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Digital subtraction angiography of carotid artery dissection A coronal view and B sagittal view with the arrows showing a tapering high-grade stenosis often referred to as a “string sign” or “flame sign” (Images courtesy of David Pasquale, MD, Loyola University Medical Center.)
Source publication
Purpose of Review
Cervical artery dissection (CAD) is rare, yet it is a common cause of stroke in young and middle-aged adults. Historically, some senior clinicians favored anticoagulation in the prevention of stroke due to CAD. Choosing the optimal antithrombotic treatment with either antiplatelet (AP) or anticoagulant (AC) medications remains a c...
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Purpose of review
Recurrent stroke after ischemic stroke (IS) or high-risk transient ischemic attack (TIA) increases morbidity and mortality. Secondary stroke prevention strategies include modification of behavioral and vascular risk factors and antithrombotic use, including single or dual antiplatelet therapy (DAPT). In this review, we focus on DA...
Citations
... When the stroke etiology is determined to be cardioembolic or due to a thrombophilia, anticoagulation is typically recommended [43]. In the case of cervical arterial dissection, there are no pediatric data to guide the choice of antithrombotic agent, and there remains equipoise in adults as well [227,228]. The presence of an intraluminal thrombus may prompt the clinician to opt for anticoagulation, while a large associated stroke may make antiplatelet therapy more appropriate. ...
Though rare, stroke in infants and children is an important cause of mortality and chronic morbidity in the pediatric population. Neuroimaging advances and implementation of pediatric stroke care protocols have led to the ability to rapidly diagnose stroke and in many cases determine the stroke etiology. Though data on efficacy of hyperacute therapies, such as intravenous thrombolysis and mechanical thrombectomy, in pediatric stroke are limited, feasibility and safety data are mounting and support careful consideration of these treatments for childhood stroke. Recent therapeutic advances allow for targeted stroke prevention efforts in high-risk conditions, such as moyamoya, sickle cell disease, cardiac disease, and genetic disorders. Despite these exciting advances, important knowledge gaps persist, including optimal dosing and type of thrombolytic agents, inclusion criteria for mechanical thrombectomy, the role of immunomodulatory therapies for focal cerebral arteriopathy, optimal long-term antithrombotic strategies, the role of patent foramen ovale closure in pediatric stroke, and optimal rehabilitation strategies after stroke of the developing brain.
... A characteristic finding in dissection is eccentric signal enhancement in the vessel wall in the fat-suppressed T1 sequences, representing the mural hematoma. This signal enhancement, due to methemoglobin in the hematoma, is often absent in the first 72 hours after the onset of dissection (24). As the signal intensity of the mural hematoma changes over time, multisequence MRI can help date the dissection (25). ...
... Findings of wall thickening are harder to classify by CT/CTA than by MRI. A mural hematoma may be difficult to tell apart from vasculitis or atherosclerosis by CT alone and can be more reliably distinguished by MRI (28,24). ...
Background:
Dissections of the cervical brain-supplying arteries are a leading cause of ischemic stroke in young adults, with an annual incidence of 2.5-3 / 100 000 for carotid artery dissection and 1-1.5 / 100 000 for vertebral artery dissection. It can be assumed that many cases go unreported. We present the clinical features here to help physicians diagnose this disease entity as rapidly as possible.
Methods:
This review is based on pertinent publications retrieved by a selective search in PubMed.
Results:
Spontaneous dissection of the internal carotid or vertebral artery is characterized by a hematoma in the vessel wall. It often arises in connection with minor injuries; underlying weakness of the arterial wall (possibly only temporary) may be a predisposing factor. Acute unilateral pain is the main presenting symptom. In internal carotid dissection, the site of the pain is temporal in 46% of cases, and frontal in 19%; in vertebral artery dissection, it is nuchal and occipital in 80%. Pain and local findings, such as Horner syndrome, are generally present from the beginning, while stroke may arise only after a latency of hours to days. If the diagnosis is made early with MRI, CT, or ultrasound, and anticoagulation or antiplatelet drugs can help prevent a stroke, yet none of these methods can detect all cases. Recurrent dissection is rare, except in patients with connective tissue diseases such as Ehlers-Danlos syndrome or fibromuscular dysplasia. Spontaneous dissection of the great vessels of the neck must be differentiated from aortic dissection spreading to the supra-aortic vessels and from traumatic dissection due to blunt or penetrating vascular trauma.
Conclusion:
Dissection of the cervical brain-supplying vessels is not always revealed by the imaging methods that are used to detect it. Stroke prevention thus depends on the physician's being aware of the symptoms and signs of this disease entity, so that early diagnosis can be followed by appropriate treatment.
Cervical Artery Dissection (CeAD) is a frequent stroke etiology for patients younger than 50 years old. The most common immediate complications related to CeAD are headache and neck pain (65-95%), TIA/ischemic stroke (>50%), and partial Horner's syndrome (25%). The prevailing hypothesis regarding the pathogenesis of sCeAD is that the underlying constitutional vessel wall weakness of patients with sCeAD is genetically determined and that environmental factors could act as triggers. The stroke prevention treatment of CeAD remains controversial, involving anticoagulation or antiplatelet therapy and potentially emergent stenting and/or thrombectomy or angioplasty for selected cases of carotid artery dissection with occlusion. The treatment of headache associated with CeAD depends on the headache phenotype and comorbidities. Radiographically, more than 75% of CeAD cases present with occlusion or non-occlusive stenosis. Many patients demonstrate partial and complete healing, more commonly in the carotid arteries. One-fifth of the patients develop dissecting pseudoaneurysm, but this is a benign clinical entity with an extremely low rupture and stroke recurrence risk. Good recovery is achieved in many CeAD cases, and mortality remains low. Family history of CeAD, connective tissue disorders like Ehlers-Danlos syndrome type IV, and fibromuscular dysplasia are risk factors for recurrent CeAD, which can occur in 3-9% of the cases. This review serves as a comprehensive, updated overview of CeAD, emphasizing etiopathogenesis and management.
