15 Spontaneous Vertebral Arterial Dissection

10.1055/b-0038-162144

15 Spontaneous Vertebral Arterial Dissection

J. Scott Pannell, Mihir Gupta, Jason Signorelli, and Alexander A. Khalessi

Abstract

Spontaneous vertebral artery dissection represents an important cause of ischemic stroke, particularly in young patients. This chapter describes the workup, management, and operative considerations in treating these lesions. Initial workup should include noncontrast head computed tomography, vascular imaging, and magnetic resonance imaging of the brain. Therapy primarily aims to prevent ischemic sequelae of the dissection. Management is guided by randomized trials as well as emerging studies that highlight the critical roles of the patient′s presenting neurological condition and dissection morphology. Neurologically unstable patients, such as those with hypoperfusion syndromes, are candidates for emergent endovascular recanalization and repair. In neurologically stable patients, a limited course of antiplatelet therapy is generally adequate in the setting of non-flow-limiting stenosis or vessel occlusion. Patients with breakthrough infarcts on antiplatelet therapy and neurologically stable patients presenting with flow-limiting stenosis may experience better outcomes with systemic anticoagulation therapy. Some patients may fail maximal medical therapy, and thus, such patients may benefit from either endovascular sacrifice to prevent further embolic strokes or stent reconstruction to prevent vertebrobasilar insufficiency. Nuances of endovascular therapy and selection of optimal devices for stenting or sacrifice are discussed in detail in this chapter.

Introduction

Spontaneous cervical artery dissection is responsible for up to 2.5% of all strokes, and over 20% of strokes in young and middle-aged patients. Spontaneous vertebral artery dissections (SVADs) comprise approximately one-third of these lesions. Although the pathophysiology underlying spontaneous dissections remains poorly understood, risk factors including hypertension, migraine, recent infection, and connective tissue disorders have been identified. SVADs may present as asymptomatic lesions, neck pain, ischemic strokes, subarachnoid hemorrhage (SAH), or space-occupying lesions with mass effect on adjacent structures. Successful management of SVADs, like all stroke syndromes, depends on consideration of both the clinical syndrome and the anatomical nature of the dissection.

Major controversies in decision making addressed in this chapter include:

Important clinical and anatomical considerations in the management of SVAD.
Antiplatelet therapy versus anticoagulation in treatment of SVAD.
Endovascular management in patients refractory to medical therapy.

Whether to Treat

Initially, the degree and severity of ischemic stroke must be considered in the management of SVAD. Over two-thirds of SVAD patients experience embolic ischemic stroke or transient ischemic attack (TIA) (▶ Figs. 15.1 and 15.2 ). On presentation, most patients will present in a neurologically stable state with either no deficits or fixed deficits that correspond to embolic ischemic strokes seen on imaging, owing to the vast potential collateralization of the posterior circulation. Beyond management considerations, the degree of presenting deficit along with the patient′s age is important in the patient′s overall prognosis. Rarely, SVAD patients may present in a neurologically unstable state with a posterior circulation hypoperfusion syndrome; these patients tend to harbor an isolated posterior circulation. Hypoperfusion syndromes may manifest as a pressure-dependent neurological examination, watershed strokes cerebellar strokes, or mismatch between the neurological deficits and anatomical strokes on magnetic resonance imaging (MRI).

**Fig. 15.1** Spontaneous vertebral artery (VA) dissection/occlusion. A 41-year-old male weightlifter presented to the emergency department with dysarthria, imbalance, and severe nausea after practicing at the gym. **(a)** CT scan (not shown) and MRI of the brain demonstrated an acute ischemic stroke at the left cerebellum. **(b–d)** CT angiogram of the neck demonstrated acute dissection and thrombus (*arrow*) formation of the VI segment of the left VA, the contralateral VA is hypoplastic. **(c)** Notice the minimal amount of contrast throughout the length of the left VA compared to the right VA, suggesting dissection and occlusion (*arrows*). **(d)** The intracranial V4 segment (*arrow*) of the left VA reconstituted by the right VA. The patient was treated with continuous heparin for 72 hours and a diagnostic cerebral angiography (DSA) was then performed. **(e–g)** DSA demonstrated complete spontaneous recanalization and opening of the left VA, no signs of residual stenosis, and no intracranial vessel occlusion. (Images provided courtesy of Leonardo Rangel-Castilla, MD, Mayo Clinic, Rochester, MN.)

**Fig. 15.2** Vertebral artery (VA) dissection. A 59-year-old man presented to the emergency department with subacute onset of headaches, dysarthria, vertigo, and imbalance. **(a)** CT scan of the brain demonstrated multiple chronic and subacute ischemic strokes at the left cerebellum. **(b)** CT angiogram of the neck demonstrated dissection and narrowing of the VI segment of the left VA (*arrow*); the contralateral right VA is occluded. The patient was treated with dual antiplatelet therapy but continued to have symptoms. **(c)** A diagnostic cerebral angiography was then performed demonstrating progression of the dissection and narrowing of the left VA. **(d)** A drug-eluding stent was placed obtaining adequate reconstruction of the diseased segment of the artery. (Images provided courtesy of Leonardo Rangel-Castilla, MD, Mayo Clinic, Rochester, MN).

Pathophysiology

The morphology of the dissection is also an important distinguishing factor in SVAD management. Dissections may present with non-flow-limiting intimal injury (▶ Fig. 15.2 ), flow-limiting stenosis, occlusion (▶ Fig. 15.1 ), or pseudoaneurysm (PSA). Although most SVADs result in embolic strokes, hypoperfusion syndromes can occur in the setting of flow-limiting stenosis or collusion. Ischemic strokes associated with non-flow-limiting intimal injury are typically the result of embolic debris from the intima at the initial injury or thrombus formed by the activation of the platelets by the exposed basement membrane underlying the intima. Ischemic strokes in the setting of a flow-limiting stenosis may result from embolic debris and platelet activation as well. However, flow-limiting stenosis may also result in embolic strokes due to fibrin-based clot formation owing to activation of the coagulation cascade in the setting of stagnant blood flow over the exposed basement membrane. Additionally, the slower flowing blood allows more time for larger clots to form. Though occlusive lesions may result in fibrin clot formation, the absence of antegrade flow limits distal embolization from the affected vertebral artery. Fibrin clot in the affected distal vertebral artery may activate platelets in the blood flowing through the contralateral V4 segment or in the blood flowing retrograde through the ipsilateral V4 to ipsilateral (posterior inferior cerebellar arter) PICA, resulting in stump emboli.

Anatomical Considerations

Finally, there are multiple important anatomical considerations important in the management of SVADs. Dissection of the dominant vertebral artery has a higher risk of presenting as a hypoperfusion syndrome and may limit treatment options in the absence of adequate collateral circulation. The vast majority of spontaneous SVADs occur in the pars transversaria (V2) or the atlas loop (V3) segments. Although intracranial V4 segment dissection is less common, the distinction between intracranial dissections and cervical dissections remains critical. Extracranial SVADs present most commonly with pain and/or ischemic symptoms referable to the posterior circulation (▶ Figs. 15.1 and 15.2 ). Intracranial SVADs may present with similar symptoms, but may also present with SAH, headache, mass effect upon brainstem, or mass effect on the spinal cord, which must be taken into consideration in choosing the treatment and management strategy.

Workup

Clinical Evaluation and Imaging

Initial workup of SVAD should include routine lab studies, noncontrast head computed tomography (CT), vascular imaging, and MRI of the brain. Labs should at least include complete blood count, complete metabolic panel, and a coagulation panel. The head CT is obtained to primarily evaluate for SAH as MRI is not as sensitive or specific as CT in the identification of acute subarachnoid blood. MRI of the brain is preferred for evaluation of presence of infarcts due to the increased sensitivity for detection of acute infarct on diffusion-weighted imaging. Initial vascular imaging may be performed by CT angiography (CTA), MR angiography (MRA), or conventional catheter angiogram. Conventional angiography is the gold standard for SVAD diagnosis and characterization. MRA is overall less sensitive than CTA or conventional cerebral angiography, but is often preferred as an initial noninvasive modality since it involves no ionizing radiation and can provide additional information. The MRA should include time-of-flight (TOF) angiography, contrast-enhanced angiography, and T1 fat saturated images. The TOF angiogram can be used to identify flow-limiting lesions prior to cerebral angiography. The T1 fat saturated images help improve the specificity of noninvasive vascular imaging with the detection of intramural hematomas, which are the sine qua non of arterial dissections. Finally, contrast-enhanced MRA improves the delineation of the morphology of the dissection, as dissections often result in turbulent flow obscuring the morphology on the TOF MRA. Vascular imaging of the intracranial vasculature should also be performed on presentation to exclude intracranial large vessel occlusions as the causative etiology in the patient′s stroke and to evaluate intracranial collaterals.

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