A 58-year-old woman with a history of thyroid nodule presented to the emergency department complaining of a headache that started a day earlier. She said the left side of her neck hurt after getting a massage a week before. She woke up sweaty and feeling ill that morning, but denied tingling, ringing in her ears, fever, gait problem, and slurred speech. She took Aleve at home, which helped a little.
Her oxygen saturation was 96%, pulse was 72 bpm, blood pressure was 140/91 mm Hg, and her temperature was 36°C. She was alert and oriented to person, place, and time, she had normal finger to nose, no pronator drift, normal gait, normal strength, sensation to soft touch, normal speech, and normal heel to toe with walking.
Consider the initial CT angiogram of her neck and an MRI of her brain. What does this patient have? What imaging should she receive? What treatment is appropriate?
Find the diagnosis and case discussion on p. 10.
Diagnosis: Internal Carotid Artery Dissection
Arterial dissections occur when there is a disruption in the arterial wall. Blood can collect when this happens, forming a hematoma or an aneurismal dilatation of the artery. This disruption can lead to serious neurologic events, such as a stroke from thromboembolism or decreased perfusion. Emboli seem to be the biggest concern in these patients. One study found that most infarcts related to ICAD were cortical or large subcortical strokes. (Stroke 1998;29:2646.)
The most common initial symptoms are headache and neck pain, found in 60 percent to 90 percent of cases. (Neurology 2006;67:1809.) The pain is thought to come from nociceptors triggered on the vessel being distended from the hematoma. (J Neurol Neurosurg Psychiatry 2006;77:1021.) Patients can also present with ptosis and miosis (partial Horner syndrome) on the same side as the injury, and this is usually accompanied by pain. This occurs in about 25 percent of cases. (Neurology 2006;67:1809.) They can also have pulsatile tinnitus, decreased taste, focal weakness, migraine-like symptoms, or amaurosis fugax. Many complaints can be nonspecific, however, so it is important to keep a high level of suspicion.
These dissections can occur spontaneously or as a result of trauma. Many sports activities may cause ICAD. (Br J Sports Med 2006;40:e10.) The main mechanisms of injury are rotation and hyperextension of the neck or full flexion of the neck. (J Emerg Med 2000;19:35.) Underlying features can predispose patients to ICAD, and a range of trauma and mechanical trigger events have been associated with it in around 40 percent of cases. (Neurology 2013;80:1950.) The American Heart Association and American Stroke Association noted a strong potential association between cervical manipulation and cervical arterial dissection. (Stroke 2014;45:3155.)
Spontaneous ICAD is not as common, but about 15-20 percent are associated with fibromuscular dysplasia. (Circulation 2014;129:1048.) Ehlers-Danlos syndrome type IV is found in less than two percent of cases. (Curr Mol Med 2009;9:210.) Other connective tissue disorders including Marfan syndrome have rare cases of cervical arterial dissection, and some studies show no occurrence. (Stroke 2002;33:680.)
You should consider imaging if you are concerned for ICAD. The best starting imaging is an MRI with MRA or a cranial CT with CTA. (AJR AM J Roentgenol 2009;193:1167.) One study did show that CT/CTA might be better for vertebral artery dissection but no different from MRI/MRA for ICAD. (AJNR AM J Neuroradiol 2008;29:1753.) An MRI also might be necessary to look for evidence of stroke. About 80 percent of ischemic sequelae arise within the first week, but latency periods of up to five months have been reported. (J Neurol Neurosurg Psychiatry 1998;65:136.)
The management of these patients depends on whether they have any neurologic sequelae as a result of the ICAD. Stroke guidelines should be followed if they have had a stroke. If not, antiplatelet therapy and or anticoagulation is necessary. Two nonrandomized meta-analysis studies from 2012 and 2015 did not show any difference in outcomes or complication rates when comparing anticoagulation with antiplatelet therapy. (Neurology 2012;79:686.)
No clear data specify how long to continue the therapy. One study did show that “recanalization” of spontaneous ICAD usually occurred within six months. (Stroke 2009;40:499.) Clinicians often recommend that patients obtain repeat imaging in three to six months.
This patient had a negative MRI brain, and her symptoms resolved. She was started on aspirin. At her one month checkup by neurosurgery, she was doing well without symptoms, and she was scheduled for a repeat CTA to evaluate her ICA.
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