Internal carotid artery dissection is a separation of the layers of the artery wall supplying oxygen-bearing blood to the head and brain and is the most common cause of stroke in young adults.
Cervical artery dissection accounts for only 1–2% of all ischemic strokes, but in young and middle-aged people it accounts for 10–25% of strokes 1).
Internal carotid artery dissection (ICAD) can be classified based on various criteria including etiology, location, extent, and imaging characteristics.
| Type | Description |
|---|---|
| I | Narrowing of the lumen with an intimal flap or double lumen. |
| II | Irregular lumen narrowing without an apparent intimal flap. |
| III | Pseudoaneurysm formation due to vessel wall weakening. |
| IV | Complete occlusion due to thrombosis in the false lumen. |
| V | Dissection extending into distal branches. |
The causes of internal carotid artery dissection can be broadly categorised into two classes: spontaneous or traumatic.
Once considered uncommon, spontaneous carotid artery dissection is an increasingly recognised cause of stroke that preferentially affects the middle-aged.
The incidence of spontaneous carotid artery dissection is low, and incidence rates for internal carotid artery dissection have been reported to be 2.6 to 2.9 per 100,000.
Observational studies and case reports published since the early 1980s show that patients with spontaneous internal carotid artery dissection may also have a history of stroke in their family and/or hereditary connective tissue disorders, such as Marfan syndrome, Ehlers-Danlos syndrome, autosomal dominant polycystic kidney disease, pseudoxanthoma elasticum, fibromuscular dysplasia, and osteogenesis imperfecta type I.
However, although an association with connective tissue disorders does exist, most people with spontaneous arterial dissections do not have associated connective tissue disorders. Also, the reports on the prevalence of hereditary connective tissue diseases in people with spontaneous dissections are highly variable, ranging from 0% to 0.6% in one study to 5% to 18% in another study.
Carotid artery dissection is thought to be more commonly caused by severe violent trauma to the head and/or neck. An estimated 0.67% of patients admitted to the hospital after major motor vehicle accidents were found to have blunt carotid injury, including intimal dissections, pseudoaneurysms, thromboses, or fistulas.
Of these, 76% had intimal dissections, pseudoaneurysms, or a combination of the two.
The probable mechanism of injury for most internal carotid injuries is rapid deceleration, with resultant hyperextension and rotation of the neck, which stretches the internal carotid artery over the upper cervical vertebrae , producing an intimal tear.
After such an injury, the patient may remain asymptomatic, have a hemispheric transient ischemic event, or suffer a stroke.
Arterial dissection of the carotid arteries occurs when a small tear forms in the innermost lining of the arterial wall (known as the tunica intima). Blood is then able to enter the space between the inner and outer layers of the vessel, causing narrowing (stenosis) or complete occlusion. The stenosis that occurs in the early stages of arterial dissection is a dynamic process and some occlusions can return to stenosis very quickly.
When complete occlusion occurs, it may lead to ischaemia. Often, even a complete occlusion is totally asymptomatic because bilateral circulation keeps the brain well perfused. However, when blood clots form and break off from the site of the tear, they form emboli, which can travel through the arteries to the brain and block the blood supply to the brain, resulting in an ischaemic stroke, otherwise known as a cerebral infarction. Blood clots, or emboli, originating from the dissection are thought to be the cause of infarction in the majority of cases of stroke in the presence of carotid artery dissection.
Cerebral infarction causes irreversible damage to the brain. In one study of patients with carotid artery dissection, 60% had infarcts documented on neuroimaging.
Embolism from thrombus forming at the dissection site is thought to play the major part in stroke pathogenesis.
This suggestion is supported by transcranial Doppler studies showing cerebral micro- emboli soon after dissection, and by the distribution of infarcts after dissection, which suggests an embolic pattern.
The signs and symptoms of carotid artery dissection may be divided into ischemic and non-ischemic categories:
Headache or neck pain
Decreased pupil size with drooping of the upper eyelid (Horner syndrome)
Temporary vision loss
Ischemic stroke
see Hypoglossal nerve palsy due to internal carotid artery dissection.
If a diagnosis of spontaneous internal carotid artery dissection is under consideration, laboratory studies are largely irrelevant for diagnostic purposes. However, if contrast-enhanced computed tomography (CT) or arteriography is planned, it is appropriate to obtain a baseline creatinine concentration.
With the use of noninvasive imaging, including magnetic resonance and computed tomography angiography, the diagnosis of carotid dissection has increased in frequency
Treatment options include thrombolysis, antiplatelet or anticoagulation therapy, endovascular or surgical interventions. The choice of appropriate therapy remains controversial as most carotid dissections heal on their own.
The goal of treatment is to prevent the development or continuation of neurologic deficits.
The risk of early recurrence of stroke has led many clinicians to advocate the use of anticoagulation from presentation until 3 or 6 months after dissection. However others believe that antiplatelet drugs might be sufficient.
Anticoagulants might prevent embolism from a fresh thrombus but they are also more hazardous than antiplatelet drugs and can result in extension of the intramural haemorrhage, which occurs in a third of patients according to MRI 2).
see Cervical Artery Dissection in Stroke Study (CADISS)
Endovascular management of acute ischemic stroke (AIS) in the setting of carotid artery dissection (CAD) is a feasible, safe, and promising strategy 3).
Some studies suggest a significantly increased risk of stroke in patients presenting with dissection either with local symptoms, such as headache and Horner’s syndrome, or with stroke or transient ischaemic attack, with estimates of the risk of secondary stroke after presentation of 15–20% 4) 5) 6) although other studies have reported a much lower proportion 7).
A patient with transient left hypoglossal nerve palsy caused by mechanic compression from intramural hematoma in higher extracranial portion of dissected carotid artery confirmed in MRI and CT scans 8).