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Table 34-8 Stroke associated with genetic disorders
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(%) 2 15 01 02 04 003 013 10 Rare
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(%) 5 20 1 5 3 6 1 5 25 3 8
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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
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Key: AD, autosomal dominant; AR, autosomal recessive; v, venous; a, arterial; ao, aorta; h, heart
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AR AR AR AR AR AR AR AR AR AR AR AR Complex AD AR AR AR Maternal AD AD Complex
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v v v v v v v v v,h,ao v v,a v v v a a a a a a
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20 in young
noid, and intracerebral) and cerebral venous thrombosis may also complicate sickle cell anemia, and perhaps because of autosplenectomy there is an increased incidence of pneumococcal meningitis Treatment of the cerebral circulatory disorder, based presumably on sludging of red blood cells, is with intravenous hydration and transfusion Cerebral venous sinus thrombosis in young children and neonates represents a special problem, dif cult to diagnose, and with a poor prognosis (see de Veber et al) Certain hereditary metabolic diseases (homocystinuria and Fabry angiokeratosis) and the mitochondrial disorder MELAS (mitochondrial encephalomyopathy, lactic acidosis, and stroke), discussed on page 839, may give rise to strokes in children or young adults; investigation of these causes is undertaken if the aforementioned diagnoses have been excluded
Overall, in children and young adults with ischemic stroke, the main diagnoses to be considered are carotid and vertebral dissection, drug abuse (mainly cocaine), thrombosis induced by birth control pills (see below), antiphospholipid antibody syndrome, and patent foramen ovale (PFO) Migraine might be added to this list, but it is a diagnosis by exclusion in these circumstances and CADASIL, albeit rare, should also be considered if migraine headaches and TIAs precede a stroke Inherited prothrombotic states such as those caused by the various clotting factor de ciencies discussed above, Fabry disease, moyamoya, and Takayasu arteritis arise in the younger age group and require exploration if clinical circumstances suggest on the basis of unusual TIAs (orthostatic or hyperventilation induced), Down syndrome, or strong family history of strokes in youth
Oral Contraceptives, Estrogen, and Cerebral Infarction The early studies of Longstreth and Swanson and of Vessey et al clearly indicated that women who take oral contraceptives in the childbearing years particularly if they are older than 35 years of age and also smoke, are hypertensive, or have migraine are at increased risk of cerebral infarction as well as of ischemic heart disease and subarachnoid hemorrhage Cerebral infarction in these cases is due to arterial occlusion, occurring in both the carotid middle cerebral and vertebrobasilar territories In most of the reported fatal cases, the thrombosed artery has been free of atheroma or other disease This has been taken to indicate that embolism is responsible for the strokes, but the source of embolism can rarely be demonstrated Cerebral and noncerebral venous thromboses are other relatively rare complications These observations, coupled with evidence that estrogen alters the coagulability of the blood, suggest that a state of hypercoagulability is an important factor in the genesis of contraceptive-associated infarction The vascular lesion underlying cerebral thrombosis in women taking oral contraceptives has been studied by Irey and colleagues It consists of nodular intimal hyperplasia of eccentric distribution with increased acid mucopolysaccharides and replication of the internal elastic lamina Similar changes have been found in pregnancy and in humans and animals receiving exogenous steroids, including estrogens Whether these promote in situ thrombosis is not known Mainly at increased risk of stroke are women taking high-dose (050-mg) estrogen pills; lowering the estrogen content has substantially reduced this risk The use of progestin-only pills (POPs) or of Norplant (subcutaneously implanted capsules of progestin) alone has not been associated with an increased risk of stroke (Petitti et al) It has also become clear that mutations of the prothrombin gene are far more frequent in patients who have cerebral venous thrombosis while on oral contraceptive pills These genetic abnormalities are thought by Martinelli and associates to account for 35 percent of idiopathic cases of cerebral vein thrombosis; they contend that contraceptives increase the risk 20-fold
Amniotic uid embolus may also cause stroke in this manner and should be suspected in multiparous women who have had uterine tears In the latter, there are almost invariably signs of acute pulmonary disease from simultaneous occlusion of lung vessels A rare peripartum cardiomyopathy is yet another source of embolic stroke
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