Auditory Sector Thalamocortical Dysrhythmia as the Mechanistic Basis of Tinnitus: A W2 Spurious-Completion Account and Derived Therapeutic Hypotheses

Tinnitus — the perception of sound in the absence of external acoustic stimulation — affects approximately 14.4% of the adult population globally (Jarach et al., 2022, JAMA Neurology), with 1–2% reporting severe, disabling symptoms. Despite extensive research, no pharmacological treatment has demonstrated consistent efficacy, and the mechanistic gap between peripheral auditory pathology and central phantom sound generation remains incompletely bridged. The thalamocortical dysrhythmia (TCD) framework, established by Llinás et al. (1999), identified auditory TRN disfacilitation as the thalamic mechanism of tinnitus: loss of peripheral auditory excitatory input hyperpolarises auditory thalamic relay neurons, activating T-type calcium channels and producing theta-range burst oscillation that drives phantom auditory cortical activation via the edge effect. This mechanism has since been confirmed at single-unit level in awake animals (Kalappa et al., 2014) and in comprehensive physiological reviews (Shore et al., 2020). Dai et al. (2024) provided direct experimental confirmation that chemogenetic activation of the auditory TRN suppresses tinnitus-related cortical activity in animal models, establishing the TRN as a validated therapeutic target and constituting a CDL Class 5 independent confirmation of the gate mechanism (rated CCT-3.5 Harvey-Level Established programme-wide). The present paper applies the Return Constraint Model (RCM) — a framework applied across twelve neurological conditions — to develop a formally precise account of tinnitus as a W2 spurious-completion phenomenon at Level 7 of a ten-level failure mode taxonomy. Three falsifiable therapeutic hypotheses are derived and presented as untested predictions. No therapeutic claim made in this paper has been confirmed in a clinical trial; all carry CCT-2 Provisional ratings and pre-specified falsification conditions.