Vertebral artery dissection (VAD) is a rare cause of stroke in the general population; however, represents one of the more common causes of stroke in patients younger than 45 years of age. Its signs and symptoms can be vague, and diagnosis can be elusive.  Spontaneous dissections have been reported. However, incidental minor trauma often precipitates this potentially dangerous condition. Often some neck distortion such as chiropractic manipulation, bending of the neck or blunt trauma causes the dissection. The dissection of the artery may ultimately lead to a stroke which often can be delayed for days following the acute dissection.
Patients typically report minor, rather innocuous precipitating events before the onset of symptoms. Coughing, vomiting, chiropractic procedures, and blunt trauma are likely initiating events. It is estimated that 1 in 20,000 cervical spine manipulations causes a stroke. Blunt trauma to the neck is the most common reported precipitating event. Patients with connective tissue disorders are also at increased risk. Ehlers-Danlos syndrome is the most the most common connective tissue disorder that can cause vertebral artery dissection. When patients with serious cervical cord injury or spine fractures are screened for vertebral artery injury approximately 20% to 40% will demonstrate traumatic occlusion. Interestingly, this occlusion tends to be asymptomatic, as opposed to dissection, and its management is controversial.
It is estimated that vertebral artery dissection is the cause of approximately 2% of all ischemic strokes. However, in middle-aged and younger patients (30 to 45 years of age) it is believed to be as high as 10% to 25%, representing a significant population affected by this condition. The combined incidence of both vertebral artery and carotid artery dissections is estimated to be 2.6 per 100,000. Carotid artery dissections are more three to five times more common than vertebral artery dissections. It should be noted that chiropractors dismiss the association between manipulation and vertebral artery dissection on the grounds that the dissection is the cause of the neck pain and the reason why the patients seek out chiropractic care. There is no conclusive evidence linking the two leading some medical associations only to suggest a causative link.
The arterial anatomy consists of three layers named the intimal (innermost), the media (middle), and the adventitia (outermost layer). Dissection occurs when the structural integrity of the arterial wall is compromised. Intimal tears lead to arterial blood dissecting between the layers of the arterial wall. The blood within the arterial wall precipitates hematoma and clot formation. The subsequent compromise in arterial blood flow secondary to the stenosis then leads to the symptoms of vertebral artery dissection and ultimately, stroke. Vertebral artery dissection can be either extracranial or intracranial. Extracranial dissections usually involve the distal extracranial segment near the atlas and axis. Intracranial dissections are often associated with subarachnoid hemorrhage and carry a much worse prognosis. Neurological sequalae of both extracranial and intracranial dissections may result from cerebral ischemia due to thromboembolism, hypoperfusion, or a combination of both. However, thromboembolism rather than hypoperfusion is considered the major cause of ischemic symptoms.
Clinical presentation is typically acute and severe unilateral neck pain and/or a headache. Minor neck trauma often precipitates the pain. The pain is typically in the occipital-cervical area of the neck or head. Neurological symptoms are often delayed and may not be present at all. Lateral medullary syndromes (Wallenberg Syndrome) and cerebellar infarctions are the most common location for strokes. Wallenberg Syndrome is defined by sensory deficits affecting the trunk and extremities on the opposite side of the infarction and sensory deficits affecting the face and cranial nerves on the same side as the infarction. When neurological symptoms are present, dizziness, ataxia, dysarthria, diplopia, and vertigo are the predominant symptoms. Extracranial dissections often have a bruit present. The bruit has even been reported on the contralateral side secondary to increased collateral blood flow. What often distinguishes this type of patient from those with cerebellar infarctions secondary to atherosclerotic disease is the age of the patient and the presence of pain. When the dissection is intracranial, a subarachnoid hemorrhage is present 50% of the time. This group of patients has severe neurological symptoms a much worse prognosis than those with extracranial dissections.
MRI rivals angiography for establishing the diagnosis but is not readily available to most. CT and CTA are often the first investigations obtained. CT scan can demonstrate posterior fossa ischemia or subarachnoid hemorrhage. It may also identify an occluded vertebral artery or mural thrombus. CTA, however, is superior to CT scan and should be performed. CTA more easily identifies irregularity of the vascular lumen or thickening of the arterial wall. CTA is the initial test of choice. Vascular Duplex scanning demonstrates abnormal flow in 95% of patients. However, it shows evidence specific to dissection in only 20% of patients.
For those patients that survive the initial dissection, the prognosis is usually good. Approximately 10% of patients die initially. In one clinical follow-up study, 80% achieved a full recovery. Death is typically secondary to extensive intracranial dissection, brainstem infarction, or subarachnoid hemorrhage. The goal of management is to prevent stroke, which is the complication of vertebral artery dissection. Management is done with anticoagulation, typically heparin. Most dissections will resolve over time with no neurological deficits. Be advised however that when the dissection is intracranial or extends intracranially, the risk of subarachnoid hemorrhage increases significantly and anticoagulation is contraindicated. Endovascular or surgical treatments are reserved for patients with concomitant complications or those whose maximal medical therapy has been unsuccessful.
A headache or neck pain associated with vertebral artery dissection may precede the development of neurological symptoms by as long as 14 days. Patients may report vague neurological symptoms associated with the pain that may be transient. The problem for the emergency department physician is that when the workup is initiated for a severe headache or neck pain, the CT scan and lumbar puncture may be negative. These patients are often diagnosed with a headache or even transient ischemic attack (TIA), delaying diagnosis and treatment. The severe pain remains the hallmark and cannot be ignored. Further neurologic imaging with CTA or MRI must be performed if clinical suspicion is high. Patients with vertebral artery dissection must be admitted to the hospital for close neurological monitoring and if indicated, anticoagulation. Surgery is very rarely indicated.
The diagnosis and treatment of vertebral artery dissection is not simple and best managed by an interprofessional team that includes a radiologist, emergency department physician, nurse practitioner, neurologist, and vascular surgeon. Once imaging has made the diagnosis, the treatment depends on patient symptoms.
For those patients that survive the initial dissection, the prognosis is usually good. Approximately 10% of patients die initially. In one clinical follow-up study, 80% achieved a full recovery. Death is typically secondary to extensive intracranial dissection, brainstem infarction, or subarachnoid hemorrhage. The goal of management is to prevent stroke, which is the complication of vertebral artery dissection. Management is done with anticoagulation, typically heparin. Endovascular or surgical treatments are reserved for patients with concomitant complications or those whose maximal medical therapy has been unsuccessful. Most dissections will resolve over time with no neurological deficits.
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