Investigating the neural basis of self-awareness deficits following traumatic brain injury
File(s)
Author(s)
Ham, Timothy
Type
Thesis
Abstract
Self-awareness deficits are a common and disabling consequence of traumatic brain injury (TBI). ‘On-line’ awareness is one facet of self-awareness that can be studied by examining how people monitor their performance and respond to their errors. Performance monitoring, like many of the cognitive functions disrupted after TBI, is believed to depend on the coordinated activity of neural networks. The fronto-parietal control network (FPCN) is one such network that contains a sub-network called the salience network (SN). The SN consists of the dorsal anterior cingulate (dACC) and bilateral insulae cortex and is thought to monitor salient events (e.g. errors). I used advanced structure and function MRI techniques to investigate these networks and test two overarching hypotheses: first, performance monitoring is regulated by regions within the FPCN; and second, dysfunction of the FPCN leads to impaired self-awareness after TBI.
My first study demonstrated two distinct frontal networks that respond to different error types. Predictable/internally signalled errors caused SN activation; whereas unpredictable/externally signalled errors caused activation of the ventral attentional network, a network thought to respond to unexpected events. This suggested the presence of parallel performance monitoring systems within the FPCN. My second study established that the ‘driving’ input into the SN originated in right anterior insula and subsequent behavioural adaptation was regulated by enhanced effective connectivity from the dACC to the left anterior insula. In my third study I identified a large group of TBI patients with impaired performance monitoring. These patients had additional metacognitive evidence of impaired self-awareness and demonstrated reduced functional connectivity between the dACC and the remainder of the FPCN at ‘rest’, and abnormally large insulae activation in response to errors.
These studies clarified how the brain monitors and responds to salient events; and, provided evidence that self-awareness deficits after TBI are due to FPCN dysfunction, identifying this network as a potential target for future treatments.
My first study demonstrated two distinct frontal networks that respond to different error types. Predictable/internally signalled errors caused SN activation; whereas unpredictable/externally signalled errors caused activation of the ventral attentional network, a network thought to respond to unexpected events. This suggested the presence of parallel performance monitoring systems within the FPCN. My second study established that the ‘driving’ input into the SN originated in right anterior insula and subsequent behavioural adaptation was regulated by enhanced effective connectivity from the dACC to the left anterior insula. In my third study I identified a large group of TBI patients with impaired performance monitoring. These patients had additional metacognitive evidence of impaired self-awareness and demonstrated reduced functional connectivity between the dACC and the remainder of the FPCN at ‘rest’, and abnormally large insulae activation in response to errors.
These studies clarified how the brain monitors and responds to salient events; and, provided evidence that self-awareness deficits after TBI are due to FPCN dysfunction, identifying this network as a potential target for future treatments.
Version
Open Access
Date Issued
2013-10
Date Awarded
2014-05
Copyright Statement
Attribution NoDerivatives 4.0 International Licence (CC BY-ND)
Advisor
Sharp, David
Leech, Robert
Wise, Richard
Publisher Department
Medicine
Publisher Institution
Imperial College London
Qualification Level
Doctoral
Qualification Name
Doctor of Philosophy (PhD)