Functional circuitry underlying natural and interventional cancellation of visual neglect

Abstract

A large body of work demonstrates that lesions at multiple levels of the visual system induce neglect of stimuli in the contralesional visual field and that the neglect dissipates as neural compensations naturally emerge. Other studies show that interventional manipulations of cerebral cortex, superior colliculus or deep-lying midbrain structures have the power to attenuate, or cancel, the neglect and reinstate orienting into a neglected hemifield, and even into a profound cortically blind field. These results, and those derived from experiments on the behavioral impacts of unilateral and bilateral lesions, lead us to evaluate the repercussions of unilateral and bilateral deactivations, neural compensations and cancellations of attentional deficits in terms of an overarching hypothesis of neglect. The cancellations can be both striking and enduring, and they suggest that therapeutic strategies can be developed to reverse or ameliorate neglect in human patients. Animal studies show that in many instances of neglect adequate representations and the accompanying motor mechanisms are present despite the lesion and they simply need to be unmasked and brought into use to effect a remedy.

Is neuroenhancement by noninvasive brain stimulation a net zero-sum proposition?

“…A subsequent lesion of the now unconstrained and hyperactive contralesional colliculus thus removed its suppression of the ipsilesional colliculus leading to a restoration in bilateral orienting behavior. Further lesion and reversible deactivation studies have confirmed (Sprague, 1996) and extended this effect to other regions (Lomber and Payne, 2001; Payne and Rushmore, 2004). …”

Prism adaptation for spatial neglect after stroke: translational practice gaps

“…However, the intermediate and deeper, motor superior colliculus seems to have a critical role in primate eye–hand coordination, and cells in this region, 98 overlapping with the mesencephalic reticular formation, may map both gaze-dependent and gaze-independent hand movements yes, OK. In animals 34–36 and humans, 99,100 damage to the motor (deep) superior colliculus induced asymmetric spatial behaviour and spatial neglect, indicating that this structure could be a critical node in the spatial motor network. 1,3,15,41,101 Whether this region participates in modulation of interhemispheric balance of eye–hand movement bias during prism adaptation, or whether it might map frontal–subcortical spatial ‘aiming’, requires further research.…”

Monocular patching may induce ipsilateral “where” spatial bias

“…The ipsilateral superior colliculus, released from intracollicular inhibition, may induce strong contralateral orienting (the Sprague effect (Sprague, 1966). Although the mechanisms of the Sprague effect have been disputed (Wallace, Rosenquist, & Sprague, 1990), a role of intracollicular inhibition in this phenomenon is supported in recent studies in cats (Payne & Rushmore, 2004; Rushmore, Valero-Cabre, Lomber, Hilgetag, & Payne, 2006) and human stroke survivors (Weddell, 2004). …”