Examination of processing speed deficits in multiple sclerosis using functional magnetic resonance imaging

Abstract

Although it is known that processing speed deficits are one of the primary cognitive impairments in multiple sclerosis (MS), the underlying neural mechanisms responsible for impaired processing speed remain undetermined. Using BOLD functional magnetic resonance imaging, the current study compared the brain activity of 16 individuals with MS to 17 healthy controls (HCs) during performance of a processing speed task, a modified version of the Symbol Digit Modalities Task. Although there were no differences in performance accuracy, the MS group was significantly slower than HCs. Although both groups showed similar activation involving the precentral gyrus and occipital cortex, the MS showed significantly less cerebral activity than HCs in bilateral frontal and parietal regions, similar to what has been reported in aging samples during speeded tasks. In the HC group, processing speed was mediated by frontal and parietal regions, as well as the cerebellum and thalamus. In the MS group, processing speed was mediated by insula, thalamus and anterior cingulate. It therefore appears that neural networks involved in processing speed differ between MS and HCs, and our findings are similar to what has been reported in aging, where damage to both white and gray matter is linked to processing speed impairments.

Neural correlates of episodic future thinking impairment in multiple sclerosis patients

“…This allows us to reasonably interpret the patient's cerebral activation pattern as resulting from pathology, rather than arising from a too poor completion of the task (Cader et al, 2006). Consistent with the literature dealing with the functional changes associated with cognitive impairment in MS patients, we reported both increased and decreased cerebral activations in brain areas pertaining to the EFT brain network normally recruited by healthy controls, but also the recruitment of contralateral brain areas (Cader et al, 2006;Genova et al, 2009;Hulst et al, 2012).…”

“…However, previous studies investigating the neural changes associated to cognitive impairment in MS patients reported increased/decreased cerebral activations in brain areas also recruited by healthy controls and/or the recruitment of alternative (frequently contralateral) brain areas (Cader, Cifelli, Abu-Omar, Palace, & Matthews, 2006;Genova, Hillary, Wylie, Rypma, & DeLuca, 2009;Hulst et al, 2012). These findings have been obtained for working memory (Forn et al, 2012;Morgen et al, 2007), information processing speed (Genova et al, 2009), or anterograde memory (Hulst et al, 2012;Mainero et al, 2004;Morgen et al, 2007).…”

Confirming white matter fMRI activation in the corpus callosum: Co-localization with DTI tractography

“…In addition, fMRI activation in white matter may have future clinical applications. Indeed, fMRI investigations of neuropsychological tests for evaluating white matter diseases have shown (but not reported) group level activation in white matter ( [Genova et al, 2009] and [Lazeron et al, 2003]). Given the variability observed in the current study, future work is needed to determine whether this concept can be meaningfully applied at the individual patient level.…”

Multiple sclerosis-related white matter microstructural change alters the BOLD hemodynamic response

“…Such regional heterogeneity would be consistent with the heterogeneous findings of MSrelated BOLD increases and decreases reported in extant literature. [6][7][8][9][10] Advanced neuroimaging methods, such as calibrated fMRI, coupled with diverse task paradigms to evoke neural activity in different ROIs, could be employed to test this hypothesis. [16][17][18][19]21,79 MS-related alterations to functional hyperemia could also influence measurement of the temporal associations used to estimate functional connectivity at rest and during tasks.…”

“…7,9 Accounting for such MS-related BOLD signal changes by considering factors that affect neural activity, such as behavioral performance, 11 has revealed a similarly complex picture. While some fMRI studies have shown MS-HC BOLD signal differences in the presence of performance differences, 7,9 others have shown BOLD signal differences in the absence of performance differences. 8 The results of studies comparing BOLD signal between MS patients and HCs have highlighted that such differences are indexing complex phenomena related to MS pathophysiology.…”