ИСТИНА

BACKGRAUND Severe traumatic brain injury (sTBI) is characterized by a comatose condition that may be followed by the development of post-comatose unconsciousness of varying duration. Coma can be caused both by direct damage to the brainstem or by dysfunction of the ascending activating system due to brainstem compression associated with dislocation processes caused by edema, intracranial hematomas, cerebrospinal fluid circulation disorders, etc. It’s hard to verify structural brainstem lesions in acute period, which can influence the current and prognosis of sTBI. Kainate glutamate receptors are mainly localized in brainstem area. In our hypothesis they may react to the traumatic brainstem damage and serve as a biomarker. METHODS. In this prospective study 23 patients (mean age 27±3,4 years) with severe diffuse axonal traumatic brain injury (TBI) (GCS<8) were examined with 3T MRI during 21 days period after injury. Localization of structural brain damage was verified by T1, T2, fluid-attenuated inversion recovery (FLAIR), diffusion-weighted imaging (DWI), and susceptibility weighted imaging (SWI) sequences. Coma depth was ranged by Glasgow Coma Scale (GCS) and FOUR. Outcome was evaluated in 6 months by Glasgow Outcome Scale (GOS). Kainate receptor antibodies (KARab) were analyzed by ELISA kit (DRD Biotech) on 3-5 and 9-15 days after TBI. RESULTS. KARab level on 3-5 days post-injury was much higher in group of patients with structural brainstem damage then in one with intact brainstem (cut off 1,5 ng/ml) (p=0,04). Sensitivity and specificity were 72,7% and 75% accordingly. High level of KARab was observed with no difference between two groups on 9-15 days which can be explained by developing of secondary brainstem damage processes to the 2nd week. KARab level didn’t reflect damage of basal ganglia, thalamus and hemisphere structures. CONCLUSION. These preliminary data showed the significance of KARab monitoring as a biomarker of brainstem impairment in comatose patients after sTBI.