Eleonora Patitucci1, Rachael C Stickland 2, Hannah L Chandler1, Michael Germuska1, Catherine Foster1, Sharmila Khot1, Neeraj Saxena1, Valentina Tomassini1,3, and Richard G Wise1,3
1CUBRIC - Cardiff University Brain Research Imaging Centre -Psychology, Cardiff University, Cardiff, United Kingdom, 2Department of Physical Therapy and Human Movement Sciences, Northwestern University, Chicago, IL, United States, 3Institute for Advanced Biomedical Technologies (ITAB), Department of Neurosciences, Imaging and Clinical Sciences, University of Chieti-Pescara “G. d’Annunzio”, Chieti, Italy
Synopsis
Calibrated
fMRI can map the rate of cerebral oxygen consumption of the human brain,
offering an important indicator of energy dysfunction in neurodegenerative and
neuroinflammatory diseases. Previous studies investigated oxygen metabolism at
rest or in response to tasks within BOLD signal defined region of interests (ROIs).
Here, we investigate on a voxel-by-voxel basis the oxygen metabolic activity in
patients with multiple sclerosis during the execution of a task. We show the
feasibility of mapping task-induced CMRO2 changes, demonstrating
reduced oxygen consumption in the basal ganglia in MS patients that was not
otherwise evident from BOLD or CBF signals.
INTRODUCTION
fMRI BOLD signal is the most widely used measure
of changes in brain activity due to its high SNR and ease of application.
However, this is only an indirect measure of neural activity, as it reflects a
combination of changes in cerebral blood volume, cerebral blood flow and oxygen
consumption1. Under the assumption of oxidative energy release, the
rate of cerebral metabolic oxygen consumption is expected to offer a direct quantitative
measure of tissue energy consumption. In neuroinflammatory conditions such as
multiple sclerosis (MS), where the coupling between neural activity and the
vascular signal may be affected, these measures can offer
biologically-relevant information on the actual tissue state. Previous studies have also shown higher
reproducibility for calibrated fMRI technique, measuring relative
changes in oxygen consumption, compared to BOLD2. Here, using
a voxel-wise approach, we aim (I) to
investigate changes in CMRO2 on a
voxel-by-voxel basis during the execution of a motor task in MS patients and in
matched healthy controls (HC) and (II) to map differences in task-related oxygen
metabolism between groups. Changes
in CMRO2 are our primary measure of tissue activity. Therefore, we
do not rely on qualitative BOLD signal changes to identify regions of interest,
when comparing HC and MS patients.METHODS
17 relapsing-remitting MS (mean±SD 37.1±1.8 years) patients and 21
matched healthy controls (mean±SD 34.1±1.3) underwent MRI (3T Siemens Prisma) that
included a dual-excitation pseudo-continuous arterial spin labelling acquisition
(TE1: 10ms, TR1: 3600ms, TE2: 30ms, TR2: 800ms, labelling duration: 1.5s,
post-labelling delay: 1.5s, slice thickness: 7mm, and GRAPPA acceleration
factor 3)3. We used our multiparametric dual-calibrated fMRI method,
employing hypercapnic and hyperoxic calibration to map baseline (absolute)
brain oxygen consumption, and provided the calibration parameter (M)4
for estimating relative changes in oxygen consumption. The same acquisition
scheme was used during the performance of 8minute serial reaction time task
consisting of 10 task blocks of 17s interleaved with 30s rest blocks. A 2-way ANOVA
was performed in order to investigate changes in behavioural performance (accuracy
(ACC) and reaction times (RT)) during task execution and differences between
groups.
FEAT
(https://fsl.fmrib.ox.ac.uk/)
was used to fit a linear model to the voxel-wise data in order to produce maps
of significant task-induced BOLD signal change and CBF change. BOLD and CBF
maps, as well as M maps from the respiratory challenges, were transformed to MNI
space using registrations defined using T1-weighted structural scans of each
participant (FSL-FLIRT).
In order to estimate relative
CMRO2 at voxel-wise level for each subject, the BOLD and CBF signal
changes were applied in the Davis equation4,5. CMRO2 mean
relative changes to the task blocks (compared to rest) were computed.
Permutation tests (FSL-Randomise) were used to localise differences at the
group level between HC and MS patients in BOLD response, CBF response and CMRO2
consumption during task execution.RESULTS
There was no significant group difference in RT (F(1,8)=3.13, p=0.08) or in ACC (F(1,8)=0.67, p=0.41). Both groups improved their
performance with time (ACC: F(8,288)=11.67, p<0.001; RT: F(8,288)=10.61, p<0.001), with no
difference between groups in the extent of improvement ( ACC: F(8,288)=1.23, p=0.28; RT: F(8,288)=1.27, p=0.25).
Both
groups showed task-induced increases in CMRO2 consumption with a
similar spatial distribution of CMRO2 compared to task-related BOLD
signal change and CBF increases (Figure 1). Areas of main activation included the
postcentral gyri, superior parietal lobules, cerebellum and basal ganglia
bilaterally. MS patients showed significantly lower CMRO2 consumption
during task execution compared to HC in the thalami and caudate nuclei (Figure
2), with no between group differences in BOLD and CBF responses to the task.DISCUSSION/CONCLUSION
Using
quantitative fMRI we demonstrate the feasibility of mapping task-induced
changes in CMRO2 on a voxel-by-voxel basis to investigate tissue energy
changes during motor-task execution in MS patients and in controls; as well as the
differences between groups. The regional group difference
were
not defined by regions of altered BOLD signal response,
but by
CMRO2 maps directly.
Overall,
our results represent a methodological step forward when seeking to understand
the tissue energetics, as they indicate that more commonly applied functional
MRI methods are not sufficiently sensitive to changes in tissue
energy consumption during task execution. Also, the voxel-wise investigation of
energy dysfunction in MS may provide more sensitive and physiologically
relevant markers of tissue damage for the evaluation of therapeutic strategies.
Acknowledgements
The study was funded by the Wellcome Trust and MS Society UK.References
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