Irene Voldsbekk1, Daniel Roelfs1, Atle Bjørnerud1, Inge Groote1, and Ivan Maximov2
1Department of Diagnostic Physics, Oslo University Hospital, Oslo, Norway, 2Norwegian Centre for Mental Disorders Research, Oslo University Hospital, Oslo, Norway
Synopsis
There is an increasing awareness of time-of-day (TOD)
effects in MRI. The underlying causes of these fluctuations may be related to diurnal
physiological variations, reflecting the processes that govern transition
between sleep and wake. We probed TOD effects in a prospective manner, scanning
47 healthy individuals in the morning and the same evening using a five-shell
diffusion-weighted imaging protocol at 3T, where a number of important Zeitgeber signals were rigorously
controlled. We found significant changes in an number of derived DWI parameters
(FA, MD, AWF, MK), and speculate that these changes are pointing towards
underlying mechanisms of sleep-wake homeostasis.
Introduction
The role of diurnal
fluctuations in the human brain derived by magnetic resonance imaging (MRI) is
receiving increasing attention. However, little is known about the
physiological changes underlying these fluctuations. Transition between stages
of sleep and wake is regulated by circadian and homeostatic processes1. Contemporary
theories of sleep regulation emphasise accumulation of learning-induced
increases in synaptic strength2 and metabolic waste3 during wakefulness,
which sleep then serves to renormalise. Diurnal fluctuations in MRI measures
may thus reflect sleep regulating processes, and as such represent MRI-derived biomarkers
of sleep pressure. Recent evidence suggests that structural measures by
diffusion tensor imaging (DTI)4 change as a function
of time-of-day (TOD), both in the white matter (WM) skeleton5, the whole cerebrum6 and at the interface
of grey matter and cerebrospinal fluid (CSF)7. However, these
studies lack rigorous experimental control between scans and only Elvsåshagen
and colleagues5 assessed changes
spanning more than a few hours. In contrast, the current study addressed the
impact of TOD from morning to evening in a prospective controlled
within-subject experimental design in which participants were continuously
monitored from the first to the second scan. Moreover, the current study
included estimations of non-Gaussian diffusion metrics obtained from diffusion
kurtosis imaging (DKI) 8 and WM tract
integrity9 in addition to
classic DTI-derived parameters,
in order to probe underlying axonal properties.Methods
Participants were
47 healthy adults (30 women) who underwent diffusion-weighted (DWI) MRI in the
morning and evening of the same day. The imaging protocol consisted of a
multi-shell full-brain multiband-accelerated 2 mm isotropic acquisition with b
[0, 500, 1000, 2000, 3000]; directions [5, 12, 30, 40, 50]. Between scans,
they stayed at the hospital premises
under constant supervision and followed a standardised protocol of physical activity,
food and fluid intake. Diffusion data were preprocessed in accordance with the
following steps: noise correction10, Gibbs ringing corrections11, topup/eddy application12, B1 field normalisation and
spatial smoothing with Gaussian kernet 1mm3. All diffusion metrics
were then estimated using the Veraart and colleagues approach13. MRI images were analysed with voxel-wise tract
based spatial statistics14,
threshold free cluster enhancement15 and
permutation testing in FSL16,17,
correcting for multiple comparisons and thresholded at p < .05.Results
A
full day of wakefulness was found to be associated with widespread increases in
fractional anisotropy (FA), mean kurtosis (MK) and axonal water fraction (AWF),
in addition to widespread decreases in mean diffusivity (MD). See figures 1-4. These
changes were adjusted for age, gender and chronotype. Chronotype did not show a significant relationship with changes in any of the diffusion parameters. Moreover, changes spanned most
of the WM skeleton, suggesting a global effect.Discussion
These
findings indicate a temporal component to DWI-derived structural measures, in
which white matter microstructure fluctuate as a function of TOD. These
fluctuations may reflect physiological changes underlying accumulating sleep
pressure, as the fluctuation is prevalent as a global change in WM
microstructure. Importantly, we
found an increase in estimations of WM integrity and specifically in axonal
density, which suggest wakefulness may accommodate activity-dependent
structural plasticity in WM. Specifically, this could reflect processes related
to the activity-dependent accumulation of synapse strength2 and metabolic
waste3. However, caution must be exerted in interpreting specific underlying
biology on the basis of DTI and DKI18.
Although the increases in the
estimation of axonal density from AWF is a promising preliminary finding, introducing
more complex diffusion models will afford more detailed investigation of this
relationship. Despite this, these findings highlight the potential of
MRI derived measures to probe sleep regulating processes in the human brain.
Moreover, these findings have important implications for experimental
considerations, as diurnal fluctuations would confound any design in which one
experimental group is consistently scanned at a different TOD than another
experimental group.Conclusion
The
WM microstructure of the human brain is not static and fluctuate as a function
of TOD. The fluctuations detected by DWI parameters may represent biomarkers of
accumulating sleep pressure.Acknowledgements
We would like to thank the great team who helped with data collection.
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