Traumatic Damage to the Nodal Axolemma: an Early, Secondary Injury

Gennarelli, Thomas A.; Tipperman, R.; Maxwell, William L.; Graham, David I.; Adams, J. Hume; Irvine, A

doi:10.1007/978-3-7091-9266-5_7

Cited by 7 publications

(6 citation statements)

References 10 publications

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“…However, repetitive mTBI at 3 days apart significantly enhanced the tissue bleeding at 24 hours post 2 nd mTBI compared to that of first mjTBI (P = 0.034). Consistent with the findings from (Giza and Hovda, 2001), which can enhance brain vulnerability to a secondary insult (Jenkins et al, 1989;Hovda et al, 1991;Gennarelli et al, 1993). Second-impact syndrome has been associated with athletes who suffer repeated concussions when playing contact sports.…”

Section: Resultssupporting

confidence: 82%

Neuroprotective effect of hyperbaric oxygen therapy in a juvenile rat model of repetitive mild traumatic brain injury

et al. 2016

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Repetitive mild traumatic brain injury (rmTBI) is an important medical concern for adolescent athletes that can lead to long-term disabilities. Multiple mild injuries may exacerbate tissue damage resulting in cumulative brain injury and poor functional recovery. In the present study, we investigated the increased brain vulnerability to rmTBI and the effect of hyperbaric oxygen treatment using a juvenile rat model of rmTBI. Two episodes of mild cortical controlled impact (3 days apart) were induced in juvenile rats. Hyperbaric oxygen (HBO) was applied 1 hour/day × 3 days at 2 atmosphere absolute consecutively, starting at 1 day after initial mild traumatic brain injury (mTBI). Neuropathology was assessed by multi-modal magnetic resonance imaging (MRI) and tissue immunohistochemistry. After repetitive mTBI, there were increases in T2-weighted imaging-defined cortical lesions and susceptibility weighted imaging-defined cortical microhemorrhages, correlated with brain tissue gliosis at the site of impact. HBO treatment significantly decreased the MRI-identified abnormalities and tissue histopathology. Our findings suggest that HBO treatment improves the cumulative tissue damage in juvenile brain following rmTBI. Such therapy regimens could be considered in adolescent athletes at the risk of repeated concussions exposures.

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Section: Resultssupporting

confidence: 82%

Neuroprotective effect of hyperbaric oxygen therapy in a juvenile rat model of repetitive mild traumatic brain injury

et al. 2016

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“…However, in addition to the significant cytoskeletal contact at axo-glial paranodal junctions, elevated adhesion occurs between apposing extraceullar membranes of an oligodendroglial myelinating process that is wrapped concentrically around an axon, forming a so-called glycosynapse, and perhaps causing adhesion between separate oligodendrocytes to additionally 'glue' the oligodendrocytes together. Both the myelin-myelin interactions and, especially, the paranodal axo-glial adhesions would place the Nodes of Ranvier at risk for deformation from a stress concentration, and elongation of the Nodes of Ranvier has been observed following non-disruptive stretch injury of the guinea pig optic nerve (Gennarelli et al 1993). …”

Section: Discussionmentioning

confidence: 97%

Probing the influence of myelin and glia on the tensile properties of the spinal cord

Shreiber

Hao

Elias

2008

Biomech Model Mechanobiol

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Although glia have been historically classified as the structurally supporting cells of the central nervous system, their role in tissue mechanics is still largely unstudied. The influence of myelin and glia on the mechanical properties of spinal cord tissue was examined by testing embryonic day 18 chick embryo spinal cords in uniaxial tension following disruption of the glial matrix using either ethidium bromide (EB) or an antibody against galactocerebroside (alphaGalC) in the presence of complement. Demyelination was confirmed by myelin basic protein immunoreactivity and quantified using osmium tetroxide staining. A substantial loss of astrocytes and oligodendrocytes concurrent with demyelination was observed following EB injection but not alphaGalC injection. No morphological changes were observed following injection of saline or IgG with complement as controls for EB and alphaGalC. Demyelinated spinal cords demonstrated significantly lower stiffness and ultimate tensile stress than myelinated spinal cords. No significant differences were observed in the tensile response between the two demyelinating protocols. The results demonstrate that the glial matrix provides significant mechanical support to the spinal cord, and suggests that myelin and cellular coupling of axons via the glial matrix in large part dictates the tensile response of the tissue.

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“…Although any region of the axon may be affected, the axon at the nodes of Ranvier exhibits the earliest features of ultrastructural disorganization and appears to be the area of the axon most vulnerable to mechanical injury.59 In addition, axons appear to be vulnerable where they make abrupt turns-at decussations, for example, or near blood vessels.54 That these axonal changes occur without disruption of adjacent vessels, glial processes, dendrites or neuronal cell bodies indicates unique vulnerability of the axon to the injurious forces encroaching on the brain. 13,14,54,57,58 Damaged axons may reside immediately adjacent to intact axons.…”

Section: Diffuse Axonal Injurymentioning

confidence: 99%

Pathologic Changes in Mild Head Injury

1994

Semin Neurol

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Physical injury of the brain constitutes a major cause of loss of life and productivity. Populations at highest risk for such injuries include children, men in late adolescence and early adult life, and the elderly. Head injuries most commonly result from assaults, vehicular accidents, and falls. T h e neuropathology of severe injury has been described extensively and constitutes much of the lore of clinical neurosurgery, forensic neuropathology, and critical care neurology.' T h e neuropathology of mild head injury is much less well explored, reflecting the low mortality of these injuries. Experimental head injury models originally developed to facilitate research in severe trauma have proven valuable in understanding the neurobiologic basis of the numerous and debilitating symptoms that follow mild head injury and have focused attention on diffuse axonal injury (DAI) as the primary neuropathologic mechanism underlying these sympt o m~.~ This review sequentially covers experimental models of head injury, neuropathology of human head trauma, with a detailed discussion of DAI, and ends with a discussion of the regenerative response to head injury and possible role of neuroplasticity in the genesis of posttraumatic symptomatology.

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Traumatic Damage to the Nodal Axolemma: an Early, Secondary Injury

Cited by 7 publications

References 10 publications

Neuroprotective effect of hyperbaric oxygen therapy in a juvenile rat model of repetitive mild traumatic brain injury

Neuroprotective effect of hyperbaric oxygen therapy in a juvenile rat model of repetitive mild traumatic brain injury

Probing the influence of myelin and glia on the tensile properties of the spinal cord

Pathologic Changes in Mild Head Injury

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