Early ultrastructural changes of diffuse axonal injury in patients with severe head injury
Qifu Tan
Abstract
Qifu Tan
Abstract
Objective To obtain more knowlege about the pathogenesis of diffuse axonal injury(DAI) via observing the ultrastructural axonal changes in the patients with DAI after traumatic brain injury. Methods 14 bioptic samples of the cerebral white matter in 12 patients with DAI were examined with transmission electratic microscope. Results We found that traumatically induced axonal pathological changes in humans may be summarized as follows: (1) cytoskeletal abnormalities; (2) disruption and infolding of the axolemma; (3) swelling and focal accumulation of mitochondria and endoplasmic reticula; (4) infolding and blebbing of myelin sheath and separation of myelin lamellae; (5) axonal swellings and disconnection giving rise to proximal axonal bulbs. Conclusion Possibly, there are differing patterns of mechanism involved in the pathogenesis of traumatically induced axonal injury. It is suggested that fragmentation of small calibre axons can occur immediately after the time of injury and then progressive axonal swelling and delayed axotomy takes place in the other injured axons, in which focal cytoskeletal perturbation and axolemmal disruption followed by permeabilization possibly are the most important factors resulting in impairment of axoplasmic transport and secondarily axonal disconnection.
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Objective To obtain more knowlege about the pathogenesis of diffuse axonal injury(DAI) via observing the ultrastructural axonal changes in the patients with DAI after traumatic brain injury. Methods 14 bioptic samples of the cerebral white matter in 12 patients with DAI were examined with transmission electratic microscope. Results We found that traumatically induced axonal pathological changes in humans may be summarized as follows: (1) cytoskeletal abnormalities; (2) disruption and infolding of the axolemma; (3) swelling and focal accumulation of mitochondria and endoplasmic reticula; (4) infolding and blebbing of myelin sheath and separation of myelin lamellae; (5) axonal swellings and disconnection giving rise to proximal axonal bulbs. Conclusion Possibly, there are differing patterns of mechanism involved in the pathogenesis of traumatically induced axonal injury. It is suggested that fragmentation of small calibre axons can occur immediately after the time of injury and then progressive axonal swelling and delayed axotomy takes place in the other injured axons, in which focal cytoskeletal perturbation and axolemmal disruption followed by permeabilization possibly are the most important factors resulting in impairment of axoplasmic transport and secondarily axonal disconnection.
Key concepts: Diffuse axonal injury, Axolemma, Axoplasm, Axon, Myelin, Axoplasmic transport, White matter, Ultrastructure