Sina Straub1, Julian Emmerich1,2, Stephanie Mangesius3, Elisabetta Indelicato4, Mark E. Ladd1,2,5, Sylvia Boesch4, and Elke R. Gizewski3
1Division of Medical Physics in Radiology, German Cancer Research Center, Heidelberg, Germany, 2Faculty of Physics and Astronomy, Heidelberg University, Heidelberg, Germany, 3Department of Neuroradiology, Medical University Innsbruck, Innsbruck, Austria, 4Department of Neurology, Medical University Innsbruck, Innsbruck, Austria, 5Faculty of Medicine, Heidelberg University, Heidelberg, Germany
Synopsis
Friedreich’s ataxia is a rare disease involving
degenerative processes within white matter fiber tracts, spinal nerves and the
cerebellum. A correlation of patients’ clinical status and superior cerebellar
peduncle atrophy has been shown in MR volumetry studies. The ongoing ultra-high
field study presented here assesses the degeneration of the superior
cerebellar peduncle in Friedreich’s ataxia with quantitative MR
parameters – susceptibility, diffusion anisotropy, and T2 and T1
relaxometry. Statistically significant differences between fractional
anisotropy as well as T2 values in patients and healthy controls
could be observed, indicating that these quantitative MRI methods potentially provide valuable
biomarkers to assess the course of Friedreich’s ataxia.
INTRODUCTION
Despite the fact that Friedreich’s ataxia is a rare
disease, it is the most common inherited ataxia with early onset of clinical
manifestations.1 A correlation of superior cerebellar peduncle (SCP)
atrophy and patients’ clinical status has been shown in magnetic resonance
imaging (MRI) studies assessing SCP volume.2,3 However, pathological
white matter changes in Friedreich’s ataxia have not been assessed using
quantitative MRI methods such as relaxometry, susceptibility mapping and
diffusion tensor imaging. Moreover, assessing fine fiber structures, such as
the superior cerebellar peduncle, benefits from ultra-high field MRI due to the
higher resolution and higher contrast-to-noise ratios achievable, thereby
minimizing partial volume effects and facilitating better structural
delineation.METHODS
The study was conducted in accordance with the
Declaration of Helsinki. Institutional review board approval was obtained and
all subjects provided written informed consent. Eight Friedreich’s ataxia
patients (mean age 38 ± 15 years; four female) and six healthy controls (mean
age 46 ± 16 years; four female) were scanned on a 7 T whole-body MR system
(Magnetom 7 T, Siemens Healthcare, Germany) with a 8Tx/32Rx-channel head coil
(Nova Medical Inc., Wakefield, MA, USA) driven in CP+ mode by use of an
in-house-constructed Butler matrix. The following sequences were acquired: a monopolar
3D gradient-echo (GRE), a multi-echo turbo spin echo (ME-TSE) with turbo factor
5, a 2D readout segmentation of long variable echo-trains (RESOLVE)4,5
in stimulated echo acquisition mode (STEAM)6,7 with two diffusion
weightings (b = 50 s/mm2, b = 800 s/mm2) and 20 diffusion
directions, a MP2RAGE with inversion times of 900 ms and 2750 ms, and a pre-saturation‐based 2D turbo flash for B1 mapping. All other
sequence parameters are shown in Table 1.
For susceptibility map generation, phase data were
combined on the scanner using ASPIRE8, and brain masks were
generated from the first echo of the magnitude images using FSL-BET9.
Phase images were unwrapped using Laplacian-based phase unwrapping10-12,
and the background field was removed with V-SHARP11,12 with
kernel size up to 12 mm. Susceptibility maps were calculated in Matlab
(R2017b, MathWorks, Natick, USA) using the STAR-QSM algorithm13.
Susceptibility maps were referenced to cerebrospinal fluid in the atrium of the
lateral ventricles.
T2 maps were generated form the ME-TSE data
and the B1 map using a dictionary-based method14. For T1
mapping and diffusion fractional anisotropy, vendor-provided maps were used.
Volumes of interest (VOIs) (see Figure 1) in the
superior cerebellar peduncle were manually drawn on each contrast using the Medical
Imaging Interaction Toolkit (MITK)15,16. Differences observed for
susceptibility values, diffusion fractional anisotropy, and T2 and T1
values were assessed using a two sample t-test in Matlab. A p-value of less
than 0.05 was considered statistically significant.
RESULTS
Figure 2 shows box plots of
susceptibility values, diffusion fractional anisotropy values, and T2
and T1 values of the superior cerebellar peduncle in Friedreich’s
ataxia patients and healthy controls. The SCP had a median susceptibility of
−0.023
ppm for patients and
−0.043 ppm for controls, median diffusion fractional
anisotropy of 0.71/ 0.85 for patients/ controls, median T2 values of
60/ 72 ms for patients/ controls, and median T1 values of 1382/ 1289
ms for patients/ controls. For diffusion anisotropy (p=0.0003) and for T2
values (p=0.005) the differences between healthy controls and patients were
statistically significant; for susceptibility values (p=0.067) and T1
values (p=0.160) the differences were not statistically significant.
In Figure 3, representative slices of susceptibility
maps, color-coded diffusion fractional anisotropy maps, and T2 and T1
maps of one healthy control and one patient of the same age and same sex are
shown. An atrophy of the superior cerebellar peduncles can be observed in all patient
images (second column). In QSM and in diffusion images, SCP (arrow heads) can
be clearly depicted in the healthy control showing more diamagnetic
susceptibility and higher fractional anisotropy than in the patient. In T2
maps, higher values can be observed in the heathy control than in the patient
as well as lower T1 values in T1 maps.
DISCUSSION AND CONCLUSION
MRI can not only visualize the degeneration of the
superior cerebellar peduncle in Friedreich’s ataxia but can also quantitatively
assess its degeneration. In this ongoing study, already at a rather early stage
with a relatively small number of participants, diffusion fractional anisotropy
and T2 values were statistically significantly different between
Friedreich’s ataxia patients and healthy controls. In future, these methods
could become reliable biomarkers for the assessment of disease stage in Friedreich’s
ataxia, for example in the evaluation of therapy efficiency.Acknowledgements
The provision of the ASPIRE gradient echo sequence and
corresponding ICE program for coil combination of the 7 T GRE data by Korbinian
Eckstein and Simon D. Robinson is kindly acknowledged.References
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