This is a summary of the recently published article in the Journal Lancet
Structural brain changes in patients with post-COVID fatigue: a prospective observational study.
Published February 27 2023 DOI: https://doi.org/10.1016/j.eclinm.2023.101874
Fatigue is a complex phenomenon at the interplay of central regulation and psychological factors like mood and motivation.
In Post-COVID Syndrome (PCS), the experience of fatigue is frequently accompanied by muscle fatigue and fatiguability and correlates with biomarkers for inflammation and hypoperfusion.
A subset of patients with PCS fulfills the diagnostic criteria for myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), a complex disease in which fatigue is accompanied by exertional intolerance and post-exertional malaise. Environmental stressors may additionally contribute to fatigue through changes in the neuroendocrine stress response, altering the hypothalamic-pituitary-adrenal and norepinephrine systems.
Central fatigue impacts psychosocial and cognitive functions and is often perceived as most distressing by patients. Fatigue is one of the main contributors to post-COVID disease burden. A recent meta-analysis estimated that ∼30% of patients with COVID-19 develop post-COVID fatigue.
Fatigue is more than twice as common after COVID-19 as in matched non-COVID controls. Importantly, fatigue frequently affected younger patients and patients with only mild or moderate acute COVID-19. In addition, post-COVID cognitive deficits are observed in up to 20% of patients, especially in older age groups.
These deficits can span multiple domains, including short-term and episodic memory, attention, and language and they can occur with a delay of several weeks or months after infection.
The prominent neurological symptoms in acute COVID-19 and PCS indicate a direct or indirect involvement of the central nervous system, potentially mediated by direct virus effects or virus-induced autoimmunity.
Patients with mild acute COVID-19 and without hospitalisation were found to have reduced volumes and aberrant diffusion markers of the thalamus and basal ganglia that correlated with fatigue severity and impairment in daily activities, daytime sleepiness, and short-term memory problems.
Importantly, this pattern of pathological changes emerged even though this cohort is relatively young, most patients were not hospitalised during their acute infection, and patients were in overall good health before COVID-19.
The finding – that post-COVID fatigue is associated with structural brain damage – highlights the importance of consequent therapeutic management of this postinfectious syndrome.