A relationship between Central Nervous System and coagulation has been known since the work by Goodnight et al5. When an encephalic injury occurs tissue damage causes the release of thromboplastin-related products, mainly the Tissular Factor. This release produces an activation of the coagulation system specially through its extrinsic path. With this physiopathologic basis we attempt to improve the knowledge of this relation by performing a prospective study at the Intensive Care Unit of our Hospital. The study included 67 patients with cranioencephalic trauma alone, with an average Glasgow coma scale score of 10 and a control group consisting of 40 healthy subjects. Two peripheral vein blood extractions were performed, at admission and 24 hours later. Global coagulation parameters (prothrombin time, activated partial thromboplastin time, platelet count and fibrinogen), hypercoagulability markers (prothrombin fragments F1+2 and thrombin-antithrombin complex (TAT)) and thrombolisis markers (D-dimer) were determined. Our results show that early after head trauma an increase in fragments F1+2, TAT and Ddimer occur. After the first 24 hours a significant decrease in hypercoagulability markers levels is detected. Modification of the global coagulation parameters was also detected. In conclusion, early after a cranioencephalic trauma a simultaneous state of hypercoagulability and thrombolysis occur which may have the purpose of improving the hemostatic balance.