Tactile discrimination performance deficits following neglect-producing unilateral lateral hypothalamic lesions in the rat

Spatial neglect increases hospital morbidity and costs in around 50% of the 795,000 people per year in the USA who survive stroke, and an urgent need exists to reduce the care burden of this condition. However, effective acute treatment for neglect has been elusive. In this article, we review 48 studies of a treatment of intense neuroscience interest: prism adaptation training. Due to its effects on spatial motor ‘aiming’, prism adaptation training may act to reduce neglect-related disability. However, research failed, first, to suggest methods to identify the 50–75% of patients who respond to treatment; second, to measure short-term and long-term outcomes in both mechanism-specific and functionally valid ways; third, to confirm treatment utility during the critical first 8 weeks poststroke; and last, to base treatment protocols on systematic dose–response data. Thus, considerable investment in prism adaptation research has not yet touched the fundamentals needed for clinical implementation. We suggest improved standards and better spatial motor models for further research, so as to clarify when, how and for whom prism adaptation should be applied.

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“…Consistent with neglect demonstrated in animal models across the mammalian class, dissociable from spatial attention and perception 104,105 …”

Section: Prism Adaptation Studiessupporting

confidence: 55%

Prism adaptation for spatial neglect after stroke: translational practice gaps

2012

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“…The tactile adhesive removal test is analogous to the clinical test of double simultaneous discriminations, which has often been used to detect "neglect," a deficit in attention or orientation mediated by damage to the frontal cortex and/or striatum (Feeney and Wier, 1979;Heilman, 1979;Heilman and Valenstein, 1972;Heilman and van den Abell, 1980;Hoyman et al, 1979;Mesulam, 1981). Neglect or sensory inattention is defined as the failure to respond to salient sensory stimuli in the absence of any apparent sensory or motor deficit.…”

Section: Discussionmentioning

confidence: 99%

Dissociable Long-Term Cognitive Deficits after Frontal versus Sensorimotor Cortical Contusions

Lindner¹,

Plone²,

Cain³

et al. 1998

Journal of Neurotrauma

106

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Cognitive deficits are the most enduring and disabling sequelae of human traumatic brain injury (TBI), but quantifying the magnitude, duration, and pattern of cognitive deficits produced by different types of TBI has received little emphasis in preclinical animal models. The objective of the present study was to use a battery of behavioral tests to determine if different impact sites produce different patterns of behavioral deficits and to determine how long behavioral deficits can be detected after TBI. Prior to surgery, rats were trained to criteria on delayed nonmatching to position, radial arm maze, and rotarod tasks. Rats received sham surgery (controls), midline frontal contusions (frontal TBI, 2.25 m/sec impact), or unilateral sensorimotor cortex contusions (lateral TBI, 3.22 m/sec impact) at 12 months of age and were tested throughout the next 12 months. Cognitive deficits were more robust and more enduring than sensorimotor deficits for both lateral TBI and frontal TBI groups. Lateral TBI rats exhibited transient deficits in the forelimb placing and in the rotarod test of motor/ambulatory function, but cognitive deficits were apparent throughout the 12-month postsurgery period on tests of spatial learning and memory including: (1)reacquisition of a working memory version of the radial arm maze 6-7 months post-TBI, (2) performance in water maze probe trials 8 months post-TBI, and (3) repeated acquisition of the Morris water maze 8 and 11 months post-TBI. Frontal TBI rats exhibited a different pattern of deficits, with the most robust deficits in tests of attention/orientation such as: (1) the delayed nonmatching to position task (even with no delays) 1-11 weeks post-TBI, (2) the repeated acquisition version of the water maze--especially on the first "information" trial 8 months post-TBI, (3) a test of sensorimotor neglect or inattention 8.5 months post-TBI, and (4) a DRL20 test of timing and/or sustained attention 11 months after surgery. These results suggest that long-term behavioral deficits can be detected in rodent models of TBI, that cognitive deficits seem to be more robust than sensorimotor deficits, and that different TBI impact sites produce dissociable patterns of cognitive deficits in rats.

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“…Implicit in the stimulation and lesion studies cited above is the assumption that there exist hypothalamic mechanisms for modulating the incentive value of stimuli associated with the satisfaction of specific motivational states. These mechanisms are not thought to exert their influence directly on sensory or motor systems, but rather to facilitate sensorymotor integration [29,56]. The view that hypothalamic stimulation only increases responsiveness to relevant stimuli, however, has been challenged by evidence that stimulation produces a nonspecific increase in reactivity even to neutral stimuli [1,8].…”

Section: Discussionmentioning

confidence: 99%

Strain differences in eating and drinking evoked by electrical stimulation of the hypothalamus

Mittleman

Valenstein

1981

Physiology & Behavior

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Strain differences in eating and drinking evoked by electrical stimulation of the hypothalamus. PHYSIOL. BEHAV. 26(3) 371-378, 1981.-Electrical stimulation of the lateral hypothalamus (ESLH) has been shown to produce individual response differences that cannot be attributed to the neuroanatomical locus of the electrode. The purpose of the present experiment was to investigate strain differences in the incidence of eating and drinking evoked by ESLH. The responses of 49 Long-Evans and 51 Spragne-Dawley male rats implanted with bilateral hypothalamic electrodes were studied. Animals from these two strains do not differ in their normal food or water consumption. Analysis of the responses to ESI~H demonstrated that a significantly greater number of Long-Evans rats ate food and/or drank water during ESLH than did the Spragne-Dawley rats. These results could not be attributed to differences in electrode placements, or rearing conditions. In addition to strain differences, the importance of individual differences within each strain was demonstrated by the fact that both electrodes in a given animal commonly evoked the same behavior. Hypotheses to explain these results are discussed. Electrical stimulation Lateral hypothalamus Strain differences Evoked eating and drinking Stimulus-bound behavior Long-Evans Sprague-Dawley

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Tactile discrimination performance deficits following neglect-producing unilateral lateral hypothalamic lesions in the rat

Cited by 40 publications

References 22 publications

Prism adaptation for spatial neglect after stroke: translational practice gaps

Prism adaptation for spatial neglect after stroke: translational practice gaps

Dissociable Long-Term Cognitive Deficits after Frontal versus Sensorimotor Cortical Contusions

Strain differences in eating and drinking evoked by electrical stimulation of the hypothalamus

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