My 2 cents: Their approach is an experimental technique without any efficacy literature to support it, and those who are doing the technique need to get their approach into the efficacy literature before we can actually start to tease out the underlying factors and mechanisms.

There are only semantic differences between SCP, infra-slow EEG and cortical DC field potential recordings, as they all are part of the same phenomenon.

I’d be happy to discuss the Othmer’s work, but their outcomes have not been published in peer reviewed material to actually start to be able to really evaluate what their work actually is. Their explanation of the effect has changed over time from a coherence phenomenon to phase shifts… they need to get their story illustrated with real outcome data and EEG recordings to identify the actual effect before teaching classes about it as though it is a standard approach in NF. It is experimental.

The recent edition of NeuroConnections has a good discussion of the factors influencing the DC or infra-slow activity, and I’d point you there for any current discussion bsed on actual EEG data and not just theory.

Once they actually get their material researched with data being published, then we will be able to discuss what it is they are doing. Right now they teach theories about how it works, but the data doesn’t support their conclusion, as the signals change due to coherence, power and phase changes when it is actually examined by Richard Souter with real data and not just a thought experiment.

I’m fine with thought experiments when actual data collection is not feasible (like the train at the speed of light experiements by Einstein), but when we can easily collect real EEG data so easily for actual data analysis, thought experiments are inexcusable.

The slow activity could be skin contact shifting, electrode drift, thermal drift, amplifier drift, pulse artifact, respiratory artifact, eye movements, or even actual EEG activity… but until it is researched with appropriate designs to make efficacy claims, it is experimental and merely based on anecdote.

Good luck in your search!

Jay

Gray matter damage decreases alpha initially, and also has beta and gamma decreases. as the very neuroplastic gray m atter heals and is not re-engaged with function, the alpha will return and even be seen as an excess idling of the cortical area… until it is re-engaged in function, when the beta and gamma will return and the alpha will regain a normal dynamic, and no longer be in excess.

White matter damage increases slowing due to a decreased inhibition of the sheet dipoles due to the lack of (or decrease in) cortical input.

I hope this helps clarify the issue for you… let me know if you need a more in-depth answer.

Jay

It was good that you question the opinion of normalcy of “14 and 6″ but unless I see what you actually have recorded, I’m not sure you actually have “14 and 6 positive spikes” You report an atypical “14 and 7” and do not discuss the distribution ir polarity of the spike portion…. So I am not really confident what you have identified.

I can’t comment on the specifics in your case due to this uncertainty… however, in general what Niedermayer is saying is that there is no specific pathology… no epilepsy, nop strokes, tumors, vascular lesions, demyelination, etc…

The importance of this difference in what “normal” means was the basis for the split in the field of EEG and the AES splinter group forming AMEEGA (now ECNS) by Gibbs and Gibbs, Duffy, Hughes and others.

The actual 14 and 6 is identified as a non-specific marker in behaviorally disordered children according to the Gibbs and Gibbs view… not a form of epilepsy, though that is a group in which it was originally seen as well…

I hope this note helps… even if I can’t comment on the case itself directly due to the lack of an EEG to review.

Jay

Commonly either a slow pattern, alpha excess, or a beta spindle… but the frontal lobe regulation of the motor strip will be compromised by whatever pattern it is, and often hypocoherence fronto-centrally (or Sterman’s fronto-central disconnect) will be seen in the “connectivity, though it is obviously not a cortical-cortical connection, but a cortical subcortical-cortical loop.