Dr John L Whiting explains why he thinks the term DOPE is better than PEM or PENE:
One of the biggest nuisances that ME/CFS sufferers have to contend with is the post exertional fatigue component.
This issue was an aspect of my own questionnaire for CFS in 1992, and that I presented a poster on the this as one of the 4 main CFS fatigue subtypes that I had recognized at the time in Dublin, Ireland to the International Symposium there in 1994. This information was inadvertently missed by attendees at the time.
Post exertional malaise etc now has been recognised as a cardinal problem in more recent years by those who study the disease, but it does not appear to have gained the traction that it deserves as a key issue in this setting by many of those who you would expect to know better.
My own acronym for this strange phenomenon (before the acronym PENE etc came into being at a rather late juncture in the 30 year history of CFS) was and still is the term DOPE.
DOPE stands for:
Delayed Onset Post Exertional fatigue.
DOPE contrasts significantly with other fatigue subtypes in that there is a time gap of 1-3 days (occasionally longer) between the exertion (or even exertion WITHOUT a sense of any intra-activity difficulties, such as having an enjoyable night out and not recognising it as exertion) and the symptoms that follow later.
This unusual GAP IN TIME
… is the diagnostic giveaway in terms of saying ah-ha, this is CFS/ME.
… is not part of normal physiology
What is strange is that the exertion in question may be FULLY tolerated symptomatically AT THE TIME of activity, with no clues or forewarning as to what is to follow later.
Thus, it does not necessarily feel like exertion in real time, but the body interprets the activity as exertion nevertheless. Consequently, caution or care with ones energy envelope are not considered during the activity, especially in patients who are new to the illness.
DOPE is a nuisance because it takes the patient by surprise. In addition, observers before the fact (of observing the consequences) see such patients activities as representing normality and assume or fail to consider any delayed onset penalty effects.
The more troublesome issue is that WHEN DOPE hits, it happens in such an unexpected way that it is difficult for patients to keep to previous promises, which in turn then creates the impression of unreliability in that person – for all the wrong reasons. Appointments have to be cancelled at the last minute, as there were no advanced warning symptoms. This can be and often is socially unacceptable and is a strike against ones own character in many home and work settings.
In my clinical notes, I record DOPE in my patients in this manner:
DOPE 1, DOPE 2-3, and so on, where the numeral represents the day of onset of symptoms and also their duration. I also circle the number when symptoms peak, say Day 3 for example.
I do not believe that there are immune mediators involved in DOPE. I have multiple sentinel markers of inflammation that I use routinely, that can indicate immunological changes, none of which I have observed to ever alter in the course of DOPE, either before, during or after DOPE occurs.
My feeling is that DOPE is either neurotransmitter related, metabolically mediated, or microcirculatory in origin. There are ways to reduce or prevent DOPE, that support my theories on the matter.
Iron status is one of the most critical factors of all, and has been totally neglected in ME/CFS research.
Simply calling the problem post exertional malaise says absolutely nothing to the novice in this field as to what is being implied. For example, when does exertion NOT have after-effects in a normal population? Is it not true that immediately after exertion it is normal to notice the body is tired, exhausted or in a state of recovery (catching ones breath, say). Agreed that malaise is not the same as catching ones breath, but who is to say WHAT this malaise we talk about, is, how it is defined, and what is its underlying mechanisms and/or pathology?
If PENE is to be characterised as pathognomonic of ME/CFS, surely its phenomenology should be described in the utmost detail in the published literature by now? This is a very very serious and very odd omission.
I much prefer the acronym DOPE over PENE as it is more specific and more correct. It more accurately highlights the issue at hand, which PENE does not unambiguously do.
This is very relevant. For example, the idea of walking distance as in the PACE trial, does not take DOPE into consideration. A person could easily exceed his/her safe exertion limits and then experience severe DOPE a number of days later, and fail to have this recorded in the study.
Furthermore, DOPE is highly unlikely to be psychosomatic, as there is neither primary nor secondary gain, as just about no one is sympathetic to the individual who seemingly has performed ‘well’ a few days before, and then says “Sorry, I’m not up to doing what you just asked me to do”. In other words, DOPE has the opposite effect to what psychosomatic theory argues to be true.
How does one characterise a person who can do something ‘normally’ (in the visually overt behavioural characterisation of what the term normal means) but who is sick in bed or housebound several days later?
Is such a person sick or is this person well? It all depends on the day one is evaluated, and whether or not the phenomenon is typical or atypical for such a person. If it is a regular occurrence, DOPE MUST be taken into account. I have seen many many clinical and medicolegal or welfare instances where DOPE is ignored, is dismissed or is considered irrelevant, simply because the evaluator SEES nothing wrong with the patient at the time.
Another noteworthy point is that the test-retest exercise testing protocol of Stevens et al. is on the money but may miss many patients where day 3 is the day of DOPE onset. Also, DOPE is itself unreliable in that sometimes it does not eventuate as expected – thus, testing for it with exercise tests may miss these uncommon absences of DOPE.
Finally, weakness post exertion, exhaustion post exertion, somnolence post exertion, apathy post exertion as well as orthostatic fatigue, cumulative fatigue and cyclical fatigue are all phenomenological subsets of fatigue, each of which has DIFFERENT pathophysiological underpinnings and treatments. What happens instead, is that the research community lumps these all together as one (!!!), diluting the chances of identifying anything meaningful from within the data collected. There is so much in this field of science that needs to be rectified. If we as experts can’t get it right, then how can we expect anyone else to accurately understand what ME/CFS is all about?
Therefore, in any research project or research paper, the type of fatigue (as subsumed into the diagnosis of ME/CFS) MUST be specified if anything is to be gained from such work.
Dr Whiting Summarises Some of the Latest Research into CFS, 30 September 2015