Structural MRI correlates of cognitive and neuropsychiatric symptoms in Long COVID: a pilot study, 2024, Joshi et al.

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Structural MRI correlates of cognitive and neuropsychiatric symptoms in Long COVID: a pilot study
Joshi, Shantanu H.; Siddarth, Prabha; Lavretsky, Helen

Approximately 7% of COVID-19 patients (1.3% children) have exhibited symptoms of post-acute sequelae of SARS-CoV-2 infection (PASC), or Long COVID, and 20% of those present with neuropsychiatric symptoms. While a large number of MRI-based neuroimaging studies in this population have shown cortical atrophy in terms of gray matter volume and cortical thickness in patients, there is a growing body of work showing brain volume enlargements or thickness increases in patients compared to COVID negative controls.

To investigate this further, we used structural magnetic resonance imaging (MRI) to examine differences in gray matter thickness for the cortical limbic and the dorsolateral prefrontal cortical regions between patients with Long COVID and healthy controls.

Results showed increased cortical thickness in the caudal anterior, isthmus, and the posterior cingulate gyrus as well as the rostral middle frontal gyrus respectively along with higher gray matter volume in the posterior cingulate and the isthmus cingulate in patients with Long COVID. Cortical thickness and gray matter volumes for regions of interest (ROIs) were also associated with the severity measures, clinical dementia rating, and anxiety scores in the Long COVID group.

Our findings provide supporting evidence for cortical hypertrophy in Long COVID.

Link | PDF (Frontiers in Psychiatry) [Open Access]
 
Our findings of group differences in structural neural changes contrast with some prior studies.

The disparity in the direction of the effects may be a consequence of the heterogeneous sample of participants with varying levels of symptoms as well as acute- and non-acute presentation of illness. Among several possible reasons, brain tissue swelling due to neuroinflammation and the resulting migration of immune cells or from persistent neurovascular injuries has been suggested to be a putative cause. Alternatively, a compensatory mechanism resulting in neurogenesis and hypertrophy or persistent neuroinflammation may also be considered as explanations for thickness increase.
 
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