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I cannot determine whether sensory-cortex stimulation studies (CCEP/TMS/MEG) show that 20–30 s working-memory-like persistence tracks directed feedback latency asymmetry more strongly than feedforward projection strength, because the provided research excerpts do not contain any CCEP/TMS/MEG measurements of (i) feedback/feedforward projection strength or (ii) directed latency asymmetry during ~20–30 s persistence.
What I can extract numerically from your dataset are (a) simulation “persistence” time constants under rhythmic vs arrhythmic input and (b) an fMRI effective-connectivity example using Granger causal modeling during a working-memory task—neither is the specific CCEP/TMS/MEG directed-latency design requested.
If you want the exact numbers you asked for, we need raw CCEP/TMS/MEG articles that report latency asymmetry for bidirectional pathways and a separate metric for feedforward/direct projection strength, ideally tied to ~20–30 s “maintenance/persistence”.
Long Answer
Novel DHSC test (CCEP/TMS/MEG → 20–30s persistence ↔ directed feedback latency asymmetry vs feedforward strength)
Requested comparison: persistence (20–30 s, “working-memory-like”) vs (1) directed feedback latency asymmetry (re-entry/reciprocal timing) and (2) feedforward direct projection strength.
Evidence availability check: The provided research excerpts do not include sensory-cortex raw stimulation paradigms (CCEP/TMS/MEG) that quantify either directed latency asymmetry or feedforward projection strength for bidirectional pathways over ~20–30 s persistence. Therefore, I cannot report the requested “numbers for each component” from what you supplied.
1) What your provided data actually contains (numerical anchors we can use)
Rhythmic temporal working-memory simulation: reports a memory-persistence time constant (tau) under rhythmic vs arrhythmic inputs, plus perturbation results on synaptic vs neural-state contributions. (No sensory-cortex CCEP/TMS/MEG latency asymmetry.)
Source:
EEG/ERP trait biomarker schizophrenia: reports oscillatory and PLF differences during working memory, but not stimulation-based directional latency asymmetry or projection strength.
Source:
Effective connectivity (Granger causal modeling) in working memory: provides directed effective connectivity values (CPC) but from fMRI, not sensory-cortex CCEP/TMS/MEG, and not latency asymmetry for re-entry vs feedforward projections.
Source:
2) The only “persistence-like” numbers present here: tau under rhythmic vs arrhythmic input
The simulation excerpt reports memory-persistence time constants (tau) for Item 2, rhythmic vs arrhythmic. This is not a sensory-cortex stimulation metric, but it is the closest persistence-like numerical component in your provided data.
Citation: tau values are reported in the provided simulation excerpt.
3) How strongly does “direct neural activity” vs “synaptic efficacy/state” matter (still not projection-latency asymmetry)
Your excerpt reports a perturbation comparison indicating synaptic perturbation reduces accuracy more than neural-activity perturbation. This helps connect “persistence” to the mechanisms maintaining it, but it still does not provide the directed feedforward vs feedback latency asymmetry requested.
Important: your excerpt does not provide numeric effect sizes for these perturbations—only qualitative p-value thresholds.
4) Why this still does not answer your CCEP/TMS/MEG directed-latency-asymmetry question
Your question requires, specifically, sensory cortex stimulation studies that separately estimate:
Directed feedback latency asymmetry (e.g., reciprocal pathway timing difference) linked to ~20–30 s persistence.
Feedforward direct projection strength (a distinct measurement/parameter).
Tracking strength: which component correlates more with persistence.
None of the provided excerpts include directed latency asymmetry or feedforward vs feedback projection strength from CCEP/TMS/MEG.
5) What we can do instead with your data: a “what would be needed” check
Re-entry/reciprocal pathway perturbation measures yielding latency (or latency-derived asymmetry) for feedback vs feedforward direction.
A separate metric of feedforward direct projection strength (e.g., coupling magnitude in the forward direction, or direct projection weights/effects).
An operational definition and quantification of 20–30 s persistence (e.g., sustained firing/phase-alignment/decoding stability during the delay) measured in the same dataset.
A reported statistical association between persistence and each directional component (or sufficient raw data to compute it).
6) Links to deeper BGPT queries (to actually find the CCEP/TMS/MEG latency-asymmetry numbers)
Key limitation (scientific skepticism)
Because the provided sources do not include the required CCEP/TMS/MEG directed-latency asymmetry metrics, any attempt to supply “numbers for each component” would require searching other raw full-text papers.
I’m not doing that here; I’m staying strictly within the evidence you provided.
Run the Science AI agent (to fetch the missing CCEP/TMS/MEG numbers)
It will extract tau/persistence and connectivity metrics from the provided sources, compute effect-size rankings, and generate component-wise tables/plots; it will also flag missing CCEP/TMS/MEG latency-asymmetry metrics.
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Hypothesis Graveyard
A common failure mode would be to conflate any directed connectivity change (e.g., fMRI Granger CPC) with latency-asymmetry mechanisms; without actual latency-resolved bidirectional stimulation, that “equivalence” hypothesis is unsupported by the provided sources.
Another weak option is that persistence is fully explained by feedforward strength alone; your provided simulation suggests synaptic/effective state maintenance can dominate over neural-activity perturbations, challenging a pure feedforward-only explanation (though not the latency-asymmetry framing you requested).
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