Developing a common framework to approach cervical arterial dissection: current evidence and remaining challenges

Dissections involving the extracranial internal carotid or vertebral arteries are a notable cause of ischemic stroke, particularly in younger individuals. Cervical artery dissections can be broadly classified into two categories: those associated with major trauma and those that occur in its absence. Our focus pertains to cervical artery dissections that arise without major trauma. In the literature, such cases are often termed "spontaneous" or "non-traumatic". However, these labels can be somewhat misleading, as it is hypothesized that minor trauma may act as a precipitating factor for the dissection in cases where major trauma is absent. For simplicity, non-major trauma-associated cervical artery dissections are referred to as cervical artery dissection (CAD).

CAD accounts for approximately 2% of all ischemic strokes and up to 25% of ischemic strokes in adult patients under 50 years old, contributing significantly to morbidity and disability in this age group.

In this statement by the AHA titled "Treatment and Outcomes of Cervical Artery Dissection", Yaghi et al. address the current state of acute stroke treatment and secondary stroke prevention in the context of CAD.  The consensus statement was collaboratively authored by eleven experts from the USA and Switzerland, hailing from a diverse array of disciplines that include Neurology, Neurosurgery, Neuroradiology, Interventional Radiology, Emergency Medicine, and Epidemiology. The group members reviewed randomized controlled trials, prospective and retrospective observational studies, meta-analyses, opinion papers, case series, and case reports from 1990-2022 and composed a scientific statement based on the available evidence on diagnosis and management of CAD.

Several takeaway points from this scientific statement can be highlighted.

In addressing acute stroke care for CAD, current practices, including intravenous thrombolysis and mechanical thrombectomy, draw heavily from general stroke guidelines. The effectiveness of acute procedural treatments of the dissection, such as stenting, remains controversial. Additional randomized or longitudinal studies are essential to address existing gaps in the evidence of procedural interventions.

Based on the available evidence, patients with CAD who experience acute ischemic stroke are recommended to complete three to six months of antithrombotic therapy to prevent recurrent stroke (with the selection of antithrombotic at the discretion of the provider, either antiplatelet alone/in combination, or vitamin K antagonists). These recommendations are largely based on the results from CADISS (a United Kingdom-based randomized control trial from 2019 comparing antiplatelets against vitamin-K antagonists) and TREAT-CAD (a multi-center, randomized controlled, non-inferiority trial comparing aspirin against vitamin-K antagonists). Because there are no data on the utility of the direct oral anticoagulants (DOACs), no recommendations on DOACs are included in the statement.

Post-acute care in CAD, mostly focusing on secondary stroke prevention, is recommended to address any condition associated with recurrence, such as migraines, genetic predisposition, or lifestyle factors. Tailored treatments or precautions for these specific conditions are advised based on individual patient needs.

It is crucial to highlight that CAD is a complex topic within stroke, due to its distinctive type of vessel wall injury, differentiating it from other causes of stroke. While the statement primarily addresses acute ischemic stroke, there are still numerous unknowns concerning the underlying vascular injury itself.

There is evidence to suggest patients with CAD have an underlying arteriopathy; several observational studies suggest over 50% of patients with CAD, even those testing negative for a known genetic predisposing condition, have ultrastructural connective tissue aberrations (i.e., composite collagen fibrils and elastic fiber fragmentation) ^1-7. As a field, it will be important that we develop a better understanding of the underlying arteriopathy in these patients (at the tissue and even molecular level). Collaborative efforts that include researchers in the mechanisms of vascular function and dysfunction, researchers in the genetics of connective tissue disorders, and vascular surgeons would be necessary. A better understanding of the underlying pathophysiology of dissection would hopefully allow us to identify novel targets for prevention and treatment of CAD. An example of the importance of understanding the underlying cause of dissection, are patients with vascular Ehlers-Danlos syndrome (vEDS). These patients have defective collagen type III, making their blood vessels extremely fragile. Standard anticoagulation and procedural interventions may exacerbate dissections, intramural hematomas, or cause new vessel injuries, leading to severe complications such as vessel rupture and massive hemorrhage. Treatment decisions for this population should be approached cautiously, considering the high risk of vascular injury and bleeding. The recommendations by Yaghi et al. do not specifically address the unique challenges faced by vEDS patients in the context of CAD treatment.

Another challenge in post-acute care in CAD, besides optimal prevention of recurrence of stroke, is rehabilitation. Special considerations in this population include potential limitations in engaging in specific exercises, like weight lifting, which could impact the delivery and dosage of therapy, potentially constraining recovery in terms of motor impairments and other functional domains. Collaborating with neurorehabilitation specialists is crucial for tailoring optimal therapeutic interventions for this heterogeneous population, addressing individual patient needs.

Dissections serve as a poignant illustration of the existing gaps in our understanding, not just within the realm of stroke care but also in the broader field of vascular care. These gaps underscore the imperative need for further research dedicated to comprehending the intricate pathophysiology of dissections. A nuanced exploration of the underlying mechanisms and contributing factors is essential to inform more precise and tailored management strategies, encompassing not only acute interventions but also extending to rehabilitation protocols. By delving deeper into the unique challenges posed by CAD, future research endeavors can pave the way for advancements in comprehensive patient care and ultimately enhance outcomes in this domain of vascular pathology.