Pathophysiological Mechanisms Leading to the Development of Late Radiation-Induced Damage to the Central Nervous System

Hopewell, J. W.; Kogel, Albert J. van der

doi:10.1159/000061239

Cited by 87 publications

(45 citation statements)

References 18 publications

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“…Glial hypothesis and vascular hypothesis are considered two possible mechanisms of radiation-induced WM damage (20). Glial hypothesis suggests that progressive demyelination and necrosis in WM is related to a gradual loss of oligodendrocytes or their precursors postradiation (20).…”

Section: Discussionmentioning

confidence: 99%

Longitudinal Diffusion Tensor Magnetic Resonance Imaging Study of Radiation-Induced White Matter Damage in a Rat Model

et al. 2009

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Radiation-induced white matter (WM) damage is a major side effect of whole brain irradiation among childhood cancer survivors. We evaluate longitudinally the diffusion characteristics of the late radiation-induced WM damage in a rat model after 25 and 30 Gy irradiation to the hemibrain at 8 time points from 2 to 48 weeks postradiation. We hypothesize that diffusion tensor magnetic resonance imaging (DTI) indices including fractional anisotropy (FA), trace, axial diffusivity (L // ), and radial diffusivity (L ? ) can accurately detect and monitor the histopathologic changes of radiation-induced WM damage, measured at the EC, and that these changes are dose and time dependent. Results showed a progressive reduction of FA, which was driven by reduction in L // from 4 to 40 weeks postradiation, and an increase in L ? with return to baseline in L // at 48 weeks postradiation. Histologic evaluation of irradiated WM showed reactive astrogliosis from 4 weeks postradiation with reversal at 36 weeks, and demyelination, axonal degeneration, and necrosis at 48 weeks postradiation. Moreover, changes in L // correlated with reactive astrogliosis (P < 0.01) and L ? correlated with demyelination (P < 0.01). Higher radiation dose (30 Gy) induced earlier and more severe histologic changes than lower radiation dose (25 Gy), and these differences were reflected by the magnitude of changes in L // and L ? . DTI indices reflected the histopathologic changes of WM damage and our results support the use of DTI as a biomarker to noninvasively monitor radiation-induced WM damage.

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Section: Discussionmentioning

confidence: 99%

Longitudinal Diffusion Tensor Magnetic Resonance Imaging Study of Radiation-Induced White Matter Damage in a Rat Model

et al. 2009

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“…13 It is likely that both damage to vascular endothelium and the neuroglial cell progenitors are involved in the pathogenesis, although the primary site of cellular damage is a subject of some controversy. [14][15][16] Endothelial cells have been shown to exhibit a time-dependent and dosedependent pathologic response following irradiation to rat CNS with subsequent disruption of the blood-brain barrier. 17 The depletion of vascular endothelial cells after radiation has also been documented in the human optic nerve.…”

Section: Pathogenesismentioning

confidence: 99%

Radiation-induced optic neuropathy

Danesh‐Meyer¹

2008

Journal of Clinical Neuroscience

190

108

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“…It caused necrosis in the cortex and subcortical area in the brain 46 . This because white matter tissue is more affected than gray matter tissue 47 .…”

Section: Electrophoretic Peroxidase Patternmentioning

confidence: 99%

Ameliorative Effect of Salicin Against Gamma Irradiation Induced Electrophoretic Changes in Brain Tissue in Male Rats

Abdalla¹,

Sharada²,

Abulyazid³

et al. 2015

PBJ

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Pathophysiological Mechanisms Leading to the Development of Late Radiation-Induced Damage to the Central Nervous System

Cited by 87 publications

References 18 publications

Longitudinal Diffusion Tensor Magnetic Resonance Imaging Study of Radiation-Induced White Matter Damage in a Rat Model

Longitudinal Diffusion Tensor Magnetic Resonance Imaging Study of Radiation-Induced White Matter Damage in a Rat Model

Radiation-induced optic neuropathy

Ameliorative Effect of Salicin Against Gamma Irradiation Induced Electrophoretic Changes in Brain Tissue in Male Rats

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