Patients and Methods/Material and Methods: C57/BL6 male mice, aged 3-4months induced brain trauma (TBI) using controlled cortical impact (CCI) model were treated with CRAC channel inhibitor (CM, 5μg/kg IP) or vehicle control every day (maximum 7days). As a positive control for neuroinflammation, a separate set of mice were given endotoxin (lipopolysaccharide [LPS], 5mg/kg IP). Brains were extracted 3 and 14 days after brain injury (1 day for LPS, n=2/group). Neurological functions were evaluated by swing test and adhesive removal test. Injury lesion and hemorrhage were evaluated from cresyl violet or hematoxylin & eosin staining. We also evaluated the microglia & monocytes activation, anti-inflammatory marker, and CRAC channel activated marker from histology (isolectin B4) & immunohistochemis- try (cluster of differentiation 68, inducible nitric oxide synthase, nuclear factor-kappa B, and stromal interaction molecule 1). Results: Mice exposed to CCI were survived 3 days (n=6/group) & 14days (n = 7/group), respectively. Neurological functions were significantly improved in CM treatment group. CM also reduced injury lesion and hemorrhage volume was significantly decreased 14 days after TBI. From histology & immunohistochemistry findings, the activation of microglia & monocytes was suppressed by CM 3 days after TBI. Conclusion: CRAC channel relates to neuroinflammation in brain and its inhibition protects neuron via blockade of microglial activation by preventing calcium influx. doi:10.1016/j.jns.2017.08.2138 2108 WCN17-2098 SHIFT 5 - TRAUMATIC BRAIN INJURY History of diagnosed and undiagnosed concussions at baseline had differential impact on neurocognitive performance and symptom scores K. O'Connor a , D. Allred b , K. Cameron c , D. Campbell b , C. D’Lauro d , M. Houston c , B. Johnson d , G. McGinty b , P. O'Donnell e , K. Peck c , S. Svoboda c , T. McAllister f , M. McCrea g , S. Broglio a . a University of Michigan, School of Kinesiology, Ann Arbor, USA; b United States Air Force Academy, Athletics, Colorado Springs, USA; c United States Military Academy, Keller Army Community Hospital, West Point, USA; d United States Air Force Academy, Behavioral Sciences and Leadership, Colorado Springs, USA; e United States Coast Guard Academy, Coast Guard Academy Regional Clinic, New London, USA; f Indiana University School of Medicine, Psychiatry, Indianapolis, USA; g Medical College of Wisconsin, Neurology, Milwaukee, USA Background: Concussion’s prevalence and possible long-term con- sequences are an increasing concern facing the U.S. military. Objective: The current investigation tested the independent impact of diagnosed and undiagnosed concussions on baseline neurocognitive and symptom scores years after injury. Patients and Methods/Material and Methods: Data were collected as part of the Concussion Assessment, Research and Education (CARE) Consortium. All consenting cadets at the military service academies completed a baseline Immediate Post-Concussion Assess- ment and Cognitive Test (ImPACT), the Brief Symptom Inventory-18 (BSI-18), and Standard Concussion Assessment Tool (SCAT) symp- tom inventory. Linear regressions modeled the effect of diagnosed and undiagnosed concussion on ImPACT scores. Due to the high proportion of zeroes on baseline BSI and SCAT, zero inflated negative binomial models estimated the effect of diagnosed and undiagnosed concussion. Results: Cadets (N=10,265, 19.38y (SD=1.5y), 23.6% Female, 3.3y (SD=3.1y) following concussion) completed baseline assessments. Cadets reported at least one diagnosed (n=1598, 15.5%) or undiagnosed (n=584, 5.7%) concussion. Diagnosed concussion (p=0.0002) was significantly associated with better ImPACT verbal memory and motor scores. Diagnosed or undiagnosed concussions were not significantly associated with visual memory or reaction time (p’s N 0.05). BSI-18 scores were not influenced by diagnosed concussion (p’s N 0.05). However, cadets with undiagnosed concus- sions had significantly elevated BSI scores (p’s b 0.05). SCAT symptom severity scores significantly increased by 1.6 points for those with a previously undiagnosed concussion (p b 0.001). Conclusion: Diagnosed concussions do not appear to have a negative effect on neurocognitive performance while undiagnosed concus- sions negatively affect symptom scores. Undiagnosed concussions may have greater lasting impact on cadets due to inadequate clinical management. doi:10.1016/j.jns.2017.08.2139 2109 WCN17-3490 SHIFT 5 - TRAUMATIC BRAIN INJURY Apraxia of lid opening with frontal lobe dysfunction after traumatic brain injury: A slowly progressive delayed complication M.Y. Park. Yeungnam University Medical Center, Neurology, Daegu, Republic of Korea Background: Apraxia of lid opening (ALO) has been suggested to be a dysfunction of the supranuclear control of the levator palpebrae superioris caused mainly by basal ganglial lesion. The hypometabolism of the medial frontal lobe may be a one of pathophysiologic mechanism in ALO with a frontal cognitive impairment. Objective: We report two ALO patients with frontal cognitive impairment who developed these symptoms as a delayed complica- tion after traumatic brain injury (TBI). Patients and Methods/Material and Methods: Those symptoms of both patients were developed 4 ~6years after TBI, and slowly progressed. Results: Their MRI showed encephalomalacia in the Rt. medial frontal cortex, which was not shown in initial brain CT scans, and tensor image show low signal intensity in same area which suggests loss of cortico-spinal tract fibers. And their neuropsycologic tests showed frontal cognitive impairment. Their difficulties in eyelid opening diagnosed pretarsal motor persistence (PMP) as one of subtypes of ALO, and were improved by repeated botulinum toxin type A injection. Conclusion: Delayed pathologic changes after TBI may contribute to the development of ALO, and frontal lobe dysfunction in these cases. doi:10.1016/j.jns.2017.08.2140 2110 WCN17-1539 SHIFT 5 - TRAUMATIC BRAIN INJURY On management of optimal cerebral perfusion pressure in severe traumatic brain injury patients V. Petkus a , A. Preiksaitis b,c,d , S. Krakauskaite a , E. Zubaviciute c , S. Rocka c,d , S. Vosylius c , D. Rastenyte b , R. Arminas a . a Kaunas University of Technology, Health Telematics Science Institute, Kaunas, Lithuania; b Lithuanian University of Health Sciences, Department of Neurology- Academy of Medicine, Kaunas, Lithuania; c Vilnius University, Clinic of Neurology and Neurosurgery- Faculty of Medicine, Vilnius, Lithuania; d Republic Vilnius University Hospital, Department of Neurosurgery, Vilnius, Lithuania (2017) 757–944 758 Abstracts / Journal of the Neurological Sciences 381