Against cortical reorganisation

Abstract

Neurological insults, such as congenital blindness, deafness, amputation, and stroke, often result in surprising and impressive behavioural changes. Cortical reorganisation, which refers to preserved brain tissue taking on a new functional role, is often invoked to account for these behavioural changes. Here, we revisit many of the classical animal and patient cortical remapping studies that spawned this notion of reorganisation. We highlight empirical, methodological, and conceptual problems that call this notion into doubt. We argue that appeal to the idea of reorganisation is attributable in part to the way that cortical maps are empirically derived. Specifically, cortical maps are often defined based on oversimplified assumptions of ‘winner-takes-all’, which in turn leads to an erroneous interpretation of what it means when these maps appear to change. Conceptually, remapping is interpreted as a circuit receiving novel input and processing it in a way unrelated to its original function. This implies that neurons are either pluripotent enough to change what they are tuned to or that a circuit can change what it computes. Instead of reorganisation, we argue that remapping is more likely to occur due to potentiation of pre-existing architecture that already has the requisite representational and computational capacity pre-injury. This architecture can be facilitated via Hebbian and homeostatic plasticity mechanisms. Crucially, our revised framework proposes that opportunities for functional change are constrained throughout the lifespan by the underlying structural ‘blueprint’. At no period, including early in development, does the cortex offer structural opportunities for functional pluripotency. We conclude that reorganisation as a distinct form of cortical plasticity, ubiquitously evoked with words such as ‘take-over’’ and ‘rewiring’, does not exist.