Thank you, pegleg, . . . indeed Parkinson's and Amyotrophic Lateral Sclerosis have many similar symptoms; both affect the motor nervous 'system' . . . but the 'dopamine' rather than 'glutamate' neurons are affected in Parkinson's. Advances in medical or biological science may help heal both disorders.

Thelma is one of my favorites, I only wish they would post more!

One of neurology's biggest problem is insufficient precision, . . . is the data sufficiently precise the conclusion validly follows therefrom? Such is the problem I think in the case of the question of whether females are at greater risk if they develop the disorder, even though they are believed to have a significantly lower risk incurring Amyotrophic Lateral Sclerosis.

There appear to be at least fourteen cases who have used the pacer and exceeded 'ten years alive' post-symptom onset . . . so far, . . . many remain candidates thereto . . . the expected number is seventeen (10% of patients are expected to reach ten years).

One of the standards for including a case in statistical calculations is completeness of the needed case. I counted forty-seven cases (from data patients provided on the web) this weekend who are either on a trach or passed away and left complete data for the basics . . . twelve bulbars and thirty-five limb onset . . . thirty-five is approximately two pilot samples (. . . 2x16 patients or 32 patients . . .). Of these thirty-five, two _probably_ are limb onset and another may not have correctly specified their onset date. Whether thirty-five or thirty-three, the median survival is seventy or seventy-four months, respectively. Regarding the possibly inadequately specified onset date, the patient is in the weaker half of the sample and correction, if appropriate, would move them well into the stronger half of the sample and therefore would only strengthen the median for the set. The bulbar median is under review will be further discussed in this thread (there are at least 56 but only twelve pacing and without missing completion data - hence we do not yet have a pilot sample):

http://neurotalk.psychcentral.com/thread224801.html

In principle, pacing patients should be more valuable in clinical studies because the researchers could collect dEMG data from them:

Identification of unexpected respiratory abnormalities in patients with amyotrophic lateral sclerosis through electromyographic analysis using intramuscular electrodes implanted for therapeutic diaphragmatic pacing

http://www.americanjournalofsurgery....598-4/fulltext

In the aforereferenced paper Dr. Onders provides more insight into patients of the original study.

Evaluations including all cases will likely show lower results because they always include all the least successful cases and remain in wait for completion data from those who continue advancing. Early studies are more likely to include patients who are later in the disease process because the treatment was not available to them before they were eligible. As time goes on, patients in the vicinity of a new implant site will be increasingly likely to receive timely implant.

Dehydration:

https://en.wikipedia.org/wiki/Dehydration

How might the highlights be made in the case for ALS patients?

Electrical device allows paralyzed man to breathe
http://web.archive.org/web/200503061...ML/000662.html

Acetylcholine neurons - the ones that contact the mucle
http://web.archive.org/web/200311031...ML/002172.html

Its hard to believe I am approaching my sixteenth 'anniversary' since formally engaging the ALS 'battle.' I was indirectly involved years before because the research area where I work can help many individuals, including those with ALS. According to the rules, six to seven years are required to validate a new molecule for treatment in a particular disease but numerous "Big Pharma" types have publically advised aspiring scientists they will need at least ten to fifteen years: if they are lucky. At present, as the DiPALS study evidences, the pacer is not yet ready for a Phase III study but how far away are we? Thankfully patients may obtain the pacer via the HUD/HDE but what about the guidance physicians and patients need on perfecting the timing or elucidating the therapeutic value seen in the report of Dr. Onders in last year's American Journal of Surgery? Bad medicine can save time but good medicine can save lives! The question whether there is a case against the pacer is of course an important one; I often review the cases I have discovered to appraise whether the weakest cases can be selected, and construed as a pilot study - are there inferences validly drawn therefrom working against the treatment? The ordinary media can make the task more difficult by failing to be careful in its choice of words. We still need to work on the question of 'it seems to work in many cases but why?'

Indeed, why do people get ALS to begin with?

At present, I am not sure whether those who would pursue a case against the pacer deserve 'a turn at bat' and I will develop this thought later but I wanted to point out the significance of Dr. Onder's paper as a showing of a de-facto biomarker, or even better than a biomarker. The ability to read the diaphragm's EMG signals live and continuously for long periods of time ought to make efficacy studies less expensive and faster to achieve preliminary insight as to prospective molecule's value. Patients may find they could enter studies based on the extent of the involvement of their diaphragm muscles and whether they are using the pacer as satisfying entry criteria . . . such can be a little better than the 'recently 'diagnosed'' standard; I shall also try to explain why such ought to be so.

I wish to restate an important point, . . . pacing ALS patients ought to be valuable in medical research studies even if they are not freshly diagnosed. Where their diaphragm remains unaffected or the impact has begun but the impact is not extensive, researchers ought to find ALS patient candidacy for studies valuable even if the study is not directed at the ALS patient because the data obtainable from dEMG may show evidence valuable in their immediate research interest or valuable to ALS researchers if the dEMG data shows some affect on the ALS disease processes.

Experts Hack for Lyme Disease Solutions in Boston and Berkeley

https://www.morningstar.com/news/pr-...-berkeley.html


Lyme disease is often portrayed as 'falsing' the symptoms of ALS and those who try to determine whether they have Lyme disease are often frustrated the tests for Lyme are not very reliable.

see also:

Hacking Lyme Disease
https://www.massbio.org/news/blog/ha...disease-122003

I thought this event already happened . . . :

Lyme Innovation: Three Day Hackathon Jun 17-19, 2016
http://lymeinnovation.org/upcoming-events/

Although it probably will not stay there, for the first time the set of patients I am following achieved sufficient days to exceed the 'maximum' life expectancy . . . the data set has deficiencies such as inadequent date specifications and patients who have not been heard from in a long time. I detected several of these long lost cases recently; although most did not change the data much, some did. I am currently reviewing the data set from the point of view of 'false positive' . . . the chance these results are 'false positive' is? . . . I expect it to be small, I am hoping it will be smaller than one would likely guess.

Discovered Charley remains with us:

http://iydlify.blogspot.com/

due to post dated April 23. Was implanted in 2009.