Distributed changes in default-mode resting-state connectivity in multiple sclerosis

Abstract

Relapsing-remitting multiple sclerosis patients show a consistent dysfunction of DMN at the level of the anterior node. DMN distribution changes in the posterior node may reflect a possible compensatory effect on cognitive performance.

Principal components of functional connectivity: A new approach to study dynamic brain connectivity during rest

“…However, we also confirmed the bilateral parahippocampal gyri, right amygdala, left thalamus and left midtemporal pole as more strongly connected in RRMS patients (Richiardi et al, 2012). Such selective increased FC has been reported by several other studies as well (Bonavita et al, 2011;Dogonowski et al, 2013;Hawellek et al, 2011;Richiardi et al, 2012;Rocca et al, 2012;Roosendaal et al, 2010) and has been interpreted as a compensatory mechanism (Bonavita et al, 2011;Roosendaal et al, 2010) because activation studies have shown increased activity in regions devoted to the task and the recruitment of additional regions in MS patients (Pantano et al, 2002;Rocca et al, 2005). It is however also possible that these increases originate from a loss of flexibility in functional interactions, rather than as a compensatory mechanism (Hawellek et al, 2011).…”

“…The importance of these regions suggests that the dynamic FC of at least part of the DMN is altered in patients. These results add to, and complement, several studies which have reported disturbed stationary FC in different parts of the DMN in MS patients (Bonavita et al, 2011;Hawellek et al, 2011;Richiardi et al, 2012;Rocca et al, 2012). The distinction between posterior and anterior/temporal DMN regions seen in eigenconnectivity 6 is similar to the DMN fragmentation observed in Allen et al (in press) and would be missed in conventional stationary FC analyses.…”

“…The identified brain regions are largely consistent with those in a previous study by our group, which aimed at discriminating between HC subjects and RRMS patients based on stationary FC (Richiardi et al, 2012); i.e., the left Heschl's gyrus, right rolandic operculum, and right superior parietal gyrus, were identified as being more strongly connected in HC subjects in both studies. Reduced stationary FC in MS patients is indeed commonly observed and is thought to stem from structural damage (Bonavita et al, 2011;Lowe et al, 2002;Richiardi et al, 2012;Roosendaal et al, 2010). However, we also confirmed the bilateral parahippocampal gyri, right amygdala, left thalamus and left midtemporal pole as more strongly connected in RRMS patients (Richiardi et al, 2012).…”

“…Alternative imaging methods, such as resting-state fMRI, have started to address the issue of hidden damage and shown disrupted stationary FC. While some studies restricted their analysis to the DMN or motor regions (Bonavita et al, 2011;Dogonowski et al, 2013;Lowe et al, 2002;Rocca et al, 2010), others have reported changes in several large-scale resting state networks, including the sensorimotor and executive control networks (Hawellek et al, 2011;Richiardi et al, 2012;Rocca et al, 2012;Roosendaal et al, 2010). Together, these results are very promising for characterizing the functional pathology of MS, but the relationship between structural damage and functional changes is still poorly understood (Schoonheim and Filippi, 2012).…”

Classifying minimally disabled multiple sclerosis patients from resting state functional connectivity

“…Rocca et al (2010) found reduction of activity in the anterior cingulate cortex (ACC) at rest in MS patients relative to controls, and in cognitively impaired MS patients related to cognitively intact MS patients. Weaker DMN connectivity in the ACC of MS patients was also reported by Bonavita et al (2011) using independent component analysis of fMRI resting-state data. Roosendaal et al (2010) investigated fMRI restingstate networks in patients with clinically isolated syndrome (CIS) and patients with RRMS and observed an increased synchronisation of some resting-state networks in CIS patients which disappeared in those with RRMS, suggesting initial functional compensation that is lost with disease progression.…”