PEM – or post-exertional malaise – means different things to different people, but it’s often treated as if it were a single phenomenon, and that undermines diagnoses, treatment, and research. A better, minimally systematic approach would:
- distinguish different types of PEM by timing
- clarify the number and kind of symptoms required for PEM
- investigate triggers beyond muscular exertion.
Differences in timing
One difference in PEM is timing: For a sizeable minority of pwme, PEM always occurs directly after overexertion. But, for most pwme, it generally occurs a day or more after overexertion. (The exception is that, if a person with delayed PEM is already in PEM, the worsening might be immediate.)
So – if PEM is a single thing, how can such a wide difference in timing occur? It seems much, much more likely that these are two separate processes that require different handling in diagnosis, treatment, and research.
Any worsening will do?
A second problem is PEM’s vague definitions, which in some cases admit any worsening of symptoms after overexertion. We have many symptoms! If my muscles ache after a walk but everything else remains the same, is that PEM? I would say that this isn’t PEM because PEM involves a general worsening that:
- includes multiple symptoms
- comes on after a delay
- always includes exhaustion.
In contrast, a pwme who was advising prominent researchers argued that I was wrong, citing her favored definition’s vague reference to any worsening.
How can we move forward without a more specific threshold for what constitutes PEM? Or maybe we need to consider different subtypes of PEM. In any case, the definition should be specific enough that it captures a process of worsening common to all pwme – or at least the process that’s shared among sufferers of a particular subtype of ME.
In truth, an increasing number of sources address these critiques. Just today, I saw a fine one that reads, “PEM involves delayed, multisystem symptom worsening and prolonged recovery following exertion.” The same source notes, however, that not all studies apply this definition, leading to the unwitting inclusion of different types of patient and thus muddying the results.
Unfortunately, there’s more.
Disparate triggers?
Descriptions of PEM often list cognitive, emotional, and physical overexertion as triggers. This presents two problems. First, no research that I know of has tested whether cognitive or emotional exertion leads to PEM at all. It seems like a cognitive challenge would be easy to design; an emotional stressor might raise ethical issues, but I think it could be done around something that would happen anyway, such as blood draws for lab tests. In any case, I personally doubt that cognitive exertion leads to delayed PEM, and I posit that, instead, for some it triggers immediate worsening due to problems with the autonomic nervous system. Hey, researchers – let’s find out!
Furthermore, by what shared mechanism might such disparate triggers lead to the same problem? If they actually do cause the same problem, probing these two unstudied triggers (emotional and cognitive) in the same way that exercise-induced PEM has been tested should greatly narrow down the possible causes of PEM and possibly of the disease itself.
In short, all researchers need to adhere to a more systematic approach to defining and understanding PEM – or PEMs. Better diagnoses and treatments will follow.
Tracy Duvall 