Why BCIs work poorly with the patients who need them the most?

TL;DR

This paper investigates why brain-computer interfaces are less effective for severely impaired patients, proposing that negative plasticity affects their covert attentional processes, which impairs BCI performance.

Contribution

It introduces a hypothesis that negative plasticity in attentional processes explains BCI inefficacy in severely impaired patients, linking neuroimaging and clinical findings.

Findings

Severely impaired patients show reduced BCI performance compared to healthy subjects.

Negative plasticity may extend impairment from overt to covert attention.

The control principle in BCI relies on attentional commands, which are affected by plasticity.

Abstract

A major objective of Brain-Computer interfaces (BCI) is to restore communication and control in patients with severe motor impairments, like people with Locked-in syndrome. These patients are left only with limited eye and eyelid movements. However, they do not benefit from efficient BCI solutions, yet. Different signals can be used as commands for non-invasive BCI: mu and beta rhythm desynchronization, evoked potentials and slow cortical potentials. Whatever the signal, clinical studies show a dramatic loss of performance in severely impaired patients compared to healthy subjects. Interestingly, the control principle is always the same, namely the replacement of an impossible (overt) movement by a (covert) attentional command. Drawing from the premotor theory of attention, from neuroimaging findings about the functional anatomy of spatial attention, from clinical observations and from recent computational accounts of attention for both action and perception, we explore the hypothesis that these patients undergo negative plasticity that extends their impairment from overt to covert attentional processes.