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. 1. Introduction A closed head trauma may result in traumatic brain injury (TBI), and its consequences constitute a large burden for the victims, their families, and the society [1–5]. The relation between the external loading of the head and the response in the brain, resulting in damage, during an impact lasting just milliseconds needs further clarification. Inertial shearing deformation of the brain is considered to be a primary cause of injury [6–14] and generates temporary pressures in the brain parenchyma, as demonstrated in, for example, postmortem human subjects and in nonhuman primates [15–17]. Anderson et al. [18] reported correlations between applied force, dynamic pressures, and histopathological changes at a lateral head impact. The forces applied at a closed head impulse have been proposed to possibly induce cavitation at interfaces [19–23]. The aim of the present study was to elucidate the importance of the direction of a sagittal plane rotational acceleration trauma to the head and neck for the deformation of the brain, which thereby induces brain concussion, also named mild traumatic brain injury (TBI) [10, 12–14, 17]. We consider that the direction of the force at a head trauma is likely to
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