Spatial Working Memory Deficits Research Articles

Spatial working memory deficits in adolescents at clinical high risk for schizophrenia

Identifying endophenotypic markers is crucial to schizophrenia research for finding appropriate preventive strategies. Working memory (WM) deficit has been suggested as a marker for schizophrenia but its presence in adolescents at high risk is understudied. We piloted a test of spatial WM function in adolescents at clinical high risk (CHR) for schizophrenia and in age- and IQ-matched low-risk control subjects. CHR adolescents showed deficits in spatial WM compared with controls but showed intact performance on a non-WM-demanding spatial control task. Although based on a small pilot study, the results strongly suggest that WM deficit may be a risk factor for psychosis.

Revisiting unilateral neglect

Unilateral neglect, a neurological disorder in which patients fail to detect or respond to contralesional stimuli, has long been considered a failure of attentional orienting mechanisms. This review provides a selective overview of the prominent biases in spatial orienting and exploratory motor behaviour observed in these patients before considering the impact of other factors on the presentation of the disorder and how those factors might inform current neurological models of neglect. In the latter part of the review, we intend to suggest that neglect is likely to be a combination of distinct but interacting impairments including biases in attentional orienting, exploratory motor behaviours and a deficit of spatial working memory. That is, we suggest that the cardinal symptom of neglect – a loss of awareness for contralesional stimuli and events – arises as a result of a combination of these impairments rather than being associated solely with the more dramatic and immediately evident biases in spatial attention.

Dissociation between physical and mental number line bisection in right hemisphere brain damage

To compare numeric quantities, humans make use of a 'mental number line' with smaller quantities located to the left of larger ones; it is unclear, however, whether orienting along the number line is like orienting along a physical line. We found that in brain-damaged subjects with defective leftward orienting, rightward deviation in the bisection of numeric and physical intervals is doubly dissociated. Deviation in numeric interval bisection was associated with prefrontal damage and spatial working memory deficit.

Deficits of visual search and spatial working memory after cerebellar infarction

In recent studies the cerebellum has been discussed to be involved not only in motor but also in cognitive functions. Particularly in fronto-executive functions patients with cerebellar lesions showed deficits. Similar to a previous study on hemi-neglect patients, 3 visual search tasks (implying feature and conjunction search for colour and shape) was applied to investigate 8 patients with isolated infarction of the cerebellum compared to a group of 10 age-matched controls. The cerebellar patients showed longer search durations, associated with a higher number of repeated saccades towards the same items. Systematic geometric search strategies were similar in both groups. Concluding, basic mechanisms of visual search are not affected by cerebellar lesions while patients' search behaviour is generally less efficient, due to redundant saccades, indicating a mild deficit of spatial working memory.

Septal co-infusions of glucose with a GABA B agonist impair memory

Septal infusions of glucose exacerbate memory deficits produced by co-infusions of drugs that increase γ-aminobutyric acid (GABA) A receptor activity. To further understand the interaction between glucose and GABA, this experiment tested whether glucose would also potentiate spatial working memory deficits produced by septal infusions of the GABA B receptor agonist baclofen. Fifteen minutes prior to assessing spontaneous alternation (SA), male Sprague–Dawley derived rats were given septal infusions of vehicle, glucose (33 nmol), baclofen (0.1 nmol), or glucose combined with baclofen in one solution. Septal co-infusions of glucose with baclofen, at doses that individually had no effect, significantly impaired SA. Thus, the memory-impairing effects of glucose are observed with either GABA A or GABA B receptor ligands. This raises the possibility that glucose may impair memory by increasing synaptic levels of GABA and subsequent activation of these different receptor subtypes. These effects of glucose could contribute to the memory-impairing effects of hyperglycemia.

Generalized and Specific Cognitive Performance in Clinical High-Risk Cohorts: A Review Highlighting Potential Vulnerability Markers for Psychosis

Cognitive deficits are a core feature of established psychotic illnesses. However, the association between cognition and emerging psychosis is less understood. While there is some evidence that cognitive deficits are present prior to the onset of psychosis, findings are not consistent. In this article we provide an overview of the more general cognitive findings available from genetic high-risk studies, retrospective studies, and birth cohort studies. We then focus the review on neuropsychological performance in clinically "at-risk" groups. Overall, general cognitive ability as assessed by established batteries appears to remain relatively intact in these ultra-high risk cohorts and is a poor predictor close to illness onset relative to other vulnerability factors. Further decline may occur with illness progression, more consistent with state relative to trait factors. In addition, most established cognitive tasks involve several relatively discrete cognitive subprocesses, where findings from general batteries of subtests may mask specific deficits. In this context, our review suggests that relatively specific olfactory identification and spatial working memory deficits exist prior to illness onset and may be more potent trait markers for psychosis than cognitively dense tasks such as verbal memory. Suggestions for further research address the importance of standardization of inclusion criteria and the maintenance of basic neuropsychological assessment to allow better comparison of findings across centers. Further, in order to better understand the aetiopathology of cognitive dysfunction in psychosis, more experimental, hypothesis-driven measures of discrete cognitive processes are required. Delineation of the relationship between specific cognitive ability and symptoms from data-driven approaches may improve our understanding of the role of cognition during psychosis onset.

Spatial Working Memory Function in Twins with Schizophrenia and Bipolar Disorder

Family studies are in conflict as to whether schizophrenia and bipolar disorder have independent genetic etiologies. Given the relatively low prevalence (approximately 1%) of these disorders, the use of quantitative endophenotypic markers of genetic liability might provide a more sensitive strategy for evaluating their genetic overlap. We have previously demonstrated that spatial working memory deficits increase in a dose-dependent fashion with increasing genetic proximity to a proband among the unaffected co-twins of schizophrenic patients. Here, we evaluated whether such deficits might also mark genetic susceptibility to bipolar disorder. The Wechsler Memory Scale-Revised Visual Memory Span and Digit Span subtests were administered to 46 schizophrenic patients, 32 of their unaffected co-twins, 22 bipolar patients, 16 of their unaffected co-twins, and 100 control twins, representing unselectively nationwide twin samples. Schizophrenic patients and their unaffected co-twins performed significantly worse than control subjects on the spatial working memory task, whereas only the schizophrenic patients performed significantly below the control subjects on the verbal working memory task. Neither bipolar patients nor their unaffected co-twins differed from control subjects on these measures. Our findings support the hypothesis that impairment in spatial working memory might effectively reflect an expression of genetic liability to schizophrenia but less clearly to bipolar disorder.

Visual spatial and visual pattern working memory: Neuropsychological evidence for a differential role of left and right dorsal visual brain

According to neurophysiological, neuroimaging, and behavioural evidence, visual working memory (WM) can be separated into a “what” and a “where” component, reflecting the duality of visual processing. Whereas a wealth of empirical data suggests a right-sided fronto-parietal network critical for the maintenance of spatial information, the cortical structures underlying maintenance of object information have remained controversial. Although visual object processing depends on ventral, inferior temporal areas, recent neuroimaging results suggest that maintenance of visual object information involves a left-sided or bilateral fronto-parietal network. The aim of the present study is to further clarify the role of the left and right parietal lobes for pattern and spatial visual WM. Seven patients with left-sided, seven with right-sided parietal brain injury, and two age-matched healthy control groups performed a delayed-matching-to-sample task using either pattern (shape) or spatial (location) information or both. In addition, eight patients with left-sided injury sparing parietal areas were tested to further examine the specific role of the left parietal cortex in pattern WM. Left parietal injury resulted in pattern WM impairment, only, while right parietal injury was associated with pattern and spatial WM deficits. Non-parietal injury was not associated with comparable deficits. These results suggest that visual spatial WM depends critically on right parietal areas; in contrast, pattern WM depends on both, left and right parietal areas.

Spatial working memory deficit correlates with disorganization symptoms and social functioning in schizophrenia

Both spatial working memory deficit and disorganization symptoms have been considered significant components of schizophrenic impairment involved with the dorsolateral prefrontal cortex. The purpose of the present study was to investigate the relationships among spatial working memory, psychiatric symptoms including disorganization symptoms, and social functioning in schizophrenia. Fifty clinically stable patients with schizophrenia and 34 healthy controls participated in the study. Patients were rated with the Brief Psychiatric Rating Scale and the Rehabilitation Evaluation Hall and Baker. The Advanced Trail Making Test was used to evaluate spatial working memory. Patients demonstrated significantly reduced spatial working memory compared to that of healthy controls. Spatial working memory in patients correlated significantly with social functioning such as self-care skills, community skills and speech disturbance, and with disorganization symptoms. Disorganization symptoms also correlated with these aspects of social functioning. In conclusion it is suggested that both spatial working memory deficit and disorganization symptoms, which are impairments involved with the dorsolateral prefrontal cortex dysfunction, can serve as effective predictors of social functioning.

Abnormal auditory N400 in a case of zolpidem dependence, during a working memory test

Zolpidem is a GABA (A) agonist, which is indicated for the short-term management of insomnia. Recent research provide evidence suggesting that zolpidem produces spatial working memory (WM) deficits and dependence; however, the underlying mechanisms of these effects are unknown. Since the auditory N400 component of event-related potentials (ERPS) is considered as an index of memory use of context processing, the present study focused on N400 waveform of ERPs elicited during a WM task in a case suffering from zolpidem dependence. The patterns of N400 waveform of this case were compared to the patterns obtained from healthy controls. This comparison revealed that zolpidem dependence is accompanied by reduced amplitudes located at posterior brain areas and diffuse prolongation of N400. These findings may indicate that zolpidem dependence manifests alterations with regard to the memory use of context processing, involving or affecting a wide-ranging network of the brain's structures.

Alpha-2 Adrenoceptor Activation Inhibits Phencyclidine-Induced Deficits of Spatial Working Memory in Rats

N-methyl-D-aspartate (NMDA)/glutamate receptor antagonists, such as phencyclidine (PCP), induce behavioral abnormalities (locomotor hyperactivity, sensorimotor gating deficits, impairments of cognition) in animals that are thought to model aspects of schizophrenia. The administration of PCP increases noradrenaline transmission in the rat prefrontal cortex, a brain structure required for normal cognitive processes. Noradrenaline, in turn, works through a set of receptors that have themselves been implicated directly in NMDA antagonist-induced deficits; we recently reported that the alpha-2 agonist, clonidine, is effective at preventing PCP-induced deficits of working memory and visual attention in rats. Here, we further investigated the role for alpha-2 adrenoreceptors in the effects of PCP on spatial working memory performance. The alpha-2 agonist clonidine (0.001-0.01 mg/kg, subcutaneously (s.c.)) produced a significant amelioration of PCP-induced working memory deficits; the effects of PCP (1.0 mg/kg, s.c.), but not clonidine, were reduced in noradrenaline-depleted rats. In addition, the alpha-2A-preferring agonist guanfacine (0.05-1.0 mg/kg, s.c.) dose-dependently prevented the deficits of spatial working memory performance produced by PCP. Although the highly selective alpha-2 receptor antagonist, atipamezole (ATI), failed to affect spatial working memory on its own, at the doses studied (0.1-0.5 mg/kg, s.c.), it dramatically enhanced the working memory deficit produced by PCP. These data indicate that alpha-2 adrenoreceptors tonically inhibit PCP-induced deficits of spatial working memory, suggesting an important role for these receptors in cognitive deficits associated with NMDA receptor hypofunction.

Orexin-saporin lesions of the medial septum impair spatial memory

The medial septum and diagonal band of Broca (MSDB) provide a major input to the hippocampus and are important for spatial learning and memory. Although electrolytic MSDB lesions have prominent memory impairing effects, selective lesions of either cholinergic or GABAergic MSDB neurons do not or only mildly impair spatial memory. MSDB neurons are targets of orexin-containing neurons from the hypothalamus. At present, the functional significance of orexin afferents to MSDB is unclear, and the present study investigated a possible involvement of orexin innervation of the MSDB in spatial memory. Orexin-saporin, a toxin that damages neurons containing the hypocretin-2 receptor, was administered into the MSDB of rats. Rats were subsequently tested on a water maze to assess spatial reference memory and a plus maze to assess spatial working memory. At 100 ng/μl, orexin-saporin destroyed primarily GABAergic septohippocampal neurons, sparing the majority of cholinergic neurons. At 200 ng/μl, orexin-saporin almost totally eliminated GABAergic septohippocampal neurons and destroyed many cholinergic neurons. Spatial reference memory was impaired at both concentrations of orexin-saporin with a dramatic impairment observed for 24-h retention. Short-term reference memory was also impaired at both concentrations. Rats treated with 200 ng/μl, but not 100 ng/μl, of orexin-saporin were also impaired on a spontaneous alternation task, showing a deficit in spatial working memory. Our results, together with previous studies, suggest that orexin innervation of the MSDB may modulate spatial memory by acting on both GABAergic and cholinergic septohippocampal neurons.

Genetic ablation of the mammillary bodies in the Foxb1 mutant mouse leads to selective deficit of spatial working memory

Mammillary bodies and the mammillothalamic tract are parts of a classic neural circuitry that has been implicated in severe memory disturbances accompanying Korsakoff's syndrome. However, the specific role of mammillary bodies in memory functions remains controversial, often being considered as just an extension of the hippocampal memory system. To study this issue we used mutant mice with a targeted mutation in the transcription factor gene Foxb1. These mice suffer perinatal degeneration of the medial and most of the lateral mammillary nuclei, as well as of the mammillothalamic bundle. Foxb1 mutant mice showed no deficits in such hippocampal-dependent tasks as contextual fear conditioning and social transmission of food preference. They were also not impaired in the spatial reference memory test in the radial arm maze. However, Foxb1 mutants showed deficits in the task for spatial navigation within the Barnes maze. Furthermore, they showed impairments in spatial working memory tasks such as the spontaneous alternation and the working memory test in the radial arm maze. Thus, our behavioural analysis of Foxb1 mutants suggests that the medial mammillary nuclei and mammillothalamic tract play a role in a specific subset of spatial tasks, which require combined use of both spatial and working memory functions. Therefore, the mammillary bodies and the mammillothalamic tract may form an important route through which the working memory circuitry receives spatial information from the hippocampus.

Spatial working memory capacity in unilateral neglect

It has been proposed recently that a deficit in keeping track of spatial locations may contribute to the severity of unilateral neglect in some right hemisphere stroke patients. However, performance on traditional spatial working memory (SWM) tasks (e.g. Corsi blocks) might be confounded by failure to encode leftward locations, rather than a true deficit of maintaining locations in SWM. Here we introduced new procedures for circumventing this to measure SWM capacity in neglect. In a first experiment, 20 right hemisphere stroke patients (10 with and 10 without neglect) were tested on a computerized vertical variant of the Corsi task. Sequences of spatial locations in a vertical column were displayed and participants had to tap out the remembered sequence on a touchscreen. Patients with left neglect were impaired on this vertical SWM task compared with all control groups. However, poor performance on this task (as for Corsi blocks) might involve impaired memory for stimulus sequence, or poor visuomotor control of manual responding, rather than reduced SWM capacity per se. A second experiment therefore employed a purer measure of vertical SWM. After the displayed sequence, a single location was now probed visually, with observers judging verbally (yes/no) if it had been in the preceding sequence. Hence order no longer mattered, and no spatial motor response was required. Again, the neglect group was impaired relative to all others, now with very little overlap between the performances of individual neglect patients versus individuals in control groups. Poor performance on the second task, which provides a purer measure of SWM capacity, correlated with severity of left neglect on cancellation tasks (but not on line bisection), consistent with recent proposals that SWM deficits can exacerbate left neglect on visual search tasks when present conjointly. Lesion anatomy indicated that neglect patients with a SWM deficit were most likely to have damage to parietal white matter, plus, in the second experiment, to the insula also. These findings demonstrate that an impairment in SWM capacity can contribute to the neglect syndrome in patients with stroke involving regions within the right parietal lobe and insula.

Deficits in saccadic eye-movement control in Parkinson's disease

In contrast to their slowed limb movements, individuals with Parkinson's disease (PD) produce rapid automatic eye movements to sensory stimuli and show an impaired ability to generate voluntary eye movements in cognitive tasks. Eighteen PD patients and 18 matched control volunteers were instructed to look either toward (pro-saccade) or away from (anti-saccade) a peripheral stimulus as soon as it appeared (immediate, gap and overlap conditions) or after a variable delay; or, they made sequential saccades to remembered targets after a variable delay. We found that PD patients made more express saccades (correct saccades in the latency range of 90–140 ms) in the immediate pro-saccade task, more direction errors (automatic pro-saccades) in the immediate anti-saccade task, and were less able to inhibit saccades during the delay period in all delay tasks. PD patients also made more directional and end-point errors in the memory-guided sequential task. Their inability to plan eye movements to remembered target locations suggests that PD patients have a deficit in spatial working memory which, along with their deficit in automatic saccade suppression, is consistent with a disorder of the prefrontal-basal ganglia circuit. Impairment of this pathway may release the automatic saccade system from top-down inhibition and produce deficits in volitional saccade control. Parallel findings across various motor, cognitive and oculomotor tasks suggest a common mechanism underlying a general deficit in automatic response suppression.

Principles of Experimental Psychopathology: Essays in Honor of Brendan A. Maher

Back to table of contents Previous article Next article Book Forum: PsychologyFull AccessPrinciples of Experimental Psychopathology: Essays in Honor of Brendan A. MaherLAURA A. FLASHMAN, Ph.D., LAURA A. FLASHMANSearch for more papers by this author, Ph.D., Lebanon, N.H.Published Online:1 Aug 2004https://doi.org/10.1176/appi.ajp.161.8.1515AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail This book examines, in a broadly defined way, the work of Brendan A. Maher, Ph.D., the Edward C. Henderson Professor of the Psychology of Personality, Department of Psychology, Harvard University. For those unfamiliar with Dr. Maher’s work, he is a primary architect of experimental psychopathology, a leading scholar in schizophrenia research, a teacher and mentor of many, and an academic statesman-at-large. The book is a Festschrift, referring directly to Brendan Maher’s methodological contributions to the study of mental illness and alluding to his landmark book on the topic (1), supported in part by the American Psychological Association Science Conference and the Decade of the Brain series.The book is composed of chapters written by prominent scholars and researchers who have had the opportunity to work with Dr. Maher as colleagues, collaborators, and former students, as well as a chapter by Dr. Maher himself. Early on in his career, Dr. Maher established that, despite the challenges encountered in working in the field of psychopathology, methodological concerns applied to this field were not inherently different from the principles already worked out in the experimental laboratory. By continuing to focus on the questions of how one conducts a particular study and how to measure the phenomenon of interest, empirical study of issues in experimental psychopathology has become more methodologically rigorous and scientifically sound. The contributing authors not only explain how Dr. Maher’s work and ideas have contributed to the development of their own research efforts but also describe the broader impact he has had on those who have had the privilege of knowing him personally.The volume is divided into five parts. The first part is written by Dr. Maher himself and contains a discussion of his views on delusional thought and the methodological approach he has taken to study these beliefs. Many of his methodological principles are described; these lay the groundwork for the other parts of the book. In the second section, a variety of scholars who have worked with Dr. Maher describe their work in schizophrenia. Topics include genetics (Gottesman and Reilly), motor dysfunction (Manschreck), neuromotor abnormalities (Dworkin et al.), spatial working memory deficits (Park and Lee), and models of vocational support (Blyler) in the emergence and development of schizophrenia.Part 3 includes chapters with distinct methodological foci, with an emphasis on the methodology of interest within the context of schizophrenia research. These include chapters on the study of neuropsychological function (Strauss and Summerfelt), signal-detection-based assessment of somatosensory dysfunction (Lenzenweger et al.), and pain insensitivity (Hooley and Chung). Part 4 describes methodological and technological advances in the study of psychopathology, including reductivism (Holzman), event-related brain potentials (Deldin et al.), magnetic resonance methods (Yurgelun-Todd and Gruber), and functional neuroimaging of working memory (Manoach). Part 5 concludes with three chapters related to temperament (one by Kagan and one by Fowles) and cognition (McNally) in experimental psychopathology and developmental psychological sciences.In the introduction, the editors state,Thirty-five years ago, Maher urged psychopathologists to bring psychopathology into the laboratory with the hope that the power of experimental methods…might help researchers resolve more clearly a variety of fundamental processes in the study of mental illness. In so doing, his vision helped transform the manner in which psychopathology research was carried out. It continues to implicitly guide the manner in which experimental psychopathology research is conducted, regardless of one’s specific focus. We believe that the chapters in this volume celebrate the spirit and implementation of that seminal vision. (p. 6)They do! In addition, they celebrate the spirit and influence of a wonderful man, with warm tributes and charming and amusing anecdotes related to both professional and personal development of those with whom he has come in contact. The editors should be very proud—this Festschrift accomplishes its goal with a perfect blend of autobiography, science, and real-world implications.Edited by Mark F. Lenzenweger, Ph.D., and Jill M. Hooley, D.Phil. Washington, D.C., American Psychological Association, 2003, 472 pp., $49.95.Reference1. Maher B: Principles of Psychopathology: An Experimental Approach. New York, McGraw-Hill, 1968Google Scholar FiguresReferencesCited byDetailsCited ByNone Volume 161Issue 8 August 2004Pages 1515-1515 Metrics PDF download History Published online 1 August 2004 Published in print 1 August 2004

The effects of ethanol and silymarin treatment during gestation on spatial working memory.

BackgroundUsing a rat model we have found that the bioflavonoid silymarin (SY) ameliorates some of the negative consequences of in utero exposure to ethanol (EtOH). In the current study our aim was to determine if spatial working memory (SWM) was impaired in offspring whose mothers were maintained on a liquid diet containing EtOH during different gestational weeks. We also determined if SWM was altered with a concomitant administration of SY with EtOH during specific gestational weeks.MethodsWe provided pregnant Fischer/344 rats with liquid diets containing 35% EtOH derived calories (EDC) during specific weeks of the gestational period. A silymarin/phospholipid compound containing 29.8% silybin co-administered with EtOH was also administered during specific weeks of the gestational period. We tested SWM of the offspring with a radial arm maze on postnatal day (PND) 60. After testing the rats were sacrificed and their brains perfused for later analysis.ResultsWe observed SWM deficits, as well as a significantly lower brain weight in female offspring born of mothers treated with EtOH during the third week of gestation in comparison to mothers treated during either the first or second weeks of gestation. Rats from any group receiving EtOH in co-administration with SY showed no significant deficits in SWM.ConclusionEtOH treatment during the last week of gestation had the greatest impact on SWM. The addition of SY to the EtOH liquid diet appeared to ameliorate the EtOH-induced learning deficits.

An investigation of the effect of tacrine and physostigmine on spatial working memory deficits in the olfactory bulbectomised rat

The olfactory bulbectomised (OB) rat is being increasingly used as a model of impaired learning and mnemonic functioning. In this study the model has been utilised to determine the effect of the acetylcholinesterase inhibiting compounds tacrine and physostigmine on spatial working memory deficits associated with the OB rat. One-hundred and twenty male rats were randomly allocated to OB or sham operated groups and received chronic i.p. treatment with either saline, physostigmine (0.1 mg/kg) or tacrine (0.1 and 0.3 mg/kg). Two weeks after beginning treatment animals were tested on the Morris water maze and open field test. The results indicated that the OB surgery was associated with spatial working memory disturbances that were effectively attenuated with both doses of tacrine, but not physostigmine. Increased hyperactivity and defacation was observed in OB animals in the Open-field test, however, these changes were not ameliorated by either drug treatment. The ability for tacrine but not physostigmine to attenuate OB cognitive deficits may be associated with the different half-life of these compounds. This study provides further support for the use of the OB rat as a drug discovery model for the investigation of novel therapeutic compounds that target the cholinergic system.

Impaired Spatial Working Memory: One Component of the Visual Neglect Syndrome?

Both impaired spatial working memory (SWM) and unilateral neglect may follow damage to the right parietal lobe. We propose that impaired SWM can exacerbate visual neglect, due to failures in remembering locations that have already been searched. When combined with an attentional bias to the ipsilesional right side, such a SWM impairment should induce recursive search of ipsilesional locations. Here we studied a left neglect patient with a right temporoparietal haemorrhage. On a nonlateralised, purely vertical SWM task, he was impaired in retaining spatial locations. In a visual search task, his eye position was monitored while his spatial memory was probed. He recursively searched through right stimuli, re-fixating previously inspected items, and critically treated them as if they were new discoveries, consistent with the SWM deficit. When his recovery was tracked over several months, his SWM deficit and left neglect showed concurrent improvements. We argue that impaired SWM may be one important component of the visual neglect syndrome.

Impaired Working Memory for Location but not for Colour or Shape in Visual Neglect: a Comparison of Parietal and Non-Parietal Lesions

Patients with spatial neglect due to right hemisphere pathology may show ‘revisiting’ behaviour during visual search and cancellation tasks, such that previously encountered targets are treated as if they are new discoveries. Revisiting behaviour is particularly evident when no visible trace is left to inform patients that a particular target has already been detected (Husain et al., 2001; Wojciulik et al., 2001), implying that spatial working memory may be impaired in neglect. To test whether working memory for location is selectively impaired relative to memory for colour and shape, we compared performances of right hemisphere neglect patients with parietal (n = 4) and non-parietal (n = 4) lesions on a change detection task. Patients were presented with a matrix containing four objects in different positions, and required to detect a change in the location, colour or shape of one of the objects following presentation of a brief visual mask. Parietal patients were selectively impaired in detecting location changes, regardless of the horizontal position of the object in the matrix, relative to colour and shape changes. This deficit of spatial working memory was not apparent for neglect patients with lesions that spared the parietal cortex. We conclude that the human parietal cortex is crucially involved in the updating and maintenance of spatial representations across saccades, and that neglect arising from parietal damage causes impairment in these re-mapping mechanisms.