Joe Landson authors this guest post on the chasm between patient experiences and the people who need to understand them.
We suffer through many devastating symptoms, but today I’m only thinking of one. It’s perhaps the most devastating effect of this illness, while not actually being a symptom at all.
It’s the sensation of being surrounded by idiots – the feeling that we have described our symptoms over and over, documented them, even proposed peer-reviewed literature-based explanations for them, only to hear the response: “So… you feel tired?” On orthostatic intolerance: “So, you feel dizzy?” On irritable bowel: “So, you have a tummyache?” It’s such fun I could go on, but I’ll stop there.
This non-symptom that probably all of us experience has led to the distinct impression that only other patients and caregivers get it, that we must cling to each other to keep from losing it completely. Indeed, our cliquishness has prompted many psychiatrists and social scientists to theorize that we suffer from mass hysteria. (Of course that’s impossible; we’re much too socially isolated to have mass anything.)
Of course, clinicians and government health officials must sympathize with our plight, because they have the mirror image of this condition. With a group of us in a room, they apparently experience the unshakable sensation of being surrounded by catastrophizing hypochondriacs. At least they act like they are, based on referral patterns, research funding levels, and non-adherence to the FACA. It’s the best explanation I can think of for how we’re treated – regardless of whatever sympathetic lip service we receive in meetings and conferences.
And so we float past each other, health workers and patients & advocates; trapped in our respective knowledge bubbles.
The problem, of course, is not limited to us. There has long been a chasm between how patients experience an illness on one hand, and how medical professionals define and treat it on the other. It’s a recognized problem that several efforts try to address. One of these efforts is patient-centered outcomes research, pursued by the Food & Drug Administration (FDA), amongst others.
Towards this goal, the FDA revised their guidelines for ME/CFS treatment research. The way I read the FDA’s instructions is this: Don’t have a validated outcome? Make one up. Make up anything, validate it statistically, and show that your proposed intervention moves the outcome score upwards on a graph. Show that the intervention is otherwise safe (to the patient and the graph), and we’ll strongly consider approving it. I hope I’m misreading it, but that’s how I see it, and it does not bode well for serious research. On the other hand, it may get a treatment approved in our lifetimes. Time will tell.
I have other doubts. Is patient-centered research really the best way to fill the chasm between the illness we have, and the one others (don’t) see? Probably some medical professionals equate patient-centered anything to putting the patients in charge of the asylum. (Given some of the doctors we’ve met, wouldn’t this be an improvement anyway?) For me, the phrase patient-centered research recalls Count Rugen (the six-fingered man) testing his suction-based torture device on Westley and asking, “And remember, this is for posterity so be honest. How do you feel?” (What could be more patient-centered than that?)
Speaking of doctors we’ve met, I will never forget the Veterans Affairs rheumatologist calmly explaining to me that while he treated fibromyalgia, which was real because it had a pressure point test, he could not treat chronic fatigue syndrome, which was just a form depression. Interestingly, he made this pronouncement shortly before his colleagues dropped the pressure point diagnostic test for fibromyalgia, and replaced it with a revised definition that sounds an awful lot like a functional disorder. Reality comes and goes, doesn’t it?
In Brain on Fire: My Month of Madness, Susannah Cahalan describes her experience with NMDA Receptor Autoimmune Encephalitis (AE). Its symptoms are utterly indistinguishable from psychosis or schizophrenia; brain scans show nothing. Moreover, doctors’ approach to the illness is a self-fulfilling prophecy. If treated as a psychiatric disorder, AE gets worse and becomes permanent or fatal. If treated as the autoimmune disease it is, AE may ameliorate and even remit to a full recovery, as it did for Cahalan. She acknowledges she was lucky, and that society really has no firm idea how many are unlucky, given a vague psychiatric label, and left to rot or die.
AE may or may not have specific medical answers for us. However the situation is absolutely the same. If health care providers continue to treat us as if we have belief issues, then their own belief will self-fulfill. Our condition will effectively become permanent, and more of us will succumb to paranoia and despair.
Of course, correcting doctors’ beliefs will not suddenly make us well. The best it might do, in the short term, is end the graded exercise and other “treatment” imposed by Count Rugen Peter White and others.
Our beliefs must change, too. Not about our illness per se: Rather, we have start believing that no matter how few or poorly funded, folks genuinely are trying to help us. There is no conspiracy; instead, there is a giant chasm in medical knowledge that has swallowed us up, along with other diseases, too.
And I have to stop being so snarky. Tomorrow.
NIH funding of ME/CFS research has bumped up against a deadline that could have dire consequences for 2015 and beyond. The primary mechanism for grant applications has expired.
PEM Differential
Correct diagnosis is critical for clinical care and research. Overly broad groups of subjects can produce misleading research results, and incorrect diagnoses harm patients. For years, advocates and experts alike have pointed to post-exertional malaise as the symptom that distinguishes our disease from other fatiguing illnesses. PEM was a focus of the Voice of the Patient report from FDA, and is also one of the core symptoms identified by Dr. Leonard Jason’s research as essential for diagnosis. The IOM agreed, and made PEM mandatory for diagnosis with SEID.
The IOM report described PEM as:
The IOM also found PEM to be a characteristic symptom of ME/CFS:
The IOM report cites several papers finding PEM in major depressive disorder and multiple sclerosis, but interpreted them with caution because the prevalence of PEM depends on how it is defined and assessed. If these papers did not define PEM as the exacerbation of multiple symptoms after physical or cognitive exertion, then the findings would not be applicable given how IOM defined PEM.
Unlike the Canadian and International Consensus Criteria, the IOM lists no exclusionary conditions. Many people seem to have interpreted this to automatically mean the criteria are too broad. But the IOM explained that people can have SEID and other diseases, whether it is obesity, hypothyroidism, or cancer. Under Fukuda, any of those diseases would preclude diagnosis with CFS, but comorbidities are a fact of life.
For example, I have obstructive sleep apnea that arose after my diagnosis under Fukuda. Technically, this should disqualify me from diagnosis under those criteria. However, my sleep apnea is perfectly controlled by use of a CPAP machine. The data from the machine show that I do not have sleep apnea when I am using the machine (which I do, every single night). Yet I am still sick. So why should having sleep apnea, especially if it is well-controlled, exclude me from diagnosis? Certainly, the sleep apnea should be taken into account if I participate in a research study, and could possibly disqualify me from some studies. But it should not exclude me from diagnosis with the disease.
The same is true of other comorbidities. Why should someone with hypothyroidism which is being adequately treated be denied diagnosis with SEID if they have PEM, sleep problems and cognitive dysfunction? If someone has PEM, severe fatigue that prevents them from working, unrefreshing sleep and orthostatic intolerance, what difference does it make if they also have depression? Doesn’t that person deserve treatment for depression as well as management of SEID?
In my opinion, comorbidities are not the concern. The legitimate concern is whether SEID would, like Oxford and Fukuda, be applied to patients who have only depression or only anxiety (or only other fatiguing illnesses). Research has shown that Oxford and Fukuda both erroneously include people with “just” depression (and I do not mean to minimize the suffering of depression) and not the distinct disease described by ME or SEID criteria. This would be a fatal flaw of SEID criteria, because we know that studies like PACE have included high numbers of people with fatigue but not our disease, and this could account for the small signal of CBT and GET effectiveness reported in PACE (notwithstanding all the other legitimate criticisms of how PACE was conducted and analyzed).
But unlike Oxford and Fukuda, SEID requires the hallmark characteristic of PEM. If post-exertional malaise is unique to our illness, then correctly applied SEID criteria should not misdiagnosis people with other fatiguing illnesses as having SEID. Why? Because if a patient does not have PEM, they would not be diagnosed with SEID. And if a person has PEM and the other core SEID symptoms, then they have our disease regardless of what other conditions they may have. Therefore, if a person has only clinical depression or only hypothyroidism or only multiple sclerosis, that person does not qualify for SEID because he/she would not have PEM and the other core symptoms.
The IOM committee is staking the position that PEM is so distinct that no differential diagnosis is required, because differential diagnoses are needed only when multiple diseases present with similar symptoms. Once a clinician has established that a patient not only has severe debilitating fatigue, but also has PEM, unrefreshing sleep, and cognitive dysfunction and/or orthostatic intolerance, there is no need to exclude other conditions. This is a distinct symptom presentation, and will not – if correctly applied – result in people who do not have the disease being included in the patient population. Remember that Dr. Jason’s research identified PEM, unrefreshing sleep and cognitive dysfunction as the core symptoms of the disease, especially when frequency and severity cutoffs are applied (as IOM also recommended).
The real issue, in my mind, is whether these criteria will be correctly applied. Chapter 7 of the IOM report and the materials for clinicians both include questions and tests to determine if a person has PEM. However, given the misinformation already extant about our disease, and the outright prejudice among some in the medical profession, we cannot take it as a given that healthcare professionals will suddenly be able to recognize PEM correctly. That is why the educational recommendations of the IOM report are so critical, and why I believe we should be vigilant about whatever materials HHS ends up creating as part of an education campaign. It is unquestionable that many healthcare professionals need remedial education, and CDC’s current education materials are grossly inadequate. But this is a different problem from the fear that the SEID criteria themselves are not sufficiently specific to exclude those who do not have the disease.