Synopsis
In the treatment of gliomas, radiation therapy
(RT) is associated with long-term effects including vascular injury in the form
of cerebral microbleeds (CMBs), and changes in the white matter and thickness
of cortex. Ultra high-field MRI techniques were used to characterize RT-induced
changes across serial scans in support of ongoing investigations of the role of
anti-angiogenic therapies in minimizing treatment effects. Steady increases in
the number of CMBs was observed decades post-RT. CMB foci were characterized by
increased isotropic diffusion when compared to surrounding white matter, which showed
signs of degradation in as few as two months between serial scans.
Purpose
While radiation therapy (RT)
remains a standard practice in the upfront treatment of high-grade gliomas and
low grade gliomas at the time of recurrence, it is often associated with
long-term side effects including vascular injury and cognitive decline.1
With current treatment strategies, survival for WHO (world health organization)
grades II and III gliomas is between 6 and 10 years,2 thus measures
of quality-of-life (QOL) serve as a relevant endpoint for these patients who
live substantially longer than patients with glioblastoma. Towards maximizing
patient QOL, a co-primary goal next to survival should be to minimize the
deficits incurred through treatment. RT-induced vascular injury
typically manifests as size-varying hemosiderin deposits in the brain called cerebral
microbleeds (CMBs), which are capable of being detected with Susceptibility-Weighted
Imaging (SWI) as early as 8 months following treatment.3 Usually accompanying
CMBs are changes in the integrity of the white matter (WM) pathways and
thickness of the cortex.4,5 While it has been shown that the number
of CMBs progressively increases, and that the WM degrades and cortex thins
following treatment, there is scant data evaluating both global and regional
changes simultaneously, or at ultra-high field strengths where visualization is
enhanced6. Understanding the chronology of RT-induced changes in the
brain, and more thoroughly characterizing serial changes in the distribution
and density of CMBs, will support ongoing work investigating the use of
anti-angiogenic or other radiosensitizing agents to alter RT-induced processes
leading to injury.3Methods
Thus far, data have been evaluated for eight of
the eighteen (5 male, 3 female; mean age 47.1 ± 9.8) who were treated with RT approximately 4
to 20 years’ prior for a glioma brain tumor (Figure 1). Patients were scanned
on a 7T scanner with a 32 channel receive coil. High-resolution SWI data, 2-shell,
24- and 55-directional DTI, and T1-weighted images of brain anatomy were acquired
across two serial scans. The time between scans varied across patients from 2
months up to 3 years. CMBs were detected using an in-house automated CMB
detection algorithm7,8, recently updated to perform CMB volume
quantification9. The number and volume of CMBs were quantified
across serial scans; between-patient comparisons were made with respect to radiation
dose, time since RT, and time between serial scans. Diffusion parameters,
including fractional anisotropy (FA), mean, longitudinal, and radial
diffusivity (MD, LD, RD) were evaluated at the CMB foci as well as within the
surrounding WM. Mean values for the CMB foci and WM were contrasted, and
assessed across serial scans. The orientation dispersion index (ODI) and free
water volume fraction (FISO) from the NODDI (neurite orientation dispersion and
density imaging) toolbox were evaluated in the same manner. Tissue contrast on
the T1-weighted anatomical images was first corrected with an optimized N4 bias
field correction algorithm, then segmented with FreeSurfer (version 5.3.0) to
quantify cortical thickness. Regional changes in cortical thickness were
assessed, and associated with CMB characteristics. Results
The number and mean volume of CMBs ranged
between 6 and 125 CMBs, and 1.87 and 8.24 mm3 respectively, but were
uncorrelated with time since CRT (Figure 2). The influence of radiation dose is
displayed in Figure 2 for two patients treated 4 and 5 years prior with 60Gy
and 54Gy, respectively. The fold increase in CMBs, was positively correlated
with time between serial scans. A weaker trend held for the fold increase in
mean volume of CMBs, however, there were observable changes in CMB volumes
overtime (Figure 3). When compared with the surrounding WM, CMB foci were predominately
characterized by decreased LD and FA, and increased MD, RD, ODI and FISO (Figure
4). Identical trends were observed in the surrounding WM across serial scans. Regional
changes in cortical thickness varied between patients, with no direct
association to tumor location where the majority of CMBs were detected.Discussion/Conclusion
Preliminary findings here suggest that there is a steady increase in the number of CMBs even decades following treatment, and confirms that radiation dose is a determinate of CMB evolution. Diffusion parameters can be used to characterize CMB foci, demonstrating increased isotropic diffusion and structural degradation over the surrounding WM. Serial changes in these parameters can be observed in as few as two months between scans. Data from the present cohort, augmented by added serial scans and data from the remaining 10 patients, will enable a more thorough investigation of these RT-induced changes. This includes the rate of CMB growth, refining the relationship between dose and CMB presence, evaluating changes in the distribution of CMBs according to dose maps, and relating CMB characteristics to structural and functional connectivity. Acknowledgements
The study was supported by NIH grant RO1HD079568 and a GE Healthcare investigator initiated grant.References
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