SPECIAL NOTE: The American Journal of Physical Medicine and Rehabilitation stopped accepting and publishing letters to the editor not long after this was submitted to them. Bradly Johns, of the Journal, encouraged me to submit this in the form of an original scientific research paper. but he also said "Time from receipt of submission to publication is currently one year."
Dear Mr. Johns:
In the July-August issue of the American Journal of Physical Medicine and Rehabilitation you published, "Word Finding Difficulty as a Post-Polio Sequelae" by Dr.s Bruno and Zimmerman. In that I co-manage the largest Post-Polio related email list on the Internet (Post-Polio-Med, www.skally.net/ppmed/) and maintain a huge post-polio data base on the World Wide Web, (Post-Polio Syndrome Central , www.skally.net/ppsc/), I search daily for newly published research which might be of use to polio survivors and health professionals dealing with post-polio patients. Frequently, an item will strike me as worth further investigation due to its topic or resources.
During this past week I've emailed and/or phoned a number of the most respected post-polio experts and polio survivors regarding this paper. I respectfully submit, in the included Letter to the Editor, only the most important of the many questions and concerns expressed regarding the above-mentioned paper.
Considering the seriousness of these concerns, it is my hope that the Journal will publish this Letter to the Editor with or without response from Dr.s Bruno and/or Zimmerman.
Thanking you in advance,
Cleo Kiernan, Co-Owner Post-Polio-Med (PPMed) and Post-Polio Syndrome Central (PPS-C)
Dear Mr. Johns:
I respectfully submit the following questions and concerns regarding Word finding difficulty as a post-polio sequelae. Bruno RL, Zimmerman JR, Am J Phys Med Rehabil 2000 Jul-Aug; 79(4):343-8
Word finding difficulty as a post-polio sequelae. Bruno RL, Zimmerman JR, Am J Phys Med Rehabil 2000 Jul-Aug;79(4):343-8 references four citations for the statistics used in the first paragraph of the paper: "..76% of the 1.8 million North American polio survivors report post-polio sequelae ..". None of these citations support the statement made and none respond to a continental survey. Where did these statistics come from?
"The1990 National Polio Survey" is referenced, again with statistics. The citation given does not lead to any solid information on this survey nor could this survey be found via a search of the literature. Although a small, two-page, non-population based survey, was sent out by one of the investigators in 1990, with apparently 373 polio survivors responding, it has never been published. It would be helpful to know how the "The 1990 National Polio Survey" was administered and where the information on the full survey, methods, statistics and conclusions can be found and evaluated.
"Post-polio 'brain fatigue' is referenced with citations back to two papers, neither of which sufficiently document that this condition exists beyond hypothesis. Are there citations to document the existence of "Post-polio Brain Fatigue" as fact, as stated in this paper, from others besides either of the authors?
Were any of the subjects actually given physical or psychological exams to verify that they did not have one or more of the many conditions or diseases that could affect the results? If not, were there reasons not to check beyond self-reporting for conditions such as hypothyroidism, anemia, depression, or poor physical conditioning which is expected in the polio population and could be corrected for with control subjects?
"The Post-Polio Fatigue Questionnaire" was given to the subjects to self-evaluate fatigue. The citation given does not describe the test, nor could this instrument be found beyond mention, in the literature. Why wasn't the standard Fatigue Severity Scale [FSS] used instead, as it has been in accepted use for some time, and allows for comparisons among several other populations? Where can complete information on the "The Post-Polio Fatigue Questionnaire be found for evaluation?
There are other possible explanations for the test results investigated. For example, it would have been illuminating to see people who have lived with spinal cord injury for more than 30 years, who now experience profound fatigue, evaluated along with these polio patients. Spinal cord injured patients would not be expected to have viral injury to the brain areas mentioned and could buttress or weaken the writers' conclusions. Nevertheless, the authors apparently chose not to use controls during this experiment.
Extreme fatigue is expected to effect word finding, animal naming, and other variables studied in this paper. This fact and the lack of controls mentioned above cast doubt on the validity of the authors' conclusion that in polio fatigued patients the cause of dysfunction is decreased dopamine secretion possibly secondary to poliovirus brain damage.
Prolactin levels fluctuate throughout the day. There were no baseline plasma prolactin levels taken and the prolactin results for all of the subjects are reported to be well within normal limits - none were reported to be even high normal. It seems flimsy to use normal range prolactin levels for 33 people, and come to conclusions about abnormal endogenous dopamine. Prolactin increases occur when there is low dopamine fixed by the D 2 receptor and not necessarily for other brain dopamine receptors. Frankly, not enough is known about the effects of low endogenous dopamine for other receptor types. Using this prolactin level to infer pathologically low endogenous dopamine is unfounded. Further, to espouse a cause to this pathology: poliovirus damage to endogenous dopaminergic cells, is less than a hypothetical.
Although autopsies of the late '40s and early '50s showed some scattered damage to the brain resulting from polio, given the known regenerative ability of the brain, what direct, conclusive evidence do the authors have that there is in fact, rather than hypothesis, clinical consequence to "poliovirus damage to the basal ganglia" in those who survived 10-30 years post-acute polio as stated in the paper?
It is difficult to understand how the authors conclude polio brain damage underlies difficulties in word finding 10-30 years post-acute polio and not in the intervening period since acute polio. What is the mechanism for activating this damage since this Brain Fatigue, in this and the authors' previous papers, is a new symptom?
When dopamine is chronically low, new receptors for them are produced. How much damage has to occur to the dopaminergic areas to produce changes in prolactin?
What kinds of feedback operate between denervated voluntary muscles in post-polio syndrome, overworked giant motor units, physical exhaustion, and the dopamine secretion/prolactin system? Physiological affects derived from the known aspects of post-polio motor neuron damage were not mentioned in this work.
Finally, the authors mention the use of bromocryptine to alleviate symptoms of brain fatigue yet clinical trials for post-polio fatigue have been done for only 2 drugs, amantadine and pyridostigmine, and both were found to lack benefit. Bromocryptine was never studied in clinical trials for post-polio syndrome. There was only one small (5-subject) non double-blind pilot study done, and yet it is recommended at the end of the article by the authors as an efficacious drug. Bromocryptine is known as an agonist that works at the D2 dopamine receptors and has therapeutic potential for hyperprolactinaemia. None of the test subjects in this study, as reported, suffer from hyperprolactinaemia.
Co-Owner, Post-Polio-Med (PPMed) and Post-Polio Syndrome Central (PPS-C)
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