Stroke and Neurodegeneration Induce Different Connectivity Aberrations in the Insula

Abstract

T he insular cortex (InsC) is a main structural-functional hub of the brain.1 It features widespread connections with cortical and subcortical regions, and it is implicated in varied domains, such as body sensation, language, emotion, and social cognition.2 Notably, the InsC abounds in von Economo neurons, which facilitate rapid integration of information. Together with its topological centrality, 1 these features render the InsC as a core region for overall brain dynamics and cognition.InsC damage after stroke or neurodegeneration can considerably impair cognitive function. Stroke can disturb behavioral, emotional, and sensory domains, 3 whereas early neurodegeneration (including the InsC) in behavioral variant frontotemporal dementia (bvFTD) 4 usually leads to social and emotional dysfunction.5 Despite such general differences, little is known about the distinct insular connectivity alterations caused by each of these causes. A direct comparison of InsC connectivity patterns in patients affected by stroke and neurodegeneration 6 may reveal theoretically and clinically relevant differences between each pathophysiological process.In fact, at the molecular level, these conditions differ in timing and physiopathology. Stroke involves tissue loss, neuronal reorganization, and plasticity.7 Instead, neurodegeneration in bvFTD results from protein aggregation, inducing physiopathological events (eg, axonal degeneration, synapse loss, and dendritic retraction) and propagation of misfolded proteins.8 These differences at the molecular level suggest that InsC connectivity may be differentially affected by stroke and bvFTD.Previous studies have reported aberrant long-range connectivity (mostly hypoconnectivity) in both stroke and bvFTD. 4,7 Nevertheless, local connectivity is a key featureBackground and Purpose-Stroke and neurodegeneration cause significant brain damage and cognitive impairment, especially if the insular cortex is compromised. This study explores for the first time whether these 2 causes differentially alter connectivity patterns in the insular cortex. Methods-Resting state-functional magnetic resonance imaging data were collected from patients with insular stroke, patients with behavioral variant frontotemporal dementia, and healthy controls. Data from the 3 groups were assessed through a correlation function analysis. Specifically, we compared decreases in connectivity as a function of voxel Euclidean distance within the insular cortex. Results-Relative to controls, patients with stroke showed faster connectivity decays as a function of distance (hypoconnectivity). In contrast, the behavioral variant frontotemporal dementia group exhibited significant hyperconnectivity between neighboring voxels. Both patient groups evinced global hypoconnectivity. No between-group differences were observed in a volumetrically and functionally comparable region without ischemia or neurodegeneration. Conclusions-Functional insular cortex connectivity is affected differently by cerebral ischemia and neurodegeneration, ...

Feeling, learning from and being aware of inner states: interoceptive dimensions in neurodegeneration and stroke

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“…Motion parameters did not differ among groups (see electronic supplementary material, §1.3.4). Following previous reports of functional connectivity in stroke and neurodegeneration [8,63], images were preprocessed with the Data Processing Assistant for Resting-State fMRI (DPARSF). For details, see electronic supplementary material, §1.3.4.…”

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Integration of Intention and Outcome for Moral Judgment in Frontotemporal Dementia: Brain Structural Signatures

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