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As indicated in Table 34-2, it is probable that ischemic necrosis of cerebral tissue can occur in utero The resulting stroke is usually referred to as congenital hemiplegia However, very little is known about the underlying vascular lesions, so that nothing further can be said about them here The occurrence of acute hemiplegia in infants and children is a well-recognized phenomenon In a series of 555 consecutive postmortem examinations at the Children s Medical Center in Boston, there were 48 cases (87 percent) of occlusive vascular disease of the brain (Banker) The occlusions were both embolic (mainly associated with congenital heart disease) and thrombotic, and the latter were actually more common in veins than in arteries Similarly, stroke is not an uncommon event in young adults (15 to 45 years) This group accounts for an estimated 3 percent of cerebral infarctions In terms of causation, this group is remarkably heterogeneous In a series of 144 such patients, more than 40 possible etiologies were identi ed (H P Adams et al) Nevertheless, 78 percent of the group could be accounted for by three categories, more or less equal in size: atherosclerotic thrombotic infarction (usually with a recognized risk factor); cardiogenic embolism (particularly in association with rheumatic heart disease, bacterial and verrucous endocarditis, paradoxic embolism through patent foramen ovale, and prosthetic valves); and nonatherosclerotic vascu-

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lopathies (arterial trauma, dissection of the carotid artery, moyamoya, lupus erythematosus, drug-induced, vasculitis) Hematologically related disorders use of oral contraceptives (see further on), the postpartum state, and hypercoagulable states were the probable causes in 15 percent of the 144 patients The presence of antiphospholipid or anticardiolipin antibodies (lupus anticoagulant) appears to explain some of these cases and is discussed further under Stroke as a Complication of Hematologic Disease ; the majority of these patients are women in their thirties without manifest systemic lupus erythematosus Despite the attention they have received as a cause of strokes in the juvenile period, the frequency of thrombophilic disorders due to inherited de ciencies of naturally occurring anticoagulant factors is low The main inherited prothrombotic clotting defects are summarized in Table 34-8 They predispose primarily to cerebral venous clotting Most arise from partial protein de ciencies due to heterozygous mutations in the genes encoding proteins that are important factors in the clotting cascade (antithrombin III, proteins S and C) and those due to disturbances of clotting balance (resistance to activated protein C, or factor V Leiden mutation, and prothrombin mutations as well as excess factor VIII) (see discussion by Brown and Bevan) However, when they are homozygous, these mutations may be associated with devastating neonatal hemorrhagic conditions In some series that report cases of strokes in youth, such that of Becker and colleagues, up to half of the cases had one of these disorders, the commonest being the factor V Leiden mutation, but others have found this mutation to be much less frequent, and that is consonant with our experience Nevertheless, in children with unexplained stroke, particularly venous and especially if there has been a previous thrombosis or if the strokes are recurrent, it is advisable to carry out an extensive hematologic investigation, especially including testing for antiphospholipid antibody (an acquired defect), as described on page 735 Establishing a diagnosis of a prothrombotic clotting gene variant has therapeutic signi cance, since strokes are prone to occur in the setting of such additional risks as the use of oral contraceptives or smoking In adults, the evaluation for inherited clotting defects is far less fruitful Furthermore, it should be kept in mind that the levels of proteins C and S and of antithrombin are temporarily depressed after stroke, so that any detected abnormalities must be con rmed months later Persistent cerebral ischemia and infarction may occasionally complicate migraine in young persons The combination of migraine and the Pill is particularly hazardous, as detailed below Similarly, despite the common occurrence of mitral valve prolapse in young adults, it is probably only rarely a cause of stroke (see comments on page 710) Stroke due to either arterial or venous occlusion occurs occasionally in association with ulcerative colitis and to a lesser extent with regional enteritis Evidence points to a hypercoagulable state during exacerbations of in ammatory bowel disease, but a precise defect in coagulation has not been identi ed Meningovascular syphilis and fungal and tuberculous meningitis and other forms of chronic basal meningitis are considerations in this age group; the strokes are usually of the cavitary lacunar type, resulting from infectious-in ammatory occlusion of small basal vessels Sickle cell anemia is a rare but important cause of stroke in children of African ancestry; acute hemiplegia is the most common manifestation, but all types of focal cerebral disorders have been observed The pathologic ndings are those of infarction, large and small; their basis is assumed to be vascular obstruction associated with the sickling process Intracranial bleeding (subdural, subarach-.

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Causes of arterial or venous infarction Activated protein C resistance Leiden factor V mutation Prothrombin 20210 Prothrombin Protein C de ciency Protein C gene Protein S de ciency Protein S gene Increased Factor VIII von Willebrand factor de ciency Antithrombin III de ciency Antithrombin III Plasminogen de ciency Plasminogen activator-1 Lipoprotein (a) Apolipoprotein (a) Marfan syndrome Fibrillin 1 Fabry disease Alpha-galactosidase Sickle cell syndrome Globin genes Heparin cofactor II Heparin cofactor II Platelet collagen receptor Platelet collagen receptor Factor XII Factor XII Phosphodiesterase 4D Phosphodiesterase 4D CADASIL Notch 3 Hyperhomocysteinemia Methylene tetrahydrofolate reductase Homocysteinemia Cystathione beta-synthase Homocysteinemia Homocysteine methyl transferase Ehlers Danlos disease MELAS (mitochondrial): mtDNA Causes of cerebral hemorrhage associated with congenital diseases von Hippel-Lindau (Chap 31) pVHL Cavernous malformations Cerebral cavernous malformations (CCM1) Cerebral amyloidosis Apolipoprotein E4 Cerebral hemorrhage with amyloidosis Dutch type Amyloid precursor protein Icelandic type Cystatin C Hereditary hemorrhagic Endoglin telangiectasia Hereditary hemorrhagic Activin receptor-like kinase telangiectasia (ALK-1) Polycystic kidney disease Polycystin 1, 2