Axonal damage associated with DTBI

In addition to diffuse neuronal perturbation and death described above, diffuse axonal injury is also a distinguishing feature of DTBI, occurring across the spectrum of brain injury ranging from mild through severe. Historically, the histological identification of diffuse axonal injury was based upon the use of silver salts to detect, within the first days of injury, grossly swollen axonal bulbs that lacked continuity with their downstream axonal partners (Strich, 1956). This suggested their mechanical transsection resulting in axonal retraction and axoplasmic pooling at the site of disconnection (Strich, 1956; Adams, 1982). More contemporary studies, however, have shown that in large part, this premise of transsection and retraction

Diffuse Axonal Injury Pathological

Fig. 1. This figure illustrates the phenomenon of mechanically induced neuronal membrane disruption and its consequences for the neuron. Via double labeled confocal images, panels A-C show neurons flooding with both dextrans with evidence of concomitant cellular injury, reflected in their irregular, distorted profiles and vacuolization (arrows). In those cells showing the most severe damage, note that the dextrans are also typically found within the nucleus (arrowhead). Note that other double-labeled neurons (D) demonstrate little or no pathological damage and that despite homogenous tracer uptake no nuclear accumulation or vacuolization occurs (arrows). Scale bars: 100 mm. Panel E illustrates three tracer flooded neurons, confirmed by routine fluorescent microscopy and followed via EM. The most severely damaged neuron (asterisk) demonstrates increased electron density, organelle vacuolization (arrows) and perisomatic glial ensheathment (arrowheads). The two other cells (double and triple asterisks) demonstrate little or no pathological change. Note that the surrounding neuropil demonstrates little overt pathologic change consistent with the confocal observations. Scale bar: 5 mm.

Fig. 1. This figure illustrates the phenomenon of mechanically induced neuronal membrane disruption and its consequences for the neuron. Via double labeled confocal images, panels A-C show neurons flooding with both dextrans with evidence of concomitant cellular injury, reflected in their irregular, distorted profiles and vacuolization (arrows). In those cells showing the most severe damage, note that the dextrans are also typically found within the nucleus (arrowhead). Note that other double-labeled neurons (D) demonstrate little or no pathological damage and that despite homogenous tracer uptake no nuclear accumulation or vacuolization occurs (arrows). Scale bars: 100 mm. Panel E illustrates three tracer flooded neurons, confirmed by routine fluorescent microscopy and followed via EM. The most severely damaged neuron (asterisk) demonstrates increased electron density, organelle vacuolization (arrows) and perisomatic glial ensheathment (arrowheads). The two other cells (double and triple asterisks) demonstrate little or no pathological change. Note that the surrounding neuropil demonstrates little overt pathologic change consistent with the confocal observations. Scale bar: 5 mm.

is not correct. Rather, it has been shown in multiple animal studies, as well as limited human investigations, that the forces of injury diffusely alter focal axonal segments. This results in a local impairment of axonal transport, with progressive local axonal swelling followed by detachment over a post-traumatic course ranging from several hours up to a day (Povlishock and Jenkins, 1995). Given

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