A study of more than 1.25 million people diagnosed with COVID-19 reports a higher two-year risk of developing certain neuropsychiatric conditions after contracting COVID-19 than for other respiratory infections.
Increased risk of developing certain neurological and psychiatric conditions (such as dementia, psychosis,brain fog‘and seizures) are higher two years after COVID-19 than other respiratory illnesses, suggests an MQ-funded observational study of more than 1.25 million patient health records published in Lancet Psychiatry magazine. increased risk of infection depression And the worry In adults less than two months before, rates return to similar to those after other respiratory infections.
in Another recent paper Posted in brain connections By the same researchers, they found support for the hypothesis that brain fog, or cognitive decline, is linked to damage to the small blood vessels in the brain, caused by COVID-19.
Since the COVID-19 pandemic began, there has been mounting evidence that survivors may be at increased risk of developing neurological and psychiatric illnesses. previous study She reported that COVID-19 survivors are at increased risk of developing several neurological and mental health conditions in the first six months after infection. However, to date, there have been no large-scale data looking at the risks of these diagnoses over a longer period of time. This study was also the first large-scale study to look at the risk of neurological and mental illness after COVID-19 in children and to assess how risks change as new variables emerge.
Professor Paul Harrison, lead author of the study, from the University of Oxford, UK, says:
In addition to confirming previous findings that COVID-19 can increase the risk of developing certain neuropsychiatric conditions in the first six months after infection, this study indicates that some of this increased risk can persist for at least two years. The findings have important implications for patients and health services because they indicate new cases of neurological conditions associated with COVID-19 infection that are likely to occur long after the epidemic has subsided. Our work also highlights the need for more research to understand why this occurs after COVID-19, and what can be done to prevent or treat these conditions.
The study analyzed data from 14 neuropsychiatric diagnoses collected from electronic health records, mostly from the United States, over a two-year period. Of these, 1,284,437 people had confirmed infection with SARS-CoV-2 on or after January 20, 2020, and were included in the study: 185,748 children (under 18 years of age), and 856,588 adults aged ≥18 years. 18 and 64 years old, and 242,101 adults over 65. These individuals were matched with an equal number of patients with other respiratory infections to serve as a control group.
The records of infected COVID-19 patients during different epidemic waves were also compared to investigate differences in the impact of alpha, delta, and omicron variables on the risk of neuropsychiatric diagnoses. People who were first diagnosed with COVID-19 during the period when a given variant was prevalent (alpha: 47,675 people, delta: 44,835 people, omicron: 39,845 people) were compared to a control group of the same number of individuals who had a first diagnosis of COVID-19. 19 in the period immediately preceding the emergence of this variant.
The study found that the risk of developing depression or a diagnosis of anxiety in adults initially increased post-SARS-CoV-2 infection but returned to what it was with other respiratory infections after a relatively short time (depression at 43 days, anxiety at 58 days). After the initial increase, the risk of being diagnosed with depression or anxiety fell below that of the control group, which means that after two years, there was no difference in the overall incidence of depression and anxiety between the COVID-19 group and the other respiratory infection group (in adults aged Between the ages of 18 and 64 in both groups, within two years after injury, there were approximately 1,100 depressive episodes per 10,000 people and about 1,800 anxiety episodes per 10,000 people).
However, the risk of being diagnosed with some other neurological and mental health conditions was higher after COVID-19 than for other respiratory infections at the end of the two-year follow-up period. Adults aged 18-64 who had COVID-19 up to two years prior were at increased risk of cognitive deficits, or ‘brain fog’ (640 cases per 10,000 people), and muscle disease (44 cases per 10,000 people) , compared with those who had other respiratory infections two years earlier (550 cases per 10,000 people with ‘brain fog’ and 32 cases per 10,000 muscle disease). In adults over 65 years of age who had COVID-19 two years earlier, there was an increased incidence of ‘brain fog’ (1,540 cases per 10,000 people), dementia (450 cases per 10,000 people) and psychotic disorder (85 cases per 10,000 people). 10,000 people). 10,000 people) compared with those who previously had a different respiratory infection (1230 cases per 10,000 ‘brain fog’, 330 cases per 10,000 cases of dementia and 60 cases per 10,000 cases of psychotic disorder).
The likelihood of most neuropsychiatric diagnoses after COVID-19 was lower in children than in adults, and they were no more at risk of anxiety or depression than children with other respiratory infections. However, like adults, children were more likely to develop some conditions, including seizures (260 cases per 10,000 children for the COVID-19 group; 130 cases per 10,000 for the control group) and psychotic disorders (18 cases per 10,000 children for the COVID-19 group). ; 6 cases per 10,000 for the control group), over the two years following COVID-19.
Little change in the risk of neuropsychiatric diagnoses was observed six months after COVID-19 before and immediately after the onset of the alpha variant. However, onset of the delta variant was associated with significantly higher six-month risks of anxiety (10% increased risk), insomnia (19% increased risk), cognitive deficits (38% increased risk), and epilepsy or seizures (3% increased risk). 26%. risk), and ischemic strokes (27% increased risk) but lower risk of dementia (40% lower risk) compared to those diagnosed with COVID-19 just prior to the delta wave. The risks during an omicron wave were similar to those when delta was the dominant alternative.
Our findings shed new light on the long-term consequences for the mental health and brain health of people after contracting COVID-19 infection. The good news is that the increased risk of depression and anxiety diagnoses after COVID-19 is relatively short-lived and there is no increased risk of these diagnoses in children. However, it is worrying that some other conditions, such as dementia and seizures, continue to be diagnosed frequently after COVID-19, even two years later.
Dr Max Takee from Oxford University, who led the analyses, says. “The emergence of the delta variant has been associated with increased risk for several conditions; however, it is important to note that the overall risk for these conditions remains low. With omicron as the predominant variant, although we see milder symptoms soon after infection, similar rates of diagnoses have been observed. Neuropsychiatric as with Delta, suggesting that the burden on the health care system may persist even with less severe variables in other respects.”
in A separate study found that a specific type of anticonvulsant medication, called phenytoin, reduced the risk of cognitive defects by 22-27%. In persons with COVID-19 infection, provided they are administered in a timely manner.
According to this research, which was also funded by MQ, this may indicate that brain fog is due, at least in part, to damage to the small blood vessels in the brain. Maxime Takee, lead author of that study says:
These findings shed light on the possible causes of brain fog, and how it can be prevented in the future. We certainly aren’t suggesting that people start taking phenytoin if they have COVID. The aim of this study was to identify possible mechanisms, not possible treatments.