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 »  Patients and Methods
 »  Results
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Table of Contents    
Year : 2010  |  Volume : 58  |  Issue : 6  |  Page : 869-874

Spontaneous vertebral artery dissection: Report of 16 cases

Southwest Hospital, Third Military Medical University, & Chongqing Intervention, Institute of Cerebrovascular Disease, Chongqing, P.R.China

Date of Acceptance04-Oct-2010
Date of Web Publication10-Dec-2010

Correspondence Address:
Kang-Ning Chen
Department of Neurology, Southwest Hospital, Third Military Medical University, and Chongqing Intervention Institute of Cerebrovascular Disease, Gao Tan Yan Street, Chongqing 400038, P.R. China.

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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.73749

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 » Abstract 

Background and Objectives: Spontaneous vertebral artery dissection (sVAD) is a rare condition and can potentially cause a stroke, particularly in young to middle-aged people. Patients and Methods: The clinical manifestations, medical imaging characteristics, treatment, and prognosis of 16 patients with sVAD were analyzed. Results: None of the 16 patients had a history of head or neck trauma. The most common clinical manifestation was headache with symptoms of posterior-circulation ischemia (63%). Diagnosis of VAD was definitive in one patient at autopsy, and in the remaining it was established by magnetic resonance angiography, computer tomography angiography, or digital subtraction angiography. Treatment modalities included: thrombolysis with urokinase (1), antiplatelet therapy (6), and endovascular stenting (9). There was one death and the remaining 15 patients were followed up for 3-48 months and did not have recurrence of cerebral events. Conclusions: Rapid and accurate diagnosis of sVAD and proper treatment are crucial for good outcomes. This study shows that antiplatelet therapy and endovascular treatment are effective treatments for sVAD.

Keywords: Dissection, interventional treatment, posterior-circulation ischemia, vertebral artery

How to cite this article:
Gui L, Shi GS, Li GJ, Fan WH, Huang HQ, Zhou ZH, Chen KN. Spontaneous vertebral artery dissection: Report of 16 cases. Neurol India 2010;58:869-74

How to cite this URL:
Gui L, Shi GS, Li GJ, Fan WH, Huang HQ, Zhou ZH, Chen KN. Spontaneous vertebral artery dissection: Report of 16 cases. Neurol India [serial online] 2010 [cited 2020 Nov 24];58:869-74. Available from:

 » Introduction Top

Spontaneous vertebral artery dissection (sVAD) is a rare condition; it is one of the common causes for posterior-circulation ischemic (PCI) stroke in people aged between 30 and 50 years. [1],[2] If the condition is not recognized early and managed promptly, some of the patients may have significant disability or death. [3],[4] Because of its low incidence, there is often delay in the diagnosis of sVAD. This report presents the clinical characteristics of 16 patients with non-traumatic VAD seen over a period of six years.

 » Patients and Methods Top

Sixteen patients with sVAD who were admitted to the Chongqing Intervention Institute of Cerebrovascular Disease (Southwest Hospital of The Third Military Medical University) between January 2003 and October 2009 and included in the Center's Prospective Stroke Registry, were the subjects of this study.

Clinical data

Vascular risk factors were analyzed in detail in all the patients and the patients were asked to recall for any abnormal movements or trauma of the neck or any physical exercise within the few weeks prior to the onset of symptoms. All patients had detailed neurologic examination. Stroke severity was assessed using the National Institute of Health Stroke Scale (NIHSS). On admission, all patients had detailed workup for vascular risk factors including lipid profile, thrombophilic states, and plasma homocysteine, and also electrocardiography, cranial computed tomography (CT) or magnetic resonance imaging (MRI). All patients underwent magnetic resonance angiography (MRA), computed tomography angiography (CTA), or digital subtraction angiography (DSA) to demonstrate vertebral artery dissection or dissecting aneurysm. Anatomically, the vertebral artery is divided into four arbitrary parts, designated V1 to V4. [5]

Treatment and follow-up

The treatment modalities included: thrombolysis (1) antiplatelet therapy, aspirin 300 mgday for 6 months, (6), and endovascular intervention (9). The endovascular intervention was for posterior-circulation ischemia and serious hemodynamic disturbances in seven, for subarachnoid hemorrhage in one and for a long tear in VA and headache in one. Endovascular procedures included: stinting with coated stent in two and coronary arterial stent in four, and three patient had stent-assisted coil embolization. All the patients had NIHSS scoring at the time of discharge. Patients were followed up 3 months later by neurologists at the outpatient department or over the phone, and all patients were recorded for modified rank score (mRS).

 » Results Top

There were 13 males and 3 females and age ranged between 16 and 57 years (39.2 ± 13.0) years). The clinical features are shown in [Table 1]. None of the patients had a history of head or neck trauma. The initial symptom was headache in 8 patients (53%). Thirteen patients presented with symptoms of posterior-circulation ischemia, one patient with subarachnoid hemorrhage and two patients with serious occipital lacerating pain. Of the 16 patients, serious parietooccipital pain with symptoms of posterior-circulation ischemia were the most common manifestations (n = 10, 63%). None of the patients had transient ischemic attacks (TIA) or spinal cord ischemic symptoms or signs. Most patients had neurologic deficits with the onset pf sVAD (n = 14, 88%), and symptoms of posterior-circulation ischemia were apparent within 4 days of onset of headache.
Table 1: Clinical manifestations in 16 sCVD patients

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CT or MRI showed acute infarcts in 13 (81%) patients. Angiographic findings (MRA, 1 patient; CTA, 1 patient; DSA, 13 patients; CTA and DSA, 1 patient) are shown in [Table 2]. Of the 16 patients, 4 (25%) had lesions on V1 segment, 5 (31%) on V2 segment, 4 (25%) on V3 segment, and 4 (25%) on V4 segment of the VA. In one patient, the lesions extended from V4 segment to the basilar artery.
Table 2: Radiological and outcome data in 16 sCVD patients

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The patient who was treated with intra arterial thrombolysis for acute basilar artery occlusion, deteriorated post-procedure and died. [4] All the six patients treated with antiplatelets had significant improvement in their NIHSS scores (2.00 ± 0.63) when compared to the admission NIHSS scores (5.50 ± 2.81) (P<0.01). The nine patients who underwent endovascular interventions had significant improvement in their NIHSS scores (4.17 ± 1.47) when compared to the admission NIHSS scores (12.50 ± 7.06) (P<0.05). Patient with subarachnoid hemorrhage was conscious and headache free at the time of admission. At 3-month follow-up the mRS scores were no or mild to moderate disability in 14 (88%): mRS = 0 in 8 patients (50%), mRS = 1 in 4 patients (25%), mRS = 2 in 2 patients (13%), and mRS = 3 in 1 patient (6%). None of the patients had recurrence of stroke at 3-48 months follow-up [Table 2].

Typical cases

Case 4

A 39-year-old woman presented with sudden loss of consciousness. Physical examination revealed altered mental status with bilateral pyramidal signs, Cranial MRI showed multiple infarcts in the bilateral thalami, occipital lobes, and the left cerebellum [Figure 1]. She was put on aspirin and showed gradul improvement in her neurological status and muscle strength was grade 4 in the left limbs, grade 1 in the right upper limb, and grade 3 in the right lower limb. DSA performed on day-19 revealed a 1.8 Χ 0.8 mm dissecting aneurysm in the V3 segment of the right VA and non-visualization of the distal end of the left postero-inferior cerebellar artery. The aneurysm was obliterated by a coated stent (4.0Χ12 mm, 210CG1240, Cordis, America) [Figure 2]. At the time of discharge she was alert with normal power in the left sided limbs and power 3-4 in the right sided limbs. At 3 months the mRS score was 2 and she did not have recurrence of stroke during 27 months follow-up.
Figure 1: Case 4, cranial MRI. T1, T2 weighted images reveal multiple long-T1, long-T2 signals in the left cerebellar, occipital lobes, and bilateral thalamus, a, b, c: T1-weighted images, d, e, f: T2-weighted images

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Figure 2: Case 4, cranial DSA. (a) DSA reveals a dissecting aneurysm on the V3 segment of the right vertebral artery (lateral view, black arrow). (b) After a coated stent was implanted into the site of the aneurysm, the dissecting aneurysm disappeared (lateral view, black arrow)

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Case 8

A 29-year-old male presented with severe left occipital pain radiating to the left neck and shoulder and persistent numbness in the left side of the head and face. Neurologic examination did not reveal abnormal findings. Cranial MRI was essentially normal [Figure 3]a, and transcranial Doppler suggested quickened blood flow in the right VA and basilar artery, slowed blood flow in the left VA, and abnormal morphology during the systolic phase. DSA performed at two weeks revealed double-lumen sign with extensive stenosis of V2-V3 segments of the left VA [[Figure 3]b, c]. The dissection segement of VA was obliterated with two Firebird stents (3.5 Χ 33 mm, Firebird, F3533, China) [[Figure 3]d, e]. He was symptom free and had no ischemic events during 24 months follow-up.
Figure 3: Case 8, MRI and DSA. There are no abnormal signals on T1, T2 weighted images. DSA reveals string sign on V2-V3 segments of the left vertebral artery (b: lateral view). DSA reveals a mouse tail-shaped stenosis in the lower part of V2 segment in the left, anterior oblique 32 degrees (c: black arrow), double-lumen sign on V2-V3 segments, and the lifted intima in the lumen (c: white arrow). After two Firebird stents (3.5×33mm) were implanted, the stenosis was corrected (d, e: black arrow), and double-lumen sign disappeared (e: white arrow)

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Case 16

A 50-year-old man presented with lacerating left occipital pain of two days duration and left facial numbness and bucking and dysphagia of one day duration. Physical examination revealed left Horner syndrome, left facial hypalgesia, bulbo-paralysis, and NIHSS score was 3. He was a chronic smoker (20 cigarettes/day for 20 years) and an alcoholic (250 ml/day of distillate spirit for 15 years). Cranial MRI revealed patchy ischemic lesions lateral to the left pons and the lateral cerebral ventricle [Figure 4]a. DSA showed a pearl and string stenosis and intima flap visible in the V2 segment of the left VA [Figure 4]b, c. The patient was put on aspirin only for six months. At the time of discharge, NIHSS score was 1, and three-month mRS score was 0. He had no recurrence of ischemic events during 36 months follow-up.
Figure 4: Case 16, MRI and DSA. (a) MRI indicates long-T1, long-T2 signals in the left pons (upper, T1-weighted image; lower, T2-weighted image). DSA reveals bead-like stenosis of V2 segment of the left vertebral artery (b: left, anterior oblique 41 degrees, arrow), and the lifted intima flap at the site of stenosis (c: left, arrow)

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 » Discussion Top

sVAD is not uncommon with estimated annual incidence of approximately 1-1.5/10 000. [2],[6],[7] However, neck arterial dissection is one of the main causes of ischemic stroke in young people. [2],[8] VAD occurs frequently in individuals aged between 30 and 50 years with 16% to 60% occurrence in males. [9],[10],[11],[12] The reported VA segment involvement is quite variable. Some series reported V2 or V3 segment involvement, [10],[11],[12] while others did not find such discretion [13] as seen in our series. However, in our series the dissection occurred more on the extracranial segments (V1-V3) (75%) than on intracranial segments. This may be due to the fact that the extracranial segment of the VA moves more freely, and is more liable to injury by adjacent osseous structures such as the cervical vertebrae or styloid process.

VAD patients usually have a history of neck trauma or neck procedure, and its association with injury is significantly higher than the association of internal carotid artery dissection with injury. [14] In fact, except traumatic VAD, most VAD cases are spontaneous ones or only minor, non-penetrating neck trauma just like the cases reported by Prabhakar. [14] Rome had listed 68 types of neck movement that may be related with neck arterial dissection, such as backing up a car, painting a roof, coughing, vomiting, and harmful sleeping posture.[15] As these movements are common in daily life, it is controversial whether they contribute to VAD. None of our 16 patients had any history of any type of such neck trauma. Many factors could lead to abnormal structural changes in the vascular wall, and increase the susceptibility to trauma and intimal laceration. They include: connective tissue abnormalities, [16] hyperhomocysteinemia, [17] fibromuscular dysplasia, [18] cystic medial necrosis, [2] hypertension, [19],[20] migraine, [21] oral contraceptive use, [21],[22] and cardiovascular risk factors. [23],[24] Of the 16 patients, four had hypertension, two were heavy smokers, one was alcoholic, and five had hyperhomocysteinemia. Seven had suspected slight neck movement or exertion prior to the onset of VAD. Most of the patients with sVSD may have some vascular abnormalities and a trivial physical injury may precipitated the dissection,

Most commonly patients with VAD present with symptoms of posterior-circulation ischemia. [4],[25] About 12% of patients present with only neck or/and occipital pain and 10% of patients with VAD many not have any clinical manifestations. [26] Spinal cord infarction is a rare complication of vertebral artery dissection. [14] Frisoni and Anzola divided sVAD into three stages. During Stage 1, various causes lead to vertebral arterial intimal injury. This stage may be subclinical or may progress to the other two stages. During Stage 2, slight neck movement results in sudden intima laceration, and the patient presents with serious neck and occipital pain. This stage can last for a long time period. Stage 3 is characterized by dissection, thrombosis, luminal occlusion by hematoma or hemodynamic disturbances from embolus shedding. [27] This staging of explains why patients with angiography-confirmed sVAD have a variety of clinical manifestations and also the progression.

The imaging modalities for the diagnosis of VAD include MRA, CTA, or DSA, [28] MRA has a low detection rate and a high false-positive rate and is not a reliable method for diagnosing vertebral artery dissecting aneurysm. CAT has a diagnostic sensitivity of ~100% for arterial dissection, with a positive and a negative predictive value of 98.5% and 98%, respectively [28] and is currently the primary imaging modality for the diagnosis of VAD, However, DSA is the gold standard for diagnosing arterial dissection. The characteristic DSA manifestations of dissection is intima flap or double-lumen sign. However, in VAD, double-lumen sign is not common (10%), but pearl and string sign, i.e., alternation of irregular vascular thickening and narrowing, is the most common imaging findings. Other angiographic findings of dissection include spindle-shaped luminal enlargement, contrast agent stasis and changing morphology over time. In this series, no characteristic angiographic changes of VAD were found in case 1, but pathological study suggested left vertebral artery dissection. [4] Arterial dissection should be considered if young or middle-aged patients present with vascular occlusion.

Currently recommended treatments for neck VAD include anticoagulation, antiplatelet treatment, and thrombolysis. [2],[29] The meta-analysis of 24 studies showed non-significant difference in case fatality and survival rates between anticoagulation and antiplatelet treatment. [30] Thrombolysis is an optional regimen for acute vascular occlusion. However, during arterial thrombolysis, care should be exercised to detect vascular wall hematoma and avoid advancing the wire into the vascular dissection. Of the 16 patients in this study, one patient died after thrombolysis, and six patients treated with antiplatelets and nine patients treated by endovascular procedures achieved satisfactory outcomes. This suggests that both antiplatelet therapy and endovascular stenting are effective treatments for VAD. The selection of treatment regimens should depend on the clinical manifestations and imaging findings in a given patient.

 » References Top

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2.Schievink WI. Spontaneous dissection of the carotid and vertebral arteries. N Engl J Med 2001;3442:898-906.  Back to cited text no. 2
3.Kratz SN, Butler KH. Vertebral artery dissection presenting as acute cerebrovascular accident. J Emerg Med 2008;In press.   Back to cited text no. 3
4.Shu GS, Kang LC, Xiao DG, Bing N. Lessons from the diagnosis and treatment of spontaneous vertebral arterial dissection: case report. Interv Neuroradiol 2009;15:203-8.  Back to cited text no. 4
5.Haneline MT, Rosner AL. The etiology of cervical artery dissection. J Chiropr Med 2007;6:110-20.  Back to cited text no. 5
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7.Schievink WI, Mokri B, O'Fallon WM. Recurrent spontaneous cervical-artery dissection. N Engl J Med 1994;330:393-7.  Back to cited text no. 7
8.Bassetti C, Carruzzo A, Sturzenegger M, Tuncdogan E. Recurrence of cervical artery dissection. A prospective study of 81 patients. Stroke 1996;270:1804-7.  Back to cited text no. 8
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11.Mas JL, Bousser MG, Hasboun D, Laplane D. Extracranial vertebral artery dissections: a review of 13 cases. Stroke 1987;18:1037-47.  Back to cited text no. 11
12.Arnold M, Bousser MG, Fahrni G, Fischer U, Georgiadis D, Gandjour J, et al. Vertebral artery dissection: presenting findings and predictors of outcome. Stroke 2006;370:2499-503.  Back to cited text no. 12
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21.Pezzini A, Granella F, Grassi M, Bertolino C, Del Zotto E, Immovilli P, et al. History of migraine and the risk of spontaneous cervical artery dissection. Cephalalgia 2005;25:575-80.  Back to cited text no. 21
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26.Houser OW, Mokri B, Sundt TM, Jr, Baker HL Jr, Reese DF. Spontaneous cervical cephalic arterial dissection and its residuum: angiographic spectrum. AJNR Am J Neuroradiol 1984;5:27-34.  Back to cited text no. 26
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  [Figure 1], [Figure 2], [Figure 3], [Figure 4]

  [Table 1], [Table 2]

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