General categories of experimental brain injury models are reviewed regarding their clinical significance, and two new models are presented that use different methodology to produce injury. This report describes and characterizes the pathophysiologic changes produced by a novel fluid percussion (FP) method and a controlled cortical impact (CI) technique, both developed at the General Motors Research Laboratories (GMRL). The new models are compared to prior experimental brain injury techniques in relation to ongoing physical and analytical modeling used in automotive safety research by GMRL. Experimental results from our laboratory indicate that although the FP technique, currently the most widely used method for producing brain injury, is useful for producing graded injury responses systemically and centrally, it is not well-suited for detailed biomechanical analyses. This conclusion is based on high-speed cineradiographic studies where the physiologic saline in the FP cannula was substituted with a radiopaque contrast medium (Conray 1:1 dilution/saline). High speed x-ray movies (1000 fps) were taken of the fluid percussion pulse (1.5-3.4 atm/20 msec) in sagittal, dorsal, and frontal planes of orientation. When viewed together, the cineradiography revealed a complex, dynamic interaction between the injected fluid and the skull/cranial contents. Rapid lateral and anterior/posterior epidural fluid flow suggest that the pathology and dysfunction following FP brain injury reflects diffuse mechanical loading of the brain. Because fluid is used to transfer mechanical energy to brain tissue, and because fluid flow characteristics (i.e., direction, velocity, and displacement) are dependent on the brain geometry and species used, accurate analytical and biomechanical analyses of the resultant injury would be difficult at best. In contrast, the cortical impact model of experimental brain injury uses a known impact interface and a measurable, controllable impact velocity and cortical compression. These controlled variables enable the amount of deformation and the change in deformation over time to be accurately determined. In addition, the CI model produces graded, reproducible cortical contusion, prolonged functional coma, and extensive axonal injury, unlike the FP technique. The quantifiable nature of the single mechanical input used to produce the injury allows correlations to be made between the amount of deformation and the resultant pathology and functional changes.(ABSTRACT TRUNCATED AT 400 WORDS)

The fluid-percussion technique produces experimental brain injury by rapid injection of a fluid volume into the closed cranial cavity. The experiments reported here characterize a new, more controlled technique for fluid-percussion brain injury in the rat and systematically examine systemic physiologic, histopathologic, and electroencephalographic responses in the rat at two levels of injury severity. The new technique was developed to permit independent variation of the fluid pressure pulse parameters and, thus, more accurately define the brain loading conditions associated with fluid-percussion injury. The new technique produced changes in mean arterial blood pressure similar to previous techniques; however, bradycardia was not observed. Significant increases in heart rate were produced by both injury levels and were more prolonged at the high level of injury severity. Both magnitudes of injury produced significant decreases in EEG amplitude immediately postinjury, but high severity injury produced a greater decrease in delta frequency band (1-4 Hz) activity than did low severity injury. Both levels produced hemorrhage at the site of injury, thalamus, corpus callosum, hippocampus, and fimbria hippocampus similar to previous techniques. Higher levels of injury produced more extensive cerebral hemorrhage and greater spinal involvement. In a separate group of animals, cineradiographic images were made at coronal, sagittal, and dorsal orientations during the fluid pressure pulse. Intracranial fluid movement was characterized by rapid radial movement within the epidural space. The data suggest that the distributed nature of fluid-percussion induces pathology, and dysfunction may reflect a diffuse mechanical loading of the brain surface. The model appears to give repeatable effects useful in the study of closed head injury.

Brain atlases that encompass detailed anatomical or physiological features are instrumental in the research and surgical planning of various neurological conditions. Magnetic resonance imaging (MRI) has played important roles in neuro-image analysis while histological data remain crucial as a gold standard to guide and validate such analyses. With cellular-scale resolution, the BigBrain atlas offers 3D histology of a complete human brain, and is highly valuable to the research and clinical community. To bridge the insights at macro- and micro-levels, accurate mapping of BigBrain and established MRI brain atlases is necessary, but the existing registration is unsatisfactory. The described dataset includes co-registration of the BigBrain atlas to the MNI PD25 atlas and the ICBM152 2009b atlases (symmetric and asymmetric versions) in addition to manual segmentation of the basal ganglia, red nucleus, amygdala, and hippocampus for all mentioned atlases. The dataset intends to provide a bridge between insights from histological data and MRI studies in research and neurosurgical planning. The registered atlases, anatomical segmentations, and deformation matrices are available at: https://osf.io/xkqb3/.

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Objective: Thrombocytosis has been reported in neonates and young infants, but little is known of its prevalence, timing of onset, associated conditions, sequelae and outcomes. To better understand this condition, we used the data repositories of a multi-hospital health-care system to identify all individuals p140 days old (20 weeks) who, during the past 6 years, had a platelet count of X1 000 000 ml À1 . Study Design:We identified all infants with extreme thrombocytosis (using the Sutor definition of a platelet count of X1 000 000 ml À1 ) during the period of January 2003 through December 2008 in any Intermountain Healthcare facility. We obtained the information provided in this report from electronic and paper records.Result: Among 40 471 infants who had one or more platelet counts performed in this period, 25 had extreme thrombocytosis. No cases were identified in the first week after birth, 40% were recognized between the second and fourth weeks and 40% between the fifth and eighth week. The prevalence of thrombocytosis had no relationship with birth weight or gestational age but a slight predominance of female patients (15/25) was noted. In all, 26 episodes were found among the 25 infants: 12 episodes involved an antecedent infectious disease, 8 had an antecedent surgical procedure, 4 had the anemia of prematurity and 1 each had congenital adrenal hyperplasia and opiate withdrawal syndrome. No pathological thromboses or hemorrhages or other sequelae were detected and all episodes resolved with no deaths. Conclusion:The thrombocytosis cases that we report were all consistent with reactive thrombocytosis (also known as secondary thrombocytosis); none seemed to be essential (primary) thrombocytosis. We speculate that the pathogenesis involves increased platelet production due to megakaryopoietic stimulators induced by an infectious or inflammatory condition. From this series and previous reports, young infants with platelet counts up to 1 300 000 ml À1 do not seem to have a significant risk of thrombotic or hemorrhagic problems, and do not generally require anti-platelet or cytoreductive treatment.