PROTHROMBOTIC STATES IN YOUNG-PEOPLE WITH IDIOPATHIC STROKE - A PROSPECTIVE-STUDY

Background and Purpose Although 4% of cerebral infarcts in the young c an be attributed to hematologic disturbances that predispose to thromb osis, the frequency of cerebral infarcts caused by prothrombotic state s is not known. Recently, the association between cerebral infarction and deficiencies of elements of the natural anticoagulant system has b een recognized. Methods Thirty-six consecutive patients under 40 years of age with cerebral infarction of undetermined cause were prospectiv ely studied. Quantitation of natural anticoagulants was done at least 3 months after the cerebral infarction. The following activity tests w ere performed, all by the chromogenic method: antithrombin III, protei n C, plasminogen, tissue plasminogen activator, and inhibitor of tissu e plasminogen activator. Protein S was quantified by the Laurell rocke t method. All patients underwent a complete cardiological examination, including two-dimensional echocardiography, as well as four-vessel ce rebral angiography. Some patients were also studied by transesophageal echocardiography. Results Of 36 patients, 17 were male, with a mean a ge of 28 years. Mean age for women was 25 years. Nine patients (25%; 5 women, 4 men) had 8 deficiency of one natural anticoagulant and const ituted group I. In these patients, isolated protein S deficiency was d etected in five cases (13.8%); in one case, we observed the associatio n between protein S deficiency and antiphospholipid antibodies; and de ficiency of protein C was seen in one case (2.7%), of antithrombin III in one case (2.7%), and of plasminogen in one case (2.7%). Instances of cerebral infarction without natural anticoagulant deficiency (group II) included 12 women and 15 men. There were no differences in clinic al and radiological findings between the two groups. Conclusions Consi dering the importance of prothrombotic state, especially caused by def iciency of protein S, in the development of cerebral infarcts, we sugg est that it should be looked for in every young patient affected by th is pathological entity and in whom no etiologic factors can be determi ned.