Iskindir Weldemeskel1 and Pierre LeVan2
1Biomedical Engineering, University of Calgary, Calgary, AB, Canada, 2Radiology, University of Calgary, Calgary, AB, Canada
Synopsis
Keywords: fMRI Analysis, Epilepsy, Implanted Electrodes, intracranial EEG, fMRI, Susceptibility
Motivation: Model susceptibility-induced signal degradation in fMRI in patients with implanted electrodes and reduce imaging artifacts across electrodes.
Goal(s): Develop a model to understand and mitigate susceptibility effects due to implanted electrodes in fMRI.
Approach: Model electrode (platinum sphere) and brain activation contrast (cylinders representing blood vessels) at 3T. Calculate intravoxel dephasing and assess the impact of the electrode on signal amplitude and activation contrast. Investigate the impact of echo times on signal loss.
Results: Key findings reveal signal enhancement with increased distance from the electrode and reduced contrast loss with shorter echo times.
Impact: This research could
redefine future functional diagnostics in patients with implanted electrodes
such as epilepsy or Parkinson’s disease patients, leading to more precise
surgical interventions and improved patient care. Mitigating
susceptibility-induced image artifacts will impact neuroscience research and
clinical applications.
INTRODUCTION
Many patients with neurological disorders such as epilepsy or Parkinson’s
disease may benefit from implanted intracerebral electrodes for brain activity
monitoring or brain stimulation. In these patients, functional MRI (fMRI) can
provide valuable insights into brain activity. However, this presents
challenges, primarily associated with image degradation due to susceptibility
artifacts introduced by the electrodes1,2. The objective of this study is to generate
a biophysical model of these artifacts and to quantify the potential for
artifact mitigation by multi-echo
imaging approaches3.METHODS
We have established a physical model that accounts for the susceptibility
effects introduced by an implanted electrode and blood vessels during brain
activation at 3T. To model the susceptibility artifacts in fMRI, we represented
the electrodes as platinum spheres with diameter 0.56mm (matching clinical
Ad-Tech electrodes), with a magnetic susceptibility of 2.65x10-4. The blood
vessels were modeled as randomly distributed cylinders, each with a
susceptibility of -6.93x10-6. T2* values at rest and during brain activation
were calculated using the following parameters: oxygenation fraction during
resting brain state (0.6), oxygenation fraction during active brain state
(0.7), susceptibility difference between oxygenated and deoxygenated blood (0.8x10-7),
volume fraction during the resting brain state (0.05) and the volume fraction
during the active brain state (0.06) for a 5ml blood volume per 100ml brain
volume.
To assess signal
degradation, we quantified intravoxel dephasing by subdividing 3x3x3mm3 voxels
(typical for fMRI) into 10 sub voxels along each spatial dimension. For each
sub voxel, we calculated the local magnetic field from the model described
above. The corresponding local Larmor frequency information (fig 1.A) was then
used to derive the MRI signal within each voxel (fig 1.B). RESULTS
In the presence
of the electrode, the main observable effect is a large loss in signal. At a
distance of 3, 4, and 5 voxels (9, 12, and 15 mm respectively) away from the electrode, the signal loss was
95.1%, 81.3%, and 53.7%, respectively. This suggests that useful fMRI signal may only be measured at least 15mm away from the electrode. However, in the
fMRI context, it is the contrast between rest and activation that is relevant,
rather than the absolute signal magnitude. We thus calculated this loss in
contrast and found it to be similarly large (95.2%, 83%, and 54.9% at locations
3, 4, and 5 voxels away from the electrode in a direction parallel to Bo,
respectively, and 97.2%, 92.1%, and 69% in a direction perpendicular to Bo).
Nevertheless, this loss in signal contrast may
be partially recoverable by optimizing the echo time. Figure 2 shows the
calculated loss in BOLD activation contrast at echo times of 55, 40, 30, 20,
and 10 milliseconds. We can see that despite the previously reported large
signal loss close to the electrodes, there may still be sufficient BOLD
contrast to quantify fMRI activations. For example, at a location 3 voxels away
from the electrode along B0, where signal loss is 95%, the corresponding BOLD
contrast loss is only ~75% when using a TE of 10 ms. The optimal TE is
spatially variable and depends on the distance between a voxel and the
electrode. CONCLUSION
Our research endeavors to address a critical issue when using fMRI in patients
with implanted electrodes. The modeled signal loss is consistent with
previously reported values that were measured experimentally at 3T1.
However, in fMRI, the strength of the MRI signal is less relevant than the
amplitude of the MRI signal change during brain activation. We have determined
that despite the significant loss of MRI signal in the vicinity of the
electrode, the loss in MRI contrast was less pronounced and could be partially
recovered by optimizing TE. As the optimal TE was spatially variable, this presents
an opportunity for the implementation of multi-echo fMRI approaches in the
future, which will provide optimal signal contrast at every brain location. This
avenue holds promise for enhancing our understanding of susceptibility-induced
effects and improving the sensitivity of fMRI in patients with implanted
electrodes.Acknowledgements
This work was supported by NSERC Discovery Grant RGPIN-2021-02797 and CIHR grant PJT-183825.References
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