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Project
Cognitive control over action in traumatic brain injury.
Cognitive control over action refers to ones ability to quickly changethe course of action when certain behavior is no longer appropriate. For example, cognitive control is necessary to safely move through traffic. Without it we would not be able to avoid the car that suddenly switched lanes, or stop in time for a child that runs into the street. It is also important in a social context, offensive comments would be made more often than intended if we lacked a mechanism for preventing us to act upon every impulsive thought.
This thesis aims to increase insight into the neural mechanisms underlying cognitive control over action. This is not only relevant for understanding human behavior in health, butalso in disease. Patients with neurological and psychiatric disorders, such as attention deficit hyperactivity disorder and Gilles de la Tourette, exhibit deficits in the ability to cognitively control their actions. Also patients with a traumatic brain injury (TBI) experience marked problems with effectively controlling their actions.
The experiments in this thesis are designed to investigate the two core processes for cognitive control over action: switching between tasks and response inhibition. Accumulating evidence indicates that these processes rely heavily on the interaction between the frontal cortex and subcortical structures, namely, the basal ganglia and thalamus. Therefore, the first part of this thesis addresses the hypothesis that damage to cortico-subcortical circuits can account for impairments in task switching in TBI.
Diffusion weighted magnetic resonance imaging revealed widespread damage of white matter pathways throughout the brain, indicative of diffuseaxonal injuries. Diffuse axonal injuries are caused by the accelerationand deacceleration of the brain within the skull at the moment of impact. In addition, volume of the subcortical nuclei was reduced in TBI. Thedegree of structural damage to the white matter pathways was related tothis atrophy of the subcortical structures. This suggests that localized grey matter atrophy might be the result of secondary degeneration processes associated with diffuse axonal injury.
On a behavioral level, TBI patients needed more time to implement a switch than the participants in the control group. They also made more errors while switching.Despite the widespread damage throughout the brain, specifically damageto the white matter connections between the frontal cortex, basal ganglia and thalamus was associated with worse task switching performance. Also atrophy of subregions of the subcortical structures was predictive oftask switching deficits.
To investigate whether structural damage of the brain also leads to abnormal brain function we used functional magnetic resonance imaging. Compared to a control group, TBI patients demonstrated increased recruitment of cortical regions while switching. At the same time, they showed reduced activation in the subthalamic nucleus. The subthalamic nucleus forms part of the basal ganglia and is thought to be important for braking and cancelling actions. This process is essential in task switching, since the new task cannot be implemented before the present one is aborted. Importantly, the changes in neural recruitment were associated with the degree of structural damage of the pathways connecting these regions.
Both functional and structural alterations could account for the observed behavioral deficits. Together,these results emphasize the importance of cortico-subcortical connections for successful cognitive control over action in TBI.
The second part of this thesis focuses on response inhibition. Recent literature distinguishes between two forms of inhibitory control: reactive and proactive inhibition. Reactive inhibition refers to the situation where anunexpected event triggers the need to cancel a particular action. An example that critically depends on a reactive inhibition mechanism is whena car comes around the corner just as you are about to cross the street. On the other hand, it is beneficial to set up inhibitory control in advance (i.e., proactively) when the need for stopping is anticipated. Slowing down your pace in order to find your way through a busy shopping street without bumping into someone, is an example of proactive inhibition. It has been suggested that these two forms of inhibitory control rely on distinct basal ganglia nuclei. We tested this hypothesis by directly contrasting the functional activation patterns during reactive and proactive control during successful stopping. The results showed a stronger involvement of the subthalamic nucleus during reactive inhibitory control, whereas the caudate head was more active during proactive response inhibition.
In summary, this PhD project provides new insight intothe neural mechanisms underlying cognitive control over action, both inhealthy participants and in patients with TBI. Specifically, we demonstrated that structural damage of the fronto-subcortical circuits may drive changes in neural recruitment and behavioral performance. In addition,we have demonstrated that different basal ganglia structures are critically involved in response inhibition depending on the level of anticipation of behaviorally relevant stimuli. These results provide empirical support for contemporary theories of cognitive control over action.
This thesis aims to increase insight into the neural mechanisms underlying cognitive control over action. This is not only relevant for understanding human behavior in health, butalso in disease. Patients with neurological and psychiatric disorders, such as attention deficit hyperactivity disorder and Gilles de la Tourette, exhibit deficits in the ability to cognitively control their actions. Also patients with a traumatic brain injury (TBI) experience marked problems with effectively controlling their actions.
The experiments in this thesis are designed to investigate the two core processes for cognitive control over action: switching between tasks and response inhibition. Accumulating evidence indicates that these processes rely heavily on the interaction between the frontal cortex and subcortical structures, namely, the basal ganglia and thalamus. Therefore, the first part of this thesis addresses the hypothesis that damage to cortico-subcortical circuits can account for impairments in task switching in TBI.
Diffusion weighted magnetic resonance imaging revealed widespread damage of white matter pathways throughout the brain, indicative of diffuseaxonal injuries. Diffuse axonal injuries are caused by the accelerationand deacceleration of the brain within the skull at the moment of impact. In addition, volume of the subcortical nuclei was reduced in TBI. Thedegree of structural damage to the white matter pathways was related tothis atrophy of the subcortical structures. This suggests that localized grey matter atrophy might be the result of secondary degeneration processes associated with diffuse axonal injury.
On a behavioral level, TBI patients needed more time to implement a switch than the participants in the control group. They also made more errors while switching.Despite the widespread damage throughout the brain, specifically damageto the white matter connections between the frontal cortex, basal ganglia and thalamus was associated with worse task switching performance. Also atrophy of subregions of the subcortical structures was predictive oftask switching deficits.
To investigate whether structural damage of the brain also leads to abnormal brain function we used functional magnetic resonance imaging. Compared to a control group, TBI patients demonstrated increased recruitment of cortical regions while switching. At the same time, they showed reduced activation in the subthalamic nucleus. The subthalamic nucleus forms part of the basal ganglia and is thought to be important for braking and cancelling actions. This process is essential in task switching, since the new task cannot be implemented before the present one is aborted. Importantly, the changes in neural recruitment were associated with the degree of structural damage of the pathways connecting these regions.
Both functional and structural alterations could account for the observed behavioral deficits. Together,these results emphasize the importance of cortico-subcortical connections for successful cognitive control over action in TBI.
The second part of this thesis focuses on response inhibition. Recent literature distinguishes between two forms of inhibitory control: reactive and proactive inhibition. Reactive inhibition refers to the situation where anunexpected event triggers the need to cancel a particular action. An example that critically depends on a reactive inhibition mechanism is whena car comes around the corner just as you are about to cross the street. On the other hand, it is beneficial to set up inhibitory control in advance (i.e., proactively) when the need for stopping is anticipated. Slowing down your pace in order to find your way through a busy shopping street without bumping into someone, is an example of proactive inhibition. It has been suggested that these two forms of inhibitory control rely on distinct basal ganglia nuclei. We tested this hypothesis by directly contrasting the functional activation patterns during reactive and proactive control during successful stopping. The results showed a stronger involvement of the subthalamic nucleus during reactive inhibitory control, whereas the caudate head was more active during proactive response inhibition.
In summary, this PhD project provides new insight intothe neural mechanisms underlying cognitive control over action, both inhealthy participants and in patients with TBI. Specifically, we demonstrated that structural damage of the fronto-subcortical circuits may drive changes in neural recruitment and behavioral performance. In addition,we have demonstrated that different basal ganglia structures are critically involved in response inhibition depending on the level of anticipation of behaviorally relevant stimuli. These results provide empirical support for contemporary theories of cognitive control over action.
Date:1 Oct 2009 → 30 Sep 2014
Keywords:Motor control, Traumatic brain injury, Cognitive control
Disciplines:Neurosciences, Biological and physiological psychology, Cognitive science and intelligent systems, Developmental psychology and ageing, Orthopaedics
Project type:PhD project