Biomedical subjects

R Jarrett Rushmore

Publications and source records attributed to R Jarrett Rushmore.

6 recordsLinked to original sources

PubMed2006

Functional circuitry underlying visual neglect.

Visuospatial neglect is a common neurological syndrome caused by unilateral brain damage to the posterior and inferior parietal cerebral cortex, and is characterized by an inability to respond or orient to stimuli presented in the contralesional hemifield. Neglect has been elicited in experimental models of the rat, cat and monkey, and is thought to result in part from a pathological state of inhibition exerted on the damaged hemisphere by the hyperexcited intact hemisphere. We sought to test this theory by assessing neural activity levels in multiple brain structures during neglect using 2-deoxyglucose (2DG) as a metabolic marker of neural activity. Neglect was induced in two ways: (i) by cooling deactivation of posterior parietal cortex or (ii) in conjunction with broader cortical blindness produced by unilateral lesion of all contiguous visual cortical areas spanning occipital, parietal and temporal regions. The direction and magnitude of changes in 2DG uptake were measured in cerebral cortex and midbrain structures. Finally, the 2DG uptake was assessed in a group of cats in which the lesion-induced neglect component of blindness was cancelled by cooling of either the contralateral posterior parietal cortex or the contralateral superior colliculus (SC). Overall, we found that (i) both lesion- and cooling-induced neglect are associated with decreases in 2DG uptake in specific ipsilateral cortical and midbrain regions; (ii) levels of 2DG uptake in the intermediate and deep layers of the SC contralateral to both cooling and lesion deactivations are increased; (iii) changes in 2DG uptake were not identified in the contralateral cortex; and (iv) reversal of the lesion-induced neglect component of blindness is associated with a reduction of contralesional 2DG uptake to normal or subnormal levels. These data are in accord with theories of neglect that include mutually suppressive mechanisms between the two hemispheres, and we show that these mechanisms operate at the level of the SC, but are not apparent at the level of cortex. These results suggest that the most effective therapies for visual neglect will be those that act to decrease neural activity in the intermediate layers of the SC contralateral to the brain damage.

Animals↗

PubMed2005

Functional impact of primary visual cortex deactivation on subcortical target structures in the thalamus and midbrain.

The functional relationships between the primary visual cortex and its major subcortical target structures have long been a subject of interest. We studied these relationships by using localized cooling deactivation to silence portions of primary visual cortex and measuring 2-deoxyglucose (2DG) uptake to assess neural activity in subcortical and midbrain targets. We focused analysis on the largest subcortical targets of primary visual cortex: the superior colliculus (SC), the dorsal lateral geniculate nucleus of the thalamus (dLGN), and the lateral division of the lateral posterior nucleus of the thalamus (LPL). We found that localized cooling of different regions of primary visual cortex caused specific decreases in 2DG uptake in target structures such that the location of 2DG decrease varied according to joint retinotopy, and the magnitude of the decreases in target structures was associated with the amount of cooled cortex. In addition, we found that the impact of cortical cooling was more profound on the SC than on the dLGN. The functional impact of cortical deactivations on the LPL was weak for small deactivations but approximated the impact on the SC when deactivations were large. We discuss these findings in terms of neural circuits and in terms of drivers and modulators.

Animals↗

PubMed2004

Neuroplasticity after unilateral visual cortex damage in the newborn cat.

Anatomical, electrophysiological, and behavioral studies implicate extrastriate cortex as a major contributor to the sparing of visually guided behaviors following lesions of primary visual cortex incurred early in life. Here we report considerable sparing of the ability to detect and localize stimuli in the hemifield contralateral to unilateral early lesions of all contiguous visually-responsive primary and extrastriate cortical regions (occipital, visuoparietal, and visuotemporal cortices). In the adult cat this same lesion induces a dense blindness and cats are unable to orient to any visual stimulus introduced into the contralesional hemifield. In the absence of cortical circuits, the neural sparing identified following the neonatal lesion is based on the superior colliculus and it occurs despite massive retrograde transynaptic degeneration of large numbers of retinal ganglion cells.

Animals↗

PubMed2003

Functional circuitry underlying natural and interventional cancellation of visual neglect.

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.

Animals↗

PubMed2003

Bilateral impact of unilateral visual cortex lesions on the superior colliculus.

We examined the functional impact of a long-standing, unilateral primary visual cortex lesion on the superior colliculus (SC) using radiolabeled 2-deoxyglucose (2DG) as a marker of neural activity. In accord with known corticotectal connectivity and functional influence, 2DG uptake in the superficial layers of the ipsilesional SC was decreased. We also found a decrease in the superficial layers of the contralesional SC. These data suggest that modifications in activity in one SC can have a substantial influence on activity in its contralateral partner, and that processing in one visual hemifield does not occur independently of processing of signals in the opposite hemifield. The effects are not mediated by the contralateral hemisphere but are probably mediated by intercollicular circuitry.

Animals↗

PubMed2003

Animal models of cerebral neglect and its cancellation.

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.

Animals↗