Study participants were 18 years or older tested positive for SARS-CoV-2 or had serum antibody positivity, and had no history of dementia.
Participant demographic characteristics (eg, age, race, and ethnicity) were collected via self-report. Cognitive functioning was assessed using well-validated neuropsychological measures: Number Span forward (attention) and backward (working memory), Trail Making Test Part A and Part B (processing speed and executive functioning, respectively), phonemic and category fluency (language), and the Hopkins Verbal Learning Test–Revised (memory encoding, recall, and recognition).
The Mount Sinai Health System Institutional Review Board approved this study, and informed consent was obtained from study participants. The study followed the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) reporting guideline.
The study findings were published in the peer reviewed journal: JAMA Network.
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes the coronavirus disease 19 (COVID-19). It first appeared in Wuhan, Hubei, China (1), and then spread to the rest of the world, making it a pandemic. The virus belongs to the Coronaviride family.
Over the past 10 years, there have been two other coronavirus epidemics that caused severe infections: the severe acute respiratory syndrome (SARS-CoV) epidemic in 2003 (2) and the Middle East respiratory syndrome (MERS-CoV) (3).
COVID-19 was reported to be primarily a lower respiratory tract disease, and common symptoms included fever, cough, and shortness of breath (1). At the same time, the severity varies, ranging from asymptomatic or very mild symptoms, such as a cold or pneumonia, to very severe symptoms and acute respiratory failure insufficiency (4).
Reports about anosmia (loss of the sense of smell) (5) and ageusia (loss of taste) in patients with COVID-19 infection turned attention toward possible affection of the central nervous system (CNS) (6–9). Other early complications include impaired consciousness, agitation, dizziness and headache (7).
After recovery, fatigue, anxiety, depression, insomnia have also been reported as common symptoms (10). Rogers and colleagues (11) conducted a systematic review and found a few studies that did systematic assessments of cognition in patients following SARS-CoV and MERS-CoV infection. During acute phase, around a third of the patients experienced impaired memory, concentration or attention (11).
After the illness, around one fifth of all patients had one or more of the aforementioned cognitive impairments. A letter dating from June 2020 (12) reported that a third of their discharged COVID-19 patients showed a dysexecutive syndrome consisting of “inattention, disorientation, or poorly organized movements in response to command” (Third paragraph).
As more unusual symptoms emerged it became gradually clear that COVID-19 could affect a wide variety of organs and tissue (13–15).
The etiology of the SARS-CoV-2 is certainly multifactorial, but the exact pathophysiological mechanisms leading to the neurological and psychiatric consequences of COVID-19 is still not clear. In earlier coronavirus infections, the following neurotoxic mechanisms are described:
- Neurotropism and direct ability to enter neurons and glial cells, leading to neuronal dysfunction and damage (neuroinvasion), and secondly to i.e., encephalitis. The virus may reach the CNS indirectly through the blood-brain barrier and/or directly by axonal transmission across olfactory neurons (16–20).
- Affection of cerebral blood vessels and coagulopathies causing ischemic or hemorrhagic strokes (21–23).
- Secondary negative consequences of excessive systemic inflammatory responses, “cytokine storm” and peripheral organ dysfunctions affecting the brain (24, 25).
- Global ischemia secondary to respiratory insufficiency, respirator treatment and so-called acute respiratory distress syndrome ARDS (26).
Heneka et al. (48) suggest that all the previously mentioned mechanisms could play a role in the etiology of the cognitive impairment in COVID-19 survivors. There is an ongoing discussion whether COVID-19 may cause long-term cognitive impairments. Such a theory is supported by several studies showing a link between infections with human herpes viruses and the risk of dementia development later in life (27).
Neurodegeneration could possibly emerge many years after viral infections in the CNS, which some considers was the case in encephalitis lethargica, where extrapyramidal symptoms emerged long after recovery of Spanish influenza in 1918 (28).
Evidence shows that inflammation is a risk factor for persistent cognitive decline in survivors of ARDS or sepsis (29, 30). In addition, high cytokine levels during ≪cytokine storm≫ predicts the occurrence of hippocampal atrophy (31).
There have been published a few reviews on cognitive impairment after COVID-19 infection, however none of them are – to our best knowledge–solely based on objective neuropsychological data. As there are no clear link between subjective reports of impaired cognition and findings on objective tests (32), we chose to only include studies that reported objective test data.
It is important to report and address specific cognitive impairments after COVID-19, as this enables us to adapt current and/or implement new rehabilitation programs. Early identification and properly tailored rehabilitation will most likely reduce negative health effects and address the socio-economic consequences at a population level.
reference link :https://www.frontiersin.org/articles/10.3389/fneur.2021.699582/full