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P0632 - Reduced brain integrity slows down and increases low alpha power in multiple sclerosis (ID 891)
In multiple sclerosis, the interplay of neurodegeneration, demyelination and inflammation leads to changes in neurophysiological functioning.
This study aims to characterise the relation between reduced brain volumes and spectral power in multiple sclerosis patients and matched healthy subjects.
During resting-state eyes closed, we collected magnetoencephalographic data in 67 multiple sclerosis patients and 47 healthy subjects, matched for age and gender. Additionally, we quantified different brain volumes (white matter, cortical and deep grey matter, FLAIR lesion load and volume of black holes) and calculated the power spectral density. Instead of using the traditionally used frequency bands, we calculated the source reconstructed power spectral density in frequency bins of 0.25 Hz (range: 0-40 Hz) and corrected for multiple comparisons through permutation testing.
First, a principal component analysis (PCA) of brain volumes demonstrates that atrophy can be largely described by two components: one overall degenerative component that is indicative of brain integrity and correlates strongly with different cognitive tests, and one component that mainly captures degeneration of the cortical grey matter that strongly correlates with age. As the first PC was observed both when performing the PCA on the full cohort and on the two subcohorts, we denote this component as an index of brain integrity. Logically, this component was more strongly expressed in the MS cohort.
Next, a multimodal correlation analysis indicates that reduced brain integrity is accompanied by increased alpha1 power in the temporoparietal junction (TPJ). Patients showing this local increase in alpha-peak also scored significantly worse on different cognitive tests and reduced thalamic volumes. The increase in alpha1-power comes from both a slowing of the main alpha-peak and an increase in power.
MS patients with reduced brain integrity demonstrated increased alpha1 power in the TPJ and impaired cognitive functioning.