spread neurodegeneration and is still a major worldwide health problem (2,33,44,50,51). TBI causes not only direct mechanical damage to the brain, but it also induces biochemical changes that lead to delayed neural cell loss. These biochemical changes are called secondary injury. The primary █ INTRODUCTION O ne common form of acute brain injury, traumatic brain injury (TBI), is the result of an outside force causing immediate mechanical disruption of brain tissue and delayed pathogenic events that collectively mediate wideAIm: To determine whether the serum level of glial fibrillary acidic protein (GFAP), an important indicator of neuron damage, correlates with the extent of tissue damage in the rat with induced head trauma and to obtain data in order to avoid unnecessary cranial computed tomography analyses. mATERIAl and mEThODS: Three-month-old male Sprague-Dawley rats were used. Rats were divided into 5 groups. The experimental head trauma model was examined in five groups (n=8) as follows: The control group had no intervention; Group 1: Head trauma was induced by dropping a 25 mg ball from a height of 20 cm; Group 2: Head trauma was induced by dropping a 50 mg ball from a height of 20 cm; Group 3: Head trauma was induced by dropping a 50 mg ball from a height of 80 cm; Group 4: Head trauma was induced by dropping a 100 mg ball from a height of 80 cm. Thus, according to the Newton's Law, respectively 0.05, 0.1, 0.2 and 0.4 N trauma was created. Serum GFAP levels were analyzed and the damage to cerebral tissues was evaluated in all groups.
RESUlTS:We determined that number of apoptotic cells and particularly the number of GFAP (+) protoplasmic astrocytes at the perilesional region of the cortex increased in association with the increased serum GFAP level as long as the severity of the trauma increased.CONClUSION: Serum GFAP concentration can be used as a marker of the severity of head trauma and traumatic brain injury. However, more animal studies are required to reflect this result in clinical practice.