Brain microstructural changes and fatigue after COVID-19

Abstract

Background Fatigue and cognitive complaints are the most frequent persistent symptoms in patients after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. This study aimed to assess fatigue and neuropsychological performance and investigate changes in the thickness and volume of gray matter (GM) and microstructural abnormalities in the white matter (WM) in a group of patients with mild-to-moderate coronavirus disease 2019 (COVID-19). Methods We studied 56 COVID-19 patients and 37 matched controls using magnetic resonance imaging (MRI). Cognition was assessed using Montreal Cognitive Assessment and Cambridge Neuropsychological Test Automated Battery, and fatigue was assessed using Chalder Fatigue Scale (CFQ-11). T1-weighted MRI was used to assess GM thickness and volume. Fiber-specific apparent fiber density (FD), free water index, and diffusion tensor imaging data were extracted using diffusion-weighted MRI (d-MRI). d-MRI data were correlated with clinical and cognitive measures using partial correlations and general linear modeling. Results COVID-19 patients had mild-to-moderate acute illness (95% non-hospitalized). The average period between real-time quantitative reverse transcription polymerase chain reaction-based diagnosis and clinical/MRI assessments was 93.3 (±26.4) days. The COVID-19 group had higher CFQ-11 scores than the control group (p < 0.001). There were no differences in neuropsychological performance between groups. The COVID-19 group had lower FD in the association, projection, and commissural tracts, but no change in GM. The corona radiata, corticospinal tract, corpus callosum, arcuate fasciculus, cingulate, fornix, inferior fronto-occipital fasciculus, inferior longitudinal fasciculus, superior longitudinal fasciculus, and uncinate fasciculus were involved. CFQ-11 scores correlated with microstructural changes in patients with COVID-19. Conclusions Quantitative d-MRI detected changes in the WM microstructure of patients recovering from COVID-19. This study suggests a possible brain substrate underlying the symptoms caused by SARS-CoV-2 during medium- to long-term recovery.

Neurocognitive Changes in Patients with Post-COVID Depression

“…One possible mechanism of cognitive impairment in PCD might be the disruption of connections between brain regions caused by neuroinflammation and demyelination due to COVID-19 [44,[83][84][85][86][87][88][89][90].…”

“…Most researchers believe that neuroinflammation leading to impaired connectivity might be the main cause of cognitive impairment after COVID-19. Several studies have demonstrated neuroinflammation [83,84] as well as disrupted connectivity and demyelination [44,85,86,88] in post-COVID patients. Since microglial and astroglial reactivation lead to impaired oligodendrocyte functioning and renewal [91][92][93], demyelination or decreased remyelination might also play important roles in cognitive changes in PCD patients.…”