Trauma–induced degenerative changes in brain injury: a morphometric analysis of three patients with preinjury and postinjury MR scans

Gale, SD; Johnson, SC; Bigler, E. D.; Blatter, DD

doi:10.1097/00001199-199612000-00014

Cited by 5 publications

(5 citation statements)

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“…41,42 Although the exact mechanisms that cause changes in DTI measures such as FA are not fully understood, it is generally accepted that loss of the microstructural integrity of white matter reduces FA values. 30 Disruption of the parallel organization of fiber tracts, loss of myelination, and increased permeability between internal and external axonal environments are plausible consequences of DAI.…”

Section: Evidence Of Dai In Mild Tbimentioning

confidence: 99%

Extent of Microstructural White Matter Injury in Postconcussive Syndrome Correlates with Impaired Cognitive Reaction Time: A 3T Diffusion Tensor Imaging Study of Mild Traumatic Brain Injury

Niogi¹,

Mukherjee²,

Ghajar³

et al. 2008

AJNR Am J Neuroradiol

532

392

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BACKGROUND AND PURPOSE: Diffusion tensor imaging (DTI) may be a useful index of microstructural changes implicated in diffuse axonal injury (DAI) linked to persistent postconcussive symptoms, especially in mild traumatic brain injury (TBI), for which conventional MR imaging techniques may lack sensitivity. We hypothesized that for mild TBI, DTI measures of DAI would correlate with impairments in reaction time, whereas the number of focal lesions on conventional 3T MR imaging would not.

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Section: Evidence Of Dai In Mild Tbimentioning

confidence: 99%

Extent of Microstructural White Matter Injury in Postconcussive Syndrome Correlates with Impaired Cognitive Reaction Time: A 3T Diffusion Tensor Imaging Study of Mild Traumatic Brain Injury

Niogi¹,

Mukherjee²,

Ghajar³

et al. 2008

AJNR Am J Neuroradiol

532

392

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“…The first phase is coincident with injury and is essentially necrotic (Hicks et al 1996), attributed mainly to the dysfunctional ion homeostasis and excitotoxicity characteristic of trauma (Faden et al 1987;Nilsson et al 1990) and hypoxia-ischemia (Lekieffre et al 1992). The second or delayed phase of cell death develops progressively following experimental (Smith et al 1995) and clinical head injury (Gale et al 1995), and hypoxia-ischemia (MacManus et al 1994;Du et al 1996;Vexler et al 1997). This prolonged phase of cell death can continue for up to a year (Smith et al 1995;Conti et al 1998), causing further tissue degeneration and contributing to post-injury neurobehavioral complications (Gualtieri and Cox 1991).…”

mentioning

confidence: 99%

Palmitic and stearic fatty acids induce caspase‐dependent and ‐independent cell death in nerve growth factor differentiated PC12 cells

Ulloth

Casiano

León

2003

Journal of Neurochemistry

119

117

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Apoptotic cell death has been proposed to play a role in the neuronal loss observed following traumatic injury in the CNS and PNS. The present study uses an in vitro tissue culture model to investigate whether free fatty acids (FFAs), at concentrations comparable to those found following traumatic brain injury, trigger cell death. Nerve growth factor (NGF)-differentiated PC12 cells exposed to oleic and arachidonic acids (2 : 1 ratio FFA/BSA) showed normal cell survival. However, when cells were exposed to stearic and palmitic acids, there was a dramatic loss of cell viability after 24 h of treatment. The cell death induced by stearic acid and palmitic acid was apoptotic as assessed by morphological analysis, and activation of caspase-8 and caspase-3-like activities.Western blotting showed that differentiated PC12 cells exposed to stearic and palmitic acids exhibited the signature apoptotic cleavage fragment of poly (ADP-ribose) polymerase (PARP). Interestingly, blockade of caspase activities with the pan-caspase inhibitor z-VAD-fmk failed to prevent the cell death observed induced by palmitic or stearic acid. RT-PCR and RNA blot experiments showed an up-regulation of the Fas receptor and ligand mRNA. These findings are consistent with our hypothesis that FFAs may play a role in the cell death associated with trauma in the CNS and PNS.

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“…It enables the identification of non-hemorrhagic as well as hemorrhagic lesions, and its superior Conventional MRI, however, tends to underestimate the true extent of DAI. This is supported by studies in which patients showed progressive, global cerebral atrophy on follow-up after initial imaging which did not show any pathology or showed discrete findings only (2,5). Microscopically, shear injury tends to occur at the cellular level, and this is the reason this type of diffuse damage cannot be detected through currently available imaging techniques.…”

Section: Discussionmentioning

confidence: 81%

Role of diffusion-weighted magnetic resonance imaging in diffuse axonal injury

et al. 2006

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Trauma–induced degenerative changes in brain injury: a morphometric analysis of three patients with preinjury and postinjury MR scans

Cited by 5 publications

References 0 publications

Extent of Microstructural White Matter Injury in Postconcussive Syndrome Correlates with Impaired Cognitive Reaction Time: A 3T Diffusion Tensor Imaging Study of Mild Traumatic Brain Injury

Extent of Microstructural White Matter Injury in Postconcussive Syndrome Correlates with Impaired Cognitive Reaction Time: A 3T Diffusion Tensor Imaging Study of Mild Traumatic Brain Injury

Palmitic and stearic fatty acids induce caspase‐dependent and ‐independent cell death in nerve growth factor differentiated PC12 cells

Role of diffusion-weighted magnetic resonance imaging in diffuse axonal injury

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