular risk factors, presenting local and ischemic symptoms, and patientoutcome were evaluated. Patients with CAD presented more often with a partial Horners syndrome and had a higher prevalence of fibromuscular dysplasia than patients with VAD. Patients with VAD complained more often of neck pain, more frequently reported a preceding chiropractic manipulation and had a higher incidence of

bilateral dissections than patients with CAD. Bilateral VAD was significantly related to a preceding chiropractic manipulation. Multivariate analysis showed that the variables stroke and arterial occlusion were the only independent factors associated with a poor outcome. This study emphasises the potential dangers of chiropractic manipulation of the cervical spine. Probably owing to the systematic use of forceful neck-rotation to both sides, this treatment was significantly associated with bilateral VAD. Patients with dissection-related cervical artery occlusion had a significantly increased risk of suffering a disabling stroke. s Key words vertebral artery dissection carotid artery dissection chiropractic manipulation

Introduction
Dissections of the carotid and vertebral arteries (CAD, VAD) are rare, with a reported annual incidence of 2.5 to 3 per 100000 for CAD [16, 34] and an estimated annual incidence of 1 to 1.5 per 100000 for VAD [3, 19, 35]. They account for about two percent of all ischemic strokes [12, 16, 34, 35]. However, in the younger adult population about 20 % of strokes are associated with cervical artery dissection [5, 8, 10, 18, 20, 31]. The increasing number of reported patients in recent years reflects both a growing familiarity with this complex clinical entity and a signif-

icant improvement in investigational methods. For instance, magnetic resonance imaging often yields almost pathognomonic findings such as an intramural hematoma [15, 43] or a double lumen in the affected vessel [21, 22]. In spite of this progress, the highly variable clinical course of cervical artery dissections still poses a major challenge to the treating physician. The objectives of this study were (1) to describe differences in the clinical course of VAD and CAD, (2) to define circumstances that led to bilateral arterial dissections, and (3) to determine factors that are predictive of a poor outcome.

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Patients and methods

Retrospectively, we studied 126 consecutive patients (50 women, 76 men, mean age 43.2 11.2 years) with cervical artery dissection admitted to our hospital during the period from 1992 to 2001. The diagnosis was based on clinical signs of either a local compressive syndrome or cerebral ischemia in combination with at least one confirming angiographic investigation. Diagnosis was established by digital subtraction angiography (DSA) in 47 patients (30 [38 %] with CAD and 17 [37 %] with VAD, by magnetic resonance angiography (MRA) and magnetic resonance imaging (MRI) of the neck in 72 patients (42 [54 %] with CAD, 28 [61 %] with VAD, 2 with VAD and CAD) and by CT-angiography in 7 patients (6 with CAD, 1 with VAD). Ultrasonography of the extra- and intracranial arteries was performed in 122 patients. On admission, clinical presentation distinguished between stroke, transient ischemic attack (TIA) and pure local signs. The major presenting symptoms and the applied therapy were recorded. In addition to the data presented in the patients reports, all patients were specifically interviewed regarding (1) the occurrence of warning symptoms and (2) the occurrence of preceding trauma or chiropractic manipulation. The following vascular risk factors were assessed: hypertension, diabetes mellitus, hypercholesterolemia, and regular cigarette smoking. Concerning the vascular findings on admission, the following items were taken into account: (1) affected vessel(s), (2) occlusion, stenosis or normal lumen, and (3) presence of fibromuscular dysplasia (FMD) [29]. Functional outcome after a maximum of six months was assessed using the modified Rankin Scale [42]. For estimation, the medical records of the initial clinical stay and, if available, of the rehabilitation stage and subsequent outpatient treatments were taken into account. Nonparametric quantitative data were compared with the MannWhitney U-test. For comparison of more than two groups, the Kruskal Wallis test was calculated first. To compare qualitative data between different groups (VAD versus CAD) the chi-square test was used. Multivariate regression analysis was used to identify variables significantly related to outcome. The significance level was set at p < 0.05.

Table 1 Characteristics of patients with carotid and vertebral arterial dissection CAD N = 78 Epidemiologic Data Women (%) Men (%) Age (SD) Dissection Characteristics Unilateral (%) Bilateral (%) Major presenting complaint Cerebral infarction (%) Transient ischemic attack (%) Local signs only (%) Associated features Neck pain (%) Headache (%) Tinnitus (%) Partial Horners syndrome (%) Risk factors Chiropractic manipulation (%) Trauma (%) Fibromuscular dysplasia (%) Hypertension (%) Hypercholesterolemia (%) Smoking (%) Diabetes mellitus (%) Vascular findings Occlusion (%) Stenoses (%) Normal (%) Outcome No sequelae or symptoms only (%) Mild to moderate handicap (%) Severe handicap or death (%) 30 (38) 48 (62) 43.6 (10.7) 75 (96) 3 (4)* 55 (71) 10 (13) 13 (17) 38 (49) 34 (44) 7 (9) 29 (37)* 5 (6)* 21 (27) 14 (18)* 21 (27) 31 (40) 32 (41) 3 (4) 43 (51) 35 (41) 7 (8) 54 (69) 12 (15) 12 (15) VAD N = 46 19 (41) 27 (59) 42.4 (12.1) 36 (78) 10 (22) 39 (85) 5 (11) 2 (4) 33 (72) 23 (50) 0 (0) 0 (0) 14 (30) 7 (15) 1 (2) 10 (22) 20 (43) 17 (37) 3 (7) 28 (47) 25 (42) 7 (12) 32 (70) 10 (22) 4 (9) All N = 126 50 (40) 76 (60) 43.2 (11.2) 111 (88) 15 (12) 96 (76) 15 (12) 15 (12) 73 (58) 57 (45) 8 (6) 29 (23) 20 (16) 29 (23) 16 (13) 31 (25) 51 (40) 50 (40) 6 (5) 71 (47) 60 (41) 14 (10) 88 (70) 22 (17) 16 (13)

Results
Among the 126 patients included in this study, 78 had CAD, 46 had VAD and 2 had both CAD and VAD. Clinical, angiographic and prognostic findings are stratified according to the dissections localisation in Table 1.

* p < 0.01 for the comparison of CAD and VAD; vascular findings refer to a total of 85 affected carotid arteries and 60 affected vertebral arteries

s Clinical findings
Among those 96 patients who suffered a stroke, 75 (78 %) reported preceding warning symptoms. In 54 patients (56 %), these symptoms were recognised only minutes prior to the onset of stroke, whereas 42 patients (44 %) noticed them between 12 hours and 14 days (median 3 days) before the onset of stroke. ceded dissection in 29 patients (23 %): sports activity with sudden head rotation in 15 patients, falling and hitting the head in seven patients, a car accident with whiplash injury in four patients, as well as lifting a heavy object, working for some hours with a reclined head and prolonged delivery in one patient each. In 23 of these 29 patients, cerebral ischemia or local symptoms occurred directly after the trauma, in six patients there was an interval of two to five days. Chiropractic manipulation of the cervical spine was performed prior to the diagnosis of dissection in 20 (16 %) patients, of whom 5 had CAD, 14 had VAD and one had both CAD and VAD (p < 0.01 for CAD versus VAD). The onset of symptoms occurred immediately after the procedure in

s Risk factors
The patients history revealed a possible link between the onset of dissection and specific predisposing factors in 48 patients (38 %). Different kinds of trauma pre-

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twelve patients and within two to ten days in the remaining eight patients.

s Vascular findings
On admission, 71 (49 %) of a total of 145 affected vessels were occluded, 60 (41 %) vessels showed a stenosis and fourteen (10 %) vessels had a normal lumen. The time point of angiographic examination with respect to the symptom onset was similar in patients with arterial occlusion (5.4 5.9 days), stenosis (5.6 6.9 days) or normal lumen (5.5 3.9 days). FMD of the cervical arteries was diagnosed in 16 patients (13 %) (diagnosis was based on DSA in 11 and MRA in 5 patients). Fourteen patients had CAD, one had VAD, and one had both VAD and CAD. Comparing the groups of patients with CAD and VAD, statistical analysis showed that bilateral dissections were significantly more frequent in VAD (p < 0.01). Conversely, FMD was significantly more frequent in CAD (p < 0.01). Owing to the rarity of bilateral dissections in patients with CAD, further statistical analysis was confined to patients with VAD (Table 2). Patients with bilateral VAD were significantly younger and had significantly more often a chiropractic manipulation of the cervical spine prior to dissection than patients with unilateral VAD. Additionally, women were significantly more often affected by bilateral VAD than men.

to CAD intravenous thrombolysis (IVT) was carried out within 3 hours of stroke, resulting in recanalisation of the MCA in all patients. In none of these five patients were side effects of thrombolysis due to extension of the wall hematoma noted. Two patients, both with CAD, made an excellent recovery (Rankin 0 and 1), one patient with VAD had a moderate residual handicap (Rankin 2) and two patients, one with CAD and one with VAD, were severely disabled (Rankin 4). One hundred and thirteen patients received anticoagulation with heparin that was followed by coumarin in 110 and antiplatelets in three patients. While treated with heparin, one patient had recurrent TIAs and one patient suffered symptomatic intracerebral hemorrhage. In another nine patients, initially treated with antiplatelets, six patients had recurrent TIAs.

s Outcome
After a maximum of six months 88 patients made an excellent recovery (Rankin 0 or 1), 22 patients had a mild to moderate handicap (Rankin 2 or 3), 15 patients were severely disabled (Rankin 4 or 5), and one patient (1 %) died (Table 3). In reference to the whole cohort of patients multivariate regression analysis revealed the variables arterial occlusion and stroke as being significantly related to a poor outcome (p < 0.05). On the other hand, the variables age and gender, preceding trivial or major trauma, preceding chiropractic manipulation, FMD, and chronic vascular risk factors were not related to outcome. The subgroup analysis for patients with CAD and VAD did not yield significant results. A recurrent dissection occurred in four patients (3.2 %) within the first month and in two patients (1.6 %) within the period of one month to one year. In two patients, both ICA and in two patients both vertebral arteries (Vas) were successively involved. In another two patients,VAD followed CAD. In patients with recurrent dissections, the prevalence of FMD was higher than in the whole series (33 % vs. 13 %), although this difference did not reach significance.

s Treatment
Data on the treatment during the acute stage of arterial dissection were collected for 122 patients. Two patients with VAD had basilar artery occlusion. They were treated with intra-arterial thrombolysis (IAT) within 6 hours of stroke and recanalisation was achieved in both of them. In three patients with occlusion of the MCA due
Table 2 Bilateral vertebral artery dissections VAD unilateral N = 36 Age (years) Female/male Chiropraxis Trauma FMD Hypertension Smoking Hyperlipidemia Diabetes m. 44.312.7* 12/24* 8 (22)* 6 (17) 0 (0) 10 (28) 14 (39) 16 (44) 3 (8) VAD bilateral N = 10 35.27.9 7/3 6 (60) 1 (10) 1 (10) 0 (0) 3 (30) 4 (40) 0 (0)

Discussion
s Clinical findings
As reported previously [6, 9, 13, 27, 38], stroke and TIA were the most common presenting features in our study affecting 86 % of patients without a significant difference between CAD and VAD. In accordance with other reports [39], neck pain was found more often in patients with VAD than in patients with CAD, while headache was present in approximately half of all patients irrespective of the dissections locali-

* = p < 0.05 for the comparison of unilateral and bilateral VAD

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Bad N = 16 (12%)

48.19.2 6/10 16 (100) 1 (6) 13 (81) 3 (19) 0 (0) 1 (6) 4 (25) 7 (44) 6 (38) 1 (6) 1 (6) 4 (25)

sation. Consistent with present knowledge [6, 7, 39], headache and neck pain were also important warning signs preceding the onset of stroke in nearly 80 % of patients between a few minutes and 14 days.

Moderate N = 22 (18%)

s Risk factors
42.611.4 8/14 22 (100) 2 (9) 19 (86) 3 (14) 0 (0) 2 (9) 7 (32) 9 (41) 7 (32) 1 (5) 3 (14) 6 (27)

* p < 0.05; ** p < 0.01 for the post-hoc comparison of patients with good outcome and patients with either moderate or bad outcome. In patients with multiple artery dissection the worst vascular finding is counted

In line with other studies [14, 23, 28, 40], a chiropractic manipulation of the cervical spine was performed significantly more often in patients with VAD (30 %) than in patients with CAD (6 %). As reported by others [23], the interval between the chiropractic manipulation and the onset of neurological symptoms was highly variable, ranging from a few seconds to ten days. Chronic vascular risk factors are usually judged to be rare in patients with CAD or VAD [7, 25, 28, 41]. In our study, the prevalence of smoking (40 %) and hypercholesterolemia (40 %) was at least twice as high in our study as in those reported previously. This is in line with Baumgartners recent observation [4], featuring hypercholesterolemia in 27 % and smoking in 39 %.

Outcome All (N = 126)

Good N = 88 (70%) Bad N = 4 (9%) Moderate N = 10 (18%)

38.010.1 4/6 10 (100) 2 (20) 8 (80) 2 (20) 0 (0) 0 (0) 3 (30) 3 (30) 3 (30) 0 (0) 3 (30) 2 (20)

50.012.0 1/3 4 (100) 1 (25) 4 (100) 0 (0) 0 (0) 0 (0) 1 (25) 4 (100) 2 (50) 1 (25) 1 (0) 0 (0)

42.511.4 36/52 58 (66)** 12 (14) 37 (42)** 44 (50) 7 (8) 13 (15) 20 (23) 35 (40) 37 (42) 4 (5) 16 (18) 19 (22)

s Vascular findings
In concordance with others [4, 7], on admission most dissected arteries were either occluded (55 %) or showed a stenosis (40 %). In line with data derived from the literature [4, 7, 39, 41], we found a higher frequency of bilateral dissections in patients with VAD (22 %) than in patients with CAD (4 %). Furthermore, a preceding chiropractic manipulation of the cervical spine was significantly related to bilateral VAD. The reason for this new observation may be seen in the fact that during chiropractic neck rotation a shearing force is systematically exerted to both VAs [26]. In contrast to this, abrupt rotational neck movements during for example physical exercise are more likely to be confined to one side of the neck, resulting in unilateral VAD more often. In contrast to other studies stating a prevalence of FMD in approximately 15 % of patients with both CAD and VAD [27], we observed a significant preponderance in patients with CAD (18 % versus 4 %).However,the low prevalence of FMD in patients with VAD may well be due to the overall low number of conventional angiographies performed in this study and a possible veiling effect induced by vessel occlusion.

Table 3 Demographic features, vascular findings and risk factors in patients with CAD and VAD stratified by outcome

Outcome VAD (N = 46)

Good N = 32 (70%) Bad N = 12 (15%) Moderate N = 12 (15%) Good N = 54 (70%)

Outcome CAD (N = 78)

42.710.6 21/33 31 (57)** 3 (6) 22 (41)* 28 (52) 4 (7) 11 (20) 14 (26) 22 (41) 24 (44) 2 (4) 5 (9) 13 (24)

45.512.3 4/8 12 (100) 0 (0) 11 (92) 1 (8) 0 (0) 2 (17) 4 (33) 6 (50) 4 (33) 1 (8) 0 (0) 4 (33)

47.18.8 5/7 12 (100) 0 (0) 9 (75) 3 (25) 0 (0) 1 (8) 3 (25) 3 (25) 4 (33) 0 (0) 0 (0) 4 (33)

42.812.8 14/18 25 (78) 7 (22) 14 (44)* 15 (47) 3 (9) 1 (3) 6 (19) 13 (41) 12 (38) 2 (6) 10 (31) 5 (16)

Age (years) Female/male Stroke Multiple vessels Occlusion Stenosis Normal FMD Hypertension Hyperlipidemia Smoking Diabetes m. Chiropraxis Trauma

s Treatment
As in our series, results of recently published studies suggest that thrombolysis is feasible in patients with stroke due to cervical artery dissection [1, 2, 11, 30, 32,

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33].As summarised by Arnold et al. [2], in none of 30 patients receiving IAT or IVT complications due to extension of wall hematoma were noted. To prevent thromboembolic complications, anticoagulation with intravenous heparin followed by warfarin is usually recommended [35, 36, 37, 39]. In our study of a total of 113 patients treated with heparin, recurrent TIAs occurred in one patient, while in six out of nine patients, in whom antiplatelets were initially used, recurrent TIAs were observed. However, one has to bear in mind that the use of heparin carries an increased risk of intracerebral hemorrhage [17].Additionally, up to now there have been no randomised trials comparing anticoagulants with antiplatelet drugs. Furthermore, in a meta-analysis of 24 studies including 286 patients, Lyrer and Engelter [24] found no significant difference between both treatment options in the odds of death and in the odds of being alive but disabled.

s Outcome
In our study, patients with CAD and VAD had a similar outcome. Overall 70 % had an excellent outcome, 18 % were moderately handicapped, and 12 % were severely disabled or dead. Multivariate regression analysis showed that besides the occurrence of a stroke, an arterial occlusion was significantly associated with a bad outcome, while other variables were not related to the prognosis. Although not significant, a trend towards a better outcome in patients with non-occlusive CAD than

in patients with arterial occlusion due to CAD was also observed by Milhaud et al. [26]. Interestingly, in this study patients with ICA occlusion due to dissection had a significantly worse prognosis than patients with atherothrombotic ICA occlusion. This was mainly due to a preponderance of large thromboembolic MCA infarcts in the first group. Comparably, Baumgartner et al. [4] found a significantly higher prevalence of > 80 % stenosis and occlusions in patients with ischemic events than in patients without ischemic events. Considering these findings, patients with dissection-related cervical artery occlusion are under a substantial risk of suffering a disabling stroke. In summary, the comparison of our data with known facts from the literature shows that our sample has most key features in common with large and well-studied groups of patients with cervical arterial dissections. Our main new findings were that [1] bilateral dissections, preceding chiropractic manipulations, and neck pain were more common in patients with VAD than in patients with CAD, [2] FMD was more frequent in patients with CAD, [3] patients with bilateral VAD received significantly more often a preceding chiropractic manipulation than patients with unilateral VAD, [4] besides the occurrence of a stroke, an arterial occlusion on admission was the only independent predictor for a poor outcome.
s Acknowledgement We are grateful to Anthony T. Herdman, PhD, Rotman Research Institute, Toronto, Canada, for expert help with the English language and to Esra Akova-ztrk for data management.

References
1. Ahmad HA, Gerraty RP, Davis SM, Cameron PA (1999) Cervicocerebral artery dissections. J Accid Emerg Med 16:422424 2. Arnold M, Nedeltchev K, Sturzenegger M, Schroth G, Loher TJ, Stepper F, Remonda L, Bassetti C, Mattle HP (2002) Thrombolysis in patients with acute stroke caused by cervical artery dissection. Arch Neurol 59:549553 3. Bassetti C, Carruzzo A, Sturzenegger M, Tuncdogan E (1996) Recurrence of cervical artery dissection: a prospective study of 81 patients. Stroke 27: 18041807 4. Baumgartner RW, Arnold M, Baumgartner I, Mosso M, Gnner F, Studer A, Schroth G, Schuknecht B, Sturzenegger M (2001) Carotid dissection with and without ischemic events. Neurology 57:827832 5. Bevan H, Sharma K, Bradley W (1990) Stroke in young adults. Stroke 21: 382386 6. Biousse V, DAnglejan-Chatillon J, Touboul PJ, Amarenco P, Bousser MG (1995) Time course of symptoms in extracranial carotid artery dissections: a series of 80 patients. Stroke 26: 235239 7. Bin Saeed A, Shuaib A, Al-Sulaiti G, Emery E (2000) Vertebral artery dissection: warning symptoms, clinical features and prognosis in 26 patients. Can J Neurol Sci 27:292296 8. Bogousslavsky J, Pierre PH (1992) Ischemic stroke in patients under age 45. Neurol Clin 10:113124 9. Caplan LR, Zarins CK, Hemmati M (1985) Spontaneous dissections of the extracranial arteries. Stroke 16: 10301038 10. Chancellor AM, Glasgow GL, Ockelford PA, Johns A, Smith J (1989) Etiology, prognosis, and hemostatic function after cerebral infarction in young adults. Stroke 20:477482 11. Derex L, Nighoghossian N, Turjman F, Hermier M, Honnorat J, Neuschwander P, Froment JC, Trouillas P (2000) Intravenous tPA in acute ischemic stroke related to internal carotid artery dissection. Neurology 54:21592161 12. Ducrocq X, Lacour JC, Debouverie M, Bracard S, Girard F, Weber M (1999) Accidents vasculaires cerebraux ischemiques du sujet jeune: etude prospective de 296 patients ages de 16 a 45 ans. Rev Neurol (Paris) 155: 575582 13. Fisher CM, Ojemann RG, Roberson GH (1978) Spontaneous dissection of cervico-cerebral arteries. Can J Neurol Sci 5:919 14. Frisoni GB, Anzola GP (1991) Vertebrobasilar ischemia after neck motion. Stroke 22:14521460 15. Gelbert F, Assouline E, Hodes JE, Reizine D, Woimant F, George B, Hagueneau M, Merland JJ (1991) MRI in spontaneous dissection of vertebral and carotid arteries: 15 cases studied at 0.5 Tesla. Neuroradiology 33: 111113

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16. Giroud M, Fayolle H, Andre N (1994) Incidence of internal carotid artery dissection in the community of Dijon. J Neurol Neurosurg Psychiatry 57:1443 17. International Stroke Trial Collaborative Group (1997) The International Stroke Trial (IST): a randomized trial of aspirin, subcutaneous heparin, both or neither among 19435 patients with acute ischemic stroke. Lancet 349: 15691581 18. Lanzino G, Andreoli A, Di Pasquale G, Urbinati S, Limoni P, Serrachioli A, Lusa A, Pinelli G, Testa C, Tognetti F (1991) Etiopathogenesis and prognosis of cerebral ischemia in young adults. A survey of 155 treated patients. Acta Neurol Scand 84:321325 19. Leys D, Moulin TH, Stojkovic T, Bergey S, Chavor D, DONALD Investigators (1995) Follow-up of patients with history of cervical artery dissection. Cerebrovasc Dis 5:4349 20. Lisovoski F, Rousseaux P (1991) Cerebral infarction in young people. A study of 148 patients with early cerebral angiography. J Neurol Neurosurg Psychiatry 54:576579 21. Hosoya T, Adachi M, Yamaguchi K, Haku T, Kayama T, Kato T (1999) Clinical and neuroradiological features of intracranial vertebrobasilar artery dissection. Stroke 30:10831090 22. Hosoya T, Watanabe N, Yamaguchi K, Kubota H, Onodera Y (1994) Intracranial vertebral artery dissection in Wallenberg syndrome. Am J Neuroradiol 15:11611165 23. Hufnagel A, Hammers A, Schnle PW, Bhm KD, Leonhardt G (1999) Stroke following chiropractic manipulation of the cervical spine. J Neurol 246: 683688 24. Lyrer P, Engelter S: Antithrombotic drugs for carotid artery dissection (Cochrane Review). In: The Cochrane Library, Issue 1, 2002. Oxford: Update Software

25. Mas JL, Bousser MG, Hasboun D, Laplane D (1987) Extracranial vertebral artery dissections: a review of 13 cases. Stroke 18:10371047 26. Milhaud D, de Freitas GR, van Melle G, Bogousslavsky J (2002) Occlusion due to carotid artery dissection. Arch Neurol 59:557561 27. Mokri B, Silbert PL, Schievink WI, Piepgras DG (1996) Cranial nerve palsy in spontaneous dissection of the extracranial internal carotid artery. Neurology 46:356359 28. Norris JW, Beletsky V, Nadareishvili ZG, Canadian Stroke Consortium (2000) Sudden neck movement and cervical artery dissection. Can Med Assoc J 163:3840 29. Osborn AG, Anderson RE (1977) Angiographic spectrum of cervical and intracranial fibromuscular dysplasia. Stroke 8:617625 30. Price RF, Sellar R, Leung C, OSullivan MJ (1998) Traumatic vertebral arterial dissection and vertebrobasilar arterial thrombosis successfully treated with endovascular thrombolysis and stenting. Am J Neuroradiol 19:16771680 31. Provenzale JM, Morgenlander JC, Gress D (1996) Spontaneous vertebral dissection: clinical conventional angiographic, CT and MR findings. J Comput Assist Tomogr 20:185193 32. Rudolf J, Neveling M, Grond M, Schmlling S, Stenzel C, Heiss WD (1999) Stroke following internal carotid artery occlusion: a contraindication for intravenous thrombolysis. Eur J Neurol 6:5155 33. Sampognaro G, Turgut T, Conners JJ, White C, Collins T, Ramee SR (1999) Intraarterial thrombolysis in a patient presenting with an ischemic stroke due to spontaneous internal carotid dissection. Catheter Cardiovasc Interv 48: 312315

34. Schievink WI, Mokri B, Whisnant JP (1993) Internal carotid artery dissection in a community: Rochester, Minnesota, 19871992. Stroke 24: 16781680 35. Schievink WI, Mokri B, OFallon WM (1994) Recurrent spontaneous cervical artery dissection. N Engl J Med 330: 393397 36. Schievink WI (2000) The treatment of spontaneous carotid and vertebral artery dissections. Curr Opin Cardiol 15:316321 37. Schievink WI (2001) Spontaneous dissection of the carotid and vertebral arteries. N Eng J Med 344:898906 38. Silbert PL, Mokri B, Schievink WI (1995) Headache and neck pain in spontaneous internal carotid and vertebral artery dissections. Neurology 45:15171522 39. Slaver JL, Easton JD (1998) Dissections and trauma of cervicocerebral arteries. In: Barnett HJM, Mohr JP, Stein BM, Yatsu FM (eds) Stroke pathophysiology, diagnosis, and management, third edition, New York: Churchill Livingstone, pp 769786 40. Stevinson C, Honan W, Cooke B, Ernst E (2001) Neurological complications of cervical spine manipulation. J R Soc Med 94:107110 41. Sturzenegger M (1995) Spontaneous internal carotid artery dissection: early diagnosis and management in 44 patients. J Neurol 242:231238 42. Wade DT (1992) Rankin scale. In: Wade DT (ed) Measurement in neurological rehabilitation. Oxford, Oxford University Press, pp 238239 43. Zuber M, Meary E, Meder JF, Mas JL (1993) Magnetic resonance imaging and dynamic CT scan in cervical artery dissections. Stroke 25:576581