| 1. |
- Hansson, Hans-Arne, 1939, et al.
(författare)
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Neck Flexion Induces Larger Deformation of the Brain Than Extension at a Rotational Acceleration, Closed Head Trauma
- 2014
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Ingår i: Advances in Neuroscience. - : Hindawi Limited. - 2356-6787 .- 2314-789X. ; 2014:945869
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Tidskriftsartikel (refereegranskat)abstract
- A closed head trauma induces incompletely characterized temporary movement and deformation of the brain, contributing to the primary traumatic brain injury. We used the pressure patterns recorded with light-operated miniature sensors in anaesthetized adult rabbits exposed to a sagittal plane rotational acceleration of the head, lasting 1ms, as a measure of brain deformation. Two exposure levels were used and scaled to correspond to force levels reported to cause mild and moderate diffuse injury in an adult man, respectively. Flexion induced transient, strong, extended, and predominantly negative pressures while extension generated a short positive pressure peak followed by a minor negative peak. Low level flexion caused as strong, extended negative pressures as did high level extension. Time differences were demonstrated between the deformation of the cerebrum, brainstem, and cerebellum. Available X-ray and MRI techniques do not have as high time resolution as pressure recordings in demonstrating complex, sequential compression and stretching of the brain during a trauma. The exposure to flexion caused more protracted and extensive deformation of the brain than extension, in agreement with a published histopathological report. The severity and extent of the brain deformation generated at a head trauma thus related to the direction at equal force.
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| 2. |
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| 3. |
- Krave, Ulrika, 1973
(författare)
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Modelling of Diffuse Brain Injury: Combining Methods to Study Possible Links between Transient Intracranial Pressure and Injury
- 2010
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- The objectives of this research are the study of sagittal rotational acceleration induced diffuse brain injury mechanisms. Such injuries are common in vehicle accidents in particular; the consequences range from mild to severe symptoms and may lead to persistent neurological dysfunction. The understanding of the mechanisms that lead to these injuries is not yet well established and needs to be studied further. A rabbit animal model was used to study the dynamic brain pressure response and the injury outcome. Rabbits were subjected to sagittal rotational acceleration of the head, during which the intracranial pressure changes were recorded by fibre optic pressure sensors inserted into the brain parenchyma at selected locations. Both flexion and extension were investigated for two levels of acceleration. A neuropathological investigation was carried out. In parallel, a rabbit brain FE model was developed to further understand the biomechanics of the experiments and experimental design.The direction of the acceleration applied was found to influence the intracranial pressure measurements, as disclosed by the prominent negative pressure patterns as a result of flexion of the head, which diverged from those recorded in extension. In the extension experiments an initial pressure rise followed by a pressure drop was observed. Such divergence in brain response was also found for the injury outcome. For similar low levels of acceleration, a flexion trauma induced prominent histopathological changes in the brain while an extension trauma induced minimal abnormalities. Evidence for the relative motion between the brain and skull was found for flexion loading. In these subjects, scattered ruptured bridging veins were observed and stretching of the olfactory bulbs and nerves. Such injuries were not observed in extension. The FE model was suitable for predicting pressure in extension load cases. The FE could help to refine the experimental design by suggesting new measurement locations in the brain, which are less sensitive to the measured pressure variations. This study shows that the combination of the three methods, the measurement of an internal parameter (pressure) in the brain, neuropathological investigation of the injury outcome, and finite element simulations of the experiments, could help to promote more detailed knowledge of brain injury mechanisms. Such knowledge could be used to develop countermeasures and, thereby to reduce the number and severity of brain injuries in traffic related accidents.
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| 4. |
- Krave, Ulrika, 1973, et al.
(författare)
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Rotational Acceleration Closed Head Flexion Trauma Generates More Extensive Diffuse Brain Injury than Extension Trauma
- 2011
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Ingår i: Journal of Neurotrauma. - : Mary Ann Liebert Inc. - 1557-9042 .- 0897-7151. ; 28:1, s. 57-70
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Tidskriftsartikel (refereegranskat)abstract
- Our aim was to investigate if seemingly identical head and neck trauma would generate differing types of braindamage. We experimentally evaluated induced brain injuries immediately after trauma exposure, and at 1 weekpost-injury. Anesthetized rabbits were exposed once to a sagittal rotational acceleration head and neck injury ateither a high or a low load level, using either flexion or extension. A high-load extension trauma induced scatteredmeningeal petechial hemorrhages and no deaths, in contrast to a flexion trauma of the same level, which resultedin extensive parenchymal and meningeal hemorrhages, and all animals succumbed immediately. A low-levelflexion trauma induced scattered meningeal petechiae, but no gross damage, while extension at the same forcegenerated no macroscopically visible acute brain injury. Immunohistochemical investigations carried out at 7 daysdisclosed that a low-level flexion trauma, as well as both low- and high-level extension exposures, all induceddiffuse brain injuries in the cerebral cortex and white matter, corpus callosum, hippocampus, brainstem, andcerebellum, as revealed by abnormal distribution of neurofilaments, a prevalence of b-amyloid precursor protein,and astrogliosis. The diffuse brain injury seen after a low-level flexion trauma was equal to or more extensive thanthat seen after a high-level extension trauma. A low-level extension trauma induced only minor histopathologicalabnormalities. We conclude that a sagittal rotational acceleration trauma of the head and neck induced diffusebrain injury, and that flexion caused more extensive damage than extension at the same applied load.
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| 5. |
- Krave, Ulrika, 1973, et al.
(författare)
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Transient, powerful pressures are generated in the brain by a rotational acceleration impulse to the head
- 2005
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Ingår i: European Journal of Neuroscience. - : Wiley. - 1460-9568 .- 0953-816X. ; 21:10, s. 2876-2882
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Tidskriftsartikel (refereegranskat)abstract
- A rotational acceleration impulse to a head, as occurs at traffic accidents, sport injuries, assaults and falls, induces a diffuse brain damage that eventually could result in persistent neuropsychiatric deficits and neurodegeneration. Emphasis has been concentrated on the relative motion of the brain inside the skull during head impact, whereas less attention has been paid to whether intracranial pressure changes are generated and, if so, the implications thereof. In the present experimental study we investigated in an animal model system, based on rabbits, if a sagittal, anterior-posterior rotational acceleration of a head generated intracranial pressure changes, recorded by fibre optic pressure sensors, inserted ipsilaterally in the parieto-temporal and the occipital lobes. Two levels of rotational acceleration were used in the experiments; one higher, corresponding to the threshold limit for moderate diffuse brain injury, and one lower, close to being noninjurious. Several pressure recordings were performed in each rabbit at the two acceleration levels. The pressure recordings invariably revealed the same general characteristics of rapid, positive and negative pressures; within the brain, with variations in amplitude and duration, lasting for up to 10 ms. A major finding was the generation of powerful negative pressures, as low as 0.3 bars in absolute pressure. The most prominent difference in amplitudes of the negative peak pressures between the two applied acceleration levels was demonstrated at the parieto-temporal location. The presented pressure recordings are the first to disclose the generation of transient, powerful intracerebral pressures at rotational acceleration of the head, which must be considered in studies of brain injury generation and distribution as well as prevention. © 2005 Federation of European Neuroscience Societies.
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