Etiology of Neurosis – Subneuronal Dynamics, Microtubules, and Entropic Load

This paper proposes a unified biophysical framework for the etiology of neurosis, integrating evolutionary genetics, non-equilibrium thermodynamics, and cytoskeletal information processing. We posit that the human-specific duplication of the SRGAP2C gene, known to induce synaptic neoteny and increased dendritic spine density, created a structural "over-parameterization" of the neocortex. We hypothesize that this densification necessitated a proportional expansion of the microtubule network, thereby increasing the brain’s capacity for high-dimensional state processing (potential quantum-inspired or high-dimensional classical superposition of future scenarios). However, this expanded hardware imposes a critical thermodynamic cost: an "entropic overhead" resulting from the energy required to erase (Landauer’s Principle) unselected predictive states. We model neurosis not as a psychological defect, but as a dynamic instability—a failure of the Default Mode Network (DMN) to efficiently collapse (or efficiently select among) this hyper-complex state space. Finally, we offer falsifiable predictions linking high-frequency neural noise and metabolic consumption to this evolutionary trade-off, suggesting new avenues for biophysical investigation and hypothesis-driven empirical testing. Keywords: SRGAP2C, Neurosis, Entropy, Microtubules, Landauer’s Principle, DMN, Biological Theory. Contact: hugo.tapia@neurociencia.solutions