Reorganization of brain connectivity in post-COVID condition: a 18F-FDG PET study, 2025, Verger et al.

[SNT Gatchaman]

Reorganization of brain connectivity in post-COVID condition: a 18F-FDG PET study
Verger, Antoine; Doyen, Matthieu; Heyer, Sebastien; Goehringer, François; Bruyere, Alexandra; Kaphan, Elsa; Chine, Meriem; Menard, Amélie; Horowitz, Tatiana; Guedj, Eric

A hypometabolic brain pattern has been reported in patients with post-COVID condition (PCC). The aim of this study was to investigate reorganization in metabolic connectivity in patients with PCC.

One hundred eighty-eight patients who underwent brain 18F-FDG PET for PCC were retrospectively included from two university hospital centres. These patients were age-and sex-matched to 120 healthy controls who underwent brain 18F-FDG PET before the COVID-19 outbreak. A voxel-based group comparison between patients and controls was performed (p-voxel at 0.005 uncorrected, p-cluster at 0.05 FWE corrected). Interregional correlation analyses of the identified clusters as well as sparse inverse covariance estimations at whole-brain scaling were also conducted. Both analyses were performed at the group level for all patients and then secondarily according to the postinfection delay; 88 and 100 patients, respectively, had a delay of less than or greater than 9 months (± 9 M).

Three hypometabolic clusters, namely, the right frontotemporal, right and left cerebellar, were identified from the voxel-based group comparisons of PCC patients. Within this hypometabolic PCC pattern, a modification in metabolic connectivity was observed in patients compared with controls, which was more marked in the + 9 M group than in the − 9 M group. On the other hand, the graph analysis revealed a decrease in connectivity efficiency metrics in the PCC.

Metabolic connectivity is modified in patients with PCC within the hypometabolic post-COVID-19 network, with lasting reorganization evolving over time, suggesting functional adaptation.

Link | PDF (EJNMMI Research) [Open Access]

 

[Hutan]

Definition of PCC?

We retrospectively identified patients who presented with PCC between May 2020 and December 2022, satisfied the WHO definition [1] and had a brain 18F-FDG PET scan to investigate suspected brain impairment (fatigue, anosmia/ageusia, cognitive symptoms and/or dysautonomia) at two University Hospitals [4].

So, there was a high level of selection of the cases - they had been referred for investigation of brain impairment before this study was undertaken.

I think the cases probably had brain impairment for a range of reasons. One reason might possibly be an ME/CFS-like condition. But, another reason could be having had a very severe respiratory illness e.g. hypoxia. Other reasons might be coincidental e.g. onset of dementia, or mechanical brain injury.

 

[Hutan]

Three hypometabolic clusters, namely, the right frontotemporal, right and left cerebellar, were identified from the voxel-based group comparisons of PCC patients.

Here's some examples of causes of cerebellar hypometabolism:

Cerebellar hypometabolism on FDG PET has been described in several conditions, for example, chronic alcohol abuse, antiepileptic medication use, multiple system atrophy, and cerebellar infarction. Corresponding cross-sectional examination is paramount in distinguishing possible etiologies because each condition has a relatively characteristic appearance. We present a case of an asymptomatic patient with diffuse cerebellar hypometabolism found incidentally on FDG PET/CT performed for suspected recurrence of gastric carcinoma. Accompanying CT images demonstrated calcification of the cerebellum and therefore confirmed the etiology of diffuse idiopathic cerebellar calcification.

These causes might have prompted the investigation, and not be related to the Covid infection.

 

[Utsikt]

Our study has several limitations. No longitudinal design was applied in the current study, limiting the direct comparison of metabolic connectivity. In addition, the retrospective design and bicentric nature of the current study do not allow us to correlate our metabolic connectivity findings with clinical characteristics. Indeed, data were retrieved retrospectively, and symptoms were not collected with a standardized survey within our two centres to allow a fair comparison of symptoms severity between patients from the two different groups.

 

[Utsikt]

Can anyone explain what the values mean? How large were the actual differences?