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.