Catharina Barbosa Lima, Leonardo Galli Hamamoto, Paulo Roberto Franceschini, Paulo Henrique Pires de Aguiar
Available evidence from preclinical and early clinical studies supports MGB-DBS as a mechanistically coherent, network-oriented neuromodulatory target within the framework of thalamocortical dysrhythmia. Although clinical evidence remains limited and preliminary, these findings support further prospective controlled translational studies incorporating objective neurophysiological biomarkers to establish safety, efficacy, and mechanisms of action in carefully selected patients with severe treatment-refractory tinnitus.
OBJECTIVES: Chronic tinnitus imposes considerable functional and socioeconomic burden, particularly in patients with treatment-refractory disease despite available therapies. Increasing evidence supports tinnitus as a disorder of maladaptive brain network activity rather than solely peripheral pathology, motivating circuit-based neuromodulatory interventions. This review synthesizes the neurophysiological rationale and translational evidence for deep brain stimulation (DBS) of the medial geniculate body (MGB) as a therapeutic strategy for refractory tinnitus.
MATERIALS AND METHODS: A narrative review was conducted by synthesizing preclinical, translational, and early clinical evidence on MGB-DBS for tinnitus, with reference tracking of key studies. Evidence was organized around three complementary neurophysiological frameworks-thalamocortical dysrhythmia, aberrant oscillatory activity, and dysfunctional sensory gating-to contextualize MGB stimulation within the broader spectrum of invasive neuromodulatory strategies for tinnitus.
RESULTS: Preclinical studies consistently show that high-frequency MGB stimulation suppresses tinnitus-like behavior and modulates pathologic thalamocortical activity. Proposed mechanisms include thalamocortical desynchronization, restoration of sensory gating, suppression of aberrant neural firing, and GABAergic modulation. Early clinical evidence, including a first-in-human case report and a subsequent feasibility study, suggests procedural safety and potential therapeutic benefit without significant auditory deterioration, although consistent tinnitus suppression was not observed across all participants.
CONCLUSIONS: Available evidence from preclinical and early clinical studies supports MGB-DBS as a mechanistically coherent, network-oriented neuromodulatory target within the framework of thalamocortical dysrhythmia. Although clinical evidence remains limited and preliminary, these findings support further prospective controlled translational studies incorporating objective neurophysiological biomarkers to establish safety, efficacy, and mechanisms of action in carefully selected patients with severe treatment-refractory tinnitus.