Brain Function Changes Following COVID-19 Infection
Study Details
Study Description
Brief Summary
The global COVID-19 pandemic has now led to millions of infections worldwide. It produces long-lasting changes in the general physiology of multiple organs, including the brain. Thus, this study aimed to comprehensively understand the cortical excitability and neuropsychological behavior changes in patients following SARS-CoV-2.
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Detailed Description
The global COVID-19 pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has led to millions of infections and deaths worldwide. However, many issues about the nature of some long-term infection-related symptoms have not yet been well clarified.
Several lines of evidence have shown that SARS-CoV-2 can attack multiple organs such as the lungs, heart, kidneys, liver, as well as brain. The pathophysiologic analyses have shown the impact of SARS-CoV-2 on the brain, including the virus-induced neuroinflammation, the immune reactions, and the possible presence of the coronavirus in the central nervous system in the COVID-19 cases. Indeed, patients who recovered from COVID-19 may experience several long-term symptoms related to brain health, such as fatigue, cognitive and attention deficits, anxiety, and depression, which can affect their ability to work or even daily life. Therefore, the neuropsychological behavior changes in patients following SARS-CoV-2 infection remain an ongoing study area.
In parallel, studies have shown that behavioral abnormities in COVID-19 patients are often accompanied by cortical changes. Utilizing magnetic resonance imaging, a more significant reduction in grey matter thickness and tissue contrast in the orbitofrontal cortex and parahippocampal gyrus has been identified. Other studies confirmed impairment of frontoparietal cognitive functions and frontoparietal hypometabolism by 18F-fluoro-2-deoxy-d-glucose positron emission tomography15. In addition, electroencephalogram abnormalities were also seen in patients who survived from COVID-19. In recent decades, transcranial magnetic stimulation (TMS) has been recognized as a promising and noninvasive adjuvant diagnostic tool enabling assessment of the excitatory and inhibitory properties of the motor cortex as well as brain connectivity17,18. However, the evidence of inhibitory or excitatory changes of intracortical networks in patients recovered from COVID-19 is still scarce.
In this study, we aimed to investigate whether deficits in response inhibition and decision-making could be found in patients following mild SARS-CoV-2 infection. Moreover, we also focused on the neurophysiological evaluation of excitability and neurotransmission within the primary motor cortex (M1).
Study Design
Arms and Interventions
| Arm | Intervention/Treatment |
|---|---|
| Uninfected Subjects who had recovered from SARS-CoV-2 infection |
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| Infected Subjects who had not been infected with SARS-CoV-2. |
Outcome Measures
Primary Outcome Measures
- The cortical excitability changes following COVID-19 infection. [January 2023 to March 2023]
This was assessed by single/paired pulse TMS procedures.
Secondary Outcome Measures
- The neuropsychological behaviors following COVID-19 infection. [January 2023 to March 2023]
These were assessed by Stop-signal task (SST) and Choice under risk and ambiguity task (CRA).
Eligibility Criteria
Criteria
Inclusion Criteria:
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- Age between 18 and 60 years; 2. Completed the TMS and cognitive function tests; 3. Without physical discomfort or special physiological conditions (e.g., female subjects in their menstrual cycle or ovulation)
Exclusion Criteria:
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- Had previous history of neurological or psychiatric disorders; 2. Had cognitive impairment or use of recreational or therapeutic psychoactive drugs within the past three months;3. Had severe hepatic or renal impairment.
Contacts and Locations
Locations
No locations specified.Sponsors and Collaborators
- RenJi Hospital
Investigators
None specified.Study Documents (Full-Text)
None provided.More Information
Publications
None provided.- LY2023-133