Animal Models of Cerebral Neglect and Its Cancellation

Abstract

The purpose of this perspective is twofold: 1) to alert and inform the neurospychology and neurology communities on how animal models can improve our understanding of spatial neglect in humans, and 2) to serve as a guide to rehabilitation strategies. Spatial neglect is a neurological syndrome that is inextricably linked to the ability to overtly or covertly reorient attention to new loci. Literature describing variants of neglect leads to the perception of lesion-induced neglect as a uniquely human syndrome for which there are limited treatment options. To the contrary, neglect has been reversed in laboratory animals, and results show that adequate neural representations and motor mechanisms for reversal are present despite damaged or deactivated cerebral cortex. These results and conclusions provoke thought on strategies that can be employed on humans to cancel neglect, and they suggest that long-term amelioration of neglect can be induced by training of specific bypass circuits.

Functional imaging reveals rapid reorganization of cortical activity after parietal inactivation in monkeys

“…Evidence for this proposal is derived from TMS studies in neglect patients showing that spatial extinction can be transiently alleviated by deactivating the hemisphere opposite to the lesion (19,61,62) and by demonstrating hyperexcitability of parietal-motor pathways in the intact hemisphere (18). Similarly, studies in cats have shown a restoration of spatial functions as a consequence of deactivation of homolog areas in the hemisphere opposite to the lesion (14,29,63).…”

“…Although dynamic competitive and cooperative interhemispheric interactions may coexist, the contribution of these interactions to spatial disorders and postlesion recovery remains unclear. Therefore, animal models of spatial disorders are needed because, unlike in humans, extent and location of the lesions can be systematically varied; in addition, brain activity can be measured before longterm neural and behavioral compensations can occur (1,29).…”

Causal functional contributions and interactions in the attention network of the brain: an objective multi-perturbation analysis

“…In particular, we investigated visual orienting behavior, based on the paradigm described by Lomber and Payne (Payne et al 1996a;Lomber et al 2001Lomber et al , 2002Lomber and Payne 1996;Payne and Rushmore 2003). These studies compared the visual orienting behavior in adult cats during unilateral and bilateral deactivation of posterior middle suprasylvian sulcal cortex (pMS, an area at the confluence of the temporal, occipital and parietal lobes) and unilateral and bilateral deactivation of the superior colliculus (SC).…”

“…When neural tissue is cooled by a permanently implanted cryoloop below a temperature of approximately 20°C, the spiking activity of neurons ceases, thus 'turning off' the output of the cooled region. Using reversible cooling, the group of Payne and Lomber (Payne et al 1996a;Lomber et al 2001Lomber et al , 2002Lomber and Payne 1996;Payne and Rushmore 2003) temporarily deactivated focal cortical and subcortical regions in adult cats, unilaterally and bilaterally, and investigated the resulting behavior during visual and auditory orienting tasks. Somewhat counterintuitively, some secondary lesions were found to reverse behavioral deficits resulting from initial lesions (that is, bilateral lesions appeared to cancel each other out), producing so-called paradoxical lesion effects (Hilgetag et al 1999;Kapur 1996) which indicate synergistic and competitive network interactions in attentional function.…”

“…In this context, lesion, deactivation and perturbation studies in animal models have been used to investigate attentional mechanisms and identify possible avenues for rehabilitation. Particularly, visual and auditory orienting tasks were used as a test of spatial attention in the cat (Lomber and Payne 1996;Lomber et al 2001), serving as an animal model of intact or perturbed attention and sensory perception in the human brain (Payne and Rushmore 2003).…”