Background: Longitudinal evolution of cortical thickness (CTh) in different MS phenotypes has been rarely studied.
Aim: To investigate the regional pattern and 1-year progression of cortical thinning in relapsing-remitting (RR) and progressive (P) MS.
Methods: 3T high-resolution T1-weighted magnetic resonance imaging (MRI) was obtained from 86 patients (75 RRMS, 11 PMS) and 34 healthy controls (HC) at three European sites at baseline and 1-year follow-up. Using FreeSurfer, baseline CTh between-group differences, longitudinal CTh changes and their correlations with clinical and MRI variables were assessed.
Results: Baseline frontal, parietal and sensorimotor atrophy was found in MS versus HC. Such pattern was driven by RRMS, while PMS showed additional parietal, insular and sensorimotor cortical atrophy versus RRMS. At 1-year versus baseline, additional frontal and temporal cortical thinning was detected in RRMS patients, while a widespread CTh reduction was found in PMS patients (significant at time-by-group interaction vs RRMS). In MS, baseline fronto-parietal atrophy correlated with more severe disability and higher lesion volume. Baseline inferior parietal CTh decrease and 1-year temporal cortical thinning correlated with more severe disability.
Conclusion: Parieto-temporal baseline CTh abnormalities and thinning pattern over time characterized the main MS clinical phenotypes and were associated with 1-year disability worsening.
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http://dx.doi.org/10.1177/1352458520940548 | DOI Listing |
Aust N Z J Psychiatry
January 2025
Melbourne Neuropsychiatry Centre, Department of Psychiatry, The University of Melbourne, Parkville, VIC, Australia.
Objective: Around 30% of people with schizophrenia are refractory to antipsychotic treatment (treatment-resistant schizophrenia). Abnormal structural neuroimaging findings, in particular volume and thickness reductions, are often described in schizophrenia. Novel biomarkers of active brain pathology such as neurofilament light chain protein are now expected to improve current understanding of psychiatric disorders, including schizophrenia.
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January 2025
Functional Imaging Unit, Department of Clinical Physiology and Nuclear Medicine, Copenhagen University Hospital Rigshospitalet, Valdemar Hansens Vej 1-23, Glostrup, 2600, Denmark.
Background: Accumulation of β-amyloid (Aβ) in the brain is a hallmark of Alzheimer's Disease (AD). Cerebral deposition of Aβ initiates deteriorating pathways which eventually can lead to AD. However, the exact mechanisms are not known.
View Article and Find Full Text PDFMult Scler
January 2025
Cognitive Neuroscience Division, Department of Neurology, Columbia University Irving Medical Center, New York, NY, USA.
Background: Memory decline is common in multiple sclerosis (MS), although pathophysiological mechanisms are not fully understood.
Objective: The objective was to investigate the relationship of changes in structural and functional neuroimaging markers to memory decline over 3-year follow-up.
Methods: Participants with MS underwent cognitive evaluation and structural, diffusion, and functional 3T magnetic resonance imaging (MRI) scans at baseline and 3-year follow-up.
Eur Arch Psychiatry Clin Neurosci
December 2024
IRCCS Ospedale Policlinico San Martino, Genoa, Italy.
Recent studies suggested that structural changes in the cerebellum are implicated in the pathophysiology of bipolar disorder (BD). Here, we aimed to characterize the structural alterations of cerebellar lobules in BD, evaluating their possible relation with those occurring in the rest of the brain. One-hundred-fifty-five type I BD patients were recruited and compared with one-hundred-nineteen controls subjects.
View Article and Find Full Text PDFCureus
November 2024
Department of Anatomy, National and Kapodistrian University of Athens School of Medicine, Athens, GRC.
This study aims to review the existing literature on cerebral cortical changes in craniosynostosis during the months of August and September 2023. It focuses on alterations occurring in cases of both syndromic and non-syndromic forms of the disease. In particular, variations in volume, size, and structure (e.
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