Abstract
Self-referential processing is a key cognitive process, associated with the serotonergic system and the default mode network (DMN). Decreased levels of serotonin and reduced activations of the DMN observed in amyotrophic lateral sclerosis (ALS) suggest that self-referential processing might be altered in patients with ALS. Here, we investigate the effects of ALS on the electroencephalography correlates of self-referential thinking. We find that electroencephalography (EEG) correlates of self-referential thinking are present in healthy individuals, but not in those with ALS. In particular, thinking about themselves or others significantly modulates the bandpower in the medial prefrontal cortex in healthy individuals, but not in ALS patients. This finding supports the view of ALS as a complex multisystem disorder which, as shown here, includes dysfunctional processing of the medial prefrontal cortex. It points towards possible alterations of self-consciousness in ALS patients, which might have important consequences for patients’ self-conceptions, personal relations, and decision-making.
Highlights
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease that is characterised mainly by the loss of motor neurons [1]
A significant main effect of the condition (“self”, “friend”, “celebrity”, “count”) on bandpower was found both for healthy individuals (F(3, 3983) = 9.17, p = 0.0000, Z2p 1⁄4 0:0137) and for ALS patients (F(3, 3999) = 5.94, p = 0.0005, Z2p 1⁄4 0:0081)
This agrees with previous EEG, functional magnetic resonance imaging (fMRI) and positron emission tomography (PET) studies with healthy individuals [28,29,30,31,32,33], which found that medial prefrontal cortex (MPFC) activity differs between self-referential and non-self-referential processing
Summary
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease that is characterised mainly by the loss of motor neurons [1]. ALS has long been believed to be purely a motor disease, there is a growing body of physiological evidence to suggest that neuronal degeneration in ALS is not limited to motor cortices and motor pathways [2]. Braak et al related ALS to the buildup of pTDP-43 protein agglomerations [3]; they showed that these agglomerations spread from the motor cortices to nearby areas and, eventually, to most of the cortex (with particular preponderance of the frontotemporal cortices). The broad multisite cortical damage of ALS was subsequently confirmed with a neuroimaging study by Schmidt et al [4], demonstrating alterations in functional and structural connectivity throughout the cortex.
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