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Thalamic inflammation after brain trauma is associated with thalamo-cortical white matter damage.

Scott G, Hellyer PJ, Ramlackhansingh AF, Brooks DJ, Matthews PM, Sharp DJ - J Neuroinflammation (2015)

Bottom Line: Animal models and human pathological studies demonstrate persistent inflammation in the thalamus associated with axonal injury, but this relationship has never been shown in vivo.Here, we use diffusion MRI to estimate axonal injury and show that thalamic inflammation is correlated with thalamo-cortical tract damage.These findings support a link between axonal damage and persistent inflammation after brain injury.

View Article: PubMed Central - PubMed

Affiliation: Division of Brain Sciences, Department of Medicine, Hammersmith Hospital Campus, Imperial College London, London, UK.

ABSTRACT

Background: Traumatic brain injury can trigger chronic neuroinflammation, which may predispose to neurodegeneration. Animal models and human pathological studies demonstrate persistent inflammation in the thalamus associated with axonal injury, but this relationship has never been shown in vivo.

Findings: Using [(11)C]-PK11195 positron emission tomography, a marker of microglial activation, we previously demonstrated thalamic inflammation up to 17 years after traumatic brain injury. Here, we use diffusion MRI to estimate axonal injury and show that thalamic inflammation is correlated with thalamo-cortical tract damage.

Conclusions: These findings support a link between axonal damage and persistent inflammation after brain injury.

No MeSH data available.


Related in: MedlinePlus

Correlation of thalamic microglial activation and white matter damage in relation to distance from thalamus. a Partial correlation of thalamic [11C]-PK11195 (PK) binding potentials (BP) and thalamo-cortical fractional anisotropy (FA), sampled with increasing distance from the thalamus in TBI patients. Distance of 0 mm reflects sampling from tracts involving the thalamus proper. R (red) and p values are shown, with a threshold of p = 0.05 (dotted line). b Plot of residuals after for thalamo-cortical FA (x-axis), sampled from a ring-shaped mask 2 mm from the outer border of the thalamus versus thalamic PK BP (y-axis). c Partial correlation of PK BP in cortical grey matter and thalamo-cortical FA, sampled and plotted as in a
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Fig2: Correlation of thalamic microglial activation and white matter damage in relation to distance from thalamus. a Partial correlation of thalamic [11C]-PK11195 (PK) binding potentials (BP) and thalamo-cortical fractional anisotropy (FA), sampled with increasing distance from the thalamus in TBI patients. Distance of 0 mm reflects sampling from tracts involving the thalamus proper. R (red) and p values are shown, with a threshold of p = 0.05 (dotted line). b Plot of residuals after for thalamo-cortical FA (x-axis), sampled from a ring-shaped mask 2 mm from the outer border of the thalamus versus thalamic PK BP (y-axis). c Partial correlation of PK BP in cortical grey matter and thalamo-cortical FA, sampled and plotted as in a

Mentions: In TBI, we found a significant negative correlation between thalamic PK BPND and mean thalamo-cortical tract FA (r = −0.770, p = 0.042). The strength of this correlation decreased with the distance at which FA was sampled from thalamo-cortical tracts (Fig. 2a). Thalamic PK binding was most strongly correlated with FA of voxels within 10 mm of the thalamus, maximally within 2-mm distance (Fig. 2b). There was no correlation between thalamic PK binding and FA of the corpus callosal tracts nor between cortical PK and thalamo-cortical FA, either when sampled as a whole or ROIs at different distances (Fig. 2c). We also found no significant correlation between time since injury and either mean thalamo-cortical FA or thalamic PK.Fig. 2


Thalamic inflammation after brain trauma is associated with thalamo-cortical white matter damage.

Scott G, Hellyer PJ, Ramlackhansingh AF, Brooks DJ, Matthews PM, Sharp DJ - J Neuroinflammation (2015)

Correlation of thalamic microglial activation and white matter damage in relation to distance from thalamus. a Partial correlation of thalamic [11C]-PK11195 (PK) binding potentials (BP) and thalamo-cortical fractional anisotropy (FA), sampled with increasing distance from the thalamus in TBI patients. Distance of 0 mm reflects sampling from tracts involving the thalamus proper. R (red) and p values are shown, with a threshold of p = 0.05 (dotted line). b Plot of residuals after for thalamo-cortical FA (x-axis), sampled from a ring-shaped mask 2 mm from the outer border of the thalamus versus thalamic PK BP (y-axis). c Partial correlation of PK BP in cortical grey matter and thalamo-cortical FA, sampled and plotted as in a
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4666189&req=5

Fig2: Correlation of thalamic microglial activation and white matter damage in relation to distance from thalamus. a Partial correlation of thalamic [11C]-PK11195 (PK) binding potentials (BP) and thalamo-cortical fractional anisotropy (FA), sampled with increasing distance from the thalamus in TBI patients. Distance of 0 mm reflects sampling from tracts involving the thalamus proper. R (red) and p values are shown, with a threshold of p = 0.05 (dotted line). b Plot of residuals after for thalamo-cortical FA (x-axis), sampled from a ring-shaped mask 2 mm from the outer border of the thalamus versus thalamic PK BP (y-axis). c Partial correlation of PK BP in cortical grey matter and thalamo-cortical FA, sampled and plotted as in a
Mentions: In TBI, we found a significant negative correlation between thalamic PK BPND and mean thalamo-cortical tract FA (r = −0.770, p = 0.042). The strength of this correlation decreased with the distance at which FA was sampled from thalamo-cortical tracts (Fig. 2a). Thalamic PK binding was most strongly correlated with FA of voxels within 10 mm of the thalamus, maximally within 2-mm distance (Fig. 2b). There was no correlation between thalamic PK binding and FA of the corpus callosal tracts nor between cortical PK and thalamo-cortical FA, either when sampled as a whole or ROIs at different distances (Fig. 2c). We also found no significant correlation between time since injury and either mean thalamo-cortical FA or thalamic PK.Fig. 2

Bottom Line: Animal models and human pathological studies demonstrate persistent inflammation in the thalamus associated with axonal injury, but this relationship has never been shown in vivo.Here, we use diffusion MRI to estimate axonal injury and show that thalamic inflammation is correlated with thalamo-cortical tract damage.These findings support a link between axonal damage and persistent inflammation after brain injury.

View Article: PubMed Central - PubMed

Affiliation: Division of Brain Sciences, Department of Medicine, Hammersmith Hospital Campus, Imperial College London, London, UK.

ABSTRACT

Background: Traumatic brain injury can trigger chronic neuroinflammation, which may predispose to neurodegeneration. Animal models and human pathological studies demonstrate persistent inflammation in the thalamus associated with axonal injury, but this relationship has never been shown in vivo.

Findings: Using [(11)C]-PK11195 positron emission tomography, a marker of microglial activation, we previously demonstrated thalamic inflammation up to 17 years after traumatic brain injury. Here, we use diffusion MRI to estimate axonal injury and show that thalamic inflammation is correlated with thalamo-cortical tract damage.

Conclusions: These findings support a link between axonal damage and persistent inflammation after brain injury.

No MeSH data available.


Related in: MedlinePlus