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Related Experiment Videos

Experimental concussion. Ultrastructural and biochemical correlates.

W J Brown, N Yoshida, T Canty

    The American Journal of Pathology
    |April 1, 1972
    PubMed
    Summary

    Transient coma induced by head trauma causes significant brainstem glycogen accumulation in neurons and astrocytes. This polysaccharide buildup occurs 5-7 days post-concussion, indicating altered brain metabolism after injury.

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    Area of Science:

    • Neuroscience
    • Biochemistry
    • Pathology

    Background:

    • Traumatic brain injury (TBI) can cause complex neurological and biochemical changes.
    • The brainstem reticular formation is crucial for consciousness and arousal.
    • Understanding cellular changes post-TBI is vital for developing effective treatments.

    Purpose of the Study:

    • To investigate ultrastructural and biochemical alterations in the brainstem reticular formation following induced transient coma.
    • To identify changes in neuronal and glial cells after controlled head trauma.
    • To elucidate the role of glycogen accumulation in the acute phase of post-concussive injury.

    Main Methods:

    • Induction of transient coma via controlled head blows in animal models.
    • Histochemistry and light microscopy to assess neuronal changes (chromatolysis).

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  • Electron microscopy and microchemical analysis to quantify polysaccharide and glycogen levels in brain tissue.

    • Main Results:

    • Chromatolysis observed in 10-15% of nucleus gigantocellularis neurons.
    • Significant accumulation of PAS-positive, diastase-sensitive material (polysaccharides) in neuropil, dendrites, axons, and astrocytes.
    • Peak brainstem glycogen concentrations observed 5-7 days post-concussion, with no significant change in phosphorylase activity.

    Conclusions:

    • Transient coma induced by head trauma leads to significant neuronal and glial glycogen accumulation in the brainstem.
    • The observed polysaccharide buildup suggests altered energy metabolism and cellular stress following concussion.
    • Further research is needed to explore the mechanisms linking glycogen accumulation to electrolyte balance and Krebs cycle alterations in TBI.