Does loss of gray- and white-matter contrast in injured spinal cord signify secondary injury? In vivo longitudinal MRI studies

Narayana, Ponnada A.; Abbe, Russell; Liu, Shi Jie; Johnston, Dennis A.

doi:10.1002/(sici)1522-2594(199902)41:2<315::aid-mrm15>3.0.co;2-b

Cited by 27 publications

(19 citation statements)

References 20 publications

(16 reference statements)

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“…1A) was essentially lost within the epicenter ( Fig. 1C and D), as reported previously (Bilgen et al, 2001;Narayana et al, 1999). This limitation of standard T2W sequences is currently an obstacle to the interpretation of clinical MR images after human SCI.…”

Section: Resultsmentioning

confidence: 99%

Diffusion Tensor Imaging at 3 Hours after Traumatic Spinal Cord Injury Predicts Long-Term Locomotor Recovery

Kim

Loy

Wang

et al. 2010

Journal of Neurotrauma

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Accurate diagnosis of spinal cord injury (SCI) severity must be achieved before highly aggressive experimental therapies can be tested responsibly in the early phases after trauma. These studies demonstrate for the first time that axial diffusivity (ljj), derived from diffusion tensor imaging (DTI) within 3 h after SCI, accurately predicts long-term locomotor behavioral recovery in mice. Female C57BL=6 mice underwent sham laminectomy or graded contusive spinal cord injuries at the T9 vertebral level (5 groups, n ¼ 8 for each group). In-vivo DTI examinations were performed immediately after SCI. Longitudinal measurements of hindlimb locomotor recovery were obtained using the Basso mouse scale (BMS). Injured and spared regions of ventrolateral white matter (VLWM) were reliably separated in the hyperacute phase by threshold segmentation. Measurements of ljj were compared with histology in the hyperacute phase and 14 days after injury. The spared normal VLWM determined by hyperacute ljj and 14-day histology correlated well (r ¼ 0.95). A strong correlation between hindlimb locomotor function recovery and ljj-determined spared normal VLWM was also observed. The odds of significant locomotor recovery increased by 18% with each 1% increase in normal VLWM measured in the hyperacute phase (odds ratio ¼ 1.18, p ¼ 0.037). The capability of measuring subclinical changes in spinal cord physiology and murine genetic advantages offer an early window into the basic mechanisms of SCI that was not previously possible. Although significant obstacles must still be overcome to derive similar data in human patients, the path to clinical translation is foreseeable and achievable.

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Section: Resultsmentioning

confidence: 99%

Diffusion Tensor Imaging at 3 Hours after Traumatic Spinal Cord Injury Predicts Long-Term Locomotor Recovery

Kim

Loy

Wang

et al. 2010

Journal of Neurotrauma

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“…At the epicenter, however, the contrast between GM and WM was diminished and the structural features of the cord were difficult to visualize. The loss of contrast was mainly due to the accumulation of edema in WM (21). Following Gd administration, a strong and rapid increase in the intensities of pixels at the epicenter was observed, starting with the first postcontrast images (second row in Fig.…”

Section: Injured Animalsmentioning

confidence: 94%

“…Specifically, we characterized the spatial and temporal course of dynamic enhancements in the hyperacute, acute, and chronic phases of experimental SCI on days 0, 2,4,7,10,14,17,21, 28, 35, and 42 from axial images. The signal enhancement was estimated from a decision mechanism based on statistical detection theory and combined with extensive image analysis to estimate the area and volume of enhanced regions in the cord.…”

mentioning

confidence: 99%

Dynamic contrast‐enhanced MRI of experimental spinal cord injury: In vivo serial studies

Bilgen¹,

Abbe²,

Narayana³

2001

Magnetic Resonance in Med

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The progression of experimental spinal cord injury (SCI) was followed with in vivo dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) and neurobehavioral studies on postinjury days 0, 2, 4, 7, 10, 14, 17, 21, 28, 35, and 42. Gadopentate dimeglumine (Gd) was administered IV and postcontrast, T 1 -weighted, axial images were acquired repetitively for up to 60 min. Images were analyzed to determine the spatial and temporal evolution of the intensity enhancement. A statistical decision mechanism was developed to objectively detect the enhancement. Strong and rapid enhancement was observed at the epicenter of injury, indicating a significant compromise in blood spinal cord barrier. The enhanced regions in each slice were combined to estimate the area and volume of the lesion. On the day of injury, around 85% of the total cord area at the epicenter showed enhancement within the first 15 min of Gd administration. At the same time, the enhanced volumes attained nearly 40% of the total cord volume and extended axially over 8 mm along the cord. The blood-spinal cord barrier (BSCB) maintains a highly regulated homeostatic environment in the spinal cord (SC) tissue. This regulatory function is sustained by various structures, including the capillary endothelial tight junctions. Under normal physiological conditions, BSCB protects the cord tissue by exhibiting selective permeability to the constituents of intravascular fluid (1,2). A traumatic insult to SC disrupts the structural and biochemical integrity of BSCB. The altered tight junctional patency allows vesicular transport of toxic substances from blood plasma to interstitial spaces. This makes the SC tissue environment unfavorable for neuronal survival, and inhibits tissue repair processes and neurologic recovery. By following the changes in BSCB after injury, important information may be gained about the regions of initial SC tissue damage and a time window for effective drug delivery across the barrier. Assessing BSCB in the late phases of the injury may help evaluate the progression of spinal cord injury (SCI) as well as the efficacy of potential therapeutic interventions.Changes in BSCB permeability can be followed experimentally using intravascularly administered tracers (such as plasma proteins, radiolabeled proteins, and small-molecular-weight molecules) that can cross the compromised barrier (3,4). Although these tracer-based techniques provide valuable information about the status of BSCB, they are either fully invasive, necessitating histological analysis of tissue, or less invasive but still requiring intravenous injection of radio-tracers with subsequent blood sampling along with imaging, as in the case of autoradiography. Moreover, active transport mechanisms involved in some of these tracers may introduce a bias in quantifying the BSCB permeability (4).As an alternative to the above techniques, dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI), with the exogenous paramagnetic contrast agent gadopentetate-dimeglumine (Gd, for short)...

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“…While there is a trend of increased NE area BSCB permeability in VEGF-treated animals compared to saline controls, a significant treatment difference in K ps , across all spatial regions, was only detected in the subacute time period. The lack of a significant difference in K ps between both cohorts during the other two time periods may be due to (1) increased edema in NE areas observed on MRI (Narayana et al, 1999) and increased hemorrhage (Bilgen et al, 2000) in the acute phase, and (2) endogenous semirestoration of the BSCB in the chronic phase (Cohen et al, 2009). Our spatio-temporal analysis also indicates significant treatment differences in the NE areas only in the epicenter region during the subacute (days 7-14 post-SCI) and chronic (days 28-56 post-SCI) periods.…”

Section: Effects Of Vegf On Bscb Permeabilitymentioning

confidence: 99%

Effect of VEGF Treatment on the Blood-Spinal Cord Barrier Permeability in Experimental Spinal Cord Injury: Dynamic Contrast-Enhanced Magnetic Resonance Imaging

Cohen¹,

Ahobila-Vajjula²,

Sundberg³

et al. 2009

Journal of Neurotrauma

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Compromised blood-spinal cord barrier (BSCB) is a factor in the outcome following traumatic spinal cord injury (SCI). Vascular endothelial growth factor (VEGF) is a potent stimulator of angiogenesis and vascular permeability. The role of VEGF in SCI is controversial. Relatively little is known about the spatial and temporal changes in the BSCB permeability following administration of VEGF in experimental SCI. Dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) studies were performed to noninvasively follow spatial and temporal changes in the BSCB permeability following acute administration of VEGF in experimental SCI over a post-injury period of 56 days. The DCE-MRI data was analyzed using a two-compartment pharmacokinetic model. Animals were assessed for open field locomotion using the Basso-Beattie-Bresnahan score. These studies demonstrate that the BSCB permeability was greater at all time points in the VEGF-treated animals compared to saline controls, most significantly in the epicenter region of injury. Although a significant temporal reduction in the BSCB permeability was observed in the VEGF-treated animals, BSCB permeability remained elevated even during the chronic phase. VEGF treatment resulted in earlier improvement in locomotor ability during the chronic phase of SCI. This study suggests a beneficial role of acutely administered VEGF in hastening neurobehavioral recovery after SCI.

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Does loss of gray- and white-matter contrast in injured spinal cord signify secondary injury? In vivo longitudinal MRI studies

Cited by 27 publications

References 20 publications

Diffusion Tensor Imaging at 3 Hours after Traumatic Spinal Cord Injury Predicts Long-Term Locomotor Recovery

Diffusion Tensor Imaging at 3 Hours after Traumatic Spinal Cord Injury Predicts Long-Term Locomotor Recovery

Dynamic contrast‐enhanced MRI of experimental spinal cord injury: In vivo serial studies

Effect of VEGF Treatment on the Blood-Spinal Cord Barrier Permeability in Experimental Spinal Cord Injury: Dynamic Contrast-Enhanced Magnetic Resonance Imaging

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