(Fig 1, left). The bilirubin level was 24.0 mg/100 ml, but the Coombs' antiglobulin test was negative. In the cerebrospinal fluid (CSF), the level of protein was 210 mg/100 ml. Gram stain of the CSF sediment revealed gram-negative spirochetes and numerous leuko¬ cytes. Despite supportive therapy, the infant died 39 hours after birth.The mother (para 1, grávida 2), a 22-year-old white resi¬ dent of Deschutes County, Oregon, had been completely well until three weeks prior to delivery of the infant. At thai time a low-grade fever developed which was thought to be due to infections of the upper respiratory tract and urinary 1. Bor relia spirochetes in peripheral-blood smear of in¬ fant (/eft) and mother (right) (Wright's stain, x 1,000).

To assess the time course of thrombosis and fibrinolysis after acute stroke, we measured concentrations of fibrinopeptide A (FpA), B-/3 1-42 peptide (B-0 1-42), B-0 15-42 peptide (B-/3 15-42), and crosslinked D-dimer (XDP) hi 31 patients at varying times following acute ischemic stroke and in 13 neurologically stable patients with chronic strokes. FpA levels were markedly elevated during the first week after stroke and declined slowly during the first month. Mean FpA levels were not significantly elevated in chronic stroke patients. Mean XDP levels were slightly elevated during the first week and increased during the next 2 weeks after stroke. B-/3 1-42 and B-/315-42 levels were not elevated at any time following acute stroke. Our data suggest that fibrin formation greatly exceeds endogenous fibrinolysis during the acute phase of ischemic stroke. Endogenous fibrinolysis develops slowly following stroke. Prolonged elevation of FpA concentration suggests that thrombin activity and fibrin formation continue for up to 4 weeks in some patients with ischemic stroke. (Stroke 1989;20:592-597)

Plasminogen activity and antigen, tissue-type plasminogen activator (tPA) activity and antigen, plasminogen activator inhibitor (PAI) activity, and plasmin generation rates were determined in 32 normal newborn plasmas and 25 normal adult plasmas. The newborns showed reduced levels of plasminogen activity and antigen and tPA antigen, and activity, normal levels of PAI activity, and slower plasmin generation rates. The slower generation was shown to be due to the hypoplasminogenemia. The in vitro plasmin generation studies also showed that the newborn needed 11 times the usual concentration of urokinase and 5 times the usual concentration of tPA to achieve the minimal activation rate of the adult.

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