Estimates of prekallikrein levels in plasma specimens from patients with migraine and from healthy individuals were obtained by determining the benzoyl-arginine ethyl ester (BAEe) esterase activities developed on activation with kaolin, as suggested by Costerase level- 'n the patients and in the control material, and kinetic data provided no evidence of a difference in inhibitor levels. Only very low BAEe esterase activity was registered in samples of cerebrospinal fluid obtained from the patients and no significant difference between attacks and free intervals was detected. When citrated EDTA-treated plasma was activated with acetone-incubated normal plasma containing prekallikrein activator (factor XIIf), no significant difference in BAEe esterase activity was noticed between plasma from the patients and that from the control persons. When, however, citrated plasma without EDTA was used, a significantly higher peak level of esterase activity was registered in the patient plasma. This observation might suggest the presence of a factor positioned between active factor XII and prekallikrein, and present in higher amounts in plasma from patients with migraine than in healthy individuals.