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Default-mode network dysfunction and cognitive impairment in progressive MS.

M A Rocca1, P Valsasina, M Absinta

  • 1Neuroimaging Research Unit, Institute of Experimental Neurology, Division of Neuroscience, Scientific Institute and University Ospedale San Raffaele, Milan, Italy.

Neurology
|April 21, 2010
PubMed
Summary
This summary is machine-generated.

Default-mode network (DMN) dysfunction is linked to cognitive decline in progressive multiple sclerosis (MS). Abnormalities in DMN activity correlate with white matter damage and cognitive impairment in patients with SPMS and PPMS.

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Area of Science:

  • Neuroimaging
  • Neurology
  • Radiology

Background:

  • Multiple sclerosis (MS) is a demyelinating disease affecting the central nervous system.
  • Progressive forms of MS, including secondary progressive MS (SPMS) and primary progressive MS (PPMS), are characterized by accumulating disability and cognitive impairment.
  • The default-mode network (DMN) is a network of interacting brain regions known to be active during rest and involved in self-referential thought.

Purpose of the Study:

  • To investigate default-mode network (DMN) abnormalities in patients with SPMS and PPMS.
  • To determine if DMN abnormalities correlate with cognitive impairment.
  • To assess the relationship between DMN dysfunction and white matter (WM) damage using diffusion tensor (DT) MRI tractography.

Main Methods:

  • Resting-state (RS) functional MRI and DT MRI data were collected from 33 SPMS patients, 24 PPMS patients, and 24 healthy controls.
  • Independent component analysis (ICA) was employed to identify the DMN.
  • Standardized imaging analysis software (SPM5) was used for between-group comparisons of DMN activity and DT MRI tractography.

Main Results:

  • Significant differences in DMN activity were observed in the medial prefrontal cortex (mPFC), precentral gyrus (PcG), and anterior cingulate cortex (ACC) between patient groups and controls.
  • SPMS patients showed reduced DMN activity in the mPFC and PcG compared to controls.
  • PPMS patients exhibited reduced DMN activity in the PcG and ACC compared to controls. Reduction in ACC activity was more pronounced in cognitively impaired MS patients.
  • DMN abnormalities correlated with cognitive test scores and DT MRI measures of the corpus callosum and cingulum.

Conclusions:

  • Dysfunction in the anterior components of the DMN is implicated in the development of cognitive deficits in progressive MS.
  • These findings highlight the role of DMN alterations in the pathophysiology of cognitive impairment in progressive multiple sclerosis.
  • Neuroimaging of the DMN may serve as a potential biomarker for cognitive dysfunction in MS.