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As a physician, I never thought that I would someday be lumped into the category of patients known as “not otherwise specified,” or NOS for short. This category is dominated by women suffering nonspecific symptoms that are inconsistently appreciated by clinicians who eventually conclude that the problem is entirely in the mind.

My induction into this group began on March 23. The emergency department in which I work had been seeing coronavirus patients, at first without our donning standardized personal protective equipment or following universal masking protocols. So when I developed a deep, dry cough, it was not outside the realm of possibility that I had contracted Covid-19. I notified my hospital’s occupational health department, even though I was personally convinced that my lungs were fighting a different, less serious respiratory virus, and that I would be back at work within days.

My conviction proved to be wrong. Despite testing negative for SARS-CoV-2, the virus that causes Covid-19, the course of my illness mimicked that of the “typical” coronavirus patient. The relentless dry cough and fatigue were followed by shortness of breath. My mentors, also physicians with whom I had informally consulted, were concerned that mine was a false negative test; at the time, the sensitivity of the swab was thought to be around 70%. But my chart was never flagged as “CoV-positive,” so my story was never counted in the growing statistics of employees affected by the disease.

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When I got sick, the guidelines for returning to work were that all symptoms must have resolved. After a long month of isolation, asking every week to be cleared for work, I finally insisted that I was ready. I was no longer short of breath while walking around my apartment. The remaining symptoms — weakness, muscle aches, and low energy — were nonspecific, subjective, and, therefore, things I could surmount. My persistent painful cough was given various names. Some providers definitively labeled it as postnasal drip, others said it was new-onset asthma. My colleagues and I settled on post-viral bronchospasm.

I was eager to get back to work in the intensive care unit. It was the end of April, and though Boston’s ICUs were still filled with coronavirus patients, we were beginning to think about what recovery might look like for those who had been critically ill. How many of them would suffer from long-term complications? When would they return to their normal lives?

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After working several shifts, I found myself unable to get out of bed one morning: the aches and fatigue were taking over. “Get up! Push through!” my mind scolded my body. My body and mind played this game for weeks. Every time I returned to work, hopeful to care for patients, my body protested, breathing hard and exhausted by the end of morning rounds.

Provider after provider unknowingly put me on trial, poised to accuse my body of falsification and interrogate it to discover alternate explanations. Without a positive SARS CoV-2 test, there was no simple diagnosis for my symptoms. When I asked them to look at the notes from my phone encounters with other clinicians, they used the same line I use on my patients: “It’s better for you to recount the story again, in your own words.” But I was tired of telling — and reliving — the story. I apologized for potentially wasting their time, as there might not be anything wrong with me, echoing the hesitancy of many women who are dismissed and fearful of being labeled as anxious or hypochondriacs.

Without seeing me in person or even virtually, nurses and doctors I spoke with on the phone posited the same diagnoses: post-nasal drip or asthma. Forced to take the stand, my body had to prove, to my mind and to everyone else, that it had been sick and it was still not well. “Despite my negative Covid tests, some of my mentors (who are also doctors) believe that I may have had Covid,” my body would begin its opening statement. My mind, trained by the best physicians and algorithms, was primed to prosecute. “Your story could fit, but we don’t have objective evidence. That’s why everyone is questioning; we don’t believe you.”

After all, that’s what we do to our patients. Shortness of breath could be any number of things. A productive cough might suggest pneumonia. Swelling in only one of your legs might indicate a clot there, which could mean there’s a clot in your lungs. Swelling in both legs could be fluid overload. Prove your diagnosis to me, and if your body can’t your lab work will.

Four months into my “illness,” no closer to any answers, I settled on “deconditioning, NOS.” If I took the right precautions — sleeping nine hours a night and dragging a chair around on rounds — I could last through the workday.

But around that time, clinics started to reopen and I finally met my primary care physician for the first time ever. As I walked with the medical assistant and felt short of breath again, I peeked at the oximeter: My heart rate had risen to 149, almost twice what it should have been, and my blood oxygen level gradually dropped to 79%, when it should have been close to 100%. “Is this why I’ve been feeling so tired?” my body asked.

My vital signs earned me a diagnostic work-up. It was the first time a health care provider had listened to my heart and lungs and ordered the basic bloodwork and imaging that have become standard of care for confirmed coronavirus patients. But the results of these preliminary tests, completed five months after my first symptoms, were nonspecific. I was given no clear diagnosis or treatment plan. The consensus reached by the specialists was that the oximeter readings, which repeatedly showed my oxygen levels dropping as I walked, were faulty. Case closed.

“See?” my mind retorted. “It’s always just been in your head.” Though I would advise my own patients in similar situations to seek medical evaluation, I instantly regretted visiting my primary care physician. If she had never taken my vital signs, then I would not have allowed my body to slip back into the belief that it had been sick in any way. I never wanted to be over-medicalized.

In May and June, the media began to cover a group of people calling themselves long-haulers. These people suffered coronavirus-like syndromes in March and, for months afterward, experienced prolonged symptoms of shortness of breath, fast heart rates, and fatigue. They started support groups in which they could discuss their lingering symptoms. Membership in these groups quickly expanded globally.

I held off on joining these groups, unwilling without a positive test to label myself a coronavirus patient. But curiosity eventually led me to join a long-haulers Facebook group. What I saw there was both illuminating and perplexing. I scrolled through post after post of individuals who had also gotten sick in March. Some initially had positive tests for SARS CoV-2, others did not, and many more had no access to testing at the time.

Regardless, their symptoms mirrored my own. While many complained of ongoing shortness of breath when exerting themselves (some with corresponding drops in their blood oxygen levels), they reported that their lab work and imaging, completed months after their symptoms began, were inconclusive. Most distressing, many turned to the coronavirus antibody test, which health care providers were hailing as highly sensitive, for answers, but to their surprise they tested negative. It was only at the end of July that researchers began to question whether antibodies remain detectable a few months after infection, a window many long-haulers missed.

The long-haulers circulated medical resources, but also stories of psychological anguish. Despite their symptoms seeming “typical” for Covid-19, some described feeling ashamed as their peers or health care providers dismissed their symptoms as stress-related or new asthma in the absence of positive tests. How was it possible that all of these people had strikingly similar experiences? Is our understanding of the virus’ biology lacking? Or is there another unrelated NOS condition spreading around the world?

The details of the long-haulers have been shared for months in social and popular media, but only recently entered academic medicine. We, as health care workers, have long been discussing the implications of post-Covid-19 care for critically ill patients, but we have barely addressed the needs of those who stayed home. We have not discussed how we will approach their prolonged debilitation; the financial and equity implications of their inability to work; and the psychological sequelae of feeling sick and cast aside. If we continue to reject that their symptoms warrant investigation and treatment simply because they are not understood, these people will inevitably be alienated from the medical establishment and forced, like other “NOS” patients, to seek compassion and care only from each other.

As readily admitted by many in the health care community, from clinicians on the front lines to journal editors, long-haulers evoke the same reactions that we have to patients with other medically inexplicable conditions like chronic fatigue syndrome or fibromyalgia. Namely, we assume that their symptoms are psychologically driven, perhaps implicitly by stress and explicitly by secondary gain, the advantages and attention one receives from others when physically ill. It is difficult to accept long-haulers as a group that warrants our attention.

I am still hesitant to identify myself with the long-haulers, unable to divorce my mind’s adherence to objective evidence from my body’s symptoms. But I share their struggles. Physicians are taught to weigh objective evidence over subjective experience. The patient’s history — her or his description of what is going on — is important, but the data (lab work and imaging) and the physical exam are more important. After all, patients are not always reliable historians.

But this mindset allows clinicians to write off the symptoms of those in the NOS category and, in doing so, heighten their suffering. Instead, perhaps we ought to humbly admit uncertainty and maintain the openness and curiosity required to ask the right questions. Whether the biology of Covid-19 infection turns out to be as serious as irreversible cardiac damage or as simple as profound deconditioning or stress reactions, these are all conditions that can and should be treated.

While the diagnostics we currently have for NOS conditions are imperfect, we must still care for the humans before us.

Pooja Yerramilli is a resident physician in the global medicine/internal medicine program at Massachusetts General Hospital in Boston.

  • Your opinion has factual errors. Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a neurological disease. ME was designated as neurological by the World Health Organization in 1969. Chronic Fatigue Syndrome followed in 1992. Their coding is G93.3 ICD10 and 8E49 ICD11.

    Dr. Anthony Komaroff, MD, of Harvard University said that there are 9,000 papers detailing the biological differences between ME/CFS patients and healthy controls.

    ME/CFS is a disease with double the disease burden of HIV- with no treatment.

    We live in the time of “emerging biomarkers” of ME/CFS including one from Dr. Ron W Davis’s team at Stanford called the Nanoneedle which shows a signal coming from ME/CFS patients, but not healthy controls (Esfandyarpour et al, 2019). The Nanoneedle involves stressing white blood cells with salt. Cells don’t like the salt, so they use up a lot of energy to pump it out. Healthy Controls white blood cells have no problems doing this, however, ME/CFS blood cells show an electrical signal. In a plasma swap experiment, the experimenter took white blood cells from ME/CFS patients and put it in healthy plasma and the signal went away, and when Healthy control white blood cells were put in ME/CFS plasma, the healthy white blood cells showed the signal.

    The CDC, the NIH, and the WHO have said that ME/CFS is a biological disease, not a psychological one. A cursory factual check would have revealed this.

    To date there have been four symposiums on the molecular basis of ME/CFS. The fourth was just a few weeks ago where more than 100 researchers attended a four day zoom meeting. Dr. Ron W Davis, the Director of the Stanford Genome Centre, and the Director of the Scientific Advisory Board of Open Medicine Foundation is leading the charge so I will leave you with his words from 2017.

    “We do know that ME/CFS is a molecular disease. People who now say that it is not are a fool. They are ignoring reality. And you can call them a fool with my permission.”

    There is no secondary gain to having ME/CFS. ME/CFS means losing your career, your family, your dreams. It means giving up your hobbies and the things you love to do. It means being stigmatized, ridiculed, and mocked by the people who are supposed to help you. It means receiving inadequate and prejudiced healthcare when trying to access regular health care for health problems that do have diagnostic tests and treatments. You have now experienced only a fraction of what that has been like for ME/CFS patients for decades.

    All of the prejudices, misconceptions, and lack of knowledge you have about ME/CFS are now being turned upon yourself in the worst possible way now that you are engaging with the reality of this horrible disease. The reality of ME/CFS thrust upon you because of COVID19 is creating cognitive dissonance within you because of the ignorant misconceptions you have of the disease.

    You are sick. ME/CFS is a real disease. You deserve to be taken seriously as a patient, as did all your ME/CFS patients prior to this pandemic.

    Harvard is the home of one of the Open Medicine Foundation Collaborative Centers. It is co-led by Ronald G. Tompkins, MD, ScD and Wenzhong Xiao, PhD. I suggest contacting the people there, and find a positive way through the wisdom of admitting you know nothing about ME/CFS, but that the tools to find out are literally on your doorstep.

    • I’m wondering if you misread the paragraph where the author refers to ME/CFS. She seems to be saying that COVID long-haulers are being dismissed by physicians in the same way that patients with other difficult to explain clusters of symptoms have been. The “we” here seems to refer to her profession. There are still few doctors who are prepared to diagnose and treat patients with CFS, Fibromyalgia, and Chronic Lyme Disease, among others. That’s a problem. Like so many of these patients, she has discovered how crazy-making it is to find that in the absence of biological markers, her first-hand knowledge of her own body is discredited. You seem to be setting up a straw man here.

    • Dear Ms. McEwan, No, I didn’t misread anything. This is what the author wrote. I was correcting the factual errors from this paragraph.

      “As readily admitted by many in the health care community, from clinicians on the front lines to journal editors, long-haulers evoke the same reactions that we have to patients with other medically inexplicable conditions like chronic fatigue syndrome or fibromyalgia. Namely, we assume that their symptoms are psychologically driven, perhaps implicitly by stress and explicitly by secondary gain, the advantages and attention one receives from others when physically ill. It is difficult to accept long-haulers as a group that warrants our attention.”

      Her implied “we” does not negate the factual errors in her own assumptions which she did not bother to correct after repeating them. At no point did she explicitly state that her assumption was wrong, and that her assumption is not based on the evidence.

      Facts are stubborn things. Drs, clinicians, journal editors “assuming” that ME/CFS psychological is very unscientific of them all. Repeating something false does not make it correct.

      Their assumption flies in the face of the objective biological evidence that ME/CFS has a molecular and biological basis and that needed to be pointed out. (Since clearly the Editor didn’t catch it)

      Had this been a news piece, instead of an opinion piece, a good editor would not have let the writer mislead the readers on the facts. Although, a good editor who knows these facts (which are publicly available) is just as hard to find.

      Sincerely,

      Andrea Martell

  • I’ll referred to surprise at what you did in the past. I’ll add that now, if you are truly concerned about the issue of “long haulers”, it seems like you would consider finding some way to get tested for T-Cell reactivity and whatever the most sensitive methods are for determining antibody presence beyond the standard bulk commercial tests to determine if you truly were infected and then research further to determine what other relevant factors might make your case “long haul”.

    Presumably someone claiming “My mind, trained by the best physicians and algorithms, was primed to prosecute” is indicating they have connections through those who trained you that most “long haulers” would go to the ends of the earth to get, in order to have access to more labs and testing. It would seem appropriate to focus on every available method to collect data about a condition rather than trying to “prosecute” a case without complete evidence.

  • With all due respect to the unfair dilemmas incurred by long-haulers : this story opens a can of worms. Why did this doctor not get a colleague to run some diagnostics at onset (oxymeter, heart rate etc)? And why were there no repeat Covid tests (certainly with unacceptably low 70% sensitivity)? Why did an ICU hospital physician have to wait for a clinic to finally open – to see a primary care physician? Why was there no (mention of) a Covid antibody test? So …. was this doctor actually a super-spreader in March, while at work in a hospital intensive care unit? Clearly the symptoms deserve more respect than was given by the writer’s physicians – and that applies to many, many more long haulers – of any disease.

  • re: ““we assume that their symptoms are psychologically driven,”

    The CDC has released data noting the rise in mental health concerns during the pandemic. It seems unwarranted to dismiss those too easily as a possible explanation for your case, or for the cases of many claimed “long haulers”, especially those without evidence of sars-cov-2 infection.

    Presumably as a physician you have the resources to have gotten multiple PCR tests for covid and antibody tests, and even tests that aren’t generally used like T-Cell testing. Yet you give no indication you did so beyond that first negative test. I suspect that you are hoping that just because you are a physician, and pretend reluctance (“though doth protest too much”…) to declare yourself a “long hauler”, that people will fall into the trap of assuming you are even without evidence.

    You provide no evidence that yours aren’t psychological (perhaps a need for sympathy, which goes along with writing an article about this despite not bothering to get concrete evidence you should be capable of getting), or that they aren’t caused by some completely unrelated condition. You claim you are “still hesitant to identify myself with the long haulers” and yet that seems to be the point of writing the column even if you pretend you aren’t claiming that. Just because there is a pandemic going on doesn’t mean that difficult to diagnose conditions are guaranteed to be covid-19.

  • Having had CFS from before it was labelled (and still not liking the label) and having had fibromyalgia from before men were allowed to have it, this story of dismay, and the comments, resonate for me.

    I am now 77 so new developments are a bit late for me: sequelae of decrepitude gobble. But I was heartened to follow a scientific conference in Australia in March 2019 on the biomedical basis of CFS.

    https://mecfsconference.org.au/

    … And to follow with the host organisation’s monthly newsletters further research. As noted I don’t like the CFS label but welcome work to clarify what medicine has had difficulty understanding. The opening paper of the conference was on mitochondrial dysfunction. My difficulty over two decades in getting medical support in treating cfs or whatever as mitochondrial dysfunction beginning with doctors saying it’s too hard to understand etc. Also fighting the institutionally endorsed notion that the needs were therapy and graduated exercise. That conference also addressed the damage done by graduated exercise.

    I extend sympathy and concern to the author, together with concern that whereas I had thought the affliction of persons of eminence with long Covid might bring fresh perspective and work, it’s perhaps more likely that affliction with long Covid may as with CFS meant vacancy and elimination of a competitor in careers of the ambitious.

  • RE: Objective evidence over subjective experience

    Objectively, there is a significant proportion of patients suffering from (as yet) unexplained debilitation post-Covid. Not to mention millions with ME/CFS; as well as other phenomena such as Gulf War Illness and others. These are objective problems (people are undeniably debilitated) and reasonable clinical and research categories; although it makes things trickier that we have few clues as to causes, that ultimately does not matter to these points.

    Speaking of subjectivity, we see a fine example here:
    “Namely, we assume that their symptoms are psychologically driven, perhaps implicitly by stress and explicitly by secondary gain, the advantages and attention one receives from others when physically ill.”
    This sort of outlook is based purely in feeling, not science. There is no reliable evidence that this is a remotely reasonable outlook.

    • When all the diagnostic reports say “Unremarkable Findings”, that doesn’t mean the patient is well. It just means the proper test was not ordered and/or *does not yet exist*. How is it that mere patients understand this, but physicians do not?

  • “we assume that their symptoms are psychologically driven, perhaps implicitly by stress and explicitly by secondary gain, the advantages and attention one receives from others when physically ill.”

    After 17 years of myalgic encephalomyelitis here are my precious “secondary gains from illness”:

    1. Income went from $50,000 to $12,000 per year
    2. Abandoned by domestic partner
    3. Bankruptcy
    4. Civil complaint to seize my home
    5. Abandoned by friends
    6. Complete social isolation
    7. Confined to couch 20 hours per day
    8. Complete dismissal by medical machine
    9. When I told the doc I had near-syncope and transient air hunger on standing, he said I should buy a cane

    Does this sound like Easy Street and a club everyone wants to join? Psychiatrists and psychologists who have promoted these evidence-free “secondary gains” lies have caused immense harm over many decades.

    If the corona virus finally causes physicians to wake up and stop blaming patients for being sick with poorly-understood disease, that will be a huge silver lining for millions of patients.

  • I also have many of the symptoms of long haul covid, but without any chance of a false negative as my onset was thirty years ago.
    The entire illness trajectory of the relapsing remitting fatigue and other symptoms match quite well.
    In the UK, some 20K people become ill with #mecfs per year. Perhaps one to five thousand during the covid peak, perhaps half of them with an onset which can be confused with covid.
    https://www.jstage.jst.go.jp/article/internalmedicine/48/21/48_21_1849/_article for example shows severe cardiac abnormalities in many patients sampled. There has been little research into this condition until recently.

    It would be interesting to follow a cohort of longhaulers who developed their illness atpeak of covid and compare them to seronegative longhaulers.

  • I was very sick at the end of February. I tested positive for the anti-bodies in April. We are in the last week of October and I still have no sense of smell, or should I say, when I do smell things, they all smell disgusting and sort of all the same. Just last night I was drinking Pepsi and it tasted like perfume. I consider myself to be a Covid-long hauler.

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