Quantitative susceptibility mapping at 7 Tesla in COVID-19: mechanistic and outcome associations, 2023, Rua et al.

Quantitative susceptibility mapping at 7 Tesla in COVID-19: mechanistic and outcome associations
Catarina Rua; Betty Raman; Christopher T Rodgers; Virginia F J Newcombe; Anne Manktelow; Doris A Chatfield; Stephen J Sawcer; Joanne G Outtrim; Victoria C Lupson; Emmanuel A Stamatakis; Guy B Williams; William T Clarke; Lin Qiu; Martyn Ezra; Rory McDonald; Stuart Clare; Mark Cassar; Stefan Neubauer; Karen D Ersche; Edward T Bullmore; David K Menon; Kyle Pattinson; James B Rowe

Post mortem studies have shown that patients dying from severe SARS-CoV-2 infection frequently have pathological changes in their central nervous system, particularly in the brainstem. Many of these changes are proposed to result from para-infectious and/or post-infection immune responses. Clinical symptoms such as fatigue, breathlessness, and chest pain are frequently reported in post-hospitalized COVID-19 patients. We propose that these symptoms are in part due to damage to key neuromodulatory brainstem nuclei. While brainstem involvement has been demonstrated in the acute phase of the illness, the evidence of long-term brainstem change on magnetic resonance imaging (MRI) is inconclusive.

We therefore used ultra-high field (7T) quantitative susceptibility mapping (QSM) to test the hypothesis that brainstem abnormalities persist in post-COVID patients and that these are associated with persistence of key symptoms. We used 7T QSM data from 30 patients, scanned 93-548 days after hospital admission for COVID-19 and compared them to 51 age-matched controls without prior history of COVID-19 infection. We correlated the patients’ QSM signals with disease severity (duration of hospital admission and COVID-19 severity scale), inflammatory response during the acute illness (C-reactive protein, D-Dimer and platelet levels), functional recovery (modified Rankin scale; mRS), depression (PHQ-9) and anxiety (GAD-7).

In COVID-19 survivors the MR susceptibility increased in the medulla, pons and midbrain regions of the brainstem. Specifically, there was increased susceptibility in the inferior medullary reticular formation and the raphe pallidus and obscurus. In these regions, patients with higher tissue susceptibility had worse acute disease severity, higher acute inflammatory markers, and significantly worse functional recovery. Using non-invasive ultra-high field 7T MRI, we show evidence of brainstem pathophysiological changes associated with inflammatory processes in post-hospitalized COVID-19 survivors.

This study contributes to understanding the mechanisms of long-term effects of COVID-19 and recovery.


Link | PDF (Preprint: MedRxiv)

 

I'd be lucky to get a 3T.

When I tested normal with an MRI, it was with 1.5T. The times my MRI came out funky was with a 3T.

If I had access to a 7T, I'd do whatever I could to see its results.

 

Quantitative susceptibility mapping at 7 T in COVID-19: brainstem effects and outcome associations

Published in Brain. (Has also generated some media coverage; I came across this story in the Independent.)

Link | PDF

 

Press release:
News Release 7-Oct-2024
Ultra-powered MRI scans show damage to brain’s ‘control center’ is behind long-lasting Covid-19 symptoms
Peer-Reviewed Publication
University of Cambridge
https://www.eurekalert.org/news-releases/1060117

 

article

Cause of long Covid in patients uncovered in bombshell MRI findings (msn.com)

 

"Cause of long COVID in patients uncovered..." - the media coverage is rather overhyped. The post-COVID patient population was small (n=31) and also a post-hospitalisation cohort (so likely quite different to LC-ME/CFS), the technique used is not sufficient to delineate past inflammatory injury from ongoing inflammation, and each patient was also only scanned once (at on average 219 days from admission). It's certainly an interesting result but "bombshell" is not the word I'd use.