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Axonal Injury

Axonal injuries (AI) occur both in the area of the bleeding (focal axonal injury) and at remote sites. In the latter instance they sometimes occur as diffuse axonal injury (DAI - see Povlishock 1992; Gennarelli

Fig. 9.27. Diffuse axonal injury is caused by angular and/or translational acceleration (ACA anterior communicating artery, B basal ganglia, ICA internal carotid artery, MCA middle cerebral artery)

BLOW: rotation

BLOW: rotation

Fig. 9.27. Diffuse axonal injury is caused by angular and/or translational acceleration (ACA anterior communicating artery, B basal ganglia, ICA internal carotid artery, MCA middle cerebral artery)

et al. 1998) concentrated along the midline structures, e.g., in the corpus callosum, septum pellucidum, fornix, tela chorioidea (Blumbergs et al. 1995), and in the midbrain, pons, and hippocampus (Adams et al. 1982) (Fig. 9.26). Today's immunohistochemical methods (P-APP - Gentleman et al. 1993a, b; Sheriff et al. 1994) can consistently demonstrate axonal injuries 105-180 min after wounding (Oehmichen et al. 1997). In two children, axon swelling was visualized by Gorrie et al. (2002) in the internal capsule after only 35-45 min of survival. Moreover, there is a significant correlation between axonal swelling size and survival time (Wilkinson et al. 1999) as confirmed by Leclercq et al. (2002). However, Leclercq et al. (2002) suggest the large variability in swelling size within individual cases and the heterogeneity of the original trauma seriously comprise the utility of such information in the timing of lesions.

However, axonal injuries are sometimes a delayed phenomenon due to interruption of intra-axonal transport (Povlishock 1997). Expression of P-APP in particular is not an indication of axonal transection at all and not all P-APP-positive axons are irreversibly damaged (Povlishock 1997).

DAI is caused by angular or rotational and/or translational acceleration following impact of the head, which exposes the axons to transient tensile strain (Fig. 9.27). Impact as well as acceleration of the head can generate impulsive loading of sufficient magnitude to produce DAI (Gennarelli and Meaney 1996). The severity of DAI correlates with the magnitude, duration, and speed of onset of the angular acceleration as well as the direction of head motion (Gennarelli and Meaney 1996). DAI is produced by longer acceleration loading than that which generates SDH and is caused by the head colliding with a relatively soft, broad object (e.g., an automobile dashboard - see Gennarelli and Thibault 1982). Equivalent magnitudes of angular acceleration applied to the primate head readily induced DAI if accelerated laterally, less readily upon oblique or sagittal acceleration.

DAI is the result of shear and/or tensile strains caused by the brain tissue movements in contrast to the static structures of falx and tentorium during angular acceleration occasioned by lateral movement of the brain tissue (Gennarelli and Meaney 1996). The prognosis for functional recovery depends largely on the extent and location of DAI.

Tissue-tear hemorrhages are sometimes associated with severe DAI and constitute small areas of hemorrhage located parasagittally in the deeper regions of the brain (Strich 1961). Because gray matter is denser than white matter, the interface between them is particularly susceptible to shearing forces generated by angular acceleration. Geometric irregularities of the skull, intracranial partitioning membranes such as the falx cerebri and tentorium, and the plane of motion of the head all help to determine the location of these lesions. As discussed above, tissue-tear lesions in the frontoparietal white matter are termed "gliding contusion injuries" (see Fig. 9.21).

Axonal injuries also occur secondary to hypoxic injury, which may also be the consequence of an impact (jellinger 1977; Kaur et al. 1999; Oehmichen et al. 1999a, b; Niess et al. 2002). It is sometimes impossible to determine retrospectively whether the axonal injury is primary or secondary. Secondary axotomy in most cases is delayed until some hours after wounding of the brain (Maxwell et al. 1993). In addition to axonal injuries, which have been relatively well studied, a mechanical dendrite injury is also possible but has been studied by only a few authors (Li et al. 1997).

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