The aim of this study was the determination of neurospecific proteins content, mechanisms of their formation and transfer into blood in the experimental craniocerebral trauma of medium-heavy degree. Results. The accumulation of neurospecific proteins in the blood during 21 days after the trauma is shown: S100B level increased saltatorily with two maximums – on the 1st and 7th days after the trauma, the NSE level grew gradually, the GFAP level – biphasically with maximums on the 1st and 7th days. Obviously, there was the secondary strengthening of destruction of nervous tissue and hemato-encephalic barrier permeability exactly on the 7th day. The immunohistochemical research conducted on the 7th day after the trauma showed that in the damaged neurons the S100, GFAP and NSE staining intensity disappeared or significantly diminished, which reflected sharp degenerative changes in the areas of damage. Along with this the S100 high degree staining was found around such neurons, that was characteristic for gliocytes and, in a less measure, for endotheliocytes, that can be considered as a cause of sharp increase of neurospecific proteins blood level. Conclusions. The reason of the repeated increase of S100B blood level, in our view, could be the repeated activating of its synthesis in activated gliocytes in perifocal zones and active transport through the hemato-encephalic barrier, that activated the inflammatory damage reactions and contributed to the progression of neurodestruction on the 7th day after the trauma, reflected in the increase of GFAP blood level and further NSE accumulation. These events could signify the beginning of new pathogenesis link of the traumatic brain illness – autoimmune inflammation, that contributed to the progression of posttraumatic brain damage in the late period.