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Self-Representations: Alterations in Frontotemporal Lobar Degeneration and Correlates in the Brain


Self-representations are multi-faceted and complex. Frontotemporal lobar degeneration (FTLD) is a neurodegenerative disease that selectively atrophies anterior brain regions (e.g., frontal pole, insula, anterior cingulate cortex) that are thought to subserve self-representations. While past work has extensively characterized the changes that occur in FTLD patients' comprehension of the social world, relatively little attention has been paid to the changes that occur in the self-representations of patients themselves. The present study assessed five domains of self-representations: (1) self-conscious emotion, (2) self-monitoring, (3) self-focus, (4) self-reflection, and (5) insight in individuals with a neurodegenerative disease (i.e., FTLD, Alzheimer's disease, corticobasal degeneration, supranuclear palsy) and without (i.e., healthy control participants). Multiple methods were used to evaluate participants' behavioral (i.e., emotional facial expressions and eye movements), physiological, and experiential responses. Self-representations in the FTLD and control groups were compared, and the neural correlates of self-representations were investigated across diagnostic categories.

Results supported the hypothesis of altered self-representations in FTLD, with FTLD patients exhibiting significantly lower levels of self-conscious emotion, self-monitoring, self-reflection, and insight and significantly higher levels of self-focus than controls. In terms of the neural correlates, three medial right hemisphere regions emerged as being significant predictors of self-representations. In line with expectations, smaller rostral anterior cingulate volumes predicted less self-conscious emotional responding, smaller frontal pole volumes predicted less self-monitoring, and smaller amygdala volumes predicted greater self-focus. FTLD is a disease in which changes in self are common. The present study expanded upon past work by detailing the specific domains of self-representations that are disrupted in FTLD and investigating the neural correlates of these self-representations in a sample of neurodegenerative patients and controls. The findings of the present study have implications for improving the diagnosis and treatment of FTLD and add to our basic understanding of the neural substrates of self-representations.

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