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Multimodal imaging of mild traumatic brain injury and persistent postconcussion syndrome.

Dean PJ, Sato JR, Vieira G, McNamara A, Sterr A - Brain Behav (2014)

Bottom Line: It was hypothesized that only those mTBI participants with persistent PCS would show functional changes, and that these changes would be related to reduced structural integrity and altered metabolite concentrations.There were no behavioral differences between the groups, but participants with greater PCS symptoms exhibited greater activation in attention-related areas (anterior cingulate), along with reduced activation in temporal, default mode network, and working memory areas (left prefrontal) as cognitive load was increased from the easiest to the most difficult task.Functional changes in these areas correlated with reduced structural integrity in corpus callosum and anterior white matter, and reduced creatine concentration in right dorsolateral prefrontal cortex.

View Article: PubMed Central - PubMed

Affiliation: School of Psychology, University Of Surrey Guildford, UK.

ABSTRACT

Background: Persistent postconcussion syndrome (PCS) occurs in around 5-10% of individuals after mild traumatic brain injury (mTBI), but research into the underlying biology of these ongoing symptoms is limited and inconsistent. One reason for this could be the heterogeneity inherent to mTBI, with individualized injury mechanisms and psychological factors. A multimodal imaging study may be able to characterize the injury better.

Aim: To look at the relationship between functional (fMRI), structural (diffusion tensor imaging), and metabolic (magnetic resonance spectroscopy) data in the same participants in the long term (>1 year) after injury. It was hypothesized that only those mTBI participants with persistent PCS would show functional changes, and that these changes would be related to reduced structural integrity and altered metabolite concentrations.

Methods: Functional changes associated with persistent PCS after mTBI (>1 year postinjury) were investigated in participants with and without PCS (both n = 8) and non-head injured participants (n = 9) during performance of working memory and attention/processing speed tasks. Correlation analyses were performed to look at the relationship between the functional data and structural and metabolic alterations in the same participants.

Results: There were no behavioral differences between the groups, but participants with greater PCS symptoms exhibited greater activation in attention-related areas (anterior cingulate), along with reduced activation in temporal, default mode network, and working memory areas (left prefrontal) as cognitive load was increased from the easiest to the most difficult task. Functional changes in these areas correlated with reduced structural integrity in corpus callosum and anterior white matter, and reduced creatine concentration in right dorsolateral prefrontal cortex.

Conclusion: These data suggest that the top-down attentional regulation and deactivation of task-irrelevant areas may be compensating for the reduction in working memory capacity and variation in white matter transmission caused by the structural and metabolic changes after injury. This may in turn be contributing to secondary PCS symptoms such as fatigue and headache. Further research is required using multimodal data to investigate the mechanisms of injury after mTBI, but also to aid individualized diagnosis and prognosis.

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Related in: MedlinePlus

A model illustrating how the structural and metabolic changes after injury (A) may cause the functional changes and compensation mechanisms during high cognitive load (B) which in turn may underlie some of the ongoing PCS symptoms in those participants with mTBI and ongoing PCS.
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fig07: A model illustrating how the structural and metabolic changes after injury (A) may cause the functional changes and compensation mechanisms during high cognitive load (B) which in turn may underlie some of the ongoing PCS symptoms in those participants with mTBI and ongoing PCS.

Mentions: These functional changes correlated with structural integrity (DTI) and alterations in metabolism (MRS) such that a smaller BOLD response increase in left IFG/MFG for the hardest task was associated with lower FA in the splenium of the corpus callosum as well as lower creatine concentration in rDLPFC. Reduced FA in the splenium of the corpus callosum was also seen in those with reduced BOLD response in PCC and precuneus, and increased BOLD response in ACC. Our data suggest that mTBI participants with persistent PCS are compensating for reduced capacity caused by structural and metabolic changes after injury by top-down regulation of attention and deactivation of task-irrelevant areas during difficult tasks (see Fig.7). These results and conclusions will be discussed in detail below.


Multimodal imaging of mild traumatic brain injury and persistent postconcussion syndrome.

Dean PJ, Sato JR, Vieira G, McNamara A, Sterr A - Brain Behav (2014)

A model illustrating how the structural and metabolic changes after injury (A) may cause the functional changes and compensation mechanisms during high cognitive load (B) which in turn may underlie some of the ongoing PCS symptoms in those participants with mTBI and ongoing PCS.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4321394&req=5

fig07: A model illustrating how the structural and metabolic changes after injury (A) may cause the functional changes and compensation mechanisms during high cognitive load (B) which in turn may underlie some of the ongoing PCS symptoms in those participants with mTBI and ongoing PCS.
Mentions: These functional changes correlated with structural integrity (DTI) and alterations in metabolism (MRS) such that a smaller BOLD response increase in left IFG/MFG for the hardest task was associated with lower FA in the splenium of the corpus callosum as well as lower creatine concentration in rDLPFC. Reduced FA in the splenium of the corpus callosum was also seen in those with reduced BOLD response in PCC and precuneus, and increased BOLD response in ACC. Our data suggest that mTBI participants with persistent PCS are compensating for reduced capacity caused by structural and metabolic changes after injury by top-down regulation of attention and deactivation of task-irrelevant areas during difficult tasks (see Fig.7). These results and conclusions will be discussed in detail below.

Bottom Line: It was hypothesized that only those mTBI participants with persistent PCS would show functional changes, and that these changes would be related to reduced structural integrity and altered metabolite concentrations.There were no behavioral differences between the groups, but participants with greater PCS symptoms exhibited greater activation in attention-related areas (anterior cingulate), along with reduced activation in temporal, default mode network, and working memory areas (left prefrontal) as cognitive load was increased from the easiest to the most difficult task.Functional changes in these areas correlated with reduced structural integrity in corpus callosum and anterior white matter, and reduced creatine concentration in right dorsolateral prefrontal cortex.

View Article: PubMed Central - PubMed

Affiliation: School of Psychology, University Of Surrey Guildford, UK.

ABSTRACT

Background: Persistent postconcussion syndrome (PCS) occurs in around 5-10% of individuals after mild traumatic brain injury (mTBI), but research into the underlying biology of these ongoing symptoms is limited and inconsistent. One reason for this could be the heterogeneity inherent to mTBI, with individualized injury mechanisms and psychological factors. A multimodal imaging study may be able to characterize the injury better.

Aim: To look at the relationship between functional (fMRI), structural (diffusion tensor imaging), and metabolic (magnetic resonance spectroscopy) data in the same participants in the long term (>1 year) after injury. It was hypothesized that only those mTBI participants with persistent PCS would show functional changes, and that these changes would be related to reduced structural integrity and altered metabolite concentrations.

Methods: Functional changes associated with persistent PCS after mTBI (>1 year postinjury) were investigated in participants with and without PCS (both n = 8) and non-head injured participants (n = 9) during performance of working memory and attention/processing speed tasks. Correlation analyses were performed to look at the relationship between the functional data and structural and metabolic alterations in the same participants.

Results: There were no behavioral differences between the groups, but participants with greater PCS symptoms exhibited greater activation in attention-related areas (anterior cingulate), along with reduced activation in temporal, default mode network, and working memory areas (left prefrontal) as cognitive load was increased from the easiest to the most difficult task. Functional changes in these areas correlated with reduced structural integrity in corpus callosum and anterior white matter, and reduced creatine concentration in right dorsolateral prefrontal cortex.

Conclusion: These data suggest that the top-down attentional regulation and deactivation of task-irrelevant areas may be compensating for the reduction in working memory capacity and variation in white matter transmission caused by the structural and metabolic changes after injury. This may in turn be contributing to secondary PCS symptoms such as fatigue and headache. Further research is required using multimodal data to investigate the mechanisms of injury after mTBI, but also to aid individualized diagnosis and prognosis.

Show MeSH
Related in: MedlinePlus