Vertebral Artery Dissection (VAD): Overview and Insights
Introduction to VAD
Definition: Dissection involves a tear in the wall of a major artery, leading to blood intrusion within the arterial wall layers, causing stenosis or aneurysmal dilatation.
Historical Context: VAD was traditionally seen as a rare stroke cause, often diagnosed postmortem until its features were better understood in the late 1970s.
Epidemiologic Features
Incidence: Approximately 1-1.5 per 100,000 people.
Demographics: Affects all age groups; peak in the fifth decade of life.
Importance: Significant cause of stroke in young and middle-aged patients.
Pathologic Features
Arterial Wall Structure: Composed of three layers – intima, media, adventitia.
Dissection Process: Blood collects between layers, forming an intramural hematoma.
Disagreement: Debate on which arterial wall is the primary dissection site.
Genetic Factors
Underlying Defects: Most patients have a structural defect, not fully understood.
Associated Disorders: Ehlers-Danlos syndrome type IV, Marfan's syndrome, etc.
Environmental Factors
Precipitating Events: Often linked to neck movements (e.g., yoga, chiropractic manipulation).
Infections: Respiratory tract infections can be a risk factor.
Natural History and Healing
Types: Ischemic type (stroke symptoms) and hemorrhagic type (subarachnoid hemorrhage).
Healing: Generally good prognosis for extracranial VAD, whereas intracranial VADs are more severe.
Classification
Types of Aneurysms: Classified into four types based on intimal and IEL changes.
Dissection Types: Entry-only and entry-exit types affect clinical stability.
Clinical Features
Extracranial VAD: Often follows neck trauma, with symptoms like neck pain and potential stroke symptoms.
Intracranial VAD: Frequently associated with SAH, having a poor prognosis.
Diagnosis
Imaging Techniques: MRI and MR angiography are preferred for detailed visualization.
Angiography Signs: Features like the string sign and aneurysmal dilatations indicate dissection.
Prognosis
Outcomes: Better prognosis for extracranial VADs; intracranial VADs often result in severe deficits.
Recurrence: Low, but higher in patients with genetic predispositions.
Therapeutic Considerations
Medical Treatment
Anticoagulation: Heparin and warfarin used to prevent thromboembolic events.
Follow-Up: Continued monitoring via MRI to guide therapy duration.
Surgical Interventions
When Indicated: Urgent intervention for SAH or persistent symptoms despite medical therapy.
Endovascular Therapy
Techniques: Includes parent artery occlusion and stenting, though each has risks.
Surgery
Approaches: Trapping of the dissection or bypass surgery can be options.
Summary
Key Points: VAD is characterized by arterial wall tears and can lead to ischemic or hemorrhagic strokes. Prognosis varies greatly between extracranial and intracranial VAD, with diverse treatment protocols available depending on the severity and location of the dissection.