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Unruptured Intracranial Vertebral Artery Dissection

Clinical Course and Serial Radiographic Imagings
Originally published 1997;28:370–374


    Background and Purpose Intracranial vertebral artery dissection is an increasingly recognized cause of stroke. However, little is known about its natural history and clinical manifestations, and appropriate management protocol has not yet been established. This study was performed to clarify its clinical course and determine the best management protocol.

    Methods This study is a retrospective clinical and radiographic review of 11 patients with 13 lesions who presented between 1990 and 1996. Patients with a history of trauma and those who presented with subarachnoid hemorrhage were excluded. The 11 patients comprised seven men and four women, who ranged in age from 34 to 71 years, with a mean age of 47 years. Ten patients presented with ischemic symptoms.

    Results Although recurrent ischemic attacks were observed in two patients, most (90%) subsequently made a good recovery and returned to their previous lifestyle. Five arteries showed the typical “string sign” or “pearl and string sign” on initial angiography. They changed in the follow-up examinations, which demonstrated either resolution of the stenosis or progression to complete occlusion. In contrast, the angiographic signs of complete occlusion (three arteries) or aneurysmal dilatation without luminal stenosis (four arteries) remained unchanged during the observation period of 5 months to 2.5 years. MRI was a sensitive tool for diagnosing intracranial vertebral artery dissection; intramural thrombus and intimal flap were the two major findings. MR angiography was also useful for demonstrating abnormalities of the arterial signal column such as pseudolumen or aneurysmal dilatation.

    Conclusions The natural history of unruptured intracranial vertebral artery dissection seems relatively benign, with a high probability (62%) of spontaneous angiographic cure. Some persistent aneurysmal dilatation may be amenable to intravascular coil embolization.

    Spontaneous dissection of the intracranial vertebral artery is an increasingly recognized cause of stroke. However, little is known about its natural history and clinical manifestations. Accurate diagnosis and appropriate management of the disease depend on a knowledge of its serial radiographic features and clinical course.

    Intracranial vertebral artery dissection has two major types of presentation: focal neurological deficits due to vertebrobasilar artery ischemia and subarachnoid hemorrhage (SAH). Recent observations suggested that the natural course and outcome of the patients strongly depend on the initial pattern of presentation.12345 Many patients presenting with ischemic symptoms have a favorable outcome.134 The plane of dissection remains mainly subintimal or within the medial layer, although the dissection sometimes extends to the basilar artery,5 and the risk of future hemorrhage due to unruptured dissection appears to be low.67 In contrast, a high mortality rate has been reported among patients with a ruptured vertebral artery dissection2 : the plane of dissection extends to the adventitial layer,5 and there is a tendency for recurrent hemorrhage.2 The natural course of each group should therefore be analyzed and discussed separately. In this study we documented the clinical course and serial radiographic features of unruptured intracranial vertebral artery dissection in 11 patients, and we use these findings to propose appropriate management strategies.

    Subjects and Methods

    The clinical course and radiographic features of 11 patients with a diagnosis of unruptured vertebral artery dissection between 1990 and 1996 were reviewed retrospectively. Patients with a history of trauma or who presented with SAH or had a dissection of an extracranial vertebral artery were excluded. The 11 patients studied comprised 7 men and 4 women who ranged in age from 34 to 71 years, with a mean age of 47 years.

    The diagnosis was based on the angiographic findings in association with MRI and MR angiography (MRA) and clinical features such as headache, vomiting, vertigo, and neurological deficits referable to the vertebrobasilar circulation.

    Standard treatment protocols for ischemic stroke were used to manage the patients in the acute stage after onset (eg, mild volume expansion with the use of low-molecular-weight dextran). Anticoagulant and fibrinolytic agents were not used, and no patients underwent surgical or intravascular intervention during the early stage of the disease. In the follow-up period, 9 patients received antiplatelet agents (8 received ticlopidine and 1 received aspirin). The remaining 2 patients had been given no medicine. All patients received follow-up angiography combined with serial MRI and MRA, and the sequential radiographic changes were studied. The follow-up period ranged from 6 to 77 months, with a mean of 27 months.


    Table 1 summarizes the clinical features and course of the 11 patients. Lateral medullary syndrome was a common clinical presentation of brain stem ischemia: some patients had a pure lateral medullary syndrome, while in others it was associated with additional manifestations, such as hemiparesis, diplopia, temporary loss of consciousness, and facial weakness. The ischemic symptoms recurred in 2 patients on days 4 (patient 2) and 20 (patient 5) after the first ictus. However, 9 (90%) of the 10 patients made a good recovery and returned to their previous lifestyle. The clinical courses of these patients were uneventful during the follow-up period. The remaining 1 patient also recovered quite well from the initial symptoms but died of a massive supratentorial SAH 1.5 years after the ischemic episode (patient 4). CT scan at that time showed massive intrasylvian fissure hematoma. Although the origin of SAH was unverified, we believe that the source of hemorrhage was unrelated to the vertebral artery dissection because of the distribution of SAH. One patient underwent intravascular coil embolization for persistent aneurysmal dilatation after 2.5 years of follow-up (case 11).

    Illustrative serial radiographic images are shown in Figs 1 through 4 (patients 4, 5, 6, and 11).

    Initial angiography was performed 3 to 67 days after onset. The 11 patients had 13 lesions, consisting of 10 symptomatic and 3 asymptomatic dissections. Three dissections extended to the basilar artery. All patients had follow-up angiography from 24 days to 2.5 years after the onset. The major angiographic abnormalities observed on the initial angiograms and the chronological changes are summarized in Table 2. The luminal configuration of 6 lesions changed in the subsequent angiographic studies but remained unchanged in the remaining 7 lesions.

    The findings of MRA and MRI are summarized in Table 3. MRA was valuable for demonstrating abnormalities of the arterial signal column. The pseudolumen or aneurysmal dilatation demonstrated by angiography was also identified by MRA in all 8 vessels (Fig 1c through 1e). It also confirmed the occlusion (Fig 2c and 2d), corresponding well with angiographic observations in 4 of 5 patients (80%). In contrast, it was difficult to evaluate angiographic luminal stenosis with MRA (Fig 3a and 3c). The two major MRI findings of arterial dissection were intramural thrombus (identified in 6 vessels) and an intimal flap (identified in 7 vessels; Figs 1a and 4a). Intramural thrombus on T1-weighted or proton images was demonstrated only in the subacute or early chronic stage after an ischemic insult (4 to 31 days). It could not be identified on T2-weighted images; however, disappearance of the flow void in this sequence suggests progression of a luminal stenosis to complete occlusion (Fig 2a and 2b).


    Clinical Course

    Spontaneous healing of unruptured vertebral artery dissection has often been noted, and therefore its biological behavior might be favorable.148 Although 2 (20%) of the 10 symptomatic patients had recurrent ischemic attacks during the early period after the onset in the present series, 9 (90%) of these 10 patients subsequently returned to their previous lifestyles (Table 1). Kitanaka et al1 also described six patients with intracranial vertebral artery dissection presenting with brain stem ischemia; they observed no further progression of dissection or associated SAH in any of the patients. These follow-up observations indicate that vertebral artery dissection presenting with ischemic episodes has a benign natural course. However, we cannot exclude fully the possibility that some patients with initially poor neurological conditions are not correctly diagnosed as having arterial dissection (eg, basilar artery occlusion).

    Angiographic Findings

    The angiographic findings of luminal narrowing, tapered occlusion, double lumen appearance, or aneurysm formation in our patients corresponded well with those of previous reports3910 (Table 2). A new significant observation from our study is that the chronological changes of angiographic findings depend largely on those seen on initial angiography. Narrowing of a long segment of the artery is thought to be characteristic of dissection and referred to as the “string sign” and the “pearl and string sign” if there is a distal or proximal site dilatation. These two characteristic signs showed dynamic changes on follow-up angiography: resolution of the stenosis or progression to complete occlusion. Most of the initial angiograms in these patients showed retention of contrast material in the later phase. Such patients should be carefully followed up with serial radiographic examinations. In contrast, none of the tapered occlusions on initial angiography recanalized in this series. The angiographic appearance of dissections evident as dilatation without luminal stenosis also remained unchanged on subsequent angiographic examinations, irrespective of the luminal configuration (ie, saccular, fingerlike extensions parallel to the artery or fusiform dilatation).

    MRI and MRA

    Although cerebral angiography remains the mainstay of radiographic diagnosis of intracranial arterial dissection,10 MRI and MRA are providing a new noninvasive method for evaluating arterial dissection.11121314151617 In this series, initial suspicion of vertebral artery dissection was raised by MR findings in 73% (8/11) of the patients, which prompted us to perform cerebral angiography for definitive diagnosis.

    The value of MR images is particularly due to its high resolution in the posterior fossa without bone artifacts and its direct visualization of intramural hematomas. The chronological changes of an intramural hematoma seem to correspond with those of an intracerebral hematoma.18 The intensity of an intramural hematoma on T1-weighted and proton images varies according to its age.1417 It appears isointense or slightly hyperintense for the first few days after onset and then becomes hyperintense in the subacute stage. The abnormal intensity of the hematoma resolved after several months.18 Therefore, when MRI is used for screening or follow-up, the chronological changes of signal intensity of the hematoma should be considered. T1-weighted images between 3 days and 2 months after the ischemic episodes demonstrated intramural hematoma in 7 (70%) of 10 examinations. In contrast, T2-weighted images seem to have less diagnostic value for demonstrating intramural hematoma because they merge with the hyperintense cerebrospinal fluid.14 However, disappearance of the flow void with this sequence suggests total occlusion of the affected vessel, as was seen in patient 5 in our study (Fig 2). An intimal flap is better visualized on MR images than angiography13 and was demonstrated in 7 (54%) of the 13 lesions in the present study (Figs 1a and 4a).

    MRA also seems to be useful in demonstrating abnormalities of the arterial signal column, such as pseudolumen, aneurysmal dilatation, and occlusion of the affected vessels (Figs 1c and 2d). Most of the findings corresponded with angiographic observations, although it is difficult to evaluate the luminal stenosis accurately (Fig 3a and 3c). If screening or follow-up examination is necessary, MRI or MRA appears to be the first-choice noninvasive technique for monitoring luminal configurations or arterial changes over time.1517

    Therapeutic Considerations

    The therapeutic approach for intracranial vertebral artery dissection has not yet been fully established. Because SAH subsequently occurs only rarely in patients who present with ischemic symptoms,67 surgical reinforcement of the dilated segment does not appear to be beneficial. The only possible effective surgical procedure in the acute or subacute settings may be proximal occlusion or trapping of the parent artery, which is a standard procedure for ruptured vertebral artery dissections.2919 However, such interventions have not yet proved to prevent further dissections or clinical recurrence. Additionally, the procedure per se sometimes produces neurological sequelae as a result of interrupting the blood flow.119 When the relatively benign natural course is taken into account, any consideration of surgical intervention should be cautious. Observation with serial radiographic studies, as we have described above, is the most rational approach.

    Our results suggest a high probability of spontaneous angiographic cure on subsequent angiography. This occurred in 8 (62%) of the 13 lesions, including total occlusion of the affected vessels with sufficient angiographic opacification of the basilar artery via the contralateral vertebral artery or the posterior communicating artery. Some patients, however, harbored persistent angiographic abnormalities, most of which were aneurysmal dilatation (dissecting aneurysms). Although the risk of future hemorrhage or ischemic attacks from these lesions cannot be estimated from currently available data, Caplan et al20 reported a case in which the persistent aneurysmal dilatation became a source of emboli. Another case was reported in which death resulted from an SAH during anticoagulation treatment.7 Patients in such a situation may be possible candidates for surgery.1

    In the chronic stage, however, organization of intramural thrombus or reparative changes are observed within the false lumen, with proliferation of fibrous tissues and formation of a new elastic lamina and smooth muscle fibers. The aneurysm at surgery in this stage was reported to be whitish gray in color and to have become firm.19 These changes make open surgical repair difficult with sparing of the parent artery, even though the aneurysmal configuration on angiograms appeared saccular. In such a case, an endovascular approach is probably the method of choice. In this series, one patient was successfully treated by intravascular coil embolization of persistent aneurysmal dilatation after a 2.5-year follow-up (Fig 4). Although the actual benefit of such a procedure is unknown, we believe that endovascular therapy can provide better treatment for these lesions and may play an important role in the management of this particular condition.


    We are greatly indebted to Dr Shigeru Nemoto, Tokyo Metropolitan Police Hospital, Tokyo, Japan, for undertaking intravascular coil embolization in case 11, and to Drs Soshi Okuhata, Masaru Endo, Akiyoshi Sato, Masaaki Hamano, and Toshihiko Tejima for performing angiography.

          Figure 1.

    Figure 1. Patient 4. a, T2-weighted axial MR images on day 7 after the initial ischemic attack show dilatation of both vertebral arteries (left greater than right). The linear high-intensity structures (arrows) demonstrate intimal flaps on both sides (double lumen). b, T1-weighted axial images of the lower slice reveal intramural thrombus (arrow). c, MR angiogram taken on the same day shows fusiform dilatation of both vertebral arteries (arrows). d, Anteroposterior angiogram of the left vertebral artery performed on day 20 shows sausagelike swelling of the left vertebral artery (arrow). The basilar artery is poorly opacified (arrowhead). e, Angiogram performed on day 35 shows that the left vertebral artery has become more stenotic. The basilar artery is opacified very faintly (arrowhead). The fusiform dilatation did not change (arrow). The venous phase reveals retained contrast material (not shown). f, Nine months after the onset the left vertebral artery is totally occluded (arrow) at the origin of the posterior inferior cerebellar artery (arrowhead). The right vertebral artery still shows slight fusiform dilatation, through which the basilar artery is well demonstrated (not shown).

          Figure 2.

    Figure 2. Patient 5. Serial T2-weighted axial MR images taken on days 2 (a) and 26 (b) after onset show disappearance of signal flow void of the left vertebral artery (arrows). Serial MR angiograms performed on days 2 (c) and 47 (d) also demonstrate disappearance of flow signal of the left vertebral artery (arrows). The progression from tapered stenosis to occlusion of the left vertebral artery was confirmed by angiography taken on days 3 and 24 (not shown).

          Figure 3.

    Figure 3. Patient 6. a, MR angiogram on day 24 after onset shows a filling defect of the right vertebral artery (arrow). b, The lesion has resolved by 5 months (arrow). c, Right vertebral angiogram on day 30 reveals slight fusiform dilatation (arrow, pearl sign) and poor opacification of the basilar artery (arrowhead) and the posterior inferior cerebellar artery. d, Angiography performed 4.5 months after onset shows that the stenosis has resolved. The basilar artery is well shown (arrowhead).

          Figure 4.

    Figure 4. Patient 11. a, MRI (proton image) shows a dilated right vertebral artery. An intimal flap (arrow) and the orifice are demonstrated. b, The aneurysm, which was demonstrated at the time of admission, is still evident after 2.5 years of follow-up (arrow). c, The persistent aneurysmal dilatation was successfully embolized with the use of an interlocking detachable coil (Target Therapeutics) (arrow).

    Table 1. Summary of 11 Patients With Vertebral Artery Dissection

    Pt No.Age, y/SexPast HistoryPresenting Symptoms and SignsInfarction on MRIClinical Course and Outcome
    140/FHeadache, L LMS, L IX, X CN palsy, miosis, ptosis, L hemiparesisL LM, midbrainPtosis and miosism persist, GR
    246/FMigraineHeadache, vomiting, transient LOC, L III CN palsyMidbrain, R cerebellumRecurrent attack (day 4; Weber syndrome), GR thereafter
    338/MDizziness, headache, vomiting, L hemiparesis, transient LOCGR
    440/FHTHeadache, vomiting, L LMSUneventful, but died of supratentorial SAH (1.5 y)
    534/FVertigo, vomiting, R hemihypesthesia, L VII, IX, X, XII CN palsy, cerebellar signLower pons, L cerebellumRecurrent attack (day 20), but GR thereafter
    645/MHeadache, vomiting, vertigoGR
    753/MHTHeadache, vomiting, vertigoGR
    854/MDM, HT, hyperlipidemiaDizziness, headache, dysarthria, R LMS, diplopiaR LMGR but hypesthesia persists
    971/MR hemihypesthesiaL LMGR
    1045/MSevere neck pain, vomiting, cerebellar signL cerebellumGR
    1154/MOPLL, DM, HTUneventful, coil embolization (2.5 y)

    Pt indicates patient; L, left; LMS, lateral medullary syndrome; CN, cranial nerve; LM, lateral medulla; GR, good recovery; LOC, loss of consciousness; R, right; HT, hypertension; SAH, subarachnoid hemorrhage; DM, diabetes mellitus; and OPLL, ossification of posterior longitudinal ligament.

    Table 2. Summary of Initial and Follow-up Angiography in 11 Patients With Intracranial Vertebral Artery Dissection (Involving 13 Arteries)

    Initial AngiographyNo. of PtsSubsequent AngiographyNo. of Pts
    Stenosis without dilatation (string sign)3*Occlusion2
    Resolution of stenosis1
    Stenosis with dilatation (pearl and string sign)2*Occlusion1
    Resolution of stenosis1
    Double lumen (intimal flap)1Dissection extended1
    Dilatation only (no stenosis)
     Saccular2 (1)No change2 (1)
     Fusiform2 (2)No change2 (2)
    Occlusion (tapered occlusion)3No change3

    Pts indicates patients. Numbers of asymptomatic dissections are shown in parentheses.

    *Contrast retention was seen in two patients in each group.

    Table 3. Summary of Initial and Follow-up MRA and MRI in 11 Patients With Intracranial Vertebral Artery Dissection (Involving 13 Arteries)

    Initial ExaminationNo. of PtsSubsequent ExaminationNo. of Pts
     Dilatation only7No change7
     Occlusion only (filling defect)3No change2
     Dilatation and occlusion2No change1
    Occlusion only1
     Intramural thrombus only5Normalized2
    Intimal flap1
    No follow-up2
     Intimal flap only5No change4
     Intramural thrombus and intimal flap1Thrombus only1


    Correspondence to Yuhei Yoshimoto, MD, Department of Neurosurgery, Dokkyo University School of Medicine, 880 Kitakobayashi, Mibu, Shimotsuga, Tochigi 321-02, Japan.


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