Traumatic brain injury affects the frontomedian cortex--an event-related fMRI study on evaluative judgments.
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Traumatic brain injury affects the frontomedian cortex--an event-related fMRI study on evaluative judgments. / Schroeter, Matthias L; Ettrich, Barbara; Menz, Mareike; Zysset, Stefan.
in: NEUROPSYCHOLOGIA, Jahrgang 48, Nr. 1, 1, 2010, S. 185-193.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Traumatic brain injury affects the frontomedian cortex--an event-related fMRI study on evaluative judgments.
AU - Schroeter, Matthias L
AU - Ettrich, Barbara
AU - Menz, Mareike
AU - Zysset, Stefan
PY - 2010
Y1 - 2010
N2 - Traumatic brain injuries represent the leading cause of death and disability in young adults in industrialized countries. Recently, it has been suggested that dysfunctions of the frontomedian cortex, which enables social cognition, are responsible for clinical deficits in the long-term. To validate this hypothesis, we examined brain activation in seven young adults suffering from diffuse axonal injury during a cognitive task that specifically depends on frontomedian structures, namely evaluative judgments, contrasted with semantic memory retrieval. Brain activation in patients was compared with healthy age and gender matched control subjects using event-related functional magnetic resonance imaging. Evaluative judgments were related to a neural network discussed in the context of self-referential processing and theory of mind. More precisely, the neural network consisted of frontomedian regions, the temporal pole, and the posterior superior temporal gyrus and sulcus/angular gyrus. Patients showed higher activations in this network and the inferior frontal gyrus, whereas healthy control subjects activated more dopaminergic structures, namely the ventral tegmental area, during evaluative judgments. One possible interpretation of the data is that deficits in the ventral tegmental area, and consequently the mesocorticolimbic projection system, have to be compensated for by higher brain activations in the frontomedian and anterior cingulate cortex in patients with diffuse axonal injury. In conclusion, our study supports the hypothesis that traumatic brain injury is characterized by frontomedian dysfunctions, which may be responsible for clinical deficits in the long-term and which might be modified by rehabilitative strategies in the future.
AB - Traumatic brain injuries represent the leading cause of death and disability in young adults in industrialized countries. Recently, it has been suggested that dysfunctions of the frontomedian cortex, which enables social cognition, are responsible for clinical deficits in the long-term. To validate this hypothesis, we examined brain activation in seven young adults suffering from diffuse axonal injury during a cognitive task that specifically depends on frontomedian structures, namely evaluative judgments, contrasted with semantic memory retrieval. Brain activation in patients was compared with healthy age and gender matched control subjects using event-related functional magnetic resonance imaging. Evaluative judgments were related to a neural network discussed in the context of self-referential processing and theory of mind. More precisely, the neural network consisted of frontomedian regions, the temporal pole, and the posterior superior temporal gyrus and sulcus/angular gyrus. Patients showed higher activations in this network and the inferior frontal gyrus, whereas healthy control subjects activated more dopaminergic structures, namely the ventral tegmental area, during evaluative judgments. One possible interpretation of the data is that deficits in the ventral tegmental area, and consequently the mesocorticolimbic projection system, have to be compensated for by higher brain activations in the frontomedian and anterior cingulate cortex in patients with diffuse axonal injury. In conclusion, our study supports the hypothesis that traumatic brain injury is characterized by frontomedian dysfunctions, which may be responsible for clinical deficits in the long-term and which might be modified by rehabilitative strategies in the future.
M3 - SCORING: Zeitschriftenaufsatz
VL - 48
SP - 185
EP - 193
JO - NEUROPSYCHOLOGIA
JF - NEUROPSYCHOLOGIA
SN - 0028-3932
IS - 1
M1 - 1
ER -