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Chapter 11

Stroke as a Complication of General Medical Disorders

Paul George and Gregory W. Albers

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Figure 11-1 The protein C anticoagulant pathway. Thrombin converts factor VIII and factor V to their activated forms, factor VIIIa and factor Va. A complex of thrombin with the endothelial cell receptor thrombomodulin activates protein C (APC). APC inactivates factor VIIIa and factor Va on the platelet surface, and this reaction is accelerated by APC cofactor and free protein S.(From Bauer KA: Hypercoagulability: a new cofactor in the protein C anticoagulant pathway. N Engl J Med 330:567, 1994, with permission. © 1994, Massachusetts Medical Society. All rights reserved.)

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Figure 11-2 Angiography showing a middle cerebral artery occlusion (arrow) in a young woman with anticardiolipin antibodies, the lupus anticoagulant, and myxomatous mitral valve thickening.(From Coull BM, Levine SR, Brey RL: The role of antiphospholipid antibodies in stroke. Neurol Clin 10:130, 1992, with permission.)

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Figure 11-3 Proposed mechanism of antiphospholipid antibody-induced thrombosis. Antiphospholipid antibodies in a complex with β2-glycoprotein-1 bind to platelet or endothelial membrane phospholipids, thereby causing platelet activation and endothelial damage. The ensuing platelet adhesion, aggregation, and impairment of endothelial anticoagulant function promote coagulation activation, vasospasm, and thrombosis. EDRF, endothelium-derived relaxing factor; PGI2, prostacylin.(From Coull BM, Clark WM: Abnormalities of hemostasis in ischemic stroke. Med Clin North Am 77:86, 1993; modified from Eisenberg GM: Antiphospholipid syndrome: the reality and implications. Hosp Pract 27:121, 1992, with permission.)

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Figure 11-4 A typical mitral valve lesion in a patient with lupus and nonbacterial thrombotic endocarditis (NBTE).(From Moder KG, Miller TD, Tazelaar HD, et al: Cardiac involvement in systemic lupus erythematosus. Mayo Clinic Proc 74:275, 1999, with permission.)

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Figure 11-5 Intraparenchymal hemorrhage due to aneurysm. A, Computed tomography (CT) scan obtained because of a complaint of headache in a 46-year-old chronic cocaine abuser shows a hyperintense lesion in the left frontal lobe that is probably an unruptured aneurysm. A small hemorrhage around the aneurysm is suggested. B, CT scan obtained 2 days later because of increasing headache and neurologic signs shows a large hematoma with intraventricular hemorrhage (arrow). The left lateral ventricle is markedly compressed and the midline is shifted. C, Angiogram shows two aneurysms, a larger one (arrow) in a branch of the middle cerebral artery and a smaller one (arrowhead) with associated vasospasm from a lenticulostriate artery.(From Brown E, Prager J, Lee HY, et al: CNS complications of cocaine abuse: prevalence, pathophysiology, and neuroradiology. AJR Am J Roentgenol 159:142, 1992, with permission.)

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Figure 11-6 Magnetic resonance image (MRI) of a 41-year-old woman, showing a large right parietal infarct that occurred in the setting of acute methamphetamine use. The patient had no other risk factors for stroke.

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Figure 11-7 Carotid angiograms in a patient after excessive use of sumatriptan and Midrin. A, Angiogram showing segmental arterial narrowing (arrows) at the time of stroke. B, Normalized angiogram taken 39 days later.(Modified from Meschia JF, Malkoff MD, Biller J: Reversible segmental cerebral arterial vasospasm and cerebral infarction: possible association with excessive use of sumatriptan and Midrin. Arch Neurol 55:713, 1998, with permission.)

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Figure 11-8 Relationship between alcohol and the risk of ischemic stroke. OR denotes odds ratio for ischemic stroke.(From Sacco RL, Elkind M, Boden-Albala B, et al: The protective effect of moderate alcohol consumption on ischemic stroke. JAMA 281:57, 1999, with permission. © 1999, American Medical Association.)

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Figure 11-9 Examples of vascular changes in CADASIL. A, A small white matter artery stained for NOTCH3 demonstrates a thickened wall and the aggregations of NOTCH3 around degenerated smooth muscle cells (arrows). B, An electron micrograph with multiple granular osmiophilic deposits (arrows) in the smooth muscle cells’ basement membrane.(From Chabriat H, Joutel A, Dichgans M: CADASIL. Lancet Neurol 8:643, 2009, with permission.)