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(Stroke. 1997;28:1993-1997.)
© 1997 American Heart Association, Inc.

Articles

Magnetic Resonance Angiography Demonstrates Vascular Healing of Carotid and Vertebral Artery Dissections

Scott E. Kasner, MD; Linda L. Hankins, MD; Patti Bratina, RN; Lewis B. Morgenstern, MD

From the Departments of Neurology and Radiology (L.L.H.), University of Texas at Houston.

Correspondence to Lewis B. Morgenstern, MD, Stroke Treatment Team, Department of Neurology, University of Texas at Houston, 6431 Fannin, Suite 7.044, Houston, TX 77030. E-mail lmorgens{at}neuro.med.uth.tmc.edu

	Abstract

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Background and Purpose Dissection of the carotid and vertebral arteries is most accurately diagnosed with conventional angiography. MR techniques are sensitive for detecting the abnormalities associated with dissection but may lack specificity. We hypothesized that MR may be useful for serial monitoring of dissection and may therefore guide therapy.

Methods All patients with angiographically proven carotid and/or vertebral artery dissection from July 1994 to June 1996 were followed for a median duration of 10.5 months. Of these 29 patients (44 vessels), 18 were concurrently evaluated with MR, and a target group of 9 patients (17 vessels) was prospectively followed with MR at 3-month intervals.

Results In the 18 patients with both imaging studies at baseline, angiography revealed 30 dissected vessels while MR detected 27 (90%). In the target group of 9 patients, initial MR identified 15 of the 17 dissections diagnosed with angiography. Serial MR revealed complete healing in 5 vessels, improvement in 6 vessels, no change in 4 vessels, and worsening in 2 vessels. The radiographic features most likely to resolve were stenosis and mural hematoma, while occlusion and luminal irregularity tended to persist. Late ischemic events occurred in 2 patients, both with persistent MR evidence of dissection, one while subtherapeutic on warfarin therapy and the other occurring 1 week after warfarin was discontinued.

Conclusions MR is a reliable noninvasive method for following the vascular response to treatment and may guide the course of a clinical trial comparing medical therapies for carotid and vertebral artery dissection.

Key Words: angiography • angiography, magnetic resonance • dissection • stroke

	Introduction

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Dissection of the extracranial portions of the internal carotid and vertebral arteries occurs as a result of trauma to the head and neck or may occur spontaneously. The best medical therapy for dissection is controversial and potentially includes antiplatelet or anticoagulant regimens. The appropriate duration of therapy is unknown, as are the relative risks and benefits of prolonged therapy.

Definitive diagnosis of arterial dissection classically requires conventional angiography as the radiographic gold standard,¹ but this modality is suboptimal for repeated examinations during the course of treatment because of risk of stroke, patient discomfort, and substantial expense. MRI and MRA have been reported to be reliable methods for establishing the initial diagnosis of dissection^{2 3 4 5 6 7 8 9 10 11} but have not been adequately evaluated as follow-up studies. We hypothesized that MRI and MRA may be suitable for subsequent noninvasive evaluation of the dissection and may therefore guide the choice and duration of therapy. We prospectively identified 29 patients with angiographically proven carotid or vertebral dissection. In nine of these patients, we correlated the angiographic findings with initial MR investigations and then monitored these patients serially with MR for evidence of vascular healing in response to treatment. In addition, we report clinical baseline and outcome data from this prospective series.

	Subjects and Methods

Top Abstract Introduction Subjects and Methods Results Discussion References

 
During the period from July 1994 through July 1996, all patients with angiographically confirmed dissection of the extracranial ICA and/or vertebral arteries were followed. Approval for this project was given by the Committee for the Protection of Human Subjects at the University of Texas, Houston. Traumatic and spontaneous dissections were both included in this analysis because they may represent the spectrum of a single clinical entity.^{12 13 14 15} Dissections were labeled as spontaneous when a history of head or neck injury was lacking. Iatrogenic (angiography-related) dissections were classified as traumatic.

All patients were evaluated for a history of recent or remote trauma, and all underwent complete neurological examination. Demographic characteristics of the patients, including age, sex, race, and any prior history of ischemic events, were recorded. Clinical data were collected regarding initial symptoms of the dissection, interval between trauma and symptoms, and therapeutic regimen. The choice of therapy for the dissection in each patient was made by the primary physician. Follow-up clinical evaluation was obtained either at subsequent outpatient visits or by telephone, if necessary, with a specific questionnaire designed to assess new or recurrent cerebral ischemic events. This questionnaire was standardized to minimize bias related to unblinded investigation.

A total of 30 patients with dissection were identified by conventional angiography. One patient refused to participate in this study. Among the remaining 29 patients, 18 patients were concurrently evaluated with MRA. Of those, 9 patients were prospectively monitored with repeated evaluation by MRA at approximately 3-month intervals. This set of patients represents the target group for analysis of serial noninvasive evaluation and was determined on the basis of availability for follow-up and economic feasibility of obtaining outpatient MRA studies. The patients in the target group did not differ significantly from the overall group in terms of age, etiology, or site of vascular injury.

Angiography was performed with the use of high-resolution digital technique and selected catheterization of carotid and vertebral arteries. MR examination included conventional spin-echo technique with T1-, proton-density, and T2-weighted axial images. MRA technique included 2D TOF imaging of the carotid bifurcations, 3D phase-contrast imaging of the neck, and 3D TOF imaging of the circle of Willis. Criteria for establishing the diagnosis included long stenotic segments consistent with "string sign," tapered stenosis or occlusion (Fig 1), pseudoaneurysm, intimal flap formation (Fig 2), and luminal irregularity, as suggested by Fisher et al¹⁵ for conventional angiography and by Goldberg et al⁸ and Lévy et al⁷ for MRA. In addition, the presence of crescent-shaped high signal intensity within a vessel wall (mural hematoma or double lumen) was considered indicative of dissection on standard MRI.⁸ Healing was defined by the complete resolution of a specific abnormality. All imaging studies were evaluated by two independent neuroradiologists, and any disagreement was resolved by consensus. Dissections that were identified by only one of the two imaging techniques were further evaluated retrospectively by both neuroradiologists.

View larger version (112K): [in this window] [in a new window]   Figure 1. Dissection of the ICA. a, Conventional angiography initially demonstrated a tapered stenosis of the ICA distal to the bifurcation. b, Baseline 2D TOF MRA obtained 2 days later revealed concordant evidence of a tapered stenosis. c, Follow-up 2D TOF MRA obtained 5 months later had normalized.

View larger version (103K): [in this window] [in a new window]   Figure 2. Dissection of the vertebral artery. a, Conventional angiography showed a well-defined dissection with a prominent intimal flap, mural hematoma, and luminal irregularity. b, Baseline 3D phase-contrast MRA showed a nonspecific flow abnormality in the midvertebral artery with associated luminal irregularity consistent with the diagnosis of dissection. c, Follow-up 3D phase-contrast MRA obtained 3 months later revealed a normal vertebral artery.

	Results

Top Abstract Introduction Subjects and Methods Results Discussion References

 
A total of 44 dissected vessels were identified in 29 patients (14 men, 15 women; age range, 11 to 61 years). There were 27 ICA and 17 vertebral artery dissections. Dissection was spontaneous in 5 patients (7 vessels) and traumatic in 24 patients (37 vessels). In 3 patients, the vascular injury was a complication of arteriography done for evaluation of aneurysms. Multiple arterial dissections occurred in 12 patients.

The presenting symptom of the dissection was ischemic stroke in 20 patients, isolated Horner's syndrome in 1 patient, and acute neck pain in 1 patient, but it was incidental in 7 patients who underwent imaging studies because of serious neck injury or other trauma-related reasons. Fifteen of the 20 stroke patients had traumatic dissections, and the interval between trauma and cerebral infarction ranged from a few hours to 1 year, with the majority (10 of 15) occurring within 24 hours. None of the patients had a prior history of transient ischemic attack or stroke.

Four patients died during initial hospitalization because of their severe head or systemic injuries, and 1 patient was lost to follow-up. The remaining 24 patients were followed for a median duration of 10.5 months (range, 1 to 24 months). Initially, 14 patients were anticoagulated with warfarin, 2 received aspirin, and 8 patients received no therapy for the dissection because of concerns of hemorrhage related to the recent trauma. Two patients (8%) had late ischemic events during the follow-up period. One of these patients had discontinued warfarin 1 week before the event, which occurred 2 weeks after the initial trauma, and the other was subtherapeutic on warfarin therapy (international normalized ratio=1.1) at the time of recurrence 3 months after the original injury.

For the purpose of comparison of baseline imaging techniques, 18 patients (30 vessels) were imaged with MRI/MRA in addition to conventional arteriography during their initial hospitalization. The median interval between the two studies was 1 day (range, 0 to 15 days), and MRA preceded arteriography in 8 patients. Compared with the findings on conventional arteriography, MRA correctly identified 27 of 30 dissected vessels (14 of 16 ICA, 13 of 14 vertebral artery). Three dissections were not detected prospectively, and the imaging studies were further analyzed retrospectively. One dissection was relatively subtle and was obscured by motion artifact, one was initially misinterpreted by the neuroradiologist, and one was labeled a congenitally atrophic vertebral artery on initial MRI/MRA. There was no MR suggestion of dissection in any of the vessels classified as normal on angiography.

The target group consisted of 9 patients (17 vessels) who had both angiography and MRA at baseline were evaluated by MRA at 3-month intervals. These patients were followed for a median duration of 10 months, and a mean of three MR studies were performed on each patient during this time. The initial MRA study demonstrated concordant evidence of dissection in 15 of 17 vessels (9 of 10 ICA, 6 of 7 vertebral artery). Serial MRA revealed complete healing of 5 vessels, improvement in 6 vessels, no change in 4 vessels, and worsening in 2 vessels. The resolution and progression of the specific radiographic features through the course of follow-up are summarized in the Table. Eighty percent of the tapered stenoses normalized during the course of follow-up, half of these during the first 3 months and the remaining half during the next 3 months. All of the mural hematomas/intimal flaps resolved, while luminal irregularities persisted in 44% of the cases. Two of the 4 occlusions remained stable on repeated examination, while 2 had recanalized by the first follow-up MR study at approximately 3 months.

View this table: [in this window] [in a new window]   Table 1. Target Group (9 Patients, 17 Dissected Vessels): Radiographic Characteristics at Baseline and Final Follow-up

Among the 9 target group patients, 7 were initially treated with warfarin, 1 with aspirin, and 1 received no therapy. The aspirin-treated patient had an occlusive dissection that remained unchanged, while the untreated patient had a tapered stenosis that progressed to complete occlusion on MR during the course of follow-up. One warfarin-treated patient also had worsening of the dissection. The two patients described above with recurrent ischemic events had traumatic dissections and incomplete healing on MRA at the time of their recurrence, characterized by residual tapered stenosis in one and luminal irregularity in both, and both had recently discontinued warfarin therapy. The 4 remaining warfarin-treated patients had improved or unchanged dissections on MR without recurrent clinical events.

	Discussion

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Conventional angiography is generally considered the diagnostic modality of choice for cervical arterial dissection^{1 16 17} but is associated with a risk of complications. Noninvasive vascular imaging techniques with ultrasonography,^{18 19 20} CT,^{6 21} and combined MRI and MRA^{2 3 4 5 6 7 8 9 10 11} have been reported to be reasonably sensitive for detecting dissection, although none are fully concordant with the angiographic standard.

In comparison to angiography, noninvasive techniques have several limitations. Ultrasonography requires evidence of a high-resistance flow profile or complete absence of flow to support the diagnosis, but these abnormalities may not be pathognomonic for dissection. Most carotid dissections occur well above the bifurcation and may not be adequately insonated. Depending on the specific techniques and criteria used, ultrasonography may detect from 68% to 95% of ICA dissections.^{3 22 23} Moreover, ultrasound techniques are poorly suited for evaluation of vertebral artery dissection. Dynamic CT has a sensitivity of 80% but requires prior angiography to direct attention toward the level of the dissection.⁶ Helical CT can evaluate the entire extracranial ICA with excellent accuracy in detecting dissection, but this technique requires further investigation.²¹ Vascular imaging with CT may also be limited by the requirements for intravenous contrast and ionizing radiation.

On MRI, dissection is suggested by an eccentric signal void surrounded by a crescent-shaped hyperintensity on T1- and T2-weighted images. This typical image may be detected in 70% to 100% of dissected vessels.^{4 6 7} Other MRI findings include stenosis or complete vascular occlusion, but these markers lack defined specificity for dissection. MRA provides a method for imaging the vasculature independently from the surrounding structures and may demonstrate vessel wall irregularity and aneurysmal dilatation that are not appreciated on segmental imaging studies. The combination of MRI and MRA appears to have a sensitivity approaching 100% for severe dissections in some series but can be confounded by turbulent flow, bony artifacts, and patient movement and may be unable to discern dissection from other causes of arterial narrowing or occlusion.^{2 3 4 6 7 24 25} Consequently, dissection of the vertebral arteries may be less accurately diagnosed with MR techniques.^{7 10} MR techniques may fail to identify specific vascular features such as pseudoaneurysm formation and are also relatively insensitive to mild stenoses.^{3 11} In addition, these noninvasive techniques are insufficient for detecting fibromuscular dysplasia, an important risk factor for arterial dissection in some patients.^{2 16 17}

In the present study, initial MRI and MRA prospectively detected 27 of the 30 dissections (90%) identified by conventional angiography. A retrospective analysis of the three missed dissections revealed the limitations of the MR techniques: motion artifacts, interobserver disagreements, and nonspecific flow abnormalities. In addition, many of the correct MR diagnoses of dissection were based on relatively nonspecific findings (Fig 2, for example). Severe stenosis or occlusion was observed to be tapered on angiography but was only noted by the phenomenon of "slow flow" on phase-contrast MRA, which may occur in other conditions. Therefore, despite the high sensitivity of MR techniques for arterial dissection, angiography was still required to provide the definitive diagnosis.

Jacobs and colleagues⁵ recently described three patients whose dissections were diagnosed and monitored solely with MRI and MRA They suggested that in selected patients with the typical clinical history and MR findings of dissection, conventional angiography may be obviated by the newer noninvasive technique. Based on our prospective target group of 9 patients, in which the initial MRI and MRA failed to detect 2 dissections, we support the use of angiography for primary diagnosis. However, after both angiography and MRI/MRA were obtained at baseline, the MR techniques provided a consistent and noninvasive method for repeated evaluation.

The MR features most likely to show evidence of healing are stenosis (Fig 1) and the mural hematoma/intimal flap (Fig 2). Occlusion may recanalize early but seems unlikely to improve if the radiographic appearance remains unchanged after a 3-month interval. Using conventional angiography, several authors have reported a similar pattern of vascular recovery after dissection.^{1 13 26} In addition, luminal irregularities have been described as a frequent residuum of dissection of uncertain significance.¹ Both of the patients in our series with late cerebrovascular events had persistent luminal irregularities, and one also had residual tapered stenosis. These intimal abnormalities may not be as benign as previously suggested and may be an indication for an extended course of therapy.

Since some dissections may be missed on initial MR studies, it is quite possible that some residual dissections could remain undetected on follow-up imaging. However, all vessels with normal MR images remained asymptomatic and were not associated with subsequent stroke in this study. The clinical importance of these MR-invisible dissections remains to be elucidated.

This observational study has several limitations. Patient selection for the target group may have been biased by potentially relevant prognostic or socioeconomic factors, and the sample size of the target group was too small to allow for meaningful statistical analysis. We are therefore unable to draw conclusions about the effects of any particular therapy. Although we required the use of angiography as the diagnostic gold standard to corroborate the initial MR findings, we did not obtain conventional angiography at the end of the follow-up period to confirm the final MRA. This would have made the follow-up results more robust but was unacceptable to many of our patients because of the discomfort, expense, and risk. In addition, the study personnel, including the neuroradiologists, were not blinded to the patients' clinical and radiographic data.

The ability to serially monitor cervical arterial dissections with MR techniques has potential clinical applicability. Many patients with dissection are treated with antiplatelet agents or anticoagulation for an empiric or indefinite period of time and remain exposed to potential hemorrhagic complications. Those not treated may be exposed to significant risk of ischemic stroke, although the magnitude of this risk is poorly characterized.^{15 27 28 29} The optimal management strategy remains unknown. In patients with MR evidence of either complete vascular healing or complete occlusion on repeated MR examination, prolonged therapy may not be required since each of these extremes appeared to be clinically and radiographically stable. Patients with incomplete healing on MR may be at higher risk for cerebral thromboembolic events and may benefit from continued therapy.

In conclusion, MRI and MRA are sensitive to vascular flow anomalies associated with dissection but may reveal nonspecific findings. When baseline conventional angiography and MR studies are concordant, MR can be used to serially monitor the dissection for evidence of healing or progression in response to treatment, although a larger study is required to confirm these results. The association between specific MR findings (or their absence) in dissection and the risk for late cerebrovascular sequelae must be evaluated further. Moreover, a clinical trial or multicenter registry is needed to determine the optimal choice and duration of medical therapy for dissection, and MR studies may be useful to guide therapy in such a trial.

	Selected Abbreviations and Acronyms

 

2D = two-dimensional 3D = three-dimensional ICA = internal carotid artery MRA = magnetic resonance angiography TOF = time of flight

	Acknowledgments

 
This study was supported by American Heart Association Clinician Scientist Award 96004040 (Dr Morgenstern). We wish to thank Dr James Grotta for his comments and suggestions.

Received March 27, 1997; revision received July 15, 1997; accepted July 15, 1997.

	References

Top Abstract Introduction Subjects and Methods Results Discussion References

 
1. Houser OW, Mokri B, Sundt TM, Baker HL, Reese DF. Spontaneous cervical cephalic arterial dissection and its residuum: angiographic spectrum. AJNR Am J Neuroradiol. 1983;5:27-34.[Abstract]

2. Bui LN, Brant-Zawadzki M, Verghese P, Gillan G. Magnetic resonance angiography of cervicocranial dissection. Stroke. 1993;24:126-131.[Abstract/Free Full Text]

3. Sturzenegger M. Spontaneous internal carotid artery dissection: early diagnosis and management in 44 patients. J Neurol. 1995;242:231-238.[Medline] [Order article via Infotrieve]

4. Stringaris K, Liberopoulos K, Giaka E, Kokkinis K, Bastounis E, Klonaris EC, Balas P. Three-dimensional time-of-flight MR angiography and MR imaging versus conventional angiography in carotid artery dissections. Int Angiol. 1996;15:20-25.[Medline] [Order article via Infotrieve]

5. Jacobs A, Lanfermann H, Szelies B, Schroder R, Neveling M. MRI- and MRA-guided therapy of carotid and vertebral artery dissections. Cerebrovasc Dis. 1996;6(suppl 2):80. Abstract.

6. Zuber M, Meary E, Meder J-F, Mas J-L. Magnetic resonance imaging and dynamic CT scan in cervical artery dissections. Stroke. 1994;25:576-581.[Abstract]

7. Levy C, Laissy JP, Raveau V, Amarenco P, Servois V, Bousser MG, Tubiana JM. Carotid and vertebral artery dissections: three-dimensional time-of-flight MR angiography and MR imaging versus conventional angiography. Radiology. 1994;190:97-103.[Abstract/Free Full Text]

8. Goldberg HI, Grossman RI, Gomori JM, Asbury AK, Bilaniuk LT, Zimmerman RA. Cervical internal carotid artery dissection hemorrhage: diagnosis using MR. Radiology. 1986;158:157-161.[Abstract/Free Full Text]

9. Klufas RA, Hsu L, Barnes PD, Patel MR, Schwartz RB. Dissection of the carotid and vertebral arteries: imaging with MR angiography. AJR Am J Roentgenol. 1995;164:673-677.[Abstract/Free Full Text]

10. Provenzale JM, Morgenlander JC, Gress D. Spontaneous vertebral dissection: clinical, conventional angiographic, CT, and MR findings. J Comput Assist Tomogr. 1996;20:185-193.[Medline] [Order article via Infotrieve]

11. Sue DE, Brant-Zawadzki MN, Chance J. Dissection of cranial arteries in the neck: correlation of MRI and arteriography. Neuroradiology. 1992;34:273-278.[Medline] [Order article via Infotrieve]

12. Biousse V, D'Anglejan-Chatillon J, Touboul P-J, Amarenco P, Bousser M-G. Time course of symptoms in extracranial carotid artery dissections: a series of 80 patients. Stroke. 1995;36:235-239.

13. Mokri B. Traumatic and spontaneous extracranial internal carotid artery dissections. J Neurol. 1990;237:356-361.[Medline] [Order article via Infotrieve]

14. Sherman DG, Hart RG, Easton JD. Abrupt change in head position and cerebral infarction. Stroke. 1981;12:2-6.[Abstract/Free Full Text]

15. Fisher CM, Ojemann RG, Roberson GH. Spontaneous dissection of the cervico-cerebral arteries. Can J Neurol Sci. 1978;5:5-19.

16. Anson J, Crowell RM. Cervicocranial arterial dissection. Neurosurgery. 1991;29:89-96.[Medline] [Order article via Infotrieve]

17. Hart RG, Easton JD. Dissections of cervical and cerebral arteries. Neurol Clin North Am. 1983;1:155-182.

18. Mullges W, Ringelstein EB, Leibold M. Non-invasive diagnosis of internal carotid artery dissections. J Neurol Neurosurg Psychiatry. 1992;55:98-104.[Abstract/Free Full Text]

19. Sturzenegger M. Ultrasound findings in spontaneous carotid artery dissection: the value of duplex sonography. Arch Neurol. 1991;48:1057-1063.[Abstract/Free Full Text]

20. Eljamel MSM, Humphrey PRD, Shaw MDM. Dissection of the cervical internal carotid artery: the role of Doppler/duplex studies and conservative management. J Neurol Neurosurg Psychiatry. 1990;53:379-383.[Abstract/Free Full Text]

21. Leclerc X, Godefroy O, Salhi A, Lucas C, Leys D, Pruvo JP. Helical CT for the diagnosis of extracranial internal carotid artery dissection. Stroke. 1996;27:461-466.[Abstract/Free Full Text]

22. Steinke W, Rautenberg W, Schwartz A, Hennerici M. Noninvasive monitoring of internal carotid artery dissection. Stroke. 1994;25:998-1005.[Abstract]

23. Sturzenegger M, Mattle HP, Rivoir A, Baumgartner RW. Ultrasound findings in carotid artery dissection: analysis of 43 patients. Neurology. 1995;45:691-698.[Abstract/Free Full Text]

24. McCormick GF, Halbach VV. Recurrent ischemic events in two patients with painless vertebral artery dissection. Stroke. 1993;24:598-602.[Abstract/Free Full Text]

25. Kitanaka C, Tanaka J, Kuwahara M, Teraoka A. Magnetic resonance imaging study of intracranial vertebrobasilar artery dissections. Stroke. 1994;25:571-575.[Abstract]

26. Bassetti C, Carruzzo A, Sturzenegger M, Tuncdogan E. Recurrence of cervical artery dissection: a prospective study of 81 patients. Stroke. 1996;27:1804-1807.[Abstract/Free Full Text]

27. Bogousslavsky J, Despland P-A, Regli F. Spontaneous carotid dissection with acute stroke. Arch Neurol. 1987;44:137-140.[Abstract/Free Full Text]

28. 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]

29. Cogbill TH, Moore EE, Meissner M, Fischer RP, Hoyt DB, Morris JA, Shackford SR, Wallace JR, Ros SE, Ochsner G, Sugerman HJ. The spectrum of blunt injury to the carotid artery: a multicenter perspective. J Trauma. 1994;37:473-479.[Medline] [Order article via Infotrieve]

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