
Say 'Ahhh': A Simpler Way To Detect Parkinson's - gruseom
http://www.npr.org/2012/07/21/157102978/say-ahhh-a-simpler-way-to-detect-parkinsons
======
martingoodson
The paper from the same group last year on the topic is here:
[http://rsif.royalsocietypublishing.org/content/8/59/842.full...](http://rsif.royalsocietypublishing.org/content/8/59/842.full#sec-9)

They are using random forest out-of-sample error as a metric but doing feature
selection before this step (see table 6).

As far as I can make out from a quick reading they are essentially making the
error described here: <http://www-
stat.stanford.edu/%7Etibs/sta306b/cvwrong.pdf>

and elegantly described in this recent blog post:
[http://blog.kaggle.com/2012/07/06/the-dangers-of-
overfitting...](http://blog.kaggle.com/2012/07/06/the-dangers-of-overfitting-
psychopathy-post-mortem/)

On a sample size of only 42 people, overfitting seems very likely.

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blahedo
One big issue with gathering this kind of data over the phone is the frequency
cutoff on voice-only lines—above a certain frequency (I want to say 4kHz?
maybe I'm misremembering), the information is lost. It's basically as if you
took a Fourier transform, zeroed out everything above the threshold, and then
transformed back.[0] For humans (and even computers) trying to interpret the
sound as language, that's not a huge problem, although you might lose some of
the higher formants. But for an acoustic analysis that's trying to do
voiceprinting—in this case to detect Parkinson's—this could be a big problem.

(I'm also irritated by the glib "99 percent success rate" but I just ranted
about that on a different HN post so I won't go into it here.)

[0] Why do this? So the phone company can compress and send a lot more data
over the same amount of internal bandwidth. Come to think of it, it's kind of
related to how wavelet-based compression works.

~~~
NinetyNine
The sampling frequency doesn't directly effect the audio frequencies it can
encode. Telephones do PCM encoding (meaning it has data representing the graph
of the sound wave) at 8 kh/z. Following the nyquist sampling theorem (cut your
rate by 2), this can allow frequencies up to 4 kh/z (as you said). It's not a
hard cutoff though, you can still get most of the sounds above that pitch,
they'll just sound pretty weird (as if you were talking on the telephone!)

~~~
lgeek
No, components above the Nyquist frequency are filtered out before the ADC
because you'd otherwise get aliasing.

<https://en.wikipedia.org/wiki/Aliasing>

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rouli
It's a very interesting field. Can insurance companies detect the early stages
of Parkinson's when you call their call-centers and change your rates
accordingly? Here's a related dissertation on detecting mental health
condition by using voice recordings
[http://www.eecs.berkeley.edu/Pubs/TechRpts/2012/EECS-2012-55...](http://www.eecs.berkeley.edu/Pubs/TechRpts/2012/EECS-2012-55.pdf)
(haven't read it yet, but was meaning to for quite a while)

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justinph
The NPR story has a non-obvious link to the site. Here it is:
<http://www.parkinsonsvoice.org/>

That's pretty amazing if they can detect it within the poor 8khz of a phone. I
wonder how awful cell phone reception changes the accuracy.

~~~
tspiteri
While 8 kHz is low if you look at the carrier of the speech signal, which is
something like the pitch of the speech, it is pretty high compared to the
envelope frequency of the speech signal. You do not move your jaw, tounge and
lips at anywhere near 8000 times per second. The algorithm looks at things
like how the jaw, tounge and lips move during speech, and I guess 8 kHz is
quite enough for those.

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Jim_Neath
If this works successfully then it would be great but as a 28 year old with
Parkinson's, I'm skeptical.

It took approximately 12 months, numerous blood tests, MRIs and doctor visits
to diagnose me as having YOPD, so I'm finding it hard to believe that this
could be replaced with a telephone call.

~~~
DigitalJack
If you don't mind answering, what was your path to the Parkinson's diagnosis?
I mean, what were some of the first signs that something was wrong?

~~~
Jim_Neath
I developed a slight tremor in my right hand and had trouble moving my arm as
fluidly as my other.

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azza-bazoo
I wonder what the false-negative rate of this algorithm is. 99% (which I
assume is the true-positive rate) is certainly impressive for such a simple
test, though.

It would be all kinds of awesome if this turns into something that can be done
reliably and routinely!

Edit: seems like 99% is only for later stages of Parkinson's, and the accuracy
number is just off a 50-person sample. Less impressive, but still cool.
[http://www.forbes.com/sites/singularity/2012/07/03/new-
softw...](http://www.forbes.com/sites/singularity/2012/07/03/new-software-can-
diagnose-parkinsons-disease-simply-by-listening-to-your-voice/)

~~~
pbhjpbhj
How do you get 99% accuracy for a 50 person sample? Has to be 100% or 98%
surely?

------
SoftwareMaven
Interesting that I got cut off during the "Ahh" test and asked to redo it. I'm
sure I don't have exceptional lung capacity.

~~~
Urgo
I did too the first time. Maybe that was on purpose.

------
nathan87
shameless plug of some ideas i've had about parkinson's disease; i'd be
interested to hear what others think about my reasoning:

Michael J Fox's Parkinson's Disease may have been caused by amphetamine use
and/or sleep deprivation
[http://www.nathanwailes.com/forum/viewtopic.php?f=3&t=22...](http://www.nathanwailes.com/forum/viewtopic.php?f=3&t=228)

Sleep Deprivation May Be a Common Cause of Parkinson's Dis.
[http://www.nathanwailes.com/forum/viewtopic.php?f=3&t=24...](http://www.nathanwailes.com/forum/viewtopic.php?f=3&t=248)

~~~
apl
Yeah, no offense, but all you've written is either widely known (Amphetamine-
induced DA depletion inducing Parkinson's-like motor symptoms and so on),
based on misunderstandings (some of your graph readings are horrifically
beside the point), or simply wrong.

Grab a book on neuropharmacology, or even just a neuroscience intro
("Fundamental Neuroscience" by Squire and colleagues is a good one), and
accept that armchair-bullshitting is not how progress is made.

~~~
nathan87
Hey apl, thanks for considering my ideas! I hope you won't mind if i try to
defend them against your objections:

re: "it's widely known that amph. can induce Parkinson's-like motor symptoms"
This may be widely known among neuroscientists, but it's certainly not widely
known among the general public, which is my audience for the essay.

re: "some of your graph readings are horrifically beside the point" There's
really only one graph I read from, so I'm going to assume you're talking about
the "Loss of DA Neurons After Heavy Meth Use". Why, exactly, reading that
graph beside the point? The study I cite immediately prior to that graph (from
a Michael J Fox source, no less) states my point for me: using amphetamines
can lead to fewer dopamine neurons.

re: "some of what you've written is simply wrong" Please be more specific! I
want to know what you found wrong.

re: "grab a book on neuropharmacology" I was actually a psychology major in
college and took several classes on neuroscience and neuropharmacology, so I'm
not totally new to this field.

re: "armchair bullshitting is not how progress is made" This wasn't armchair
bullshitting; I was combining the results of several different published
studies and other concrete information to arrive at a novel hypothesis. I
agree my reasoning isn't enough to remove a great deal of uncertainty about
whether the hypothesis is true, but all I'm trying to do is establish that
it's plausible enough to warrant people's attention. Many scientific advances
are made this way; for example, in physics there are often speculative
theories made that need to be verified through experiment: Einstein's theories
and the idea of a Higgs Boson, the idea of dark matter and dark energy. All of
them started off as unproven possible explanations of observed phenomena, and
all needed to be verified. But that doesn't mean they weren't worth giving
attention before they were verified.

~~~
apl
I'll give you a couple of examples.

    
    
      > is sleep a cause or a result of some other underlying 
      > factor? - Not sure what this objection means, exactly, yet.
    

It's simple, really: Say most PD patients present with sleep
dysfunctionalities. What conclusions can we draw from that? Three, actually.
That PD causes sleep dysfunction, that PD is caused by sleep irregularities,
or that both are caused by some unknown cause X. Based on correlative data,
all three are equally likely. You, however, immediately jump to the sleep
causes PD conclusion -- critically, without mentioning a mechanism for how
that could work.

If you investigated PD a bit further, you'd realize that there's dozens of
confirmed comorbidities (e.g., depression, cognitive issues, hyposmia, etc.).
That doesn't tell us anything about anything.

    
    
      > Amphetamines are drugs associated with pushing your 
      > brain to operate without sleep, and they're also 
      > associated with causing Parkinson's Disease
    

Well, you know what else amphetamines are associated with? Interference with
the dopaminergic system at a massive scale. What's the key neuronal pathology
in PD? Right, SN-focused DA cell degeneration. So it's exceedingly more likely
that DA function plays the role of causal link here than lack of sleep. Again,
common cause.

Regarding genetics and Fox: We _know_ that PD has a genetic component; there's
promising mouse models and solid epidemiological data. Fox is one data point.
His lack of family history doesn't suggest anything at all.

In summary, your whole argument rests on a flawed logical strategy. You're
connecting three semi-confirmed factoids (increased PD risk among amphetamine
users, amphetamines lessen the need for sleep and are taken by traditionally
sleep-deprived groups) by positing a direct causal connection; namely,
amphetamines -> no sleep -> PD. All this while ignoring much more sensible
connections (e.g., via dopaminergic systems).

Sure, one could test this. But that's faint praise -- it's still far away from
what cutting-edge PD research does right now and for good reason. BTW, Higgs
and Einstein developed their ideas from deep knowledge of and appreciation for
state of the art research at their time; both knew their stuff and went from
there. You're displaying very basic knowledge, tendency for random sourcing,
and ignorance of fairly basic scientific principles (experimental logic esp.).

~~~
nathan87
re: "Say most PD patients present with sleep dysfunctionalities."

I understand that idea, but the problem with it is that I'm not just saying
that PD is correlated with coexisting sleep deprivation; I'm saying that
evidence suggests PD is associated with a history of pre-existing sleep
deprivation, where the sleep deprivation is itself correlated with the demands
of a person's job/lifestyle. It seems obvious to me that the most plausible
cause-and-effect relationship there is that the sleep deprivation is causing
the PD, rather than vice versa or some third factor causing both.

re: "If you investigated PD a bit further, you'd realize that there's dozens
of confirmed comorbidities. That doesn't tell us anything about anything."

I've actually read the literature reviews that neuroscientists use to learn
about this stuff. I even include links to those journal articles. Here's the
most recent one I found: "2011.04 - Epidemiology and etiology of Parkinson’s
disease: a review of the evidence." I mention this journal article in the
essay on PD and sleep.

You're right that comorbidities don't necessarily tell us much. But the
evidence I'm talking about seems different, because the factor I'm discussing
(sleep dep / job demands) predates the PD symptoms. You could argue that an
underlying cause of PD was latent in these people earlier in life (their
20s-40s) and causing them to work longer hours and get less sleep, but it just
seems much simpler and more sensible to me to say that people were working
harder, getting less sleep, and paying a price as a result.

"it's exceedingly more likely that DA function plays the role of causal link
here than lack of sleep."

I think you misunderstood the point I was making in that section; I was
writing that for people who did not know much about how the brain works. I
agree it seems clear it's the DA neuron death that's causing the PD symptoms;
my hypothesis is that lack of sleep over a lifetime is causing gradual DA
neuron death.

re: "Fox's lack of family history doesn't suggest anything at all."

I'm not trying to establish that it's lock-tight that there was no genetic
component; I'm trying to explain to the average person out there that Fox's
situation was not a case where everyone in his family had PD and so he got PD
too. For a long time I assumed that's what had happened. Again, it isn't a
lock-tight piece of evidence, but I do think it's relevant and adds weight to
the environment-side of the scale (I'm imagining a scale where genetics is on
one side and environment is on the other). It just seems more likely to have
been caused by his environment if his family doesn't have a history of PD.
That seems totally reasonable to me, and I think it would to most people.

re: "You're connecting three semi-confirmed factoids (increased PD risk among
amphetamine users, amphetamines lessen the need for sleep and are taken by
traditionally sleep-deprived groups) by positing a direct causal connection;
namely, amphetamines -> no sleep -> PD. All this while ignoring much more
sensible connections (e.g., via dopaminergic systems)."

Again, I think you misunderstood what I was trying to get across in my essay:
I was saying that the amphetamines AND / OR sleep were causing damage to the
DA neurons. So it seems plausible to me that amphetamines are causing the DA
damage on their own and sleep dep. has no effect, or that amph. have no effect
and only cause DA damage by causing sleep dep, or that both amph. and sleep
dep. are able to independently cause DA neuron damage.

Thank you again for your feedback! There are some complicated facts here to
process (complicated for those who haven't studied this subject) and so it's
helpful for me to see when I'm not communicating my ideas as clearly as I
would like.

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laktek
Wonder whether it's possible for them to crowdsource this via web instead of
the phone lines, which would make it easier for more people to participate.

~~~
rada
Average onset of Parkinson's happens at 60 years old.

~~~
prbuckley
That is given the poor tools we have to date to diagnose the disease. I think
the really promising thing about this development is the possibility of
earlier warning and being able to test new treatments before the disease
progress's so far that someone is going in to ask the doctor what is wrong.

My father has Parkinson's, it is an awful disease.

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copyrightip
This will come as no surprise to the orthodontists in the UK and US who treat
some cases of Parkinson's as a disorder of the mandible.

<http://www.youtube.com/watch?v=VYKBPd2Kowo>

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cteng04
would be cool to see somebody build a twilio app to link on the article and
collect voice samples right off the page

