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Memory performance in multiple sclerosis patients correlates with central brain atrophy.

H Hildebrandt1, H K Hahn, J A Kraus

  • 1Department of Neurology, Klinikum Bremen-Ost, Züricher Str. 40, 28325 Bremen, Germany. helmut.hildebrandt@uni-oldenburg.de

Multiple Sclerosis (Houndmills, Basingstoke, England)
|August 12, 2006
PubMed
Summary

In relapsing-remitting multiple sclerosis (RRMS), ventricular enlargement correlates with memory decline, while cognitive function is linked to depression and fatigue, independent of brain atrophy.

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Area of Science:

  • Neuroimaging
  • Neurology
  • Cognitive Science

Background:

  • Relapsing-remitting multiple sclerosis (RRMS) is characterized by neurological deficits.
  • Brain atrophy and cognitive dysfunction are common in MS, impacting quality of life.

Purpose of the Study:

  • To investigate whole brain and central brain atrophy in RRMS patients.
  • To determine the relationship between brain atrophy, memory, cognitive performance, fatigue, depression, and quality of life.

Main Methods:

  • 45 RRMS patients underwent T1-weighted MRI for automated brain parenchymal fraction (BPF) and ventricular brain fraction (VF) calculation.
  • Neuropsychological tests and self-rating scales assessed memory, cognition, depression, fatigue, and quality of life.
  • Age-corrected partial correlations analyzed relationships between atrophy measures and clinical/cognitive outcomes.

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Main Results:

  • BPF moderately correlated with disease duration, EDSS, upper extremity motor function, and mental quality of life.
  • VF moderately correlated with EDSS, motor function (upper/lower extremities), and memory.
  • Neither BPF nor VF correlated with fatigue or depression; cognitive tests correlated with fatigue and depression.

Conclusions:

  • Ventricular enlargement in RRMS is associated with memory deficits, suggesting limbic system vulnerability.
  • Cognitive performance is linked to depression and fatigue, independent of measurable brain atrophy.
  • These findings highlight the complex interplay between structural changes, cognitive function, and emotional state in MS.