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.
Our aim was to investigate if seemingly identical head and neck trauma would generate differing types of brain damage. We experimentally evaluated induced brain injuries immediately after trauma exposure, and at 1 week post-injury. Anesthetized rabbits were exposed once to a sagittal rotational acceleration head and neck injury at either a high or a low load level, using either flexion or extension. A high-load extension trauma induced scattered meningeal petechial hemorrhages and no deaths, in contrast to a flexion trauma of the same level, which resulted in extensive parenchymal and meningeal hemorrhages, and all animals succumbed immediately. A low-level flexion trauma induced scattered meningeal petechiae, but no gross damage, while extension at the same force generated no macroscopically visible acute brain injury. Immunohistochemical investigations carried out at 7 days disclosed that a low-level flexion trauma, as well as both low- and high-level extension exposures, all induced diffuse brain injuries in the cerebral cortex and white matter, corpus callosum, hippocampus, brainstem, and cerebellum, as revealed by abnormal distribution of neurofilaments, a prevalence of β-amyloid precursor protein, and astrogliosis. The diffuse brain injury seen after a low-level flexion trauma was equal to or more extensive than that seen after a high-level extension trauma. A low-level extension trauma induced only minor histopathological abnormalities. We conclude that a sagittal rotational acceleration trauma of the head and neck induced diffuse brain injury, and that flexion caused more extensive damage than extension at the same applied load.
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 1 ms, 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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