Carotid artery dissection (CAD) is defined as a hematoma within the vascular wall, typically within the media. It can produce luminal irregularity, stenosis, occlusion and aneurysmal dilatation. Extension of the hematoma into the subadventitial region can weaken the wall of the vessel, producing pseudoaneurysms. CAD typically starts approximately 2 cm above the bifurcation and extends superiorly. CAD is a neurologic emergency because of the increased risk of cerebral infarction that is usually caused by decreased perfusion secondary to luminal stenosis rather than embolism. The mortality rate is high, possibly as great as 75%. CAD is typically divided into two categories, traumatic and spontaneous. Spontaneous CAD is not associated with any identifiable, major traumatic event. Fibromuscular dysplasia, Marfan’s syndrome, cystic medial necrosis, vigorous physical activity, have been reported as predisposing conditions to CAD. However, in most patients, no risk factor can be recognized. Once considered rare, CAD is an increasingly recognized entity due to improvements in carotid sonography and the advent of cross-sectional imaging techniques, such as MRI and CTA. CAD can occur at any age, but it is most usually seen in young and middle-aged adults, with a mean age of 32 to 45 years.
Clinical findings include new onset of otherwise unexplained unremitting headache or neck ache, especially in association with transient or permanent focal neurological deficits. Incomplete Horner’s syndrome is rare but typical. However, many patients initially may be asymptomatic.
Catheter angiography is considered the procedure of choice for depiction of CAD. The most common angiographic appearance of CAD is a region of arterial narrowing extending over a few centimeters, with a return to normal luminal diameter beyond this point. When the smoothly tapered artery terminates in an occlusion, the dissection has a “flame-shaped” appearance. Other appearances include the so called “string sign”, when arterial lumen narrows allowing only a thin trickle of contrast material, and a pseudoaneurysm. Delayed opacification of the intracranial branches can occur.
Color Doppler Ultrasonography has generally non specific findings, but raises the suspicion. The dissection is often distal to the region that can be directly visualized by ultrasonography, and the diagnosis is often based on a Doppler signal indicative of blood flow reduction due to stenosis or occlusion at a distal site.
Brain CT, although not diagnostic, is usually performed when the patient is symptomatic. The examination can show abnormal findings when infarct occurs. Only CTA can depict the luminal stenosis and confirm the diagnosis.
The role of MR imaging in detection of CAD is well established and may provide evidence of disturbed flow of the carotid artery. MRI allows direct imaging of the hematoma within the vascular wall. The characteristic appearance is a narrowed arterial flow void channel, surrounded by an eccentric periarterial rim of hypertense signal that frequently widens the external diameter of the artery. MRA is an exam of high accuracy for the evaluation of the cervical and intracranial arteries compared to catheter angiography. MRI and MRA also offer a noninvasive means of follow up study.
In our patient brain CT was normal whereas MRI showed infarct of the deep white matter, due to dissective aneurysm of the right internal carotid artery.