Serdar Çevik1, Mustafa Murat Özgenç2, Ahmet Güneyk3, Şevket Evran4, Enes Akkaya5, Fatih Çalış6, Salim Katar7, Celaleddin Soyalp8, Hakan Hanımoğlu9, Mehmet Yaşar Kaynar10. 1. Department of Neurosurgery, Bezmialem Vakıf University, Adnan Menderes Bulvarı, Vatan caddesi 34093, Fatih, Istanbul, Turkey. Electronic address: dr.serdarcevik@gmail.com. 2. Department of Emergency Medicine, Medikal Park Hospital, Antalya, Turkey. 3. Department of Biochemstry, Ağrı State Hospital, Ağrı, Turkey. 4. Department of Neurosurgery, Bahçelievler State Hospital, İstanbul, Turkey. 5. Department of Neurosurgery, University of Health Sciences, Sisli Hamidiye Etfal Training and Research Hospital, Istanbul, Turkey. 6. Deparrment of Neurosurgery, Medeniyet University, Göztepe Training and Research Hospital, Istanbul, Turkey. 7. Department of Neurosurgery, Selahaddin Eyyübi State Hospital, Diyarbakır, Turkey. 8. Department of Anesthesiology and Intensive Care, Yüzüncü Yıl University School of Medicine, Van, Turkey. 9. Department of Neurosurgery, Biruni University, İstanbul, Turkey. 10. Department of Neurosurgery, Istanbul University Cerrahpasa School of Medicine, İstanbul, Turkey.
Abstract
OBJECTIVE: To determine whether serum neurogranin (NRGN), glial fibrillary acidic protein (GFAP), and calcium-binding protein S100 beta (S100B) levels are associated with traumatic intracranial lesions compared to computed tomography (CT) findings of patients with mild traumatic brain injury (mTBI). PATIENTS AND METHODS: The cross-sectional study cohort included 48 patients who were admitted to the Emergency Department with a complaint of mTBI, a Glasgow Coma Scale score of 14-15, and at least one symptom of head trauma (i.e., post-traumatic amnesia, nausea or vomiting, post-traumatic seizures, persistent headache, and transient loss of consciousness). Blood samples and CT scans were obtained for all patients within 4 h of injury. Age-matched patients without intracranial traumatic pathology (CT-) were recruited as a control group. Blood samples were measured for NRGN, GFAP, and S100B levels. RESULTS: Of 48 patients, 24 were CT + and had significantly higher serum NRGN (5.79 vs. 2.95 ng/mL), GFAP (0.59 vs.0.36 ng/mL), and S100B (1.72 vs.0.73 μg/L) levels than those who were CT- (p = 0.001, p = 0.026, and p < 0.001, respectively). ROC curves showed that NRGN, GFAP, and S100B levels were sufficient to distinguish traumatic brain injury in patients with mTBI. At the cut-off value for NRGN of 1.87 ng/mL, sensivity was 83.3%, and specificity was 58.3%. At the cut-off value for GFAP of 0.23 ng/mL, sensivity was 75% and specificity was 62.5%. The optimal cut-off value for S100B was 0.47 μg/L (95.8% sensitivity and 62.5% specificity). CONCLUSION: This is the first study to evaluate NRGN in human serum after mTBI. We confirmed that NRGN levels were significantly higher in CT + patients than CT- patients in the mTBI patient population. Future studies of larger populations and different age groups (especially pediatric) can help reduce the number of CT scans as a reliable and noninvasive diagnostic tool for evaluating NRGN protein levels in mTBI patients with a low probability of intracranial lesions.
OBJECTIVE: To determine whether serum neurogranin (NRGN), glial fibrillary acidic protein (GFAP), and calcium-binding protein S100 beta (S100B) levels are associated with traumatic intracranial lesions compared to computed tomography (CT) findings of patients with mild traumatic brain injury (mTBI). PATIENTS AND METHODS: The cross-sectional study cohort included 48 patients who were admitted to the Emergency Department with a complaint of mTBI, a Glasgow Coma Scale score of 14-15, and at least one symptom of head trauma (i.e., post-traumatic amnesia, nausea or vomiting, post-traumatic seizures, persistent headache, and transient loss of consciousness). Blood samples and CT scans were obtained for all patients within 4 h of injury. Age-matched patients without intracranial traumatic pathology (CT-) were recruited as a control group. Blood samples were measured for NRGN, GFAP, and S100B levels. RESULTS: Of 48 patients, 24 were CT + and had significantly higher serum NRGN (5.79 vs. 2.95 ng/mL), GFAP (0.59 vs.0.36 ng/mL), and S100B (1.72 vs.0.73 μg/L) levels than those who were CT- (p = 0.001, p = 0.026, and p < 0.001, respectively). ROC curves showed that NRGN, GFAP, and S100B levels were sufficient to distinguish traumatic brain injury in patients with mTBI. At the cut-off value for NRGN of 1.87 ng/mL, sensivity was 83.3%, and specificity was 58.3%. At the cut-off value for GFAP of 0.23 ng/mL, sensivity was 75% and specificity was 62.5%. The optimal cut-off value for S100B was 0.47 μg/L (95.8% sensitivity and 62.5% specificity). CONCLUSION: This is the first study to evaluate NRGN in human serum after mTBI. We confirmed that NRGN levels were significantly higher in CT + patients than CT- patients in the mTBI patient population. Future studies of larger populations and different age groups (especially pediatric) can help reduce the number of CT scans as a reliable and noninvasive diagnostic tool for evaluating NRGN protein levels in mTBI patients with a low probability of intracranial lesions.
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