Cortical thickness estimation in longitudinal stroke studies: A comparison of 3 measurement methods

Abstract

There is considerable controversy about the causes of cognitive decline after stroke, with evidence for both the absence and coexistence of Alzheimer pathology. A reduction in cortical thickness has been shown to be an important biomarker for the progression of many neurodegenerative diseases, including Alzheimer's disease (AD). However, brain volume changes following stroke are not well described. Cortical thickness estimation presents an ideal way to detect regional and global post-stroke brain atrophy. In this study, we imaged a group of patients in the first month after stroke and at 3 months. We compared three methods of estimating cortical thickness on unmasked images: one surface-based (FreeSurfer) and two voxel-based methods (a Laplacian method and a registration method, DiRecT). We used three benchmarks for our analyses: accuracy of segmentation (especially peri-lesional performance), reproducibility, and biological validity. We found important differences between these methods in cortical thickness values and performance in high curvature areas and peri-lesional regions, but similar reproducibility metrics. FreeSurfer had less reliance on manual boundary correction than the other two methods, while reproducibility was highest in the Laplacian method. A discussion of the caveats for each method and recommendations for use in a stroke population is included. We conclude that both surface- and voxel-based methods are valid for estimating cortical thickness in stroke populations.

Reproducibility of quantitative structural and physiological MRI measurements

“…Previous efforts demonstrated high scan–rescan reproducibility of the neuroimaging included of the volumetric measurements for subcortical brain structures (Maclaren et al., 2014), cortical gray matter thickness (Dickerson et al., 2008; Han et al., 2006; Li et al., 2015), and diffusion tensor measurements (Acheson et al., 2017; Jovicich et al., 2014). Likewise, several prior studies quantified scan–rescan stability and reproducibility of the MRS measurements at 3T (Wellard, Briellmann, Jennings, & Jackson, 2005; Wijtenburg & Knight‐Scott, 2011; Wijtenburg et al., 2013).…”

Structural Plasticity of Remote Cortical Brain Regions is Determined by Connectivity to the Primary Lesion in Subcortical Stroke

“…[9][10][11] Only few studies have focused on changes of cortical gray matter after stroke using conventional volumetric measurements, 12 voxel-based morphometry, 13,14 or CT measurements. 15,16 In a recent study, Duering et al 17 showed cortical atrophy in regions with high probability of connectivity to incident subcortical infarcts in patients with CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy) showing a specific impact of subcortical lesion. Taken together, these previous studies show a general pattern of cortical atrophy mainly interpreted as secondary damage to homologous areas either via direct retrograde axonal degeneration or locally disturbed cerebral blood flow and metabolism.…”

Know your tools—concordance of different methods for measuring brain volume change after ischemic stroke

“…Cerebral volume change, particularly atrophy, has been described in a variety of neurological disorders, most notably multiple sclerosis, where it has been demonstrated to correlate with long-term disability [1][2][3] and dementia [4]. In both of these conditions, the detection of global or regional changes in brain volume has the potential to be used as a surrogate marker of disease progression or treatment response.…”

“…In both of these conditions, the detection of global or regional changes in brain volume has the potential to be used as a surrogate marker of disease progression or treatment response. Recently, there has also been growing interest in the detection of regional and global cerebral volume change after stroke [2,3,[5][6][7], particularly as this may represent part of the mechanism involved in brain recovery, or a novel treatment target for a neuroprotective agent [8,9]. However, there are concerns regarding the validity and reproducibility of automated cerebral magnetic Electronic supplementary material The online version of this article (doi:10.1007/s00234-015-1522-8) contains supplementary material, which is available to authorized users.…”

“…Furthermore, the time interval required for the robust detection of meaningful degrees of brain atrophy after stroke remains uncertain. While studies have examined differences over time frames typical of stroke clinical trials, such as 3 months [2,3,7], it may be that this relatively short timeframe does not allow sufficient volume change to be reliably detectable and that intervals of 1 year or more may be required [5,13]. On the other hand, in most clinical settings, imaging at these longer time points becomes increasingly difficult due to patient attrition and loss of follow-up.…”