Which of the Following Is a Force That Can Result in Trauma?
The interior and exterior surfaces of a car are designed to protect the occupants from injury at accidents through utilize of energy absorbing materials and clever structural solutions. The primary verification tool in the pattern process is the Head Injury Criterion (HIC) applied in a free move head-form experimental set-upwards, where a rigid dummy head is launched toward specific locations (National Highway Traffic Safety Administration, 1995). Linear accelerations in three perpendicular directions are measured in the head-form during the bear on and the performance is evaluated co-ordinate to the HIC. The test process is established internationally and thus used by automotive manufacturers all over the world. Sports and automotive helmets are also only tested for pure radial impacts to the helmet, except for the BS 6658 and EN 22.05 oblique bear upon exam for MC helmets (these tests are, however, simply used to appraise external projections and surface friction past measuring the tangential force). A pure radial touch will cause primarily linear acceleration of the head while a pure tangential touch around the head's center of gravity will cause both rotational and linear acceleration of the head. In reality, pure radial impacts are very rare and would mainly cause skull fractures and injuries secondary to those. Bicycle, motorcycle, and equestrian accidents' statistics from Frg, Canada, Belgium, and Finland have, on the other paw, plant the virtually common accident situation to exist an oblique bear upon with an average angle to the ground of xxx–forty°(Harrison et al., 1996; Otte et al., 1999; Richter et al., 2001; Verschueren, 2009). It is more likely that an oblique impact will occur that gives ascension to both linear and rotational head kinematics (Figure 1).
Figure one. Illustration of the biomechanics of an oblique touch on (lower), compared to a corresponding perpendicular one (upper), when impacted against the aforementioned padding using an identical initial velocity of six.7 m/s. Maximum principal strain (Green-Lagrange) at maximum for the brain are illustrated together with the maximum von Mises stress for the skull bone. Parts of the figure are modified from Kleiven (2007a).
The human brain is sensitive to rotational motion (Holbourn, 1943; Gennarelli et al., 1987). In a pioneering work Holbourn (1943) observed shear strain patterns in 2D gel models, and claimed that translation is non injurious, while rotation could explicate the bulk of traumatic brain injuries due to the nearly incompressible properties of brain tissue. The bulk modulus of brain tissue is roughly five to six orders of magnitude larger than the shear modulus (McElhaney et al., 1976) so that for a given impact it tends to deform primarily in shear. Therefore, distortional strain was used as an indicator of the risk of traumatic brain injury in the current written report. The maximal principal Green-Lagrange strain was chosen equally a predictor of CNS injuries since it has shown to correlate with diffuse axonal injuries (Gennarelli et al., 1989; Galbraith et al., 1993; Bain and Meaney, 2000; Morrison et al., 2003), as well as for mechanical injury to the blood-brain barrier (Shreiber et al., 1997). This gives a big sensitivity of the strain in the brain to rotational loading and a small sensitivity to linear kinematics (Kleiven, 2006). Therefore, rotational kinematics should be a better indicator of traumatic brain injury risk than linear acceleration. As well, it has been shown that the most common severe injuries, such every bit subdural hemorrhage and diffuse axonal injury (DAI), are more than hands acquired by rotational caput motion (Gennarelli et al., 1972, 1987). Gurdjian and Gurdjian (1975) suggested that a combination of skull deformation, pressures, and inertial brain lag could present a clearer motion-picture show of caput injury. Gennarelli et al. (1982) stated that all types of brain injury tin can exist produced past angular dispatch. According to Ommaya (1985), rotation can produce both focal and lengthened encephalon injuries while translation is limited to focal effects.
The aim of this perspective is to point out hereafter directions when it comes to the prediction of head injuries based on the predominant mechanism behind each type of injury. To illustrate the difference between radial and oblique impacts, perpendicular impacts through the center of gravity of the head and 45° oblique impacts were simulated (Kleiven, 2007a). It is obvious that essentially higher strain levels in the brain are obtained for an oblique bear on, compared to a corresponding perpendicular i, when impacted toward the same padding of expanded polypropylene (EPP-31 kg/m3) using an identical initial velocity of 6.7 m/s. It is also clearly illustrated that the radial impact causes substantially higher stresses in the skull with an associated higher risk of skull fractures (Figure 1, upper).
Brain Injuries Primarily Induced by Rotational Kinematics
Concussion
The classical cerebral concussion involves immediate loss of consciousness following loading (Melvin et al., 1993). This is the nearly unremarkably occurring caput injury accounting for effectually 70% of the full where more than 99% of the patients have left the hospital within xiv days (Kleiven et al., 2003). Gennarelli et al. (1972) subjected squirrel monkeys to controlled sagittal plane head motions. It was institute that the animals subjected to pure translation of the head, cerebral concussion was not obtainable. In contrast, the animals who were subjected to head rotations were all concussed. Visible brain lesions were noted in both translated and rotated groups but with a greater frequency and severity after rotation. Patton et al. (2012) suggested rotational kinematics above 4500 rad/s2 and 33 rad/s for summit resultant angular acceleration and maximum alter in resultant angular velocity, respectively, to predict concussions involving loss of consciousness lasting longer than ane min in rugby and Australian football impacts. Recently, Rowson et al. (2012) recorded 57 concussions and a large number of sub-concussive impacts during the 2007–2009 collegiate American football season, and proposed 6383 rad/southtwo in rotational acceleration associated with 28.3 rad/due south in rotational velocity to represent a 50% risk of concussion. Studies on giant squid axons (Thibault, 1993) suggested a maximal principal strain of effectually 0.10 to crusade reversible injury to the axons which could be used equally an approximate axonal strain threshold for concussion. During simulations of concussions in the National Football League (NFL), the strain magnitude in the brain was establish to be sensitive to only the rotational kinematics and not the translational motion (Kleiven, 2007b).
Diffuse Axonal Injury
Lengthened axonal injury is associated with mechanical disruption of many axons in the cerebral hemispheres and subcortical white affair, illustrated equally shear strain in Effigy ii. Severe memory and motor deficits are present, and posttraumatic amnesia may terminal for weeks (Melvin et al., 1993). At the end of 1 month, 55% of the patients are likely to take died (Gennarelli et al., 1982). High-resolution CT scans may show pocket-sized hemorrhages and axonal swelling. The maximum strain to cause damage to the axons has been estimated in previous publications. Studies have been performed with behemothic squid axons (Thibault et al., 1990) and a strain of 0.3 was suggested equally threshold of DAI. Bain and Meaney (2000) proposed a threshold of 0.2 in maximal principal strain in the brain tissue for the onset of the malfunction of the neurons in the brain, which could be seen as a first stage of DAI. Maximum primary Green-Lagrange strain of 0.2 has too been shown to correlate with cell expiry and neuronal dysfunction associated with DAI (Morrison et al., 2003). Ueno and Melvin (1995) plant, when applying kinematics to a second caput model, that the rotational acceleration has a dominant issue on shear deformation while linear acceleration is related to pressure.
Figure two. Schematical description of the biomechanics of subdural hematoma (left), concussions, contusions, intra-cerebral hematomas, and lengthened axonal injuries (right) when impacted against a surface as illustrated in Figure 1.
Contusions
Cerebral contusion is one of the most ofttimes found lesions following head injury. It consists of heterogeneous areas of necrosis, pulping, infarction, hemorrhage, and edema (Melvin et al., 1993). Contusions generally occur at the site of bear on (coup contusions) and at remote sites from the affect (contrecoup contusions) (Figure 2). In the absence of skull fracture information technology is likely induced by shearing and scratching of the brain tissue against edges and sharper ridges in the dura/skull and therefore acquired by excessive caput rotational loading (Löwenhielm, 1975). Moreover, Shreiber et al. (1997) derived a threshold of 0.19 in master logarithmic strain in the cortex for a 50% risk of cognitive contusions induced past vacuum. Every bit previously mentioned, this strain is sensitive to merely the rotational kinematics and not the translational motion (Ueno and Melvin, 1995; Kleiven, 2007b).
Subdural Hematoma
Acute subdural hematoma (SDH) together with DAI account for more than head injury deaths than all other lesions combined (Gennarelli, 1981). SDH is the nearly mutual of the severe traumatic brain injuries bookkeeping for around 50% of the total of this category in Sweden (Kleiven et al., 2003). The most common mechanism of SDH is vehement of veins that span the subdural space as they go from the brain surface to the various dural sinuses (Figure 2) (Gennarelli and Thibault, 1982). Based on previous primate experiments, Gennarelli (1983) suggested that SDH was produced by short elapsing and loftier amplitude of angular accelerations. Lee and Haut (1989) studied the effects of strain rate on tensile failure backdrop of human bridging veins and determined the ultimate strain to be almost εf = 0.5 which was found to exist independent of the strain rate (ε = 0.1–250 s−1). Before inquiry done past Löwenhielm (1974a) showed that the failure strain was markedly reduced from almost 0.8 to 0.2 equally the rate was increased. Lee et al. (1987) used a 2D sagittal model, and Huang et al. (1999) used a 3D model (previously presented in Shugar, 1977) to report the mechanisms of SDH. They found that the contribution of angular acceleration to violent of bridging veins (measured as observed modify in distance between a node in the interior of the skull and a node in the encephalon) was greater than the translational acceleration. Substantially larger relative motions betwixt the skull and the brain as well every bit higher strain in the bridging veins take been found, when switching from a translational to a rotational mode of motion using a detailed 3D head model including 11 pairs of the largest bridging veins (Kleiven, 2003).
Intra-Cerebral Hematomas
Intra-cerebral hematomas (ICH) are well defined homogeneous collections of blood inside the cerebral parenchyma. Information technology was possible, through the reconstruction of a motocross accident, to re-create the injury pattern in the brain of the injured passenger using maximal principal (Kleiven, 2007b). The strain levels at maximum for two locations of ICH were around 0.4–0.five, which is close to known thresholds for rupture of cerebral veins and arteries (Löwenhielm, 1974b; Lee and Haut, 1989; Monson et al., 2003) indicating that the take a chance of ICH tin be predicted past the pattern and magnitude of maximum principal strain.
Head Injuries Primarily Induced by Linear Kinematics
Skull Fracture
It is obvious that a purely radial impact produce higher contact forces and larger linear accelerations increasing the stresses in the skull bone which predict the risk of skull fractures (Figure i). Consistent mean fracture force levels in the range of 4.viii–five.viii kN for the frontal bone and iii.five–3.6 kN for the temporoparietal surface area of the skull accept been reported (Nahum et al., 1968; Allsop et al., 1988; Schneider and Nahum, 1972). The reported fracture forces do, even so, vary depending on the impactor surface area (Hodgson and Thomas, 1971, 1973). These force values tin can be related to the linear acceleration of the head through Newton'southward 2nd law. A report past Mertz et al. (1997) estimated a 5% risk of skull fractures for a peak acceleration of 180 gravities (thousand) and a 40% take a chance of fractures for 250 g.
Epidural Hematoma
Epidural hematoma (EDH) is a relatively infrequently occurring sequel to head trauma (0.2–6%, Cooper, 1982; Kleiven et al., 2003). It occurs as a result of trauma to the skull and the underlying meningeal vessels and is not due to brain injury (Melvin et al., 1993).
Contusions (Secondary to Skull Fracture)
Cerebral contusion at the site of impact in the presence of skull fracture it is likely induced by the direct impression of the skull against the underlying brain tissue and therefore, as for skull fracture, caused by the contact force and well predicted by the linear dispatch.
Concluding Remarks
The results presented and discussed in the present written report deal with traumatic head injuries induced by inertia or due to impacts and exclude penetrating injuries due to projectiles, fluid percussion injury systems, or boom induced TBI where the etiology is not yet well understood. Withal, it can be concluded that the following impact or inertia induced traumatic head injuries would likely exist all-time prevented by minimizing the magnitudes of rotational kinematics:
• Concussion
• Diffuse axonal injury
• Contusion (in absenteeism of skull fracture)
• Subdural hematoma
• Intra-cerebral hematoma
On the other manus, the post-obit traumatic head injuries would likely exist all-time prevented by minimizing the magnitudes of linear dispatch or the impact force:
• Skull fracture
• Epidural hematoma
• Contusions (secondary to skull fracture)
Conflict of Interest Statement
The author is a part owner of a helmet company (MIPS AB).
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Source: https://www.frontiersin.org/articles/10.3389/fbioe.2013.00015/full
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