In a recent study posted to medRxiv* Preprint server, researchers characterized the mechanisms associated with neural dysregulation in post-coronavirus disease (COVID) fatigue (pCF) by evaluating individuals who have recovered from mild severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection.
Examination: Neural dysregulation in post-covid fatigue. Image credit: fizkes / Shutterstock
The majority of SARS-CoV-2 infected people do not need hospitalization. Nevertheless, a small percentage of individuals develop long-term consequences following SARS-CoV-2 infection, known as long-term COVID. Fatigue is a frequently reported disorder among COVID 2019 (COVID-19) convalescent people and has a significant negative impact on daily quality of life. Additionally, fatigue appears to be a multisystem disorder, including hormonal, metabolic, and immunological abnormalities. However, the neural mechanisms associated with post-COVID fatigue are not yet understood.
About the study
In this study, the researchers conducted a series of non-invasive behavioral and neurophysiological assessments that evaluated the autonomic, peripheral, and central nervous system in individuals with self-reported fatigue after a mild form of COVID-19 to characterize the neural mechanisms underlying the record. . – Covid fatigue.
A total of 37 participants with no history of hospitalization during the mild SARS-CoV-2 infection underwent an approximately four-hour laboratory examination approximately six to 26 weeks after SARS-CoV-2 infection. An additional 52 age- and gender-matched individuals served as controls for the study.
The battery of well-characterized behavioral and neurophysiological tests yielded 35 measurements. Of the 35 measurements, 33 depicted the condition of various nervous system components, and the remaining two were drum temperature and blood oxygen saturation.
The results reveal that a history of mild COVID-19 was associated with reductions in activities of particular cortical circuits, dysregulation of myopathic changes in skeletal muscle, and autonomic function relative to sex- and age-matched cohorts without fatigue.
In detail, the maximum grip strength was not significantly decreased in pCF, indicating that the power generation for short contractions was intact in these cohorts. Further, the inherent motoneuron excitability and the effectiveness of transmission at the neuromuscular junction evaluated using different measurements suggested that these parameters were comparable between the control and study groups. Nevertheless, pCF patients were associated with a higher level of peripheral fatigue than the control group, while evaluating changes during prolonged maximal contraction, suggesting that pCF causes metabolic changes in muscle fibers, resulting in decreased power generation after prolonged activity.
Intracortical facilitation (ICF) was significantly lower in pCF subjects compared to the control groups, while the function of the primary motor cortex was evaluated. However, several measures of cortical inhibition did not show any notable inequalities between the study and control parties. In addition, different assessments of sensory function showed no significant variations between the pCF and control groups, indicating that disturbances in sensory feedback may not be a contributing component of pCF.
The pCF subjects showed a higher resting heart rate than the age- and gender-matched cohorts. Furthermore, variations in other assessments of autonomic functions, such as drum temperature, galvanic skin response habituation, and heart rate variability, were also seen among the study and control groups. These findings are indicators of elevated vagal tone compared to sympathetic, suggesting that pCF subjects were associated with a degree of dysautonomia.
There were differences in a minimum of three neurophysiological measurements between the pCF subjects and the control lots. In addition, a marked variation in blood oxygen saturation was also seen between the study and control batches. Nevertheless, cluster analysis showed no subgrouping, indicating that post-COVID fatigue was a single unit with interpersonal variation rather than a few discrete syndromes.
The study results connote the need for a better understanding of the physiological bases of long-term COVID, especially pCF. It is crucial to know which neural systems are affected in pCF to design effective treatments. Thus, the discrepancies in behavioral and neurophysiological tests observed in the current study among pCF individuals and controls may point to new directions for principled therapeutic intervention in pCF treatment.
Furthermore, if these abnormalities occur early after SARS-CoV-2 infection, they can serve as rapid and accurate biomarkers for diagnosing and tracking the development of fatigue over time.
Overall, the study shows that dysregulation exists in three main sections of the nervous system during pCF by using tests that are simple to perform and can be easily integrated into future studies to assess and devise treatment strategies for pCF.
medRxiv publishes preliminary scientific reports that are not peer-reviewed and therefore should not be considered essential, guide clinical practice / health-related behavior or be treated as established information.