Cardiology >  Vertebral Artery Dissection

Background

Vertebral artery dissection (VAD) refers to a tear in the intimal layer of the vertebral artery, allowing blood to enter the arterial wall and form a false lumen. This can lead to stenosis or occlusion of the vessel and may result in thromboembolism or ischemia in the posterior circulation of the brain, particularly the brainstem, cerebellum, and occipital lobes.

II) Classification/Types

By Etiology: 

• • Spontaneous VAD: Occurs without major trauma; associated with connective tissue disorders or minor neck strain. 

• • Traumatic VAD: Due to blunt or penetrating trauma to the neck (e.g., motor vehicle accidents, chiropractic manipulation). 

By Location: 

• • Extracranial VAD: More common; affects the segment from its origin to the foramen magnum. 

• • Intracranial VAD: Less common but associated with higher risk of subarachnoid hemorrhage. 

By Course: 

• • Ischemic VAD: Presents with infarcts in posterior circulation territory. 

• • Hemorrhagic VAD: May result in subarachnoid hemorrhage, particularly with intracranial dissections. 

III) Pathophysiology 
Intimal tear allows blood under arterial pressure to enter the media, forming an intramural hematoma or false lumen. This can: 

• • Narrow the true lumen → cerebral ischemia. 

• • Form thrombi → embolization. 

• • Expand → compress adjacent structures. 

• • Extend intracranially → rupture and hemorrhage. 

IV) Epidemiology

• • Age: Common in young to middle-aged adults (30–50 years). 

• • Sex: Slight male predominance in trauma; spontaneous cases more balanced. 

• • Incidence: ~1–1.5 per 100,000/year. 

• • Associated Conditions: Connective tissue disorders (e.g., Ehlers-Danlos, Marfan), recent infection, migraine, hypertension, and smoking. 

Etiology

I) Causes

• • Minor neck trauma or manipulation (e.g., chiropractic adjustments) 

• • Major trauma (e.g., motor vehicle accidents, strangulation) 

• • Spontaneous dissection (idiopathic or genetic predisposition) 

• • Fibromuscular dysplasia 

• • Connective tissue disorders (e.g., Marfan syndrome, Ehlers-Danlos syndrome) 

• • Infections and inflammation (e.g., recent respiratory infection) 

II) Risk Factors

• • Head/neck trauma 

• • Genetic arteriopathies 

• • Migraine 

• • Recent respiratory infection 

• • Smoking 

• • Hypertension 

• • Oral contraceptive use 

Clinical Presentation

I) History (Symptoms)

• • Sudden-onset, severe occipital headache or neck pain (most common initial symptom) 

• • Vertigo, dizziness 

• • Visual disturbances (e.g., diplopia, field defects) 

• • Ataxia, dysarthria 

• • Nausea, vomiting 

• • Transient ischemic attacks or posterior circulation stroke symptoms 

• • Horner syndrome (ptosis, miosis, anhidrosis) in lateral medullary infarction (Wallenberg syndrome) 

II) Physical Exam (Signs)

Neurological: 

• • Cranial nerve deficits (especially IX–XII) 

• • Limb ataxia, dysmetria 

• • Dysarthria 

• • Hemiparesis or sensory deficits (posterior circulation stroke signs) 

Ophthalmologic: 

• • Nystagmus 

• • Diplopia 

Autonomic: 

• • Horner syndrome (ipsilateral) 

Cervical Exam: 

• • Local tenderness over vertebral artery path (may be subtle) 

• • Neck stiffness (in hemorrhagic cases) 

Differential Diagnosis (DDx)

• • Ischemic stroke (posterior circulation) 

• • Subarachnoid hemorrhage 

• • Migraine with aura 

• • Multiple sclerosis 

• • Labyrinthitis/vestibular neuritis 

• • Cervical radiculopathy 

• • Giant cell arteritis 

• • Meningitis (if febrile with neck stiffness) 

Diagnostic Tests

Initial Imaging: 

• • MRI Brain with DWI: Identifies acute infarcts in posterior circulation. 

• • MRA or CTA Head and Neck: Preferred for detecting arterial dissection; shows tapering, occlusion, or pseudoaneurysm. 

• • Catheter Angiography: Gold standard but used selectively due to invasiveness. 

Additional Tests: 

• • Cervical Spine Imaging: If trauma suspected. 

• • Lumbar Puncture: If subarachnoid hemorrhage is suspected. 

• • ESR/CRP: Rule out vasculitis or temporal arteritis in older patients. 

• • Hypercoagulable panel: If multiple dissections or young stroke without clear cause. 

Treatment

I) Medical Management

Antithrombotic Therapy: 

• • Antiplatelet therapy (aspirin or clopidogrel): First-line in most cases. 

• • Anticoagulation (heparin followed by warfarin): May be used if large thrombus burden or cardioembolic concern. 

• • Duration: 3–6 months, followed by repeat imaging. 

Pain Management: 

• • NSAIDs or acetaminophen for headache and neck pain. 

• • Avoid cervical manipulation. 

Blood Pressure Control: 

• • Maintain normotension; avoid fluctuations that might worsen dissection or ischemia. 

II) Interventional/Surgical

Endovascular Stenting: 

• • Reserved for patients with progressive symptoms or failed medical therapy. 

• • Can restore vessel patency and prevent further ischemia. 

Surgical Repair: 

• • Rarely needed; used in cases of aneurysm rupture or failure of endovascular approach. 

Patient Education, Screening, Vaccines

• • Avoid high-risk neck activities (chiropractic adjustments, contact sports) during healing. 

• • Educate on stroke warning signs: sudden weakness, speech changes, vision loss. 

• • Emphasize medication adherence. 

• • Counsel on modifiable risk factors: smoking cessation, blood pressure control. 

• • No specific vaccines related to VAD, but routine vaccinations (influenza, COVID-19) recommended. 

Consults

• • Neurology: All suspected or confirmed cases of VAD. 

• • Interventional Neuroradiology: If endovascular treatment considered. 

• • Neurosurgery/Vascular Surgery: For rare surgical cases. 

• • Genetics: If connective tissue disease suspected. 

• • Physical Therapy: Safe mobilization post-dissection. 

• • Primary Care: Long-term risk factor management and follow-up. 

Follow-Up

• • Repeat MRA/CTA in 3–6 months to assess healing or resolution. 

• • Monitor for recurrent stroke or new neurologic symptoms. 

• • Assess for residual pain or headaches. 

• • Evaluate compliance with antithrombotic therapy. 

• • Gradual return to normal activities after confirmation of vessel healing. 

• • Long-term follow-up for patients with underlying arteriopathy or recurrent dissections