Single-sided deafness: EEG Study Proposes Hierarchical Plasticity Model

A new analysis posits that the brain’s response to single-sided deafness (SSD) is strictly hierarchical, altering raw sensory input while leaving higher-level cognitive processing untouched. For decades, mapping this specific neural terrain has proved frustratingly difficult. Previous attempts yielded contradictory data, often muddied by heterogeneous patient groups or inconsistent task designs that failed to isolate specific stages of neural processing.

Technical Contrast: Sensory Input vs Cognitive Processing

To clarify these prior discrepancies, the researchers distinguished strictly between early exogenous components and late endogenous ones. In EEG analysis, early markers such as N1 and P2 represent the brain's immediate, automatic reception of a stimulus—essentially the raw feed. Conversely, late components like N2 and P3 signify the cognitive labour of categorising and discriminating between those signals. The study measured a distinct reduction in the early auditory markers (N1, P2) and mismatch negativity (MMN) within the SSD cohort. Yet, the late endogenous components remained statistically indistinguishable from the normal-hearing controls. This suggests that while the 'hardware' reception of sound is dampened, the 'software' processing remains robust.

Visual Compensation and Single-sided deafness

The investigation into cross-modal plasticity—how the brain compensates for lost senses—revealed a sharp inversion when testing visual stimuli. While auditory input was dampened at the sensory stage, the SSD group displayed significantly increased amplitudes in the early visual N1 component. The brain appears to turn up the volume on sight to compensate for the lack of stereo sound. However, much like the auditory results, the higher-level visual processing (vMMN, N2, P3) showed no latency differences or anomalies. The plasticity is specific, not general. It occurs at the gate, not in the control room.

These findings rely on a homogeneous cohort of 37 congenital SSD patients, matched against 32 controls. By excluding acquired deafness, the study removes variables related to progressive hearing loss, though this limits the application of the findings to those who lost hearing later in life. The data indicates that functional plasticity is characterised by a trade-off: diminished auditory activity balanced by elevated visual vigilance, restricted entirely to the sensory stages.

Clinicians may need to reassess rehabilitation strategies based on this hierarchical framework. If higher-level discrimination remains intact, therapies might be better focused on managing the sensory load and integration rather than cognitive retraining. The brain is not broken; it has simply recalibrated its inputs.