Unilateral Damage Research Articles

Patterns of ocular oscillation in oculopalatal tremor

To determine patterns of nystagmus in oculopalatal tremor (OPT, also designated oculopalatal myoclonus) and correlate them with MRI changes in the inferior olivary nuclei (ION). Mixed torsional-vertical pendular nystagmus (PN) in OPT has been considered to signify unilateral brainstem damage and symmetric vertical nystagmus considered to indicate bilateral disease. Ocular oscillations were analyzed in 22 patients with OPT, 20 from focal brainstem lesions, with or without cerebellar lesions, and two from the progressive ataxia and palatal tremor syndrome. MRI was performed in all patients. Patients had mainly vertical oscillations with varied combinations of torsional and horizontal components. Fourteen patients had binocular symmetry of PN and eight showed dissociated PN. MRI demonstrated ION signal change, unilateral in 14 and bilateral in eight. Unilateral olivary changes were associated with symmetric PN in six and with dissociated nystagmus in eight patients. Bilateral olivary changes were visible in eight patients with symmetric nystagmus. Dissociated PN was associated with MR pseudohypertrophy of ION on the side of the eye with greater vertical amplitude of oscillation. Notably, four patients never developed palatal tremor despite ION signal change. OPT resolved in one patient after 20 years and was markedly reduced in another patients after 6 years. Dissociated pendular nystagmus predicted asymmetric (unilateral) inferior olivary pseudohypertrophy on MRI with accuracy, but symmetric pendular nystagmus was associated with either unilateral or bilateral signal changes in the inferior olivary nucleus. Instability of eye velocity to position integration from damage to the paramedian tract projections and denervation of the dorsal cap of the inferior olive are proposed mechanisms of the pendular nystagmus.

Association Between Facial Emotion Recognition and Odor Identification in Schizophrenia

The authors examine facial emotion recognition and unirhinal olfactory performance in 19 schizophrenia patients and 14 comparison subjects. In patients, right nostril odor identification performance was positively related to overall emotion recognition accuracy, specifically, sad facial expressions. Olfactory and emotion recognition abilities appear significantly linked in schizophrenia.

Changes in brain functional activation during resting and locomotor states after unilateral nigrostriatal damage in rats

To evaluate functional neuronal compensation after partial damage to the nigrostriatal system, we lesioned rats unilaterally in the striatum with 6-hydroxydopamine. Five weeks later, cerebral perfusion was mapped at rest or during treadmill walking using [14C]-iodoantipyrine. Regional CBF-related tissue radioactivity (CBF-TR) was quantified by autoradiography and analyzed by statistical parametric mapping and region-of- interest analysis. Lesions were confirmed by tyrosine hydroxylase immunohistochemistry and changes in rotational locomotor activity.Functional compensations were bilateral and differed at rest and during treadmill walking. Consistent with the classic view of striatopallidal connections, CBF-TR of lesioned compared to sham-lesioned rats increased in the ipsilateral subthalamic nucleus (STN) and internal globus pallidus, and decreased in the striatum and external globus pallidus. Contrary to the classic view, CBF-TR increased in the ipsilateral ventral lateral, ventral anterior thalamus and motor cortex, as well as in the central medial thalamus, midline cerebellum, and contralateral STN.During walking, perfusion decreased in lesioned compared to sham-lesioned rats across the ipsilateral striato-pallidal-thalamic-cortical motor circuit. Compensatory increases were seen bilaterally in the ventromedial thalamus and red nucleus, in the contralateral STN, anterior substantia nigra, subiculum, motor cortex, and in midline cerebellum. Enhanced recruitment of associative sensory areas was noted cortically and subcortically.Future models of compensatory changes after nigrostriatal damage need to address the effects of increased neural activity by residual dopaminergic neurons, interhemispheric interactions and differences between resting and locomotor states. Identification of sites at which functional compensation occurs may define useful future targets for neurorehabilitative or neurorestorative interventions in Parkinson's disease.

Risk of hypertension in primary vesicoureteral reflux

The aim of this report was to estimate the risk of hypertension in children with primary vesicoureteral reflux (VUR). Between 1970 and 2004, 735 patients were diagnosed with VUR at a single tertiary renal unit. Of 735 patients, 664 (90%) were systematically followed and had multiple measurements of blood pressure. Hypertension was defined as values persistently above 95th for age, sex, and height in three consecutive visits. Risk of hypertension was analyzed by the Kaplan-Meier method. Of 664 patients followed, 20 (3%) developed hypertension. The estimated probability of hypertension was 2% (95%CI, 0.5%-3%), 6% (95%CI, 2%-10%), 15% (95%CI, 11%-20%) at 10, 15, and 21 years of age, respectively. The prevalence of hypertension has increased with age: it was 1.7% for patients with 1 yr-9.9 yr, 1.8% for adolescents with 10 yr-14.9 yr, 4.7% for patients with 15-19.9 yr, and 35% for patients>20 years at the end of the follow-up (P<0.001). It was estimated by survival analysis that 50% of patients with unilateral and bilateral renal damage would have sustained hypertension at about 30 and 22 years of age, respectively. Hypertension increased with age and was strongly associated with renal damage at entry in an unselected population of primary VUR.

Adaptive rescaling of central sensorimotor signals is preserved after unilateral vestibular damage

Adaptive rescaling is a widespread phenomenon that dynamically adjusts the input–output relationship of a sensory system in response to changes in the ambient stimulus conditions. Rescaling has been described in the central vestibular neurons of normal cats. After recovery from unilateral vestibular damage, the vestibulo-ocular reflex (VOR) remains nonlinear for rotation toward the damaged side. Therefore, rescaling in the VOR pathway may be especially important after damage. Here, we demonstrate that central vestibular neurons adjust their input–output relationships depending on the input velocity range, suggesting that adaptive rescaling is preserved after vestibular damage and can contribute to the performance of the VOR. We recorded from isolated vestibular neurons in alert cats that had recovered from unilateral vestibular damage. The peak velocity of 1-Hz sinusoidal rotation was varied from 10 to 120°/s and the sensitivities and dynamic ranges of vestibular neurons were measured. Most neuronal responses showed significant nonlinearities even at the lowest peak velocity that we tested. Significant rescaling was seen in the responses of neurons both ipsilateral and contralateral to chronic unilateral damage. On the average, when the peak rotational velocity increased by a factor of 8, the average sensitivity to rotation decreased by roughly a factor of 2. Rescaling did not depend on eye movement signals. Our results suggest that the dynamic ranges of central neurons are extended by rescaling and that, after vestibular damage, adaptive rescaling may act to reduce nonlinearities in the response of the VOR to rotation at high speeds.

Failure analysis of tempered glass structures with pin-loaded joints

Pin-loaded joints are frequently used to assemble tempered glass plates. To prevent such structures from fracture, a holed glass plate is reinforced by a steel ring and glued to it through a soft resin layer. The present work first models and identifies the mechanical behaviour of the constituent materials and then analyzes the failure process of tempered glass structures with pin-loaded joints, in which unilateral contact, friction, damage and residual stresses are involved. The numerical results obtained by the finite element method are in good agreement with the experimental ones issuing from the real size test.

Abnormal involuntary movements (AIMs) following pulsatile dopaminergic stimulation: Severe deterioration and morphological correlates following the loss of locus coeruleus neurons

Parkinsonian patients are treated with dopamine replacement therapy (typically, intermittent administration of the dopamine precursor l-DOPA); however, this is associated with the onset of abnormal involuntary movements, which seriously impair the quality of life. The molecular mechanisms underlying abnormal involuntary movements represent an intense field of investigation in the area of neurobiology of disease, although their aetiology remains unclear. Apart from the fine cellular mechanisms, the pathways responsible for the generation of abnormal involuntary movements may involve changes in neurotransmitter systems. A potential candidate is noradrenaline, since a severe loss of this neurotransmitter characterizes Parkinson's disease, and noradrenergic drugs produce a symptomatic relief of l-DOPA-induced dyskinesia. In previous studies we found that pulsatile dopamine release, in the absence of the physiological noradrenaline innervation, produces motor alterations and ultrastructural changes within striatal neurons. In the present study we demonstrate that a unilateral damage to the noradrenaline system anticipates the onset and worsens the severity of l-DOPA-induced contralateral abnormal involuntary movements in hemi-parkinsonian rats. Similarly, ubiquitin-positive striatal ultrastructural changes occur in unilaterally dopamine-depleted, noradrenaline-deficient rats following chronic l-DOPA administration. This study confirms a significant impact of the noradrenergic system in the natural history of Parkinson's disease and extends its role to the behavioural and morphological effects taking place during pulsatile dopamine replacement therapy.

Thermographic Assessment of Inferior Alveolar Nerve Injury in Patients With Dentofacial Deformity

The purpose of this study was to evaluate the injury and recovery of the inferior alveolar nerve in orthognathic patients at 1 and 4 weeks after surgery using electronic thermography. Twenty subjects with Class III dentofacial deformity were studied. All patients underwent bilateral sagittal split ramus osteotomy. To image the temperature of the face, 1 anteroposterior view and 1 lateral view were taken from both the right and left sides. Similar images were taken at 1 and 4 weeks after surgery. The control was the presurgical temperature of the 20 patients who showed unilateral or bilateral nerve damage after surgery. In the patients with unilateral nerve damage (n = 14), on the anteroposterior views, the temperatures of the mentum on the 2 sides differed by 0.64 degrees C at 1 week after surgery, and the difference decreased to 0.23 degrees C at 4 weeks after surgery. On the lateral images, the differences in temperature between the mentum areas were 0.10 degrees C at 1 week and 0.27 degrees C at 4 weeks after surgery. In the patients with bilateral nerve injury (n = 6), on the anteroposterior views, the temperatures of the mentum on the 2 sides differed by 0.20 degrees C at 1 week after surgery and 0.13 degrees C after 4 weeks. On the lateral views, the differences were 0.18 degrees C at 1 week and 0.34 degrees C at 4 weeks after surgery. Using the repeated measurement analysis method, the anteroposterior view showed statistically significant results in the patients with unilateral nerve damage. The infrared body temperature method is an objective method that can be applied as a supplemental diagnostic method for inferior alveolar nerve injury.

Abnormalities in skilled reaching movements are improved by peripheral anesthetization of the less-affected forelimb after sensorimotor cortical infarcts in rats

Unilateral damage to sensorimotor cortical (SMC) regions can profoundly impair skilled reaching function in the contralesional forelimb. Such damage also results in impairments and compensatory changes in the less-affected/ipsilesional forelimb, but these effects remain poorly understood. Furthermore, anesthetization of the ipsilesional hand in humans with cerebral infarcts has been reported to produce transient functional improvements in the paretic hand [Floel A, Nagorsen U, Werhahn KJ, Ravindran S, Birbaumer N, Knecht S, et al. Influence of somatosensory input on motor function in patients with chronic stroke. Ann Neurol 2004;56:206–12; Voller B, Floel A, Werhahn KJ, Ravindran S, Wu CW, Cohen LG. Contralateral hand anesthesia transiently improves poststroke sensory deficits. Ann Neurol 2006;59:385–8]. One aim of this study was to sensitively assay the bilateral effects of unilateral ischemic SMC damage on performance of a unimanual skilled reaching task (the single pellet retrieval task) that rats had acquired pre-operatively with each forelimb. The second aim was to determine whether partially recovered contralesional reaching function is influenced by anesthetization of the ipsilesional forelimb. Unilateral SMC lesions were found to result in transient ipsilesional impairments in reaching success and significant ipsilesional abnormalities in reaching movements compared with sham-operates. There were major contralesional reaching impairments which improved during a 4 week training period, but movements remained significantly abnormal. Anesthetization of the ipsilesional forelimb with lidocaine at this time attenuated the contralesional movement abnormalities. These findings indicate that unilateral ischemic SMC lesions impair skilled reaching behavior in both forelimbs. Furthermore, after partial recovery in the contralesional forelimb, additional improvements can be induced by transient anesthetization of the ipsilesional forelimb. This is consistent with the effects of unilateral anesthetization in humans which have been attributed to the modulation of competitive interhemispheric interactions. The present findings suggest that such interactions are also likely to influence skilled reaching function in rats.

Amnesia and the hippocampus

Long-term memory impairments have great medical significance and a considerable health and economic burden. Understanding their cognitive and neuroanatomical underpinnings is of crucial importance. Severe amnesia is usually observed following bilateral hippocampal pathology. This review addresses the precise role of the hippocampus and related medial temporal lobe structures in amnesia. Disagreements exist over whether, following selective hippocampal damage: retrograde amnesia for episodic memories is temporally limited or extensive and ungraded; anterograde amnesia involves both recollective and familiarity processes. It is accepted that material specific impairments follow unilateral medial temporal lobe damage, with verbal and nonverbal memory lateralized to left or right, respectively. Memory for unknown faces, however, may not depend on the hippocampus. Pharmacological studies in animals, with some extension to humans, highlight promising future therapeutic interventions targeting synaptic plasticity modulation. Despite considerable progress, some issues remain unresolved. The available evidence favours the view, however, that the hippocampus, in conjunction with other cortical areas, is critical for the retrieval of remote episodic memories and for both recollection and familiarity anterograde memory processes. There are as yet no effective pharmacological treatments for medial temporal lobe amnesia, but various rehabilitative techniques may be useful.

Bilateral damage to the sexually dimorphic medial preoptic area/anterior hypothalamus of male ferrets causes a female-typical preference for and a hypothalamic Fos response to male body odors

Previous studies showed that bilateral lesions of the male ferret's preoptic area/anterior hypothalamus (POA/AH), centered in the sexually dimorphic nuclei present in this region, caused subjects to seek out a same-sex male, as opposed to a female conspecific. Male subjects with POA/AH lesions (which were also castrated and given estradiol) displayed female-typical receptive behavior in response to neck gripping by a stimulus male, implying that subjects' approaches to a same-sex conspecific were sexually motivated. We asked whether the effect of POA/AH lesions on males' partner preference reflects a shift in the central processing of body odorant cues so that males come to display a female-typical preference to approach male body odorants. Sexually experienced male ferrets in which electrolytic lesions of the POA/AH caused bilateral damage to the sexually dimorphic male nucleus (MN) resembled sham-operated females by preferring to approach body odors emitted from anesthetized male as opposed to female stimulus ferrets confined in the goal boxes of a Y-maze. This lesion-induced shift in odor preference was correlated with a significant increase in the ability of soiled male bedding to induce a Fos response in the medial POA of males with bilateral damage to the MN-POA/AH. No such partner preference or neural Fos responses were seen in sham-operated males or in other groups of males with POA/AH lesions that either caused unilateral damage or no damage to the MN-POA/AH. Male-typical hypothalamic processing of conspecifics' body odorants may determine males' normal preference to seek out odors emitted by female conspecifics, leading to mating and successful reproduction.

The Frontal Cortex and Exogenous Attentional Orienting

Normal functioning of the attentional orienting system is critical for effective behavior and is predicated on a balanced interaction between goal-directed (endogenous) processes and stimulus-driven (exogenous) processes. Although both systems have been subject to much investigation, little is known about the neural underpinnings of exogenous orienting. In the present study, we examined the early facilitatory effects and later inhibition of return effects of exogenous cues in patients with frontal and parietal lesions. Three novel findings emerged from this study. First, unilateral frontoparietal damage appears not to affect the early facilitation effects of exogenous cues. Second, dorsolateral prefrontal damage, especially lesions involving the inferior frontal gyrus, produces an exogenous disengage deficit (i.e., the sluggish withdrawal of attention from the ipsilesional to the contralesional field). Third, a subset of patients with dorsolateral prefrontal damage, with lesions involving the middle frontal gyrus, have a reorienting deficit that extends in duration well beyond established boundaries of the normal reflexive orienting system. These results suggest that the dorsolateral prefrontal cortex plays an important role in exogenous orienting and that component processes of this system may be differentially impaired by damage to different parts of the dorsolateral prefrontal cortex.

Abnormal inhibition of return: A review and new data on patients with parietal lobe damage

The study of the performance of patients with neurological disorders has been fruitful in revealing the nature and neural basis of inhibition of return (IOR). Thus, in recent years, studies have reported abnormal IOR in patients with Alzheimer's disease, patients diagnosed with schizophrenia, and brain-damaged patients. In the present study, we investigated the hypothesis that a spatial “disengagement deficit” (DD; Posner, Walker, Friedrich, & Rafal, 1984) contributed to the pattern of impaired IOR in the ipsilesional field of parietal patients, found in a previous work (Vivas, Humphreys, & Fuentes, 2003). In a first experiment, we replicated the attenuation of IOR for ipsilesional targets on those trials with a lateralized IOR procedure. With stimuli vertically aligned about fixation, we found intact IOR for both up and down targets. Most important, when we ameliorated the potential impact of a spatial DD by presenting both cues and target in the same hemifield, still we found impaired IOR in the ipsilesional field. We interpret these findings in terms of unilateral parietal damage leading to an imbalance of the relative salience of signals represented in a spatial map for directing attention.

Amygdala damage impairs emotion recognition from music

The role of the amygdala in recognition of danger is well established for visual stimuli such as faces. A similar role in another class of emotionally potent stimuli – music – has been recently suggested by the study of epileptic patients with unilateral resection of the anteromedian part of the temporal lobe [Gosselin, N., Peretz, I., Noulhiane, M., Hasboun, D., Beckett, C., & Baulac, M., et al. (2005). Impaired recognition of scary music following unilateral temporal lobe excision. Brain, 128(Pt 3), 628–640]. The goal of the present study was to assess the specific role of the amygdala in the recognition of fear from music. To this aim, we investigated a rare subject, S.M., who has complete bilateral damage relatively restricted to the amygdala and not encompassing other sectors of the temporal lobe. In Experiment 1, S.M. and four matched controls were asked to rate the intensity of fear, peacefulness, happiness, and sadness from computer-generated instrumental music purposely created to express those emotions. Subjects also rated the arousal and valence of each musical stimulus. An error detection task assessed basic auditory perceptual function. S.M. performed normally in this perceptual task, but was selectively impaired in the recognition of scary and sad music. In contrast, her recognition of happy music was normal. Furthermore, S.M. judged the scary music to be less arousing and the peaceful music less relaxing than did the controls. Overall, the pattern of impairment in S.M. is similar to that previously reported in patients with unilateral anteromedial temporal lobe damage. S.M.'s impaired emotional judgments occur in the face of otherwise intact processing of musical features that are emotionally determinant. The use of tempo and mode cues in distinguishing happy from sad music was also spared in S.M. Thus, the amygdala appears to be necessary for emotional processing of music rather than the perceptual processing itself.

Facilitation as well as inhibition of the blink reflex by a visual prepulse requires intact striate cortex

Objective The role of visual cortex in modulation of the human eye blink reflex was assessed. Methods Participants were 13 patients with unilateral striate cortex damage. Nonreflexogenic gratings were presented in their intact or blind hemifield prior to white noise or air puff blink-eliciting stimuli. Results Inhibition of reflex amplitude was observed at asynchronies ranging from about 120 to 600 ms for visible but not invisible prepulses. Facilitation by intact-hemifield gratings was observed for (1) the latency of the acoustic blink reflex, (2) the amplitude of the disynaptic cutaneous blink reflex, R1, and (3) the latency of voluntary hand-grip reactions to the reflexogenic stimuli. These facilitatory effects were absent on trials with blind-hemifield prepulses. Conclusions An intact V1 is required for prepulse facilitation as well as inhibition. Significance These results extend a popular model of sensorimotor gating deficits in schizophrenia.

Visual restoration in cortical blindness: Insights from natural and TMS-induced blindsight

Unilateral damage to visual cortex of the parietal or occipital lobe can cause the patient to be unaware of contralesional visual information due to either hemispatial neglect or hemianopia. It is now known that both neglect and hemianopia result from the disruption of a dynamic interaction between cortical visual pathways and more phylogenetically primitive visual pathways to the midbrain. We consider the therapeutic implications of these cortical–subcortical interactions in the rehabilitation of hemianopia. We start with the pheonmenon of “blindsight”, in which patients with hemianopia can be shown, by implicit measures of visual detection or discrimination, to process visual information without conscious awareness. Some variants of blindsight have been postulated to recruit subcortical processes, while others may reflect compensatory optimisation of processing of spared visual cortex. Both mechanisms may offer opportunities for innovative strategies for rehabilitation of visual field defects. We relate the neural mechanisms that have been proposed to underlie blindsight to those that have been suggested to underlie the recovery of visual function after rehabilitation. It is suggested that the similarity and overlap of the neural processes supporting blindsight and recovery of visual function might provide insights for effective rehabilitation strategies for restoring visual functions.

Left Ipsilesional Neglect for Visual Imagery: A Mental Image Generation Impairment?

In this article, we describe a patient, CN, with unilateral left posterior brain damage, who shows a rare occurrence of left ipsilesional neglect limited to mental representations. CN's clinical pattern is consistent with the hypothesis that different mechanisms underlie perceptual and representational neglect. We also discuss an interpretation of representational neglect based on the different involvement of the two hemispheres in visual imagery processes. In particular, left brain lesions do not present the typical strong contralesional bias and may lead to an impairment of mental generation of either side of the image, depending on pre-morbid and methodological factors. We thank Zorzi, Priftis and Umiltà for making available normative data of the bisection mental line test. Thanks also to Ms. Anna Stone and Rosalind Watling for amending the English of this manuscript. Special thanks to CN.

Social and emotional functions in three patients with medial frontal lobe damage including the anterior cingulate cortex

Introduction. The aim of this study was to explore social and emotional functions in patients with medial frontal damage including the anterior cingulate cortex (ACC). Methods. Three patients with medial frontal lobe lesions primarily involving the ACC performed tasks on motivational decision making, emotional facial expression recognition, and social cognition, including theory of mind (ToM). Their performance on these tasks was compared with age and education matched healthy controls. Results. Patient performance on the motivational decision making and social situations tasks did not differ from controls. Selective emotional facial expression recognition impairment for fear was evident in one patient with a unilateral right ACC lesion (patient 3). ToM impairment was present in only one patient with a bilateral ACC lesion (patient 2). In contrast, the two patients with unilateral right ACC lesions had intact ToM (patients 1 and 3). Conclusions. These findings suggest that medial frontal lobe lesions primarily involving the ACC do not appear to critically disrupt motivational decision making or social situation processing. The ACC plays a role in processing particular types of emotion (fear). Bilateral ACC damage impairs ToM processing, but unilateral damage to the right ACC is not sufficient to disrupt ToM.

Contralesional neural plasticity and functional changes in the less-affected forelimb after large and small cortical infarcts in rats

Some studies have found that unilateral cerebral damage produces significant deficits in the ipsilesional, “less-affected”, body side. Other studies have found that such damage results in a paradoxical hyperfunctionality of the ipsilesional body side and a facilitation of learning-induced neuroplastic changes in the contralesional motor cortex. The purpose of this study was to determine whether these effects co-exist and/or vary with lesion severity. After small or large unilateral ischemic lesions of the sensorimotor cortex (SMC) or sham operations, adult male rats were trained for 20 days to acquire a motor task, skilled reaching for food, for the first time with the ipsilesional forelimb. Analyses of movement patterns indicated lesion-size-dependent ipsilesional abnormalities in grasping, retrieving and releasing food pellets. Despite these impairments, success rates were significantly increased and aiming errors reduced in lesion groups compared with sham operates. Performance was best in rats with small lesions that had more minor ipsilesional impairments. In the motor cortex contralateral to the lesion and trained limb, there were significant increases in the density of dendrites immunoreactive for microtubule-associated protein-2 (MAP2) and of N-methyl- d-aspartate receptor subunit 1 (NMDAR1) immunoreactivity compared with sham operates. These effects were correlated with reaching performance. Therefore, enhanced motor skill learning in the “less-affected” forelimb and contralesional neuroplastic changes are muted after larger lesions and co-exist with ipsilesional impairments. These effects may be related to a denervation-induced neural restructuring of the contralesional cortex that both disrupts pre-existing motor engrams and facilitates the establishment of new ones.

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.