Jackson Cionek
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Finitude as Loss - when pain and memory dissolve into new consciousness - LATAN LatBrain SfN 2025 Brain Bree

Finitude as Loss - when pain and memory dissolve into new consciousness - LATAN LatBrain SfN 2025 Brain Bree

I am the consciousness that says goodbye. I feel loss arriving like a tide: at first the body tenses to protect me; then, if I allow it, it softens and dissolves the “I” that was holding the pain. Between one breath and the next, the identity that hurt begins to lose its name. In its place, a silent awareness emerges — fruition, metacognition, peace. Finitude teaches me how to fall without breaking.


1) Loss, trauma, and belonging

  • Natural loss tends toward Zone 2, dissolving tensions and reducing pain.

  • Traumatic or ideological loss pulls into Zone 3, with limbic hyperactivity (amygdala–hippocampus) and persistent vigilance.

  • Relation vs causality: evidence shows strong relations between catastrophizing and worse pain; proving causality requires interventions that reduce catastrophizing and demonstrate measurable changes in pain and brain connectivity.


2) Sleep: the natural path of dissolution

Healthy sleep fragments the tensional self step by step:

  • N1 loosens the first knot,

  • N2 stabilizes,

  • N3 gives a “provisional finitude” of the tensional self,

  • REM tonic recalibrates proprioception,

  • REM phasic refines emotions.

In chronic pain, this cycle is broken: N3 is shortened, REM becomes fragmented, micro-arousals increase pain and keep the body on alert. The relation is bidirectional — poor sleep worsens pain, pain worsens sleep — but longitudinal and interventional studies begin to show causality.


3) When the “self that hurts” grows larger than the pain

Central sensitization and cortical reorganization fuse identity with pain. EEG shows increased power in theta, beta, and gamma bands. fNIRS reveals altered prefrontal connectivity. These are relations with pain intensity, but causality needs experimental interventions (exercise, neurofeedback, tDCS) to confirm whether changes in EEG/fNIRS precede and mediate pain reduction.


4) From the Whole to measurement

Simplifying the Whole is a strategy to generate hypotheses:

  • N3 sleep → pain: more N3 may reduce next-day pain mediated by lower inflammation.

  • Prefrontal fNIRS → TENS response: connectivity predicting analgesia.

  • EEG gamma/beta → pain intensity: potential biomarkers of treatment response.

  • REM tonic → proprioception: better proprioceptive calibration on waking.

These hypotheses are possibilities; only experimental design can measure probability and causality.


5) For clinicians and caregivers

  • Pain neuroscience education to reduce fear and catastrophizing.

  • Sleep hygiene focused on deep N3 restoration.

  • Simple rituals of belonging (DANA) in palliative care.

  • Graded movement and exercise to break the identity–pain loop.


6) Indicative References (EEG/fNIRS/Sleep)

EEG and pain

  • Zebhauser et al., PAIN, 2023 – Neuropathic pain and theta/alpha/beta/gamma oscillations.

  • Ryu et al., Scientific Reports, 2024 – Prefrontal gamma activity in subjective pain.

  • Reid et al., 2023 – Advances in sleep EEG and pain mechanisms.

fNIRS and pain

  • Luo et al., 2024 – Prefrontal connectivity predicting analgesia with TENS in chronic pain.

  • Shafiei et al., 2025 – fNIRS + VR to classify cancer pain severity.

  • Liao et al., 2025 – fNIRS HbO changes to painful vs. non-painful stimuli.

  • Bae et al., 2025 – DLPFC activation reduction after manual therapy for chronic pain.

Sleep and inflammation

  • Irwin et al., PAIN, 2023 – Loss of N3 increases cellular inflammation and pain sensitivity.


Signature:
Finitude must bring peace with new Consciousness — maturity with inoscence.



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Jackson Cionek

New perspectives in translational control: from neurodegenerative diseases to glioblastoma | Brain States