In the latest Case Record of the Massachusetts General Hospital, an 18-year-old man suddenly became weak, with slurred speech. Dysarthria and ataxia were noted. Head CT was normal. The next day, he became unresponsive, with extensor posturing. A diagnostic procedure was performed.
Up to 14% of all strokes occur in children and young adults. The incidence rates are 10 to 23 ischemic strokes per 100,000 young adults (18 to 50 years of age) and 3 to 9 hemorrhagic strokes per 100,000 young adults. Unfortunately, stroke remains under recognized and often misdiagnosed in young adults, particularly those less than 35 years of age and those with abnormalities in the posterior circulation.
• What are the most common causes of stroke in young adults?
Cerebral-artery dissection and other arteriopathies are collectively the most common causes in young adults. Stroke rarely develops in young people from conditions — such as large-artery atherosclerosis or lipohyalinotic small-vessel disease — that are attributed to modifiable vascular risk factors (e.g., hypertension, diabetes, smoking, and hyperlipidemia). However, several recent studies of stroke in young people have shown a high incidence of modifiable vascular risk factors, suggesting that the presence of these risk factors increases the susceptibility to stroke from any cause.
• What is the most frequent source of cardioembolic stroke in young adults?
Patent foramen ovale is the most frequent cardioembolic risk factor for stroke in young adults. Others include congenital heart disease, infectious nonbacterial thrombotic endocarditis, rheumatic valvular heart disease, cardiac surgery or catheter intervention, arrhythmia (e.g., atrial fibrillation or sick sinus syndrome), cardiac tumors (e.g., atrial myxoma or papillary fibroestastoma), recent myocardial infarction, and dilated cardiomyopathy.
Morning Report Questions
Q: What are the clinical characteristics of basilar-artery occlusion?
A: An important consideration in managing basilar-artery occlusion in an individual patient is that the occlusion is clinically highly pleomorphic; outcomes depend on multiple variables, including the initial thrombus burden and location and the degree of collateral flow, residual antegrade flow, or both. The symptoms may be mild, even in patients with complete occlusion, because of compensatory collateral flow through the posterior communicating arteries, cerebellar pial anastomosis, or both; such patients may do well even without reperfusion. At the other extreme are patients with quadriplegia, a locked-in state, or coma who, without timely reperfusion, will nearly always have poor outcomes. CT scan may demonstrate evidence of a hyperintense basilar-artery sign. This finding has a sensitivity of 61 to 71%, specificity of 71 to 98%, and accuracy of 66 to 94% for the presence or absence of basilar-artery occlusion. The natural history of basilar-artery occlusion is grim, with close to 90% mortality rates in some studies.
Q: What is the treatment of basilar-artery occlusion?
A: Since acute basilar-artery occlusion is uncommon, accounting for only 6 to 10% of large-vessel strokes, evidence-based guidelines for management are lacking. There is one controlled trial of endovascular treatment of basilar-artery occlusion, which compared the intraarterial administration of the thrombolytic agent urokinase with anticoagulation alone; the results did not show a significant difference between the two methods. An observational multicenter study of patients with basilar-artery occlusion showed that reperfusion therapy was superior to antithrombotic therapy alone but did not show unequivocal superiority of intraarterial thrombolysis as compared with intravenous thrombolysis. Vessel recanalization protected against poor outcomes in both this and other studies, and it appears that intraarterial thrombolysis may be associated with a higher rate of recanalization than is intravenous thrombolysis.