Abstract
1) Four dry human skulls were statically compressed in fronto-occipital direction. The forces to produce bone fracture ranged between 600 and 1000kg weight. The load-deflection curves gave spring rates of 400 to 900kg/mm, average 600kg/mm.2) Semi-free fall test to give impact on twenty dry human skulls at midfrontal regions were performed using a strain-gauge load cell, an accelerometer, DC amplifiers and a cathode-ray oscilloscope. Various buffer materials including the scalp simulator were used.At fracture notching and abrupt lowering of the load curves as well as high frequency vibration of the acceleration curves were noted. The rise time at fracture became shorter compared to those when fracture did not occur. The dynamic load level for frontal bone fracture was between 400 and 1300kg, was independent of acceleration, energy, buffer materials as well as rise times. The peak loads at the moment of fracture were closely related to the weights of dry skulls. These results indicate that human skulls have the characteristics of brittle fracture both statically and dynamically.3) Based on the above conclusions the tolerance limits against brain damage was theoretically considered and the Wayne State Human Tolerance Curve was criticized.Postulating a head falling brow-down on a hard flat surface without the effect of the body, the threshold for fracture in terms of peak acceleration and rise time is very close to the Wayne State Human Tolerance Curve (H. T. C.). Above this threshold or even when higher energy is applied, the head does not give rise to a higher acceleration but fracture should occur at the same peak acceleration and possibly shorter rise time. This means transition to the safe zone of the H. T. C. Clinically, however, severer brain damage is expected. The H.T.C. and the pressure gradient theory due to translational acceleration should not be applied to brain damage in the presence of fracture. Instead, skull deformation and possibly snap-back of the deformed skull should be considered as the mechanism of the brain damage associated with skull fracture.
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