Long Covid

[Woodchopper]

At 6-month follow-up after hospitalisation due to COVID-19 disease, patients displayed a wide array of neurological symptoms, being fatigue (34%), memory/attention (31%), and sleep disorders (30%) the most frequent. Subjects reporting neurological symptoms were affected by more severe respiratory SARS-CoV-2 infection parameters during hospitalisation. At neurological examination, 37.4% of patients exhibited neurological abnormalities, being cognitive deficits (17.5%), hyposmia (15.7%) and postural tremor (13.8%) the most common. Patients with cognitive deficits at follow-up were comparable for age, sex and pre-admission comorbidities but experienced worse respiratory SARS-CoV-2 infection disease and longer hospitalisation. Conclusions: long term neurological manifestations after hospitalization due to COVID-19 infection affects one third of survivors. Multiple neurological abnormalities including mild cognitive impairment are associated with severity of respiratory SARS-CoV-2 infection.

https://www.medrxiv.org/content/10.1101 ... 20248903v1

[Woodchopper]

Postacute COVID-19: An Overview and Approach to Classification
https://academic.oup.com/ofid/article/7 ... 09/5934556

[Woodchopper]

How COVID-19 Attacks The Brain And May Cause Lasting Damage
https://www.npr.org/sections/health-sho ... ing-damage

[Woodchopper]

6-month consequences of COVID-19 in patients discharged from hospital: a cohort study

At 6 months after acute infection, COVID-19 survivors were mainly troubled with fatigue or muscle weakness, sleep difficulties, and anxiety or depression. Patients who were more severely ill during their hospital stay had more severe impaired pulmonary diffusion capacities and abnormal chest imaging manifestations, and are the main target population for intervention of long-term recovery.

https://www.thelancet.com/journals/lanc ... 8/fulltext

[Woodchopper]

Article summarizes likely long-term effects of Covid on the brain and central nervous system: https://alz-journals.onlinelibrary.wile ... /alz.12255

[Woodchopper]

Abstract
Objectives: The epidemiology of post-COVID syndrome (PCS) is currently undefined. We quantified rates of organ-specific impairment following recovery from COVID-19 hospitalisation compared with those in a matched control group, and how the rate ratio (RR) varies by age, sex, and ethnicity.

Design: Observational, retrospective, matched cohort study.
Setting: NHS hospitals in England.

Participants: 47,780 individuals (mean age 65 years, 55% male) in hospital with COVID-19 and discharged alive by 31 August 2020, matched to controls on demographic and clinical characteristics.

Outcome measures: Rates of hospital readmission, all-cause mortality, and diagnoses of respiratory, cardiovascular, metabolic, kidney and liver diseases until 30 September 2020.

Results: Mean follow-up time was 140 days for COVID-19 cases and 153 days for controls. 766 (95% confidence interval: 753 to 779) readmissions and 320 (312 to 328) deaths per 1,000 person- years were observed in COVID-19 cases, 3.5 (3.4 to 3.6) and 7.7 (7.2 to 8.3) times greater, respectively, than in controls. Rates of respiratory, diabetes and cardiovascular events were also significantly elevated in COVID-19 cases, at 770 (758 to 783), 127 (122 to 132) and 126 (121 to 131) events per 1,000 person-years, respectively. RRs were greater for individuals aged <70 than ≥70 years, and in ethnic minority groups than the White population, with the biggest differences observed for respiratory disease: 10.5 [9.7 to 11.4] for <70 years versus 4.6 [4.3 to 4.8] for ≥70 years, and 11.4 (9.8 to 13.3) for Non-White versus 5.2 (5.0 to 5.5) for White.

Conclusions: Individuals discharged from hospital following COVID-19 face elevated rates of multi- organ dysfunction compared with background levels, and the increase in risk is neither confined to the elderly nor uniform across ethnicities. The diagnosis, treatment and prevention of PCS require integrated rather than organ- or disease-specific approaches. Urgent research is required to establish risk factors for PCS.

https://www.medrxiv.org/content/10.1101 ... 1.full.pdf

[Woodchopper]

Regarding the above 313614 people have been admitted to hospital in the UK already. It seems like there may be circa 100 000 people with chronic long term conditions that have required another stay in hospital. I expect that there will be many more who are affected but didn’t need to go to hospital.

[Woodchopper]

Abstract

Background.

Neurologicaland psychiatric sequelae of COVID-19 have been reported, butthere are limited data on incidence rates and relative risks.

Methods.

Using retrospective cohort studies and time-to-event analysis, we estimated the incidence of ICD-10 diagnosesin the 6 months after a confirmed diagnosis of COVID-19: intracranial haemorrhage;ischaemic stroke;Parkinsonism;Guillain-Barré syndrome;nerve/nerve root/plexus disorders;myoneural/muscle disease;encephalitis;dementia;mood, anxiety, and psychotic disorders;substance misuse;and insomnia. Data were obtained from the TriNetX electronic health records network (over 81 million patients). We compared incidences with those in propensityscore-matched cohorts of patients with influenza or other respiratory infections using a Cox model. We investigated the effect on incidence estimates of COVID-19 severity, as proxied by hospitalization and encephalopathy (including delirium and related disorders).

2Findings.

236,379 patients survived a confirmed diagnosis of COVID-19. Among them, the estimatedincidence of neurologicalor psychiatric sequelae at 6 months was 33.6%, with 12.8% receiving their first such diagnosis.Most diagnostic categorieswere commoner after COVID-19 than afterinfluenza or other respiratory infections(hazard ratios from 1.21 to 5.28), including stroke, intracranial haemorrhage, dementia, and psychotic disorders.Findings were equivocal for Parkinsonism and Guillain-Barré syndrome. Amongst COVID-19 cases, incidences and hazard ratios for most disorders were higher in patients who had been hospitalized,and markedly so in those who had experienced encephalopathy. Results were robust to sensitivity analyses, including comparisons against an additional four index health events.

Interpretation.

The study provides evidence for substantial neurologicaland psychiatric morbidityfollowing COVID-19infection.Risks were greatest in, but not limited to,those who had severe COVID-19. The information can help in service planning and identification of research priorities.

https://www.medrxiv.org/content/10.1101 ... 21249950v1

[Woodchopper]

Results Six months after the infection, 67% of the study participants reported at least one symptom as a consequence of COVID-19. Exertional dyspnea (30% of participants), fatigue (25%) and diminished sense of taste/smell (19%) were the most common individual symptoms. At least one symptom, exertional dyspnea, and fatigue were reported more often after a severe acute illness, but diminished sense of taste/smell was unrelated to acute severity. Age group and sex did not associate with the frequency of symptoms at 6 months. Conclusions Based on this study, the prevalence of COVID-19-related symptoms 6 months after the infection is high. Some bias for overestimation may have affected this result. Nevertheless, ′long COVID′ requires attention in medical care and a better scientific understanding.

https://www.medrxiv.org/content/10.1101 ... 21251619v1

[Woodchopper]

Although direct infection like this can occur, many experts now believe that systemic inflammation originating from the infected lungs or blood vessels, not myocyte infection, explains most myocardial injury findings among patients hospitalized with COVID-19. Immune cell messengers called cytokines circulating through the body could induce heart muscle inflammation. Systemic inflammation could also trigger arrhythmias and destabilize coronary plaques, leading to plaque rupture and type 1 myocardial infarction (MI), or heart attack—the most common cause of elevated troponins.

A recent study involving Rhesus macaques supports the role of systemic inflammation. Researchers at Emory University led by cardiologist Rebecca Levit, MD, discovered more scar tissue in the hearts of monkeys they infected with SARS-CoV-2 two weeks prior than in an uninfected control group. Yet they detected no virus or white blood cells in the infected monkeys’ hearts.

“We hypothesize that support cells in the heart, fibroblast, may be responding to the systemic inflammation,” Levit said in an email. “The activation of these cells may lead to fibrosis.”

Additionally, several other COVID-19 manifestations could injure the heart muscle, including an oxygen supply-and-demand imbalance in the heart (type 2 MI), blood clots, sepsis, stress-induced cardiomyopathy, and multisystem inflammatory syndrome. Troponin levels could also represent COVID-19 severity because a critical illness can hasten preexisting cardiovascular disease.

Sorting out the source of myocardial injury could steer treatments to safeguard the heart. Going forward, novel research tools like stem cell–derived cardiovascular cells will be used to model how SARS-CoV-2 infection causes cardiac damage. Researchers have begun to infect these lab-grown cells to understand the precise mechanisms of heart cell injury.

https://jamanetwork.com/journals/jama/f ... o.linkedin

[Woodchopper]

In this cohort of individuals with COVID-19 who were followed up for as long as 9 months after illness, approximately 30% reported persistent symptoms. A unique aspect of our cohort is the high proportion of outpatients with mild disease. Persistent symptoms were reported by one-third of outpatients in our study, consistent with a previously reported study,4 in which 36% of outpatients had not returned to baseline health by 14 to 21 days following infection. However, this has not been previously described 9 months after infection.

Consistent with existing literature, fatigue was the most commonly reported symptom.2-4 This occurred in 14% of individuals in this study, lower than the 53% to 71%2-4 reported in cohorts of hospitalized patients, likely reflecting the lower acuity of illness in our cohort. Furthermore, impairment in HRQoL has previously been reported among hospitalized patients who have recovered from COVID-19; we found 29% of outpatients reported worsened HRQoL.5

Notably, 14 participants, including 9 nonhospitalized individuals, reported negative impacts on ADLs after infection. With 57.8 million cases worldwide, even a small incidence of long-term debility could have enormous health and economic consequences.6

Study limitations include a small sample size, single study location, potential bias from self-reported symptoms during illness episode, and loss to follow-up of 57 participants. To our knowledge, this study presents the longest follow-up symptom assessment after COVID-19 infection. Our research indicates that the health consequences of COVID-19 extend far beyond acute infection, even among those who experience mild illness. Comprehensive long-term investigation will be necessary to fully understand the impact of this evolving viral pathogen.

https://jamanetwork.com/journals/jamane ... le/2776560

[Woodchopper]

Delayed-onset myocarditis following COVID-19

A multisystem inflammatory syndrome occurring several weeks after SARS-CoV-2 infection and that can include severe acute heart failure has been reported in children (MIS-C).1, 2 In adults with acute severe heart failure, we have identified a similar syndrome (MIS-A) and describe presenting characteristics, diagnostic features, and early outcomes. Our data also complement reports of MIS-A.3

https://www.thelancet.com/journals/lanr ... 0/fulltext

[Woodchopper]

Long COVID neuropsychological deficits after severe, moderate or mild infection

Background: There is growing awareness that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection can include long-term neuropsychological deficits, even in its mild or moderate respiratory forms. Methods: Standardized neuropsychological, psychiatric, neurological and olfactory tests were administered to 45 patients (categorized according to the severity of their respiratory symptoms during the acute phase) 236.51 (SD: 22.54) days post-discharge following SARS-CoV-2 infection. Results: Deficits were found in all the domains of cognition and the prevalence of psychiatric symptoms was also high in the three groups. The severe performed more poorly on long-term episodic memory and exhibited greater anosognosia. The moderate had poorer emotion recognition, which was positively correlated with persistent olfactory dysfunction. The mild were more stressed, anxious and depressed. Conclusion: The data support the hypothesis that the virus targets the central nervous system (and notably the limbic system), and support the notion of different neuropsychological phenotypes.

https://www.medrxiv.org/content/10.1101 ... 21252329v1

[Woodchopper]

Estimating the burden of post-COVID-19 syndrome in a population-based cohort study of SARS-CoV-2 infected individuals: Implications for healthcare service planning


Results Symptoms were present in 385 (89%) participants at diagnosis and 81 (19%) were initially hospitalised. At six to eight months, 111 (26%) reported not having fully recovered. 233 (55%) participants reported symptoms of fatigue, 96 (25%) had at least grade 1 dyspnoea, and 111 (26%) had DASS-21 scores indicating symptoms of depression. 170 (40%) participants reported at least one general practitioner visit related to COVID-19 after acute illness, and 10% (8/81) of initially hospitalised individuals were rehospitalised. Individuals that have not fully recovered or suffer from fatigue, dyspnoea or depression were more likely to have further healthcare contacts. However, a third of individuals (37/111) that have not fully recovered did not seek further care.

Conclusion In our population-based study, a relevant proportion of individuals suffered from longer-term consequences after SARS-CoV-2 infection. Our findings indicate that a considerable number of individuals affected by post-COVID-19 syndrome is to be expected, and that a wide range of additional healthcare services and integrative approaches will be required to support the recovery of these individuals. Thus, the timely planning of resources and services for post-COVID-19 care will be necessary alongside public health measures to mitigate the effects of the pandemic.

https://www.medrxiv.org/content/10.1101 ... 21252572v1

[jimbob]

Is that 55% reported fatigue during the course the illness?
I'm guessing it's not at 6-8 months... because the numbers wouldn't fit...

On s phone so can't easily read the paper

[jdc]

Is that 55% reported fatigue during the course the illness?
I'm guessing it's not at 6-8 months... because the numbers wouldn't fit...

On s phone so can't easily read the paper

442 individuals agreed to participate in our study (participation rate 34%). Five individuals never completed the baseline questionnaire and were excluded from analysis. Furthermore, we excluded six individuals who had a suspected reinfection

So it's out of a total of 442. Minus 11 exclusions.

I checked the percentages and it looks like all but one of the first seven figures given are out of the 431 (though there are rounding errors on the 233 fatigue and 170 GP visits - they should be 54 and 39 rather than 55 and 40). The 96 with dyspnoea is out of 385 rather than 431 for no apparent reason. I assume this is a mistake and they meant to do 96/431.

The only other figures given are shown as proportions (8/81 hospitalised and 37/111 not fully recovered but did not seek further care).

[jdc]

I mean, you can tell just from eyeballing the 385 (89%) and the 233 (55%) that the fatigue figure is out of the total participants rather than the subgroup who had long-lasting symptoms but I thought I might as well get the figures checked. It's not like I'm going anywhere.

Actually, you might as well ask me another while I'm here.

[jimbob]

I mean, you can tell just from eyeballing the 385 (89%) and the 233 (55%) that the fatigue figure is out of the total participants rather than the subgroup who had long-lasting symptoms but I thought I might as well get the figures checked. It's not like I'm going anywhere.

Actually, you might as well ask me another while I'm here.

That was why I said the numbers didn't fit, but it seemed an odd mishmash

[Woodchopper]

When Putrino looked at the data, he saw the same symptoms that Chen saw. To Putrino, they looked like those of patients who suffer from a poorly understood and often misdiagnosed condition, one that he happens to know a lot about because his wife lives with it: dysautonomia, or impairment of the usual functioning of the autonomic nervous system, which controls blood pressure, temperature regulation, and digestion. Dysautonomia is itself an umbrella term for a host of different conditions, many of whose causes have yet to be fully pinned down. In common manifestations of it, a patient’s autonomic nervous system has trouble regulating the heart’s response to exertion, changes in posture, or variations in temperature, sending the body into an inappropriate fight-or-flight response. Some patients’ systems have trouble adjusting blood pressure or constricting blood vessels to send blood to the brain. Blood can pool in the legs and peripheries of the body; the heart might compensate by increasing its rate, while the body releases surges of adrenaline in a fruitless attempt to correct the problem. As a result, patients can experience some blend of fatigue, headaches, digestive problems, heart palpitations, difficulty breathing, and cognitive issues such as brain fog.

[...]

In a group of patients, they theorized, either the virus or the immune system’s reaction to it had caused dramatic dysregulation of the autonomic nervous system. In the absence of clear data, Putrino told me, they decided to study how patients responded to treatment. Patients with cardiac or pulmonary problems typically react well to rehab that pushes them physically (“if you can take a little more, we’ll push you a little more,” as Putrino put it). But that push-through-it model can dramatically exacerbate dysautonomia patients’ symptoms, causing exhaustion and a racing heart. So standard rehab usually doesn’t work.

Experimentation with POTS over the past decade has yielded a paradoxical axiom that the group used as a guiding principle: Very gentle rehab is important, if you can tolerate it. The regimen involves doing short bursts of cardiac exertion while lying down or seated (so as not to tax the nervous and cardiovascular systems), wearing compression garments (to reduce blood pooling), hydrating, and taking salt (to increase blood volume). Studies, including an ongoing one conducted by Kontorovich’s lab, have found that in dysautonomia patients, the heart is smaller, and has less blood-volume capacity, than would be expected. No one knows if these patients’ hearts have actually shrunk in response to illness or other stresses—the phenomenon turns up in endurance athletes who suddenly stop training—or if people with smaller hearts are just more vulnerable to dysautonomia and related conditions. But studies have shown that targeted rehab can safely help the heart increase in size, improving symptoms. Putrino and Kontorovich theorized that the same might be true for the patients they were seeing.

Their hypothesis was borne out in a preliminary study, which found that a majority of their patients’ hearts were smaller than expected. And in rehab, people responded “more like we expected them to respond if they had autonomic issues than if they had cardiac or lung injuries,” Putrino said.

The patients’ symptoms were too varied to be lumped under an established label; in some ways the condition resembled dysautonomia, and POTS in particular—but it was not textbook. (Some clinicians began calling it post-COVID POTS.) In other ways, it closely resembled myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), in which people also demonstrate exercise intolerance and profound fatigue, but it was likewise not textbook. Same for autoimmune disorders. A commonality stood out: These are all poorly understood conditions that, evidence suggests, can be triggered by the body’s response to infections, with clusters of system-roaming symptoms that get grouped under one name.

In conjunction with a group of physicians in the U.K., Putrino’s team came up with a name, “post-acute COVID syndrome,” to distinguish between this manifestation of long COVID and the ongoing symptoms caused by observable organ damage from the virus.

Putrino’s team partnered with immunologists and researchers at Mount Sinai, as well as the National Institutes of Health and Yale, to try to identify the biological markers of post-acute COVID syndrome, and to understand the role the immune system was playing—but that kind of research takes months, if not years, to complete. In the meantime, the Mount Sinai teams struggled to find treatment protocols that worked for everyone to whom the new label seemed to apply. Some of their patients were so sick that even gentle rehab worsened their symptoms (much as people with ME/CFS have long reported). In others, rehab worked, but only up to a point, or patients overexerted themselves and relapsed.

[...]

missing piece of the puzzle, the Mount Sinai teams soon found, was right in front of them: breathing. Everyone knew, of course, about severely sick COVID‑19 patients on ventilators. What the researchers and doctors at Mount Sinai hadn’t realized was that even mild cases might be affecting respiration after the acute phase of the disease. Evidence began to accrue that long-COVID patients were breathing shallowly through their mouths and into their upper chest. By contrast, a proper breath happens in the nose and goes deep into the diaphragm; it stimulates the vagus nerve along the way, helping regulate heart rate and the nervous system. Many of us breathe through our mouths, slightly compromising our respiration, but in patients with post-acute COVID syndrome, lung inflammation or another trigger appeared to have profoundly affected the process. In these cases, patients’ breathing “is just completely off,” McCarthy told me.

[...]

Similar symptoms (fatigue, shortness of breath, racing heart) occur in people who have low carbon-dioxide levels in their blood—a condition known as hypocapnia, which can be triggered by hyperventilation, or shallow, rapid breathing through the mouth. Duntz wondered if perhaps these long-COVID patients, so many of whom suffered from dizziness and tachycardia, were also breathing shallowly, because of either lung inflammation even in mild cases or viral damage to the vagus nerve. The theory seemed plausible to Putrino: Oxygen is key to our health, but carbon dioxide plays an equally crucial role, by balancing the blood’s pH level. Mount Sinai was able to launch a breathwork pilot program swiftly because of “how desperate people were—the hospital was so overwhelmed,” Duntz said. The program also didn’t have to pass FDA clearance.

After a week, everyone in the pilot program reported improvement in symptoms like shortness of breath and fatigue. (No double-blind randomized controlled trial has yet been conducted, so it is not possible to know what percentage of the improvement was due to the placebo effect.) The patients’ responses were “game-changing,” Putrino told me.

[...]

The key was the realization that the diaphragm and the nervous system had to be coached back to normal function before further reconditioning could start. “You cannot rehabilitate someone when their symptoms are completely out of control,” Putrino said. Although patients still faced an unfolding array of unpredictable symptoms, breathwork helped get them to a “place where the healing can start.”

https://www.theatlantic.com/magazine/ar ... id/618076/

[Woodchopper]

COVID Symptoms, Symptom Clusters, and Predictors for Becoming a Long-Hauler: Looking for Clarity in the Haze of the Pandemic

The purpose of this study was to assess for symptoms at days 0-10 and 61+ among subjects with PCR-confirmed SARS-CoV-2 infection. The University of California COvid Research Data Set (UC CORDS) was used to identify 1407 records that met inclusion criteria. Symptoms attributable to COVID-19 were extracted from the electronic health record. Symptoms reported over the previous year prior to COVID-19 were excluded, using nonnegative matrix factorization (NMF) followed by graph lasso to assess relationships between symptoms.

A model was developed predictive for becoming a long-hauler based on symptoms. 27% reported persistent symptoms after 60 days. Women were more likely to become long-haulers, and all age groups were represented with those aged 50 ± 20 years comprising 72% of cases. Presenting symptoms included palpitations, chronic rhinitis, dysgeusia, chills, insomnia, hyperhidrosis, anxiety, sore throat, and headache among others. We identified 5 symptom clusters at day 61+: chest pain-cough, dyspnea-cough, anxiety-tachycardia, abdominal pain-nausea, and low back pain-joint pain.

Long-haulers represent a very significant public health concern, and there are no guidelines to address their diagnosis and management. Additional studies are urgently needed that focus on the physical, mental, and emotional impact of long-term COVID-19 survivors who become long-haulers.

https://www.medrxiv.org/content/10.1101 ... 21252086v1


Notably, about a third of the long haulers didn’t experience symptoms during the first ten days of the infection (though they tested positive).

[Nero]

I really hope this doesn't end up messy again:

https://www.theguardian.com/society/202 ... se-therapy

Dr Joanna Herman is right to call out the lack of care being offered to sufferers of long Covid (People with long Covid urgently need help. Why can’t we access it?, 10 March). The willingness of doctors to speak out as patients has done much to highlight the long-term effects of Covid-19.

We know that long Covid is more than one disease, all of which will need different treatments. But we do not know that graded exercise therapy is detrimental to recovery from the post-Covid fatigue syndrome. There are no such studies.

In contrast, we know that graded exercise therapy is an effective treatment for chronic fatigue syndrome (or ME), a clearly related condition. Moreover, no trials of graded exercise have shown harm to patients. We need trials of this treatment in post-Covid fatigue. In the meantime, let us not discourage patients from accessing what may be a helpful treatment, so long as it is provided by physiotherapists trained to properly deliver it.

Dr Alastair Miller Cumberland Infirmary, Carlisle, Prof Paul Garner Liverpool School of Tropical Medicine, Prof Peter White Queen Mary University of London

[jimbob]

COVID Symptoms, Symptom Clusters, and Predictors for Becoming a Long-Hauler: Looking for Clarity in the Haze of the Pandemic

The purpose of this study was to assess for symptoms at days 0-10 and 61+ among subjects with PCR-confirmed SARS-CoV-2 infection. The University of California COvid Research Data Set (UC CORDS) was used to identify 1407 records that met inclusion criteria. Symptoms attributable to COVID-19 were extracted from the electronic health record. Symptoms reported over the previous year prior to COVID-19 were excluded, using nonnegative matrix factorization (NMF) followed by graph lasso to assess relationships between symptoms.

A model was developed predictive for becoming a long-hauler based on symptoms. 27% reported persistent symptoms after 60 days. Women were more likely to become long-haulers, and all age groups were represented with those aged 50 ± 20 years comprising 72% of cases. Presenting symptoms included palpitations, chronic rhinitis, dysgeusia, chills, insomnia, hyperhidrosis, anxiety, sore throat, and headache among others. We identified 5 symptom clusters at day 61+: chest pain-cough, dyspnea-cough, anxiety-tachycardia, abdominal pain-nausea, and low back pain-joint pain.

Long-haulers represent a very significant public health concern, and there are no guidelines to address their diagnosis and management. Additional studies are urgently needed that focus on the physical, mental, and emotional impact of long-term COVID-19 survivors who become long-haulers.

https://www.medrxiv.org/content/10.1101 ... 21252086v1


Notably, about a third of the long haulers didn’t experience symptoms during the first ten days of the infection (though they tested positive).

And that is also about 8.5% of those who were asymptomatic at PCR test, if I'm reading that right.

[Woodchopper]

I really hope this doesn't end up messy again:

https://www.theguardian.com/society/202 ... se-therapy

Dr Joanna Herman is right to call out the lack of care being offered to sufferers of long Covid (People with long Covid urgently need help. Why can’t we access it?, 10 March). The willingness of doctors to speak out as patients has done much to highlight the long-term effects of Covid-19.

We know that long Covid is more than one disease, all of which will need different treatments. But we do not know that graded exercise therapy is detrimental to recovery from the post-Covid fatigue syndrome. There are no such studies.

In contrast, we know that graded exercise therapy is an effective treatment for chronic fatigue syndrome (or ME), a clearly related condition. Moreover, no trials of graded exercise have shown harm to patients. We need trials of this treatment in post-Covid fatigue. In the meantime, let us not discourage patients from accessing what may be a helpful treatment, so long as it is provided by physiotherapists trained to properly deliver it.

Dr Alastair Miller Cumberland Infirmary, Carlisle, Prof Paul Garner Liverpool School of Tropical Medicine, Prof Peter White Queen Mary University of London

Yes, the Long Covid symptoms do seem to resemble ME CFS in many ways, and as far as I know its widely assumed that ME CFS can be a post-viral syndrome. Long Covid could just be a form of ME CFS.

[Nero]

Yes, the Long Covid symptoms do seem to resemble ME CFS in many ways, and as far as I know its widely assumed that ME CFS can be a post-viral syndrome. Long Covid could just be a form of ME CFS.

I was more thinking of the ME CFS advocacy groups that riled against the use of graded therapy in a somewhat "robust" manner. If they started the same line and the same "robustness" within the Long Covid support groups it could end up being a bit of a re-run.

[shpalman]

Some long-haul covid-19 patients say their symptoms are subsiding after getting vaccines