[Eeglablist] Critical pitfall of spectral power analysis?

[Makoto Miyakoshi]

Hello Mate and all,

I became curious about the 1/f^n issue, so I spent a whole day today
investigating this problem.
Following Cedric's obsession, I uploaded simulation code and results to
Github, YouTube, and SCCN Wiki page.
https://urldefense.com/v3/__https://github.com/MakotoMiyakoshi/cableTheoryDemo/tree/main__;!!Mih3wA!CORpSZkbn8mntguT3SylRvIRIqrj-8phD2Bm9zBE0rNFZZa8DMJcfa0mXv2pG2xDJfbgRregAtjdLfj53TBo4g-7dEc$ 
https://sccn.ucsd.edu/wiki/Makoto%27s_preprocessing_pipeline#Where_does_power_distribution_come_from.3F_.28For_510.2C000_page_views.2C_Added_on_09.2F17.2F2025.29 
https://urldefense.com/v3/__https://www.youtube.com/watch?v=SitmGp8LYtY__;!!Mih3wA!CORpSZkbn8mntguT3SylRvIRIqrj-8phD2Bm9zBE0rNFZZa8DMJcfa0mXv2pG2xDJfbgRregAtjdLfj53TBosE7VLyc$ 
https://urldefense.com/v3/__https://www.youtube.com/watch?v=iaRQsaU1_2s__;!!Mih3wA!CORpSZkbn8mntguT3SylRvIRIqrj-8phD2Bm9zBE0rNFZZa8DMJcfa0mXv2pG2xDJfbgRregAtjdLfj53TBoDhtKxC8$ 

I think the mechanism you are referring to, Makoto, is what's usually just
described as "dendritic filtering", is it not? I'm aware of this process
plus the low-pass filtering that happens as a consequence of spatial
summation.


Yes, a dendritic filtering. But to be honest I was not aware of the fact
that there were actually two scenarios, one is passive (like EFB) and the
other is active (like Gao et al.)
I once asked Paul whether the subthreshold passive cable theory was
sufficient to explain the generative model of EEG signals. He said the
subthreshold model was 'good enough'. As I read Reimann et al. (2013) this
time, I found that the difference between passive vs. active cable is
present but probably not very critical after all. As we can easily imagine,
the active model with action potentials adds more power at higher
frequencies (in FOOOF terminology, 'flatter aperiodic') If I were an
American, I would say duh--action potentials are spikes. But Reimann and
colleagues also investigated the impact on laminer CSD patterns, which was
good to confirm.

As my simulation confirms, we can make testable hypotheses on modulation of
1/f-ness.
For example, selective engagement of pyramidal neurons whose soma are at L5
should show more low-pass filter effect simply because their dendrites are
longer than those that reside at L3.
Also, any preferential engagement of neural populations that are known to
use non-myelinated axons should produce more low-pass filter effects etc
etc..

I want to see a quantitative comparison between the dendritic length model
within the framework of the passive cable theory and AMPA/GABA_A model
within the framework of Gao's action potential-based model. Is the latter
so prominently larger than the former so that we can safely forget it? It's
an empirical question.

Makoto


On Sun, Aug 31, 2025 at 6:30 PM Gyurkovics, Mate <mategy at illinois.edu>
wrote:

> Thanks again for all the interesting points. I'm certianly learning a lot
> on the physics side - and also about the PSD in different animals, I was
> genuinely unaware of all this, but sounds super interesting.
>
> I think the mechanism you are referring to, Makoto, is what's usually just
> described as "dendritic filtering", is it not? I'm aware of this process
> plus the low-pass filtering that happens as a consequence of spatial
> summation. These are the two main ones I was thinking of, so you are right,
> it was very imprecise on my part to talk about the low-pass filtering
> properties of the tissue.
>
> As demonstrated in a classical study by Lopes da Silva and van
> Leeuwen (1977), alpha oscillation is generated within the cortex which is
> only 4-5 mm thick.
>
> Just out of curiosity, what point was this sentence supporting?
>
> I'm very happy to learn the conceptual distinction between trivial and
> non-trivial contributions to the changes of 1/f power distribution. Thank
> you Mate. Your works are impressive.
>
> Very nice of you to say this, Makoto - I would, however, also like to
> stress that this particular distinction just reflects how I personally
> think about this problem (i.e., the contribution of the ERP to the
> spectrum), I'm sure reasonable people could disagree. (Although this is
> basically the logic we published in the Journal of Neuroscience paper
> linked above.)
>
> @Eugen - you raise many interesting points. (I certainly agree that in
> scalp recordings at leat, oscillatory activity is sparse, and most robustly
> occurs when the brain is not engaged with a task, in the form of alpha
> activity, but that is about as bold as I can be here.)
>
> is sinusoidal (with sharp peaks in the spectrum) activity and broadband
> (not necessarily 1/f) activity generated by different mechanisms?
>
> I think, to put it very simply, this is one of the fundamental questions
> underlying this discussion here. If they are separate AND fairly
> independent, that is when the conclusions of our paper hold. If they are
> separate but interact, our conclusions will sometimes hold, other times
> maybe not. If they reflect the same underlying mechanism, our conclusions
> would likely rarely be a concern. I personally think that they likely
> reflect mechanisms that are separate at least to some extent - plus
> 1/f-like broadban activity likely reflects several, not just one,
> generative mechanisms as highlighted by Makoto and others here too.
>
> Moreover, the function 1/f may simply be the result of the Fourier
> transform of a single excitatory or inhibitory postsynaptic potential.
>
> As far as I recall, this point is covered in Gao et al. (2017), the paper
> that first linked 1/f-like features to excitation/inhibition balance.
>
> Thanks,
> Mate
>
>
>
>
>
>
>
>
> ------------------------------
> *Feladó:* Евгений Машеров <emasherov at yandex.ru>
> *Elküldve:* 2025. augusztus 30., szombat 9:07
> *Címzett:* Gyurkovics, Mate <mategy at illinois.edu>
> *Másolatot kap:* EEGLAB List <eeglablist at sccn.ucsd.edu>; Wirsing, Karlton
> <kwirsing at vt.edu>; Cedric Cannard <ccannard at protonmail.com>; 장진원 <
> jinwon06292 at gmail.com>; Makoto Miyakoshi <mmiyakoshi at ucsd.edu>
> *Tárgy:* Re: [Eeglablist] Critical pitfall of spectral power analysis?
>
> As a (naive and insufficiently substantiated hypothesis) — is sinusoidal
> (with sharp peaks in the spectrum) activity and broadband (not necessarily
> 1/f) activity generated by different mechanisms? Moreover, sinusoidal
> activity is a manifestation not of action, but of inaction of the brain.
> Physiological (alpha rhythm when closing the eyes, possibly also mu rhythm
> in the absence of proprioceptive signals, sleep spindles) or pathological
> (alpha coma and low-frequency sinusoids in the delta or theta ranges). It
> can be associated with the regulation of the level of constant potential
> and, in general, with metabolic processes carried out by the integral
> regulator generating oscillations (but we see oscillations directly only as
> an idle rhythm). Broadband activity seems to be directly associated with
> the functioning of individual neurons. Moreover, the function 1/f may
> simply be the result of the Fourier transform of a single excitatory or
> inhibitory postsynaptic potential. These mechanisms are interconnected, but
> different. Perhaps the mathematical apparatus for their study should also
> be different.
>
> Your truly
>
> Eugen Masherov,
> Burdenko Neurosurgery Institute
>
> > Thanks again everyone, for these very interesting points.
> >
> > Just to add to something that was said recently - yes, 1/f (or rather,
> 1/f^x) features are quite ubiquitous, I think practically any time series
> with some amount of autocorrelation will have a similar shape:
> https://urldefense.com/v3/__https://www.cell.com/trends/cognitive-sciences/fulltext/S1364-6613(14)00085-0__;!!Mih3wA!E0DB3LnNc6JHuXWc3N5M5iAUeusaX8LTN3dqbu9ZUeyzmDOwf3GVazliJU65YVxC6mC4VLMvHBOlkHKz4AeGoXXj$
> - its ubiquity is covered nicely in this lovely paper, as far as I remember.
> >
> > I also get most of Makoto's points about how just the location of the
> neuronal inputs, either in terms of proximity to the soma or in terms of
> cortical layers, will affect the strength of the low-pass filtering, and
> thus the shape of the 1/f scaling. This is super interesting, and this and
> dendritic filtering are certainly discussed in the literature to some
> extent. I am a bit more sceptical whether such subtle differences could
> contribute to 1/f changes in scalp recordings, but Makoto suggests they
> could and I trust his expertise.
> >
> > If you perform an ERP task, it would change 1/f power distribution, not
> surprisingly, because task-triggered cortico-cortical and thalamo-cortical
> inputs are recruited.
> >
> > This is a very interesting point. In our 2021 paper linked above, we
> also make the point that 1/f shape should change in an event-related
> design, but for a more trivial reason: ERPs are non-oscillatory (in the
> simple sense that they are transient bursts that do not repeat with a clear
> period), and will thus have a 1/f shape in the frequency domain (indeed,
> they do, there are some figures in the paper). Thus, 1/f scaling will
> change after an event trivially because there are well-known
> non-band-limited changes happening in the EEG (the ERPs). We tried to
> correct for the contribution of the ERPs and still found post-stimulus 1/f
> changes that we consider non-trivial (a steepening to be specific). These,
> then, could be explained by the mechanism that Makoto suggests (which we
> did not consider in the paper, as it seemed maybe a bit small-scale to
> explain scalp-derived effects) and/or by Gao et al.'s excitation-inhibition
> balance idea (this is the framework we used in the paper). It certainly
> cannot be explained by the general low-pass filtering properties of the
> tissue or similar more or less fixed variables, as those should not change
> so rapidly.
> >
> > I share much of your scepticism about oscillatory mechanisms (in scalp
> recordings), Makoto, but if we take the most typical generative mechanisms
> assigned to these phenomena (interplay of pyramidal cells and
> interneurons), they seem like they could potentially interact with these
> other mechanisms described above, or be fairly independent.
> >
> > So we've got this really complex picture, where there could be
> oscillations going on (maybe in alpha only), there could be (independent?)
> 1/f dynamics happening for multiple reasons, e.g., because of the location
> and/or the nature (E vs. I) of neuronal inputs changing, and there could be
> ERPs happening too, which might partly be phase-locked oscillations, and
> could also be related to where the neuronal inputs are located, so they
> "straddle" these different mechanisms quite a bit, probably. Not too sure
> about the ERPs to be honest.
> >
> > Two more minor points:
> >
> > I can't put up with the fuzziness of how the term 'oscillation' is used
> in the field now. Is a try-phasic burst, such as a classical event-related
> N1-P1 waveform, an oscillation?
> >
> > I agree completely that it is very unclear what constitutes an
> oscillation - basically, how many cycles are enough for something to be
> considered an oscillation, and how do we show that those cycles come from
> the same generative mechanism, and not just multiple successive events
> happening. This is less of a question for longer, more stable oscillations,
> e.g., alpha at rest.
> >
> > And as for Michael's question: my limited experience with this topic
> would certainly suggest that 1/f dynamics (for whatever reason) could
> change very rapidly, and often in a systematic fashion (e.g., predictably
> after a stimulus). They also do seem to change on much slower time scales
> as well, e.g., across the lifespan.
> >
> > Thanks,
> > Mate
> >
>