Study of restorative processes in brain laceration in the first seven days after traumatic brain injury

Vol. 56 No. 1, 2015


Charoula Florou, Bogdan Catalin, Oana Badea, Tudor-Adrian Balseanu, Cristina Eugenia Vasilescu, Laurentiu Mogoanta, Florin Grosu, Marius Matei, Adriana Turculeanu

Traumatic brain injuries represent the main cause of death and invalidity all over the world. Persons surviving a severe traumatic brain injury often present long-term disabilities, sensitive and motor deficits, cognitive, vegetative or mental disorders. Brain injuries are directly caused by the traumatic agent, and indirectly caused by the action of cells involved in the restorative process. The main cells involved in the restorative process are microglias and astrocytes. By using an experimental model, we investigated the reaction of these cells in the first week after a severe brain injury, followed by brain laceration. Of the two cell types, the most rapid and intense reaction was held by the macroglias, also known as resident macrophages of the central nervous system. Alongside the activation of local microglias, in the restorative process there were also involved blood monocytes that turned into macrophages. 24 hours after the injury, the number of macrophage cells/mm(2) at brain wound level increased 2-4 times, after three days - 10-12 times, and after seven days - over 20 times. The astrocyte reaction was slower, their activation being signaled no sooner than three days from injury, when their number in the perilesional brain parenchyma increased approximately two times, while after seven days - approximately 4-5 times. Both astrocytes and macrophages (microglias), besides their beneficial effects in restoring traumatic brain injuries, may have unfavorable effects upon the nervous cells in the immediate proximity of the injury. Destruction of vascular network by the traumatic agent, and the extremely slow restore of vascularization, partially explain brain neurons death on extend areas.

Corresponding author: Laurentiu Mogoanta, Professor, MD, PhD; e-mail:

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