Magnetic Resonance Imaging of Diffuse Axonal Injury: Quantitative Assessment of White Matter Lesion Volume

Plata, Carlos Marquez de la; Ardelean, Andreea; Koovakkattu, Della; Srinivasan, Priya; Miller, Anna N.; Phuong, Viet; Harper, Caryn R.; Moore, Carol; Whittemore, Anthony R; Madden, Christopher J.; Diaz‐Arrastia, Ramon; Devous, Michael D.

doi:10.1089/neu.2006.0214

Cited by 75 publications

(22 citation statements)

References 31 publications

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“…There is increasing clinicopathological MRI evidence for continued loss of central white matter in patients who survive to the post-acute and chronic phases of TBI (Bendlin et al, 2008;De La Plata et al, 2007;Kennedy et al, 2009;Kim et al, 2008;Kraus et al, 2007;Sidaros et al, 2009;Sugiyama et al, 2008;Tomaiuolo et al, 2005). A small number of experimental studies have documented neuronal and axonal loss in TBI (Bramlett and Dietrich, 2002;Rodrigues-Baez et al, 2005;Smith et al, 1997) out to about a year after injury.…”

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confidence: 99%

Stereology and Ultrastructure of Chronic Phase Axonal and Cell Soma Pathology in Stretch-Injured Central Nerve Fibers

Sulaiman

Denman

Buchanan

et al. 2011

Journal of Neurotrauma

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Magnetic resonance imaging (MRI) suggests that with survival after human traumatic brain injury (TBI), there is ongoing loss of white and grey matter from the injured brain during the chronic phase. However; direct quantitative experimental evidence in support of this observation is lacking. Using the guinea pig stretch-injury optic nerve model, quantitative evidence by stereology of damage to the optic nerve and retina was sought. Stretch injury was applied to the right optic nerve of 15 adult male guinea pigs. Three animals each at 1, 2, 3, 8, or 12 weeks' survival were killed and prepared for transmission electron microscopy (TEM). The estimated number of intact and injured axons within bins of transverse diameters 0-0.5, 0.51-1.0, 1.01-1.5, 1.51-2.0, 2.01-2.5, and 2.51-3.0 μm in the middle segment of each injured optic nerve and from 5 control animals were compared across all survival time points. The estimated numbers of intact and pyknotic retinal ganglion cells from the same animals were also compared. Loss of myelinated fibers continued throughout the experimental period. The most rapid loss was of the largest fibers; loss of intermediate-sized fibers continued, but the numbers of the smallest fibers increased from 3 weeks onward. There was hypertrophy and proliferation of glial cells within the surrounding neuropil. A relatively low-grade loss of retinal ganglion cells occurred throughout the experiment, with about 60% remaining at 12 weeks' survival. We provide quantitative evidence that after traumatic axonal injury (TAI) there is a continuing loss of nerve fibers and their cell bodies from a CNS tract over a 3-month post-traumatic interval.

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confidence: 99%

Stereology and Ultrastructure of Chronic Phase Axonal and Cell Soma Pathology in Stretch-Injured Central Nerve Fibers

Sulaiman

Denman

Buchanan

et al. 2011

Journal of Neurotrauma

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“…The literature reports worse outcomes – frequency of disability (40.0–87.5%) and dependency (20.0–41.3%) – for patients with DAI, evaluated by GOS or GOS-E at 6 months after injury (26–30). However, most participants in our study had mild (44.9%) or moderate (19.2%) DAI, and among these, only one (2.2%) was dependent during the period of the study (Table 5).…”

Section: Discussionmentioning

confidence: 99%

Diffuse Axonal Injury: Epidemiology, Outcome and Associated Risk Factors

et al. 2016

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Diffuse axonal injury (DAI), a type of traumatic injury, is known for its severe consequences. However, there are few studies describing the outcomes of DAI and the risk factors associated with it. This study aimed to describe the outcome for patients with a primary diagnosis of DAI 6 months after trauma and to identify sociodemographic and clinical factors associated with mortality and dependence at this time point. Seventy-eight patients with DAI were recruited from July 2013 to February 2014 in a prospective cohort study. Patient outcome was analyzed using the Extended Glasgow Outcome Scale (GOS-E) within 6 months of the traumatic injury. The mean Injury Severity Score was 35.0 (SD = 11.9), and the mean New Injury Severity Score (NISS) was 46.2 (SD = 15.9). Mild DAI was observed in 44.9% of the patients and severe DAI in 35.9%. Six months after trauma, 30.8% of the patients had died, and 45.1% had shown full recovery according to the GOS-E. In the logistic regression model, the severity variables – DAI with hypoxia, as measured by peripheral oxygen saturation, and hypotension with NISS value – had a statistically significant association with patient mortality; on the other hand, severity of DAI and length of hospital stay were the only significant predictors for dependence. Therefore, severity of DAI emerged as a risk factor for both mortality and dependence.

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“…Leukoaraiosis regions were identified from FLAIR images (Fig. 1e) using a semiautomatic method described previously (37). Briefly, the FLAIR images were skull-stripped and the voxels with signal intensity greater than 2 standard deviations above average were delineated as possible lesions.…”

Section: Methodsmentioning

confidence: 99%

In vivo vascular hallmarks of diffuse leukoaraiosis

Yezhuvath

Cheng

et al. 2010

Magnetic Resonance Imaging

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Purpose To characterize multiple patterns of vascular changes in leukoaraiosis using in vivo magnetic resonance imaging (MRI) techniques. Materials and Methods We measured cerebral blood flow (CBF), cerebrovascular reactivity (CVR), and blood–brain-barrier (BBB) leakage in a group of 33 elderly subjects (age: 72.3 ± 6.8 years, 17 males, 16 females). Leukoaraiosis brain regions were identified in each subject using fluid-attenuated inversion-recovery (FLAIR) MRI. Vascular parameters in the leukoaraiosis regions were compared to those in the normal-appearing white matter (NAWM) regions. Vascular changes in leukoaraiosis were also compared to structural damage as assessed by diffusion tensor imaging. Results CBF and CVR in leukoaraiosis regions were found to be 39.7 ± 5.2% (P < 0.001) and 52.5 ± 11.6% (P = 0.005), respectively, of those in NAWM. In subjects who did not have significant leukoaraiosis, CBF and CVR in regions with high risk for leukoaraiosis showed a slight reduction compared to the other white matter regions. Significant BBB leakage was also detected (P = 0.003) in leukoaraiosis and the extent of BBB leakage was positively correlated with mean diffusivity. In addition, CVR in NAWM was lower than that in white matter of subjects without significant leukoaraiosis. Conclusion Leukoaraiosis was characterized by reduced CBF, CVR, and a leakage in the BBB.

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Magnetic Resonance Imaging of Diffuse Axonal Injury: Quantitative Assessment of White Matter Lesion Volume

Cited by 75 publications

References 31 publications

Stereology and Ultrastructure of Chronic Phase Axonal and Cell Soma Pathology in Stretch-Injured Central Nerve Fibers

Stereology and Ultrastructure of Chronic Phase Axonal and Cell Soma Pathology in Stretch-Injured Central Nerve Fibers

Diffuse Axonal Injury: Epidemiology, Outcome and Associated Risk Factors

In vivo vascular hallmarks of diffuse leukoaraiosis

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