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lupus anticoagulant is not ideal, since most patients with the anticoagulant do not have lupus and the antibody has a procoagulant, not anticoagulant, property in vivo Nonetheless, the main laboratory feature of the illness is a prolonged partial thromboplastin time Further testing for antiphospholipid antibody consists of detection of both lupus anticoagulant and anticardiolipin antibody; there is a partial overlap between these 80 percent of patients with lupus anticoagulant have anticardiolipin antibody but fewer than 50 percent of those with anticardiolipin antibody have lupus anticoagulant The principal antigen involved is in fact not phospholipid but 2-glycoprotein 1, a protein that binds to phospholipid The titer of antibody correlates with the risk of thrombosis and smoking; pregnancy and the use of oral contraceptives raise the risk further There may be an increased incidence of migraine but this has been disputed The most frequent neurologic abnormality is a TIA, usually taking the form of amaurosis fugax (transient monocular blindness), with or without retinal arteriolar or venous occlusion (Digre et al) Stroke-like phenomena are more frequent in patients who also have migraine, hyperlipidemia, and antinuclear antibodies and in those who smoke or take birth control pills Almost one-third of the 48 patients reported by Levine and associates had thrombocytopenia and 23 percent had a false-positive VDRL test Some of the phospholipids with which the antibodies react are shared with clotting factors, particularly prothrombin and annexin, as well as with the lupus anticoagulant (a cardiolipin-glycoprotein complex) These antibodies are circulating serum polyclonal immunoglobulins (IgG, IgM, IgA) The vascular lesions are mainly in the cerebral white matter and are infarcts, seen well with MRI Angiography reveals occlusions of arteries at unusual sites (Brey et al) The mechanism of stroke is not entirely clear and may derive from emboli originating on mitral valve lea ets similar to nonbacterial thrombotic endocarditis; alternatively, and more likely in our view, there is a nonin ammatory in situ thrombosis of medium-sized cerebral vessels, as suggested by the limited pathologic material studied by Briley and colleagues These circulating antibodies may also cause a syndrome of transient bilateral choreal or hemichorea; some patients have an additional slight hemiparesis or other subtle focal signs Almost all of the affected patients we have seen have been women with thrombocytopenia, some of whom probably had systemic lupus, at least on the grounds of laboratory studies (see Cevera et al) A direct connection of the choreic syndrome to the antibodies, comparable to what is proposed in Sydenham chorea, may be valid but at the moment is unproven Some cases display microinfarctions in the basal ganglia, perhaps on the basis of valvular vegetations The syndrome may be precipitated in these patients by the introduction of estrogen-containing birth control pills and is improved, usually promptly, by corticosteroids or antiplatelet agents The Sneddon syndrome consists of deep blue-red lesions of livedo reticularis and livedo racemosa in association with multiple strokes; 126 cases had been reported up to 1992 Most but not all patients have high titers of antiphospholipid antibodies Although the skin lesions show a nonin ammatory vasculopathy with intimal thickening, the pathology of the occlusive disease has not been adequately studied In a report of 17 such patients by Stockhammer and coworkers, 8 had strokes and MRI showed lesions in 16 of 17 patients The age of patients with strokes was 30 to 35 years, hence this condition must always be considered in young adults with cerebrovascular disease Many of the lesions on MRI were small, deep, and multiple Although there is a tendency for strokes to recur,.

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The solution is to use the open2 function that comes as part of the IPC::Open2 module, which is part of the standard distribution:

many of the patients have remained well for years after a single stroke Skin biopsy aids in diagnosis There are instances in which the radiologic changes caused by recurrent small infarctions are dif cult to distinguish from multiple sclerosis, as discussed in several parts of Chap 36, on demyelinative diseases Associations of the syndrome with transverse myelitis, Guillain-Barre syndrome, hearing loss, and a number of other processes has been suspected but not proven Treatment Warfarin has been used with some bene t in the above conditions Khamashta and colleagues have found that the INR must be maintained close to 3 for effective prevention of stroke According to the study conducted by Crowther and colleagues, an INR of 2 to 3 conferred the same degree of protection from thrombosis as did higher levels, but the number of thrombotic events was low in both groups and there was only one stroke in 114 patients over a period of about 3 years Patients with severe thrombocytopenia and with other intrinsic coagulopathies should be treated with warfarin very cautiously Although the INR is used as a gauge of the level of anticoagulation, it maybe altered by the antibodies; no ideal method for monitoring treatment has been devised Aspirin, on uncertain grounds, is thought not to confer protection for stroke, but in only a few small series has its effect been analyzed In catastrophic cases, intravenous immunoglobulin and plasma exchange have been used with some effect It is most important to eliminate smoking and estrogen-containing compounds, since these greatly raise the risk of stroke Plasma exchange may be useful in fulminant cases Aspirin and heparin are favored in women with recurrent fetal loss related to antiphospholipid antibody (Lockshin and Sammaritano) Thrombotic Thrombocytopenic Purpura (TTP, Moschcowitz Syndrome) This is yet another uncommon but serious disease of the small blood vessels, observed mainly in young adults It is characterized pathologically by widespread occlusions of arterioles and capillaries involving practically all organs of the body, including the brain, as described by Adams and colleagues (1948) The nature of the occluding material has not been completely de ned Fibrin components have been identi ed by immuno uorescent techniques; some investigators have demonstrated disseminated intravascular platelet aggregation rather than brin thrombi TTP is caused by an acquired circulating IgG inhibitor of von Willebrand factor cleaving protease; a rarer familial form is caused by a constitutional de ciency of the protease Clinically, the main features of this disease are fever, anemia, symptoms of renal and hepatic disease, and thrombocytopenia the latter giving rise to the common hemorrhagic manifestations (petechiae and ecchymoses of the skin, retinal hemorrhages, hematuria, gastrointestinal bleeding, etc) Neurologic symptoms are practically always present and are the initial manifestation of the disease in about half the cases Confusion, delirium, seizures, and hemiparesis sometimes remittent or uctuating in nature are the usual manifestations of the nervous system disorder and are readily explained by the widespread microscopic ischemic lesions in the brain Garrett and colleagues have emphasized the presentation of nonconvulsive status epilepticus in TTP, and we have encountered two such cases Gross infarction was not observed In most patients who survive, recovery of the focal neurologic de cits can be expected unless there is an identi able infarction on CT or MRI The CSF is normal except for elevated protein in some cases To our knowledge, a mononeuritis multiplex does not occur The recommended treatment is plasma exchange or plasma infusion.

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