Transcript

MIC CAVAZZINI:              Welcome to Pomegranate Health, I’m Mic Cavazzini for the Royal Australasian College of Physicians. Today’s podcast comes from a seminar I attended hosted by the Curran Foundation at St Vincent’s Hospital, Sydney, featuring four Fellows of the RACP all in different specialties.

The Curran Foundation funds a variety of research streams and also certain needs for equipment or staff education. In 2020 it was called upon to support an ambitious project to follow cohorts of patients presenting with COVID-19. The intention of the ADAPT study was to collect wide-ranging measures in order to characterise the disease with as little bias as possible.

This was before anyone imagined that some COVID-19 patients would continue to suffer malaise long after the infection had resolved. But up to a fifth of patients would go on to report ongoing breathlessness, fatigue, chest tightness and also what’s described as brain fog. The term “Long-COVID” actually emerged first among online communities of patients, as many felt that their reported experiences were treated with shrugs or even scepticism from their doctors.

Many findings from the ADAPT study have been published already and the seminar you’re about to hear was a public-facing overview of the work up to December 2022. I’m going to flip the order of the presenting speakers so that you’ll get the bigger clinical and public health picture before we get into the research output. So first you’ll hear from Professor Steven Faux. He is Director of Rehabilitation and Pain Medicine at St Vincent’s Hospital and co-founded one of the first clinics for long COVID in Australia. His has a conjoint academic appointment between the Universities of New South Wales and Notre Dame and advises New South Wales Health's COVID-19 Clinical Council on guideline management. The panel was chaired by David Faktor who is the hospital’s director of public affairs and media.

DAVID FAKTOR:              Steven, given your role in the long COVID clinic here at St. Vincent's, what are the definitions of long COVID and how do you make that diagnosis?

STEVEN FAUX:  Well, thanks for that, David. Yeah, and thank you very much for inviting me and listening to some of our experiences our long COVID clinic. The WHO definition, which is the current one is for the persistence of symptoms for at least two months, but the definition starts at three months. Interestingly, this is underlined by the fact that you can't have these symptoms if they're caused by any other diagnosis. So it's what we call a diagnosis of exclusion—we've got to make sure that there's nothing else causing it. So that's very difficult for patients because they've got to be able to cope with not knowing what their trajectory is. But it's also difficult for the referring doctors not knowing how much to investigate or whether to just have a watchful waiting sort of approach. And what we're seeing in our clinic is at least 25% of people have seen more than one specialist prior to being referred.

And so there's a lot of fragmentation of healthcare because of this very vague definition. So a lot of specialists will say, “Look, I've had a look at the heart. There's no problem here. I don't know what the other symptoms are.” And so then the GP will be in this quandary. Because there's no or very few multidisciplinary referral clinics like ours, they're going to say, “Well, maybe I'll ask a respiratory physician to look at you. Or maybe I'll ask an infectious diseases physician. “And so a patient will move from one to another and probably having a lot of investigations, which are expensive for the patient and also for the community. So that the definition is really about the persistence of the symptoms, but it doesn't really give us a lot more than that.

DAVID FAKTOR:              So you touched on the fragmentation, but what hat would be the most common long COVID symptoms that you are seeing? And what treatment options do you have for those more common symptoms?

STEVEN FAUX:  So that the most common symptom is fatigue. It's followed by breathlessness in about a third. Fatigue in about half of the people we’re seeing. And then then it's followed by mental health disorders, which are about 25%, and then cognitive problems or brain fog in about 20%. And then you can have a whole variety of symptoms from losing your hair, which isn't a real problem for me, but a lot of other symptoms that people come through with. With fatigue, we use a multidisciplinary sort of approach. So we have physiotherapists that will show a person how to exercise very carefully with a lot of feedback. Because some people feel a bit better and then push themselves very hard and then become overly fatigued again, so we have to measure them out. Our psychologist teaches people about pacing.

And interestingly, one of the groups of people we're seeing quite commonly to present is the very high functioning person, the person who works a lot of hours, who exercises quite hard, and then has trouble coping with the long term effects of a lateral disease. And those people we need to sort of get them to slow down and to slowly meter out their recovery. We also involve an occupational therapist, because many of them, about 19%, have stop working. 25% have stopped working for more than a month. So the impact of getting people back to work is quite a challenge. So that's the next step. So we use all those people to help this one person's fatigue and to try and control it.

DAVID FAKTOR:              So I know, Steven, you've got a parliamentary delegation coming from Canberra tomorrow. So I'm going to give you an opportunity for a dress rehearsal, because I know this is the question they're going to ask you. Can you share with us a little bit about the potential scale of the public health problem that long COVID presents to us as a society? Is it true that more than 1.4 million Australians could be affected? What sort of cost to society could we expect?

STEVEN FAUX:  Well, that's a daunting question when I'm sitting amongst all these scientists. What I can tell you is that the scientific answer will be, “it's very hard to estimate”. Because the number of people who had persistent symptoms with the first wave will be different to the Delta wave, will be different to the Omicron wave. And we do know the data shows that people who are double vaccinated who got Delta, around about 10% of them in Australia continue to have symptoms. The people who got Omicron and were triple vaccinated, about 5%. The WHO says that on a global scale it's 10 to 20%. But that, of course, involves many countries that have less than ideal health systems.

10 to 20% of the Australians who've had COVID would be over a million, because 11 million Australians have had COVID. New South Wales Health have tried to model this and said at least 57,000 people in New South Wales will have long COVID. So it's not insignificant, and if you put that trajectory through to the whole of Australia, it's going to be between 250 and 300,000, which when you think about it is about the number of people have dementia. It's not a small category.

The straightforward answer is a lot of people. When we opened our clinic in March of this year, till October, we've had 700 referrals. And that's pretty good, because we can only see that eight a week. So we’re booked out until the end of next year. And even though we have rejected 300 of those referrals because they've come from interstate, or they've come from other areas with health services, there's obviously a quite a pressing need.

MIC CAVAZZINI:              Let’s go now to the conception of the ADAPT study and some of its key findings. One of the principal investigators is Professor Gail Matthews, Head of Infectious Diseases at St Vincent's Hospital Sydney and also program head of the therapeutics research and vaccine program at the Kirby Institute of UNSW. Her co-lead is respiratory clinician Dr David Darley whose other stream of research looks at predictors of lung transplant rejection and survival. Professor Matthews takes us back to the early days of the pandemic and the uncertainty hovering around this new syndrome for patients and their doctors.

GAIL MATTHEWS:          So it's really interesting the story of ADAPT, in a way, because when we set it up, and we set out really very early on in the in the pandemic—so I think our first patients were starting to be seen at St Vincent’s in April 2020—end of March and April. And we had the study actually set up and running by May, which is an amazing feat if anyone knows about research.

And the background to it was that when we started to see the patients coming to the hospital, obviously the hospital went into a sort of stand-up mode, everybody was involved. But clearly the patients were coming predominantly through to Respiratory medicine and to Infectious Diseases where we were managing all the patients in the in the community.

So those two departments, particularly—and that’s how myself and David sort of came to co-lead the study. We had no idea that long COVID was going to be a thing at this time, and we really envisioned it that start really as a fairly short-term study. My background is very much in clinical trials, and cohorts. I'm very familiar with how to set things up in a very rigorous manner so that we collect data across the board, and we collected on a standard schedule assessments, we do the same thing on everybody. And, of course, we involved colleagues, and Bruce from neurology, and immunologists, and we really wanted it to be a very collaborative study.

So we were able to set it up very quickly, which was amazing. And then we started to follow people. And any of the people who are here today or online, I think we have some of our ADAPT participants, and I want to just say a big thank you to those people—some of them we've been following for two years from those early days. And we followed everybody. We followed them whether they had symptoms or not. Whether they recovered or not.

And then clearly as time went on, after a few months, we started to see what the world was seeing, which was that some of our patients were just not getting better. And so it was really incredibly fortuitous that we already had this established cohort of patients that we were following after their infection and doing standardized assessments and from and that's one of the beauties, I think, of the study, and why it's been pretty successful in some of its findings.

The challenges, obviously, of setting a study up like this, in a pandemic are a huge because everybody is in crisis mode. The hospitals in crisis mode in terms of policies, and how things had to change. And we were all very much under the pump just trying to learn about so many different new things that were happening. I have to also have a big shout out to people in the ethics board and people in governance at the hospital, who really worked incredibly hard to push things through very quickly to get this study up and running. And usually it takes around six months from thinking about a study to actually getting it started. It took us six weeks despite all the challenges of having to work in a very pressured environment. And that's a testament everybody who was involved in the study and a lot of people were.

DAVID FAKTOR:              I remember back in the day, thinking that such a study was luxury we didn't have because we were in sink or swim mode. And to think now sitting here, how fortuitous that was on your part, and how extraordinarily swiftly you got the study up, given how multi-dimensional it was. And to think now we're sitting here, and I'm about to ask you a whole lot of very in depth questions So still Gail, how have the adapts participants and their data contributed to what we know about on COVID now.

GAIL MATTHEWS:          So it's a good question, because when you look at the literature on long COVID that's out there at the moment, it's taken a long time to come through because as I say, research is a long-term business. But what we see coming out now is very big data sets of you know, tens of thousands of people particularly from the UK in the US. And we have obviously a relatively small—it's a big study for one site, it's 200 patients, but it's actually a really small data set. But because we had collected their cells—not just their blood work, but what we call that PBMCs, the cells in their blood, which is quite difficult to do—costly and required a lot of effort from the lab to do it—but we thought it's worthwhile doing.

So what we were able to do is to marry together the cells and people's symptoms, and then do this really elegant study, which was one of the first to really try and understand what was going on in the blood of people who are suffering from long COVID, as opposed to those who were recovered. And what we saw was what we call an immunological signal, which was persisting out to four months, and then eight months in people who had long COVID symptoms, that were just wasn't there and people who were recovered. And certainly wasn't there at all, in what we call our control group of people who had other coronaviruses, which we also set up as a control group.

So it was one of the first bits of global evidence to really support this idea that there was something immunologically different about people who are suffering from long COVID, or at least a portion of those people. And that was really important because it validated for a lot of people at the time—again, a novel presentation. And I think a lot of people at the start maybe didn't think long COVID was a real thing, thought that people were just taking a long time to recover, or they were traumatized or that it’s in their heads or you know, all kinds of things and patients told us this. But for us to be able to actually measure this immunological signal and characterize it really, really carefully, was very impactful. And that paper was published in Nature immunology, one of the top nature journals, and it’s been one of the most downloaded and cited papers in long COVID.

DAVID FAKTOR:              Gail still picking on you, I understand that many of the ADAPT participants took part in qualitative interviews about their experience of long COVID. What does this tell us?

GAIL MATTHEWS:          So often, what happens with research is you'll get a group of researchers who asked a question in a certain group of people. And different researchers ask their question in a different group of people and so on around the same sort of disease area. But what we tried to do, and one of the powers of ADAPT, we still got lots of things we can look at, is that because it's the same group of patients we can link up bits of data. So we can link up the neurological data, for example, with the psychological data, with the immunological data, because we have it all in one system, if you like, and so it gives us a lot of power.

But one of the aspects of it that we involved was some of the social researchers to do some qualitative work. Which is actually really important, it's more about looking at the patient's own experience and their own journey and their own story and their own narrative of long COVID, and what it meant to them. And, you know, there were some interesting things that came out of that, but one of them was around patients learning to live with a new illness and some of the anxiety of that and how they adapted to that, and how that changed their lives. And that sort of qualitative data is really important bit of the scientific puzzle in what we started to learn about long COVID.

DAVID FAKTOR:              David, if I can pick on you now. Many patients in ADAPT underwent lung function testing, what were the main effects seen on lung function for COVID Recovery?

DAVID DARLEY: Thanks, David. And before I start, I just want to acknowledge all the participants, some of whom I can see in the room tonight. Thank you for your time and patience. It's really helped us create a really fantastic study and we've learned so much. I'd also like to thank the Curran Foundation, it's really hard to get government-funded research. And it was really amazing to get philanthropic donor funding early on to set up the study. And of course, the study team. You know, we're sitting up here we kind of get the limelight as the investigators but there's so many staff from the AMR, Chloe and Nicola and her bio-banking staff that that need to be acknowledged, there's so many cogs in the wheel that that make a study like this run. So just to give just a quick thanks.

So yeah, I mean, I'm a respiratory physician, and we had this novel respiratory virus. And I guess one of—the main question that that we had was, “what kind of effect does this virus have on people's lung function?” And so we did blowing tests at St Vincent's Hospital, over 100 patients did that. And that measures airflow in and out of the lungs, lung capacity, the efficiency of the lungs. And what was interesting is that, fortunately, the majority of patients actually had normal lung function. There was a small minority of patients who had problems with lung capacity and lung efficiency. And this was mostly related to the fact that those patients had been hospitalized for severe infection. So it was the patients who really needed to go to hospital for pneumonia, were the ones that we were seeing the lung abnormalities.

We have been following participants for up to 12 months with lung function tests. And I guess the good news for participants is that the majority of people with problems with their lung function tests are tending to show improvement over time. So this doesn't look like it's a persistent problem that gets worse in the majority of participants. And what we're seeing is scarring of the lungs in a very small number of participants. So there's a silver lining, and there's a good message, I guess.

DAVID FAKTOR:              Yeah. So I also understand that some of the adapts participants underwent cardiac MRI to measure heart function. What did we learn from this?

DAVID DARLEY: So we're very lucky at St. Vincent's to have advanced cardiac imaging on campus. And we were very lucky for one of the cardiology groups to allow us to use the cardiac MRI for 20 patients. And we mostly focused on patients who met our definition of long COVID; you know, fatigue, short of breath, chest tightness going on for months after initial infection. Fortunately, the majority of those patients had normal function of the heart. But we did see some scar in a small minority of those patients. Most of those patients then went to see a cardiologist. And fortunately, the scar wasn't causing any major functional structural problems of the heart, and we don't think is a is a long term problem with that. But the cardiac MRI component of the study has really given us a really high definition look at heart function after COVID and helping us identify those patients that might need further investigation and management with a with a specialist.

DAVID FAKTOR:              So as Gail pointed out, we're now at two years plus after initial infection. What does the general health of the ADAPT cohort look like?

DAVID DARLEY: So many patients in our study completed up to 12 months of follow up after the initial infection. But we did offer an extension for some patients to be followed up to 18 months or two years after initial infection. And our Honours student, Ben Schiavone, has analysed the data and it’s shown some interesting results. I think feedback for the participants is that the majority of patients in the study had fully recovered by two years.

There were a group of patients who would have met the definition of long COVID when they entered the study, so at three to four months after initial infection. Interestingly, for those patients, there were some mixed findings. About two thirds of those patients still did have some symptoms and some of them reported they didn't feel like they, even at two years, had fully recovered back to normal. But the flip side of that was that we did see improvements in a lot of the assessments that we were doing. So in terms of mental health, adjusting to the diagnosis, quality of life, even some of the cognitive testing and the smell testing that we were doing. Even in patients who did have long COVID we were seeing some improvements. So I think there's a kind of mixed message there. Clearly there's a cohort of patients who are still struggling at two years and we really need better prevention and treatment for long COVID. But our study has shown that there is improvement for a lot of people.

MIC CAVAZZINI:              The more common symptoms of long COVID are cognitive rather than respiratory. Mental fatigue, confusion, forgetfulness, which are often wrapped together under the label of brain fog. Fortunately, the ADAPT cohort have been undergoing neurological testing from the beginning of the study.

This has been led by Professor Bruce Brew AM, senior consultant neurologist at St Vincents and Director of the Peter Duncan Neurosciences Research Unit. He has spent years investigating the neuropsychological impacts of HIV/AIDS and its therapies with his colleague at UNSW, Associate Professor Lucette Cysique. She, in turn, chairs the neuroCOVID special interest group of the International Neuropsychological Society. Here’s Professor Brew describing the real life impact that these symptoms have for patients with long COVID.

BRUCE BREW:   So brain fog is a reasonably apt way of describing the problem. Because people complain that they can't concentrate, so can't focus on what they want to absorb. That translates into being forgetful. And they can't hold their thoughts to organize things. And so those symptoms can fluctuate. Sometimes they can be reasonably okay but after some, even just reading, a few pages can be quite taxing. And that can translate to not being able to work at all if they’re high functioning.

There's a particular patient who related that he was involved in a number of companies, and would have to sort of digest the legalese and be sure that the other party wasn't ripping him off. He could no longer do that. At a face to face level, you would think everything was fine. A brief conversation, you'd think things were fine. But getting into any sort of depth, you'd realize that there were problems and he's now employing people to actually read the documents and then go through them very slowly with him so that he can still participate in this business, but at nowhere near the functional level.

DAVID FAKTOR:              More broadly, Bruce, can you share with us the main findings of the neuro COVID sub study of ADAPT, and how these findings may impact how we treat and care for long COVID patients moving forward?

BRUCE BREW:   So I think there's several findings. Right back when we started, from a neurological perspective, we were thinking that there could be a whole host of things that we might find. And we were focused on what was happening to the patients in the context of the acute illness.  We had no idea that there was this thing called long COVID. Now, what is it? What did we find? I guess the first thing is that it's real. And that took some time. The second thing is that it's not psychologically based, it's not a mental health issue. Sure, lots of patients have mental health problems, understandably, but it's not driving the cognitive disturbance. Third, it's not, in the non-hospitalized patients, related to the severity of the acute illness. The patients who are hospitalized are a different group, they have been through a lot and they will have deficits that are related to the severity of their acute illness. But in the non-hospitalized patients, it's not related to the severity, and it's not related to their comorbidity burden.

So it's a unique disorder. And we were one of the first actually recognize that and it was like bashing your head against a brick wall to get people to understand. So the participants in ADAPT really contributed in a very, very significant way to understanding that as a true disease entity. And we wondered whether it was immune activation, given that that was related to COVID, looked at a number of markers didn't find anything. And then when we dug a bit deeper, there was a particular part of the immune system, which is a regulatory function of the body to say to the immune system, “it's time to switch off, game’s over.” It induces what's called tolerance. And it's a consequence of any insult, that insult being virus or bacteria, whatever, that send a signal the immune system, “We have to get rid of you.” And in the in the context of this particular pathway it's not switched off. This particular pathway is overactive and remains overactive produces a number of toxins. And that was the only marker, the only analyte, if you like, that was related to the degree of the presence and degree of cognitive impairment. And to my knowledge, there's no other marker that's been linked to the degree of cognitive damage. So it's very unique.

And the other—the sub sub study—some of the ADAPT patients participated in an MRI study with the radiologist, particularly Joga Chaganti who was very helpful. And what do we find from that? We use some advanced MR imaging techniques to identify a very subtle impairments of the blood-brain barrier. So there's this thing called the blood-brain barrier where the brain is semi immunologically privileged. So you don't want the brain exposed to a whole host of toxins and immune parameters that the rest of the body can take with the brain can’t. In COVID, particularly in the neurologically impaired patients, there was evidence of impairment of the blood brain barrier, and by this particularly sensitive technique, not in all of them but for the majority.

So there’s cross sectional data, then we've got a small number that we've now had several repeat studies. And again, there’s improvement, in some patients resolution, to normality, which is really encouraging. And the other aspect of the MR was looking at markers of inflammation and that was very helpful in identifying, yes there's inflammation, but it's very subtle. And that does persist for longer than we thought [under review].

Tying that back to the clinical part of the study, the neurological aspects in terms of cognitive impairment surprisingly don't budge when we analyse up to about a year. With some of them there's a small increase, which is statistically significant but probably not clinically significant. So that that's in contradistinction to a lot of the other symptoms.

DAVID FAKTOR:              And Bruce, this might me a bit of a naive question. But you've spent 40 years looking at neural pathways for neurodegenerative illnesses. In terms of some of those pathways lighting up, are you seeing commonality between these or am l my way off the mark here.

BRUCE BREW:   So yes, there are commonalities and that that isn't just interesting. At a biological level, it's clinically potentially significant, because there are certainly reports and there's an increasing appreciation that patients who are already cognitively impaired, who get COVID, are at risk—not all of them, but some of them—of impairment, which is worse. It's as though it takes them down a notch in terms of their functioning. So if they’re demented, some will get worse. And one explanation of that, maybe this link to the pathway.

DAVID FAKTOR:              Right, okay. Look, we've got we've got some time for questions, both from the audience here tonight and also, hopefully, we'll have a bit of time for questions from the audience online. But I think Craig's is going to hand you a microphone, if you could. Thanks so much.

AUDIENCE MEMBER 1: I'm just wondering if research from a long, long time ago to do with ME/ chronic fatigue syndrome contributes in any way to this because as I understand it, that can be a typical post viral trigger, Chronic Fatigue Syndrome.

GAIL MATTHEWS:          Yeah, I think it's a really good question. It's something that comes up a lot, because of the similarities between chronic fatigue any all those syndromes, and also long COVID. And I think one of the things is, we don't know a lot about chronic fatigue. And the problem is, is that it hasn't been properly studied, it's been very hard to know what was the trigger and what happened since and then, by the time people present often, it's very hard to disentangle what's going on. COVID offers us a really great opportunity, because we have these cohorts studies of people who've been followed from the start, and then are going to be followed up over long periods of time to really understand what having a virus might trigger for some people.

 So I think COVID, if done properly—and there are very large studies now being set up of people with long COVID—can actually offer and hopefully some insights into the group of people who have been suffering with ME and those post viral syndromes for some time and, and to therapy. Obviously, there has been no drug therapy that's been particularly helpful in those settings. But we're a long way off having the answers for long COVID or for CFS/ME about good therapeutic options. It's something we're all trying to think about and explore.

BRUCE BREW: So if I can just jump in. So in our control samples, we had healthy controls, coronavirus non-COVID controls, and then CF, chronic fatigue syndrome controls from collaborators in Victoria. This particular signature pathway activation was quite different—was not present in chronic fatigue. So from a from a chemical biochemical biological perspective, it's different.

STEVEN FAUX:  From a treatment perspective, we've actually learned a bit from chronic fatigue syndrome because what we saw very early on was post-exertional malaise, which has been described by chronic fatigue sufferers. So when we exercise people hard, early on, they actually stopped. I can remember a young adolescent girl, we just saw her again today after six months who couldn't complete her HSC, she was an athlete at school. And she insisted on exercising quite hard, but then would often be unable to get out of bed for three or four days. And in fact, her HSC she had to do with periods of lying down completely. So we realized that we had to tailor the exercise to constant feedback about fatigue levels, so it has actually tempered some of the treatments.

AUDIENCE MEMBER 2: Hi, I had COVID in early 2020 and I found it affected me neurologically. My, my question is, have we seen any evidence on people who have get COVID a second time or a third time whatever they've gained neurologically, whether that will erode back to the original level, or whether it will have no impact.

STEVEN FAUX:  In our experience in the clinic, people who've had long COVID from one strain, if they get a second strain, and we've seen that in about four or five cases, don't complain of long COVID a second time. So it doesn't necessarily mean if you've had it the first time that you'll get it with the other strains. Maybe it's because you've been vaccinated in between maybe because the strains are different. So it doesn't necessarily follow that if you have for one strain, you'll get it for another.

GAIL MATTHEWS: About 25% I of the ADAPT patients have been reinfected during the study. And that gives us a really nice opportunity then to look at the effect of getting reinfected on those immunological markers and so on and see whether it does trigger the same thing the second time around. But certainly from our look at the data so far, it doesn't seem to be that when you've got reinfected your parameters of whatever health that you're measuring go back down. So that sort of backs up what Steve's saying there that it doesn't necessarily happen that if you've had a long COVID once and you get reinfected again you're going to go back to your symptoms previously.

DAVID FAKTOR:              We've got someone in the audience with a question.

MIC CAVAZZINI:                           Thanks very much for such a thorough explanation. We've heard about some of the immunological markers that you picked up, some of the cardiac scarring and MRI, and the neurological pathway. I presume you weren't lucky enough to do the same assays in all the same patients to join the dots. Is it possible that those are three entirely different markers of different syndromes or….?

DAVID DARLEY: I think it's a great question. The way we set up the study was that we did most things on most patients at the same time points. So we had patients who did have long COVID symptoms, we had patients who didn't. And so we were able to compare groups with the same sorts of assessments. I think what I've seen and what others have seen in clinic is that there are different clusters of symptoms. So some patients have more of a fatigue type of presentation. Some have more of a brain fog, you know, problems with memory and thinking, some have more of a breathless, chest pain type of presentation. So I think a lot more work needs to be done to work out, you know, what are the differences or commonalities between these different clusters? Why would why would one patient get a particular symptom as opposed to another? And I think we're really there yet.

DAVID FAKTOR:              You've got a question.

AUDIENCE MEMBER 3: Hey, thanks for like, it's like outlining the treatment plans for people with fatigue. Are there similar protocols for people with things like brain fog, or like loss of smell, or I, guess, vertigo, Could you outline what those are?

STEVEN FAUX:  Loss of smell is a great one, because it is a system that can be trained—we train people to identify smells. It's been developed in the United States, and we've been using it in a number of our clinics. So that's a good question. The other about brain fog, essentially, what we do to characterize it by doing the tests. We often pull in a neurologist, we contact Bruce, if we notice that there might be other symptomatology for him to review. Then we look at what function they can't do, so mostly it's work. I mean, the loss of productivity in an environment of low unemployment and high workforce needs is huge. So we look mostly at their work, we get an occupational therapist to do that, and we try and then fashion return to work based on what cognitive power they have, as opposed to the weakness. And then we also give them some exercise because, certainly in other neurological conditions, exercise can often improve the vascular supply to the brain so we do we do some of that. And we'll also, if there is psychological phenomena—particularly if people get depressed, which often happens because they get insight into the fact they're not functioning well—we'll treat that psychological techniques or even medications. So it's a multidisciplinary approach. And we tell people not to expect too much and slowly paced their return to work. And recently we discharged a lawyer back to full time work after about six months in the program with cognitive impairment initially doing very slow return to work and working with his employer. There's only been two or three in that category, because we've not been running for very long.

MIC CAVAZZINI:              Many thanks to Gail Matthews, David Darley, Steven Faux and Bruce Brew for their important work, so clearly explained. And to the staff at the St Vincent’s Hospital Curran Foundation for recording the seminar and allowing me to share it with you. I’ll provide a link to the Foundation’s home page, and a video recording of the event at our website. That’s racp.edu.au/podcast.

You’ll find a full transcript there as well, links to some relevant academic literature, and credits to the music you’ve heard via Epidemic Sound. To log CPD credits for your time spent absorbing this information just click on the MyCPD link in the blurb describing to this episode.

I’m Mic Cavazzini and this episode was recorded on the traditional lands of the Gadigal people of the Eora nation. I pay respect to their elders past and present, and their ongoing connection to the country I’m fortunate to share.  

Thanks for listening to Pomegranate Health and best wishes over the holiday season.