Summary
Sixteen rats were killed by transcardial perfusion fixation 1 min after a non-contusing concussive head injury, and seven rats 1 day later. In each of the “1-min” animals Golgi-like neurons and long axonal segments scattered in various proportions among unstained neurons and axons were demonstrated by a new silver method both near to and far from the impact site in a parenchymal environment unaffected by contusion. The silver-stained neurons, dendrites and axons were considered to have been damaged by the trauma because they were consistently absent from control brains. In the “1-day” brains silver-stained dendrites and axons had a beaded appearence, indicating an advanced stage of morphopathological damage. From details of these findings the following conclusions were drawn: (1) trauma can directly induce some kind of morphopathological damage in neurons which manifests itself in shrinkage of the soma and tortuosity of appendages as well as in type III argyrophilia; (2) different vulnerability of various brain areas is likely due to the inhomogeneity of the trauma-induced pressure wave propagating through the brain; and (3) the somato-dendritic and axonal domains of the neuron are selectively vulnerable to different values of the parameters of the intracranial pressure wave.
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References
Adams JH, Graham DI, Gennarelli TA (1985) Contemporary neuropathological considerations regarding brain damage in head injury. In: Becker D, Povlishock JT (eds) Central nervous system trauma status report. Byrd Press, Richmond, pp 65–77
Cammermeyer J (1961) The importance of avoiding “dark” neurons in experimental neuropathology. Acta Neuropathol (Berl) 1:245–270
Gallyas F (1982) Physico-chemical mechanism of the argyrophil III reaction. Histochemistry 74:409–421
Gallyas F (1982) Equation of the mass-time relationship of the argyrophil I and argyrophil III reactions. Histochemistry 74:423–433
Gallyas F, Güldner FH, Zoltay G, Wolff JR (1990) Golgi-like demonstration of “dark” neurons with an argyrophil III method for experimental neuropathology. Acta Neuropathol 79:620–628
Gallyas F, Zoltay G, Balás I (1992) An immediate light microscopic response of neuronal somata, dendrites and axons to contusing concussive head injury in the rat. Acta Neuropathol 83:394–401
Gallyas F, Zoltay G, Horváth Z (1992) Light microseopic response of neuronal somata, dendrites and axons to postmortem concussive head injury. Acta Neuropathol 83: (in press)
Gallyas F, Zoltay G, Dames W (1992) Formation of “dark” (argyrophilic) neurons of various origin proceeds with a common mechanism of biophysical nature (a novel hypothesis). Acta Neuropathol 83: (in press)
Gennarelli TA, Thibault LE (1985) Biological models of head injury. In: Becker D, Povlishock JT (eds) Central nervous system trauma status report. Byrd Press, Richmond, pp 391–404
Horobin RW (1982) Histochemistry. An explanatory outline of histochemistry and biophysical staining. Gustav Fischer Verlag, Stuttgart New York, pp 56–110
Jenkins LW, Povlishock JT, Lewelt W, Miller JP, Becker DP (1981) The role of postischemic recirculation in the development of ischemic neuronal injury following complete cerebral ischemia. Acta Neuropathol (Berl) 55:205–220
Povlishock JT (1985) The morphopathologic response to experimental head injuries of varying severity. In: Becker D, Povlishock JT (eds) Central nervous system trauma status report. Byrd Press, Richmond, pp 443–452
Thibault LE, Gennarelli TA (1985) Biomechanics and craniocerebral trauma. In: Becker D, Povlishock JT (eds) Central nervous system trauma status report. Byrd Press, Richmond, pp 379–389
van den Pol AN, Gallyas F (1990) Trauma induced Golgi-like staining of neurons a new approach to neuronal organization and response to injury. J Comp Neurol 296:654–673
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Gallyas, F., Zoltay, G. An immediate light microscopic response of neuronal somata, dendrites and axons to non-contusing concussive head injury in the rat. Acta Neuropathol 83, 386–393 (1992). https://doi.org/10.1007/BF00713530
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DOI: https://doi.org/10.1007/BF00713530