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

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.

Structural brain development and depression onset during adolescence: a prospective longitudinal study.

OBJECTIVE: The authors sought to investigate whether the structural development of limbic, striatal, and prefrontal regions that are critically implicated in the pathophysiology of depression is associated with adolescent-onset depression. METHOD: In a longitudinal design, a risk enriched community sample of 86 adolescents (41 of them female) who had no history of depressive disorders participated in neuroimaging assessments conducted during early (age 12) and midadolescence (age 16). Onset of depressive disorders was assessed for the period spanning early to late adolescence (ages 12 to 18). Thirty participants experienced a first episode of a depressive disorder during the follow-up period. The authors assessed whether onset of depressive disorder was associated with structural change in limbic, striatal, and prefrontal cortical regions from early to mid-adolescence. RESULTS: Volumetric change in the hippocampus, amygdala, and putamen from early to mid-adolescence was associated with the onset of depression during adolescence. Attenuated growth of the hippocampus and attenuated reduction in putamen volume over time were associated with the onset of depression. Sex moderated the association between amygdala growth and depression such that exaggerated growth and attenuated growth of the amygdala were associated with depression in females and males, respectively. Across time, smaller nucleus accumbens volume was associated with depression in females only. CONCLUSIONS: These findings suggest that alterations in the developmental trajectories of limbic and striatal regions during adolescence may represent a neurobiological manifestation of a risk factor for the development of depression during this critical period and thus may provide clues as to etiological mechanisms of this disorder.

Changes in regional brain volume three months after stroke.

INTRODUCTION: Little is known about changes in regional brain volume after stroke. We investigated cortical thickness changes over 3 months in a group of stroke patients compared with controls. MATERIAL AND METHODS: Patients with acute hemispheric stroke were studied within 3h of stroke onset and serially over 3 months. We compared the acute and 3 month scans with independently acquired control images. High resolution isotropic T1 images were analyzed using FreeSurfer V5.0, comparing regional average cortical thickness, hippocampal and thalamic volumes. Stroke patient results were analyzed separately for ipsilesional and contralesional regions, whereas control results were averaged across hemisphere. Percentage change scores between the two time points were computed for each participant, and paired sample t-tests were used to assess significant change. RESULTS: 12 stroke patients (9 men, 7 left-hemispheric, mean age=65.1 years) and 10 control participants (5 men, mean age=67.2 years) were included. There were no significant differences between the 2 time points in global or regional average cortical thickness, or hippocampal and thalamic volume estimates for control subjects. Regional variability in patient data was demonstrated, particularly cortical thickness increases in contralesional paracentral, superior frontal and insular regions, areas known to be activated in functional MRI studies of motor recovery. A significant reduction in thalamic volume was also found, most apparent ipsilesionally. CONCLUSIONS: Post-stroke changes in regional cortical thickness are demonstrable even over short time-frames. Contralesional cortical thickness increases may represent compensatory mechanisms. Significant reductions in thalamic volume may represent evidence of early post-stroke atrophy. Further studies are required to confirm and extend these preliminary results.