Abstract:Hypoxia and edema are frequent and serious complications of traumatic brain injury (TBI). Therefore, we examined the effects of hypoxia on edema formation after moderate lateral fluid percussion (LFP) injury using NMR diffusion-weighted imaging (DWI). Adult Sprague-Dawley rats were separated into four groups: sham uninjured (S), hypoxia alone (H), trauma alone (T), and trauma and hypoxia (TH). Animals in Groups T and TH received LFP brain injury, with Groups H and TH undergoing 30 min of moderately severe hypo… Show more
“…At early stages, DWI is more sensitive than T2, but at subacute stages, T2 becomes more sensitive than DWI as the diffusion-weighted images undergo pseudonormalization (Schlaug et al, 1997;Copen et al, 2001;Schaefer et al, 2005). Similar changes in DWI signal characteristics over time after TBI have been observed in rats (Alsop et al, 1996;Albensi et al, 2000;Van Putten et al, 2005), pigs (Duhaime et al, 2003), and humans (Pasco et al, 2006). However, these studies did not use DTI and did not focus on white matter injury.…”
Section: Discussionmentioning
confidence: 96%
“…These studies were performed at only a single time point, 24 h after injury. It is unknown whether there are changes in the sensitivity of DTI over time, because only very limited clinical studies (Arfanakis et al, 2002;Naganawa et al, 2004;Voss et al, 2006) and none of the previous experimental animal studies (Hanstock et al, 1994;Kochanek et al, 1995;Alsop et al, 1996;Assaf et al, 1997;Albensi et al, 2000;Duhaime et al, 2003;Van Putten et al, 2005), to our knowledge, have performed DTI at multiple time points. For optimal clinical utility, a method should be robust across a variety of time points, given that it is rarely possible to scan patients at a fixed time point after injury.…”
Traumatic axonal injury (TAI) may contribute greatly to neurological impairments after traumatic brain injury, but it is difficult to assess with conventional imaging. We quantitatively compared diffusion tensor imaging (DTI) signal abnormalities with histological and electron microscopic characteristics of pericontusional TAI in a mouse model. Two DTI parameters, relative anisotropy and axial diffusivity, were significantly reduced 6 h to 4 d after trauma, corresponding to relatively isolated axonal injury. One to 4 weeks after trauma, relative anisotropy remained decreased, whereas axial diffusivity "pseudo-normalized" and radial diffusivity increased. These changes corresponded to demyelination, edema, and persistent axonal injury. At every time point, DTI was more sensitive to injury than conventional magnetic resonance imaging, and relative anisotropy distinguished injured from control mice with no overlap between groups. Remarkably, DTI changes strongly predicted the approximate time since trauma. These results provide an important validation of DTI for pericontusional TAI and suggest novel clinical and forensic applications.
“…At early stages, DWI is more sensitive than T2, but at subacute stages, T2 becomes more sensitive than DWI as the diffusion-weighted images undergo pseudonormalization (Schlaug et al, 1997;Copen et al, 2001;Schaefer et al, 2005). Similar changes in DWI signal characteristics over time after TBI have been observed in rats (Alsop et al, 1996;Albensi et al, 2000;Van Putten et al, 2005), pigs (Duhaime et al, 2003), and humans (Pasco et al, 2006). However, these studies did not use DTI and did not focus on white matter injury.…”
Section: Discussionmentioning
confidence: 96%
“…These studies were performed at only a single time point, 24 h after injury. It is unknown whether there are changes in the sensitivity of DTI over time, because only very limited clinical studies (Arfanakis et al, 2002;Naganawa et al, 2004;Voss et al, 2006) and none of the previous experimental animal studies (Hanstock et al, 1994;Kochanek et al, 1995;Alsop et al, 1996;Assaf et al, 1997;Albensi et al, 2000;Duhaime et al, 2003;Van Putten et al, 2005), to our knowledge, have performed DTI at multiple time points. For optimal clinical utility, a method should be robust across a variety of time points, given that it is rarely possible to scan patients at a fixed time point after injury.…”
Traumatic axonal injury (TAI) may contribute greatly to neurological impairments after traumatic brain injury, but it is difficult to assess with conventional imaging. We quantitatively compared diffusion tensor imaging (DTI) signal abnormalities with histological and electron microscopic characteristics of pericontusional TAI in a mouse model. Two DTI parameters, relative anisotropy and axial diffusivity, were significantly reduced 6 h to 4 d after trauma, corresponding to relatively isolated axonal injury. One to 4 weeks after trauma, relative anisotropy remained decreased, whereas axial diffusivity "pseudo-normalized" and radial diffusivity increased. These changes corresponded to demyelination, edema, and persistent axonal injury. At every time point, DTI was more sensitive to injury than conventional magnetic resonance imaging, and relative anisotropy distinguished injured from control mice with no overlap between groups. Remarkably, DTI changes strongly predicted the approximate time since trauma. These results provide an important validation of DTI for pericontusional TAI and suggest novel clinical and forensic applications.
“…23 MRI scans were analysed with National Institutes of Health ImageJ 1.43 (National Institutes of Health, Bethesda, MD), and the degree of midline shift were measured directly by constructing a straight line from the midpoint of the longitudinal cerebral fissure to the middle of the mammillary body. The length from the lateral surface of the cortex to the midline was measured and a left-to-right ratio was calculated (Fig.…”
Section: Magnetic Resonance T2-weighted Imagingmentioning
Excessive active voltage-gated sodium channels are responsible for the cellular abnormalities associated with secondary brain injury following traumatic brain injury (TBI). We previously presented evidence that significant upregulation of Na v 1.3 expression occurs in the rat cortex at 2 h and 12 h post-TBI and is correlated with TBI severity. In our current study, we tested the hypothesis that blocking upregulation of Na v 1.3 expression in vivo in the acute stage post-TBI attenuates the secondary brain injury associated with TBI. We administered either antisense oligodeoxynucleotides (ODN) targeting Na v 1.3 or artificial cerebrospinal fluid (aCSF) at 2 h, 4 h, 6 h, and 8 h following TBI. Control sham animals received aCSF administration at the same time points. At 12 h post-TBI, Na v 1.3 messenger ribonucleic acid (mRNA) levels in bilateral hippocampi of the aCSF group were significantly elevated, compared with the sham and ODN groups ( p < 0.01). However, the Na v 1.3 mRNA levels in the uninjured contralateral hippocampus of the ODN group were significantly lowered, compared with the sham group ( p < 0.01). Treatment with antisense ODN significantly decreased the number of degenerating neurons in the ipsilateral hippocampal CA3 and hilar region ( p < 0.01). A set of left-to-right ratio value analyzed by magnetic resonance imaging T2 image on one day, three days, and seven days post-TBI showed marked edema in the ipsilateral hemisphere of the aCSF group, compared with that of the ODN group ( p < 0.05). The Morris water maze memory retention test showed that both the aCSF and ODN groups took longer to find a hidden platform, compared with the sham group ( p < 0.01). However, latency in the aCSF group was significantly higher than in the ODN group ( p < 0.05). Our in vivo Na v 1.3 inhibition studies suggest that therapeutic strategies to block upregulation of Na v 1.3 expression in the brain may improve outcomes following TBI.
“…This was followed by an increase in ADC values corresponding to demyelination and decreased tissue cellularity in the long term. 10,11 Spinal cord DWI A DWI of the spinal cord is technically demanding because of the small volume of the spinal cord. Physiological motion, including cerebrospinal fluid flow and cardiac and respiratory motion, also influenced the quality of images.…”
Section: Correlation Between Pathological Changes and Adc Valuesmentioning
Objective: Magnetic resonance imaging (MRI) is useful in diagnosing spontaneous spinal epidural hematoma (SSEH). The purpose of the present study is to determine whether apparent diffusion coefficient (ADC) values could determine severity of spinal cord damage and predict functional recovery in SSEH. Methods: The study involved four consecutive patients with SSEH (two men and two women: aged 21-76 years). Using axial slices, ADC values were determined in four separate regions of the spinal cord. These areas were classified into the following three groups based on findings in T2-weighted images: normal T2 intensity; persistent T2 abnormality; and temporary T2 abnormality. ADC values among different groups were compared. The relationship between preoperative ADC values and neurological grades were also evaluated. Results: ADC values in normal T2 areas were 0.89 ± 0.10 Â 10 À3 mm 2 s À1 , whereas those for the persistent T2 abnormality group were significantly lower (0.63 ± 0.14 Â 10 À3 ). In a patient who was Frankel A on admission and in the follow-up, the ADC value was as low as 0.41 Â 10 À3 . Functional recovery was also limited in the spinal cord segments with lower ADC values. In the temporary T2 abnormality group, ADC values were significantly higher (1.05±0.10 Â 10 À3 ).
Conclusions:In SSEH, if MRI demonstrated T2-hyperintensity with lower ADC values, patients may suffer from irreversible spinal cord damages. ADC values of the spinal cord can be added as a new factor that reliably indicated the severity of spinal cord damage and predicted functional recovery.
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