Much has been said about the long-term effects of coronavirus disease 2019 (COVID-19), including neurological side effects. A new study compares the rates of occurrence of various types of neurological diseases, whether degenerative, stroke-related or immunological, after COVID-19 or other respiratory infections.
Study: Frequency of neurological diseases after COVID-19, influenza A / B and bacterial pneumonia. Image credit: Andrii Vodolazhskyi / Shutterstock
Introduction
More than 80% of COVID-19 patients hospitalized with the diagnosis have reported neurological symptoms, the most common being headache and anemia. There is also a greater tendency to coagulation and stroke has been described to occur as a complication. Some patients have developed neuropathies such as Guillain-Barré syndrome (GBS) or Parkinson’s disease (MP).
This led to the question of whether COVID-19 actually increased the risk of developing neurodegenerative or post-infectious diseases.
The current article, published online in the journal Frontiers in Neurology, examined the electronic health records (EHR) of approximately half of the Danish population, looking for people diagnosed with COVID-19 or hospitalized with acquired pneumonia in the community, during the period from February 2020 to November 2021. The researchers also included people who were tested for the flu between February 2018 and November 2019.
Discoveries
Of more than 900,000 people with a history of COVID-19 testing, more than 43,000 tested positive. During the same period, approximately 1,500 people had bacterial pneumonia. Third, during the study period, more than 8,000 had influenza.
The group of individuals with COVID-19, whether hospitalized or not, had higher rates of COVID-19 risk factors, such as high cholesterol levels, type 2 diabetes mellitus, and hypertension, than those hospitalized for influenza. Obesity was more common in people positive for COVID-19 or in those hospitalized for the flu and with a history of transient ischemic attacks (TIAs).
The latter was also more likely among patients hospitalized for pneumonia, as well as smoking, which was also more common among patients with influenza. Delirium, which is known to be a risk factor for dementia, was more common among patients with COVID-19, with twice the frequency among non-COVID-19 patients.
The risk of brain hemorrhage was 5-fold higher for outpatients with a history of COVID-19. Against this, it should be remembered that intravenous thrombolysis was seven times more common in this group, with 0.14%. Even after taking this risk factor into account, the risk remained more than four times greater.
The risk of Alzheimer’s disease (AD) increased 3.5-fold, up to a year later. This was the case even after excluding cases with delirium and those at risk of stroke, both independent risk factors for AD.
The risk of Parkinson’s disease and ischemic stroke was almost 3 times higher up to 12 months in those diagnosed with COVID-19.
However, this was put into perspective compared to rates of the same conditions among people who had been hospitalized with influenza or bacterial pneumonia, which showed equivalent rates of both AD and PD.
In this situation, the risk of stroke was almost double among outpatients with COVID-19 (but not combined with inpatients and outpatients, or only hospitalized), compared with those who did not have COVID-19, once compensated. stroke risk factors. This risk was not seen within a month, but began to become apparent from 3 months after COVID-19. The increased risk was higher among patients aged 40 to 59 years, younger than the typical ischemic stroke risk group.
Compared with influenza patients, hospitalized patients with COVID-19 also showed a 70% increase in stroke risk up to 6 months later, decreasing to 30% in one year. When stroke risk factors were considered, the risk was found to triple or more in hospitalized patients with COVID-19, even at one year.
In addition, compared to hospitalized patients with bacterial pneumonia who were over 80 years of age, the risk was almost 3-fold higher among hospitalized patients with COVID-19, but no overall increase in risk was found after taking in account for stroke risk factors.
There was no observable difference in rates of postinfectious neuropathies or neurodegenerative diseases between those with or without a history of any of these infectious conditions.
Implications
The results of this study indicate a causative role of neuroinflammation, fatigue, and negative emotions in patients with COVID-19 that may have contributed to the higher incidence of AD and PD one year after initial diagnosis. It was found that young patients who died of COVID-19 had abnormally high concentrations of the pathological β-amyloid protein in the brain.
Against this, more care should be given to patients with a history of COVID-19, which could have led to an earlier and more frequent diagnosis of these conditions in their later history, compared with COVID-19-negative patients. However, AD and PD rates were comparable to those found after hospitalization with influenza or bacterial pneumonia.
In contrast, there was a higher incidence of ischemic stroke among patients with COVID-19 compared with those with a history of influenza or bacterial pneumonia. Explanations may include the inflammatory state, the heart condition leading to a heart attack, immobilization during the hospital stay, or some unique feature of this infection.
The incidence of intracerebral hemorrhage was more frequent per month among outpatients with COVID-19, compared with people without COVID-19, but comparable to the finding after a previous flu or bacterial pneumonia. Risk factors include anticoagulant therapy, mechanical ventilation, and the use of extracorporeal membrane oxygenation (ECMO).
Even after compensating for thrombolysis, the risk of bleeding remained high, demonstrating that COVID-19 itself was a risk factor. The results here suggest that patients with a history of respiratory infections should be monitored for neurodegenerative disorders and that ischemic stroke appears to be a risk inherent in COVID-19. Subsequent studies will be needed to validate this hypothesis.