Aziel Eliab · preprint · Preprint
DOI: 10.5281/zenodo.21430082 Concept DOI: 10.5281/zenodo.21430081 Publication date: 2026-07-18 Checksum: md5:4cafffce209db593ae015f850a1c7cc8 Zenodo record id: 21430082 Post-Perturbation Integrative Neuroplasticity (PPIN) Section 4: Mechanistic Hypotheses OVERVIEW This section outlines plausible neurocognitive mechanisms underlying Post-Perturbation Integrative Neuroplasticity (PPIN). These hypotheses are grounded in established neuroscience and cognitive psychology literature and are intended to guide future empirical investigation. No single mechanism is assumed to be sufficient; PPIN is likely a convergent outcome of multiple interacting processes. 1. NETWORK-LEVEL NEUROPLASTIC REORGANIZATION PPIN is hypothesized to arise from large-scale network reconfiguration rather than focal lesion compensation. Perturbation events may disrupt habitual network dominance, allowing alternative coupling patterns to stabilize. Key networks implicated: - Default Mode Network (DMN): reduced dominance or rebalanced engagement - Salience Network (SN): altered threshold for signal relevance - Central Executive Network (CEN): preserved or strengthened top-down coordination The resulting configuration favors integrative processing across perceptual, associative, and executive domains. 2. ATTENUATED LATENT INHIBITION WITH PRESERVED EXECUTIVE CONTROL Latent inhibition refers to the brain’s tendency to filter familiar or low-salience stimuli. PPIN may involve a sustained reduction in latent inhibition, increasing access to raw perceptual and associative input. Crucially, unlike psychotic-spectrum conditions, executive control remains intact. This allows: - Increased signal intake without loss of coherence - Active hypothesis testing rather than passive belief formation - Deliberate inhibition of premature conclusions This balance is proposed as a central stabilizing factor distinguishing PPIN from maladaptive pattern over-attribution. 3. SALIENCE NETWORK RECALIBRATION Perturb
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