Dr Rhys Thomas of the COVID-19 Clinical Neuroscience Study’s research team tells HEQ about the neurological damage caused by COVID-19 and the need for further targeted research.
Patients with COVID-19 have frequently been found to suffer brain-related issues during the course of their infection, with a significant proportion left with symptoms of brain injury even once the other symptoms of the virus have passed. Identifying ‘a unique opportunity to understand how these problems occur and develop strategies to prevent and treat them’, the COVID-19 Clinical Neuroscience Study, led by Dr Benedict Michael at the National Institute of Health Research (NIHR) Health Protection Research Unit for Emerging and Zoonotic Infection and Professor Gerome Breen of King’s College London, aims to examine the triggers, risk factors and effects of neurological damage brought on by COVID-19 infection.
Dr Rhys Thomas of Newcastle University, who is part of the study’s research team, tells HEQ about the links between COVID-19 and neurological damage and the need for further targeted research.
What does the COVID-19 Clinical Neuroscience Study hope to uncover or understand?
From early 2020, we were warned to expect a respiratory virus, presenting with high temperature and a cough; and then very early on, it began to feel like it could be a bit more than that. We were scouring the Chinese literature, trying to get an idea of the symptoms reported by people who were hospitalised: some people lost their senses of smell or taste, although that is not unusual when it comes to viral infections, which can affect the nervous system; but it did make us wonder what could be next. We looked at the reports of nonspecific symptoms such as seizures, dizziness, headache, which pointed to potential neurological issues; and once the virus hit the UK, we were determined to do the best level of surveillance that we could in terms of the UK population.
In addition to conducting essential surveillance, we looked at the supporting information, such as the other illnesses COVID-19 patients have and the medications they take. The third arm is the scientific part: this allows us to look at the risk factors that people carry, using biological predictors of severe infection – particularly severe infection which could affect the brain. We know that people who survived COVID-19 whose respiratory systems were particularly affected can end up with lung scarring, while COVID-19 survivors who have been primarily affected in other parts of their body typically make a full recovery; but if a patient does not make a full recovery from something which affects their brain, they are in a lot of trouble. Stroke is a great example of this: you can rehabilitate from a stroke, but you are left with a neurological impairment, probably followed by a degree of disability.
In the course of our research we have identified a lot more psychiatric symptoms stemming from COVID-19 infection – psychosis, delirium, altered mental state – and we still don’t know whether people are making a full recovery from that. We look at the impact of COVID-19 on the brain and try to identify who is more likely to experience that impact: identifying patients who are most at risk of severe brain impact matters, because those brain problems can linger and lead to problems later in life.
What external factors – such as age, environment and previous conditions – need to be considered in a study of this nature?
This matters most for the different types of comorbid illness: outside of COVID-19, stroke is a common condition, so we are getting very sophisticated in terms of knowing who is at risk – that is why we ask people to be more active and try to keep their blood pressure low; and if a patient has an irregular heart rate, we are able to thin their blood. However, it looks as though a lot of those common risk factors do not come into play for strokes associated with COVID-19 infection. We may have been identifying the at-risk population in the wrong way, because our previous markers of risk do not make as much sense when it comes to COVID-19-related stroke.
Similarly, we may have been too guilty of thinking this is all age-related, that the older a patient is when they get it, the sicker they are going to be; because people who have presented with altered mental state – slowing of thought or psychiatric symptoms – have been predominantly working-age adults rather than older adults. It may be that working-age adults have been protected against a different manifestation of COVID-19, but they are more vulnerable in different way. Children are completely different again: children who contract COVID-19 are primarily asymptomatic, but a very small proportion of child patients get a severe inflammatory disorder, which is very different from the ways in which adults are affected.
Is there a possibility of additional longer-term neurological issues associated with COVID which have yet to be identified?
We are carrying a lot of risk at the moment: there have been a lot of changes to the healthcare system, so people may not visit their GP for symptoms they have been presenting with for the last six months, because they may not want to bother people or services may not have been open and available to them. There is the risk that comes with the economic downturn, with the country being in recession and locked down. There is the risk presented by the severing of emotional connections, because lockdown has separated people from their support networks. There is risk associated with a constant news narrative about disaster and mortality which impacts on people’s resilience; and on top of all of that, there is this new biological threat. We have not been exposed to this form of RNA virus before; and as a result, the first time we as a human species are encountering it, we are having severe and significant reactions to it. People’s brains and their nerves are affected, and it is far too early for us to know whether we are elastic and we bounce back, or whether we are going to end up with lingering symptoms – we may have a generation of people who make a recovery, but only to 95% or 98%, rather than 100% of where they should be.
What has been the progress of the study so far? What are your plans moving forward?
We are focusing now on the third stage of the study, which covers risk factors and biological predictors. This was designed to be implemented in every major neuroscience centre across the UK, in England, Northern Ireland, Scotland and Wales, involving people from the fields of psychiatry and neurology – this has to be a pan-UK and pan-brain collaboration. We have work packages looking at psychology, covering memory and behaviour following COVID-19 infection; psychiatry, which covers mood and psychosis; brain imaging, identifying certain risk factors in terms of the brain’s vulnerability towards these problems; antibodies and other biomarkers which can predict why people have a more severe outcome; and then the neurology arm, investigating what has actually happened to the brain during this acute illness. We have these centres set up across the UK; following a pilot phase in late 2020, those centres will open fully in early 2021. We aim to recruit over 800 people and 500 controls, to be able to look at these predictive factors.
Dr Rhys Thomas
COVID-19 Clinical Neuroscience Study