High-resolution intracranial vessel wall MRI in an elderly asymptomatic population: comparison of 3T and 7T.

OBJECTIVES: Several intracranial vessel wall sequences have been described in recent literature, with either 3-T or 7-T magnetic resonance imaging (MRI). In the current study, we compared 3-T and 7-T MRI in visualising both the intracranial arterial vessel wall and vessel wall lesions. METHODS: Twenty-one elderly asymptomatic volunteers were scanned by 3-T and 7-T MRI with an intracranial vessel wall sequence, both before and after contrast administration. Two raters scored image quality, and presence and characteristics of vessel wall lesions. RESULTS: Vessel wall visibility was equal or significantly better at 7 T for the studied arterial segments, even though there were more artefacts hampering assessment. The better visualisation of the vessel wall at 7 T was most prominent in the proximal anterior cerebral circulation and the posterior cerebral artery. In the studied elderly asymptomatic population, 48 vessel-wall lesions were identified at 3 T, of which 7 showed enhancement. At 7 T, 79 lesions were identified, of which 29 showed enhancement. Seventy-one percent of all 3-T lesions and 59 % of all 7-T lesions were also seen at the other field strength. CONCLUSIONS: Despite the large variability in detected lesions at both field strengths, we believe 7-T MRI has the highest potential to identify the total burden of intracranial vessel wall lesions. KEY POINTS: • Intracranial vessel wall visibility was equal or significantly better at 7-T MRI • Most vessel wall lesions in the cerebral arteries were found at 7-T MRI • Many intracranial vessel wall lesions showed enhancement after contrast administration • Large variability in detected intracranial vessel wall lesions at both field strengths • Seven-tesla MRI has the highest potential to identify total burden of intracranial atherosclerosis.

Dissociations between Spatial and Temporal Order Memory: A Neuropsychological Patient Study.

OBJECTIVES: In complex real life situations, memories for temporal and spatial information are naturally linked since sequential events coincide in time and space. Whether this connection is inseparable or instead whether these processes are functionally dissociable was investigated in this patient study. METHODS: Spatial object-location and temporal order memory tasks were administered to 36 stroke patients and 44 healthy control participants. RESULTS: On group level, patients with a stroke in the left hemisphere performed worse on temporal order memory, compared to the control participants. On individual level, using a multiple case-study approach, a clear pattern of dissociations was found between memory for temporal and for spatial features. CONCLUSIONS: These findings indicate that location and temporal order memory contain functionally separable processes. This adds to our understanding of how context information is processed in human memory. (JINS, 2017, 23, 421-430).

Mutations in BICD2, which encodes a golgin and important motor adaptor, cause congenital autosomal-dominant spinal muscular atrophy.

Spinal muscular atrophy (SMA) is a heterogeneous group of neuromuscular disorders caused by degeneration of lower motor neurons. Although functional loss of SMN1 is associated with autosomal-recessive childhood SMA, the genetic cause for most families affected by dominantly inherited SMA is unknown. Here, we identified pathogenic variants in bicaudal D homolog 2 (Drosophila) (BICD2) in three families afflicted with autosomal-dominant SMA. Affected individuals displayed congenital slowly progressive muscle weakness mainly of the lower limbs and congenital contractures. In a large Dutch family, linkage analysis identified a 9q22.3 locus in which exome sequencing uncovered c.320C>T (p.Ser107Leu) in BICD2. Sequencing of 23 additional families affected by dominant SMA led to the identification of pathogenic variants in one family from Canada (c.2108C>T [p.Thr703Met]) and one from the Netherlands (c.563A>C [p.Asn188Thr]). BICD2 is a golgin and motor-adaptor protein involved in Golgi dynamics and vesicular and mRNA transport. Transient transfection of HeLa cells with all three mutant BICD2 cDNAs caused massive Golgi fragmentation. This observation was even more prominent in primary fibroblasts from an individual harboring c.2108C>T (p.Thr703Met) (affecting the C-terminal coiled-coil domain) and slightly less evident in individuals with c.563A>C (p.Asn188Thr) (affecting the N-terminal coiled-coil domain). Furthermore, BICD2 levels were reduced in affected individuals and trapped within the fragmented Golgi. Previous studies have shown that Drosophila mutant BicD causes reduced larvae locomotion by impaired clathrin-mediated synaptic endocytosis in neuromuscular junctions. These data emphasize the relevance of BICD2 in synaptic-vesicle recycling and support the conclusion that BICD2 mutations cause congenital slowly progressive dominant SMA.

Diagnostic criteria for Susac syndrome.

BACKGROUND: Susac syndrome is characterised by the triad of encephalopathy with or without focal neurological signs, branch retinal artery occlusions and hearing loss. Establishment of the diagnosis is often delayed because the triad is complete only in a minority of patients at disease onset. This leads to a critical delay in the initiation of appropriate treatment. Our objective was to establish criteria for diagnosis of either definite or probable Susac syndrome. METHOD: The establishment of diagnostic criteria was based on the following three steps: (1) Definition of a reference group of 32 patients with an unambiguous diagnosis of Susac syndrome as assessed by all interdisciplinary experts of the European Susac Consortium (EuSaC) team (EuSaC cohort); (2) selection of diagnostic criteria, based on common clinical and paraclinical findings in the EuSaC cohort and on a review of the literature; and (3) validation of the proposed criteria in the previously published cohort of all Susac cases reported until 2012. RESULTS: Integrating the clinical presentation and paraclinical findings, we propose formal criteria and recommend a diagnostic workup to facilitate the diagnosis of Susac syndrome. More than 90% of the cases in the literature fulfilled the proposed criteria for probable or definite Susac syndrome. We surmise that more patients could have been diagnosed with the recommended diagnostic workup. CONCLUSIONS: We propose diagnostic criteria for Susac syndrome that may help both experts and physicians not familiar with Susac syndrome to make a correct diagnosis and to prevent delayed treatment initiation.

Early prediction of delayed cerebral ischemia after subarachnoid hemorrhage: development and validation of a practical risk chart.

BACKGROUND AND PURPOSE: To develop and validate a risk chart for prediction of delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage based on admission characteristics. METHODS: For derivation of the risk chart, we studied data from 371 prospectively collected consecutive subarachnoid hemorrhage patients with a confirmed aneurysm admitted between 1999 and 2007. For its validation we similarly studied 255 patients admitted between 2007 and 2009. The predictive value of admission characteristics was tested in logistic regression models with delayed cerebral ischemia-related infarction as primary outcome. Procedure-related infarctions were not included. Performance of the models was tested by discrimination and calibration. On the basis of these models, a risk chart was developed for application in clinical practice. RESULTS: The strongest predictors were clinical condition on admission, amount of blood on computed tomography (both cisternal and intraventricular) and age. A model that combined these 4 predictors had an area under the receiver operating characteristic curve of 0.63 (95% confidence interval, 0.57-0.69). This model improved little by including current smoking and hyperglycemia on admission (area under the receiver operating characteristic curve, 0.65; 95% confidence interval, 0.59-0.71). The risk chart predicted risks of delayed cerebral ischemia-related infarction varying from 12% to 61%. Both low risk (<20% risk) and high risk (>40% risk) were predicted in ≈20% of the patients. Validation confirmed that the discriminative ability was adequate (area under the receiver operating characteristic curve, 0.69; 95% confidence interval, 0.61-0.77). CONCLUSIONS: Absolute risks of delayed cerebral ischemia-related infarction can be reliably estimated by a simple risk chart that includes clinical condition on admission, amount of blood on computed tomography (both cisternal and intraventricular), and age.

Delayed cerebral ischemia after subarachnoid hemorrhage: a systematic review of clinical, laboratory, and radiological predictors.

BACKGROUND AND PURPOSE: Established predictors of delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage are large amounts of extravasated blood and poor clinical condition on admission. The predictive value of other factors is uncertain. METHODS: We searched MEDLINE (1960-2012) for clinical, laboratory, and radiological predictors routinely available within 72 hours after subarachnoid hemorrhage. The studies were categorized according to methodological quality. Crude data and effect estimates (odds ratio [OR], hazard ratios, and risk ratio) with 95% CI were extracted, (re-)calculated and pooled if possible. For every potential predictor we assessed all effect estimates on consistency (point estimates in equal direction) and clinical relevance (size and 95% CI). RESULTS: Fifty-two studies on 33 potential predictors were included. There was strong evidence (≥3 high-quality studies) for a higher risk of delayed cerebral ischemia in smokers (pooled OR, 1.2; 95% CI, 1.1-1.4), and moderate evidence (2 high-quality studies) for an increased risk in patients with hyperglycemia (OR, 3.2; 1.8-5.8 and hazard ratios, 1.7; 1.1-2.5), hydrocephalus (OR, 1.3; 1.1-1.5 and OR, 2.6; 1.2-5.5), history of diabetes mellitus (pooled OR, 6.7; 1.7-26), and early systemic inflammatory response syndrome (pooled OR, 2.1; 1.4-3.3). Evidence was limited for increased risk in women (pooled OR, 1.3; 1.1-1.6) and in patients with history of hypertension (pooled OR, 1.5; 1.3-1.7). The evidence on initial loss of consciousness, history of migraine, previous use of selective serotonin reuptake inhibitors, hypomagnesemia, low hemoglobin, or high blood flow on early transcranial Doppler was also limited. CONCLUSIONS: There is strong evidence that smoking is a predictor of delayed cerebral ischemia. For several other potential predictions the evidence is moderate, limited, or inconsistent.

Glial cell response and microthrombosis in aneurysmal subarachnoid hemorrhage patients: An autopsy study.

Neuroinflammation and microthrombosis may be underlying mechanisms of brain injury after aneurysmal subarachnoid hemorrhage (aSAH), but they have not been studied in relation to each other. In postmortem brain tissue, we investigated neuroinflammation by studying the microglial and astrocyte response in the frontal cortex of 11 aSAH and 10 control patients. In a second study, we investigated the correlation between microthrombosis and microglia by studying the microglial surface area around vessels with and without microthrombosis in the frontal cortex and hippocampus of 8 other aSAH patients. In comparison with controls, we found increased numbers of microglia (mean ± SEM 50 ± 8 vs 20 ± 5 per 0.0026 mm³, p < 0.01), an increased surface area (%) of microglia (mean ± SEM 4.2 ± 0.6 vs 2.2 ± 0.4, p < 0.05), a higher intensity of the astrocytic intermediate filament protein glial fibrillary acidic protein (GFAP) (mean ± SEM 184 ± 28 vs 92 ± 23 arbitrary units, p < 0.05), and an increased GFAP surface area (%) (mean ± SEM 21.2 ± 2.6 vs 10.7 ± 2.1, p < 0.01) in aSAH tissue. Microglia surface area was approximately 40% larger around vessels with microthrombosis than those without microthrombosis (estimated marginal means [95% CI]; 6.1 [5.4-6.9] vs 4.3 [3.6-5.0], p < 0.001). Our results show that the microglial and astrocyte surface areas increased after aSAH and that microthrombosis and microglia are interrelated.

Prothrombotic gene variants and mortality after cerebral ischemia of arterial origin.

BACKGROUND: Several functional prothrombotic gene variants have been associated with cerebral ischemia and myocardial infarction. We hypothesized that such gene variants may also be associated with mortality after cerebral ischemia of arterial origin because of an increased risk of fatal vascular events. METHODS: We performed a case-control study in 316 long-term survivors and 887 patients with recent cerebral ischemia of arterial origin. False discovery rate q values were calculated to account for multiple testing. The mean duration between occurrence of cerebral ischemia and DNA collection was 16.8 years in long-term survivors and 3.2 months in recent patients. RESULTS: Two of 23 variants were associated with mortality: the 95Arg allele of the coagulation factor XIII subunit B (F13B) His95Arg variant (OR, 1.5 for Arg/Arg and His/Arg vs. His/His genotype; 95% CI, 1.1-2.2, q = 0.29) and the 4G allele of the plasminogen activator inhibitor-1 (PAI-1) 4G/5G variant (OR, 1.5 for 4G/4G and 5G/4G vs. 5G/5G genotype; 95% CI, 1.1-2.0, q = 0.29). Both associations disappeared after accounting for multiple testing. Data analysis restricted to recently deceased patients (n = 133) yielded similar results. CONCLUSIONS: In this hospital-based study none of 23 prothrombotic gene variants were associated with long-term mortality after cerebral ischemia of arterial origin. Prothrombotic gene variants do not appear to play an important role in long-term mortality after cerebral ischemia.

Diagnosing delayed cerebral ischemia with different CT modalities in patients with subarachnoid hemorrhage with clinical deterioration.

BACKGROUND AND PURPOSE: Delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage worsens the prognosis and is difficult to diagnose. We investigated the diagnostic value of noncontrast CT (NCT), CT perfusion (CTP), and CT angiography (CTA) for DCI after clinical deterioration in patients with subarachnoid hemorrhage. METHODS: We prospectively enrolled 42 patients with subarachnoid hemorrhage with clinical deterioration suspect for DCI (new focal deficit or Glasgow Coma Scale decrease >or=2 points) within 21 days after hemorrhage. All patients underwent NCT, CTP, and CTA scans on admission and directly after clinical deterioration. The gold standard was the clinical diagnosis DCI made retrospectively by 2 neurologists who interpreted all clinical data, except CTP and CTA, to rule out other causes for the deterioration. Radiologists interpreted NCT and CTP images for signs of ischemia (NCT) or hypoperfusion (CTP) not localized in the neurosurgical trajectory or around intracerebral hematomas, and CTA images for presence of vasospasm. Diagnostic values for DCI of NCT, CTP, and CTA were assessed by calculating sensitivities, specificities, positive predictive values, and negative predictive values with 95% CIs. RESULTS: In 3 patients with clinical deterioration, imaging failed due to motion artifacts. Of the remaining 39 patients, 25 had DCI and 14 did not. NCT had a sensitivity of 0.56 (95% CI, 0.37 to 0.73), specificity=0.71 (0.57 to 0.77), positive predictive value=0.78 (0.55 to 0.91), negative predictive value=0.48 (0.28 to 0.68); CTP: sensitivity=0.84 (0.65 to 0.94), specificity=0.79 (0.52 to 0.92), positive predictive value=0.88 (0.69 to 0.96), negative predictive value=0.73 (0.48 to 0.89); CTA: sensitivity=0.64 (0.45 to 0.80), specificity=0.50 (0.27 to 0.73), positive predictive value=0.70 (0.49 to 0.84), negative predictive value=0.44 (0.23 to 0.67). CONCLUSIONS: As a diagnostic tool for DCI, qualitative assessment of CTP is overall superior to NCT and CTA and could be useful for fast decision-making and guiding treatment.

Object-location memory: a lesion-behavior mapping study in stroke patients.

Object-location memory is an important form of spatial memory, comprising different subcomponents that each process specific types of information within memory, i.e. remembering objects, remembering positions and binding these features in memory. In the current study we investigated the neural correlates of binding categorical (relative) or coordinate (exact) position information with objects in memory. Therefore, an object-location memory battery was used, including different task conditions assessing object-location memory, i.e. memory for position information per se, and binding object information with coordinate and categorical position information. Sixty-one stroke patients with focal brain lesions were examined and compared with 77 healthy matched controls. The lesion subtraction method was used to define the area of overlap. Results indicate an important role of the left posterior parietal cortex in the binding of both categorical and coordinate positions with object information. Additionally, the hippocampus seems important for categorical object-location memory. This suggests that categorical and coordinate object-location memory depend on similar cognitive and neural systems.

Brain areas involved in spatial working memory.

Spatial working memory entails the ability to keep spatial information active in working memory over a short period of time. To study the areas of the brain that are involved in spatial working memory, a group of stroke patients was tested with a spatial search task. Patients and healthy controls were asked to search through a number of boxes shown at different locations on a touch-sensitive computer screen in order to find a target object. In subsequent trials, new target objects were hidden in boxes that were previously empty. Within-search errors were made if a participant returned to an already searched box; between-search errors occurred if a participant returned to a box that was already known to contain a target item. The use of a strategy to remember the locations of the target objects was calculated as well. Damage to the right posterior parietal and right dorsolateral prefrontal cortex impaired the ability to keep spatial information 'on-line', as was indicated by performance on the Corsi Block-Tapping task and the within-search errors. Moreover, patients with damage to the right posterior parietal cortex, the right dorsolateral prefrontal cortex and the hippocampal formation bilaterally made more between-search errors, indicating the importance of these areas in maintaining spatial information in working memory over an extended time period.

Neural correlates of human wayfinding in stroke patients.

Wayfinding is a complex cognitive function involving different types of information, such as knowledge about landmarks and direction information. This variety of processes suggest that multiple neural mechanisms are involved, e.g., the hippocampal system, the posterior parietal and temporal cortical areas. Although patient studies and imaging studies have given important insights in the exact neural circuitry underlying wayfinding, many controversies remain. Therefore, the current study sets out to further examine the neuroanatomical correlates of wayfinding in a sample of 31 stroke patients with unilateral lesions, tested with a series of different wayfinding tasks, including landmark recognition, landmark ordering, route reversal and route drawing. For all patients, the exact location of their lesion was determined using CT or MRI scans. Based on existing literature, a number of relevant brain areas were demarcated, after which the extent of damage to these areas was determined for each patient separately. Performance on the landmark recognition task was impaired by damage to the right hippocampal formation, whereas a weak correlation was found between damage to the dorsolateral prefrontal cortex and processing the order of the landmarks. Several brain areas were found to be involved in retracing a route from the end to the beginning, including the right hippocampal formation, the right posterior parietal cortex, the right dorsolateral prefrontal cortex and the right temporal lobe. Finally, damage to the right temporal lobe impaired the ability to draw the route.

Painful ophthalmoplegia from metastatic nonproducing parathyroid carcinoma: case study and review of the literature.

Parathyroid carcinoma is an uncommon malignancy. Of the fewer than 400 cases reported, most have been cases of producing parathyroid carcinoma with accompanying hypercalcemia. Only 13 patients with nonproducing parathyroid carcinoma have been described. Nine of these 13 patients had metastatic disease. We report a patient with i.c. metastasis. Distal metastases of producing parathyroid carcinoma are treated surgically to prolong survival and prevent complications of hyperparathyroidism and hypercalcemia. One half of the patients with producing parathyroid carcinoma die within 5 years, mostly because of the complications of hypercalcemia. Nonproducing parathyroid carcinoma compares unfavorably with producing parathyroid carcinoma in terms of tumor progression and prognosis. Few data on choice of therapy in nonproducing parathyroid carcinoma are available. We treated our patient with a combination of radiotherapy and chemotherapy. Treatment was followed by an unexpectedly prolonged survival of 31 months after diagnosis of metastatic disease.

Endothelial cell activation after subarachnoid hemorrhage.

OBJECTIVE: Evidence from animal experiments suggests that endothelial cell activation plays a pathogenetic role in the development of cerebral ischemia after subarachnoid hemorrhage (SAH). We measured plasma concentrations of two markers of endothelial cell activation, i.e., ED1-fibronectin (ED1-fn) and von Willebrand factor (vWf), among patients with aneurysmal SAH. We analyzed the relationships of concentrations to initial clinical conditions, treatment modalities, and the occurrence of delayed cerebral ischemia. METHODS: We collected 123 blood samples from 27 patients with aneurysmal SAH. Aneurysms were treated surgically in 19 cases, were treated endovascularly in 7 cases, and remained untreated in 1 case. Twelve patients developed symptomatic delayed cerebral ischemia. RESULTS: Initial concentrations of ED1-fn (4.3 +/- 3.7 microg/ml) and vWf (17.8 +/- 8.2 microg/ml) were higher than the reference values (ED1-fn, 1.7 +/- 0.9 microg/ml, P < 0.001; vWf, 11.5 +/- 5.2 microg/ml, P = 0.003). Concentrations were higher among patients in poor clinical condition at admission, compared with patients in good clinical condition (mean difference, ED1-fn, 5.7 microg/ml, P = 0.04; vWf, 10.4 microg/ml, P = 0.02). Levels of both markers increased significantly after surgery (mean increase, ED1-fn, 7.5 microg/ml, P = 0.01; vWf, 13.2 microg/ml, P = 0.05) and after ischemic episodes (mean increase, ED1-fn, 8.3 microg/ml, P = 0.02; vWf, 5.0 microg/ml, P = 0.04). CONCLUSION: Plasma concentrations of markers of endothelial cell activation were increased early after SAH and were significantly associated with the clinical condition at admission. We also observed a significant increase in concentrations after surgery and after ischemic episodes. Whether endothelial cell activation is a causal or indirectly related factor in the pathogenesis of delayed cerebral ischemia after SAH is still uncertain.

Patterns of intracranial vessel wall changes in relation to ischemic infarcts.

OBJECTIVE: In this retrospective case series study, we used 7.0 tesla MRI to describe patterns of intracranial vessel wall abnormalities in relation to ischemic infarcts in 9 patients with different intracranial vessel wall pathologies. METHODS: A patient-specific clinical imaging protocol was obtained after regular clinical workup, including a fluid-attenuated inversion recovery and an intracranial vessel wall sequence before and after contrast administration using 7.0 tesla MRI. An attempt was made to describe patterns by grouping the patients by intracranial vessel wall abnormalities (eccentric or concentric; enhancing or nonenhancing), then on the presence of macroinfarcts and cortical microinfarcts (CMIs), and lastly on type of macroinfarct (lacunar, small macroinfarct, or large macroinfarct). RESULTS: Intracranial vessel wall abnormalities were identified in all patients, totaling 45 lesions, 12 of which enhanced after contrast administration. CMIs were found in 5 patients. Two patients had eccentric, enhancing wall thickening but differed based on presence or absence of CMIs. Four patients also had eccentric but nonenhancing wall thickening, 2 of whom showed CMIs. The 2 patients lacking CMIs could be subdivided based on the type of macroinfarct. Concentric, enhanced wall thickening was observed in 2 patients with CMIs who differed regarding macroinfarct types. One patient with previous vasculitis showed concentric, nonenhancing wall thickening. CONCLUSION: Our results suggest that the combination of intracranial vessel wall abnormalities and infarct type is related to different stroke etiologies.

Functional correlates of prospective memory in stroke.

INTRODUCTION: Prospective memory is the ability to remember actions to be performed later in time or when a certain event occurs. Multiple cognitive processes are involved in prospective memory, and the degree to which automatic or effortful processes are involved may differ for different types of prospective memory tasks. This study aimed to investigate prospective memory (dys)functioning in stroke patients, and to get more insight in which cognitive processes are involved in time- versus event-based prospective memory. METHODS: We investigated 39 community-dwelling stroke survivors and 53 matched control participants. Assessment included naturalistic and experimental event- and time-based prospective memory tasks, as well as standard neuropsychological measures of (retrospective) memory, processing speed and attention/executive functioning. RESULTS: 41% of the stroke patients performed significantly worse than control participants on prospective memory tasks. Deficits in prospective memory occurred as frequently as impairments in retrospective memory (33%, χ(2)(1, N=39)=3.4, p=.066), and more often than impairments in attention/executive functioning (15%, χ(2)(1, N=39)=5.2, p=.022) and speed of processing (23%, χ(2)(1, N=39)=6.5, p=.011). Regression analyses showed that event-based ('focal') prospective memory is supported by retrospective memory, indicating that it is a relatively simple and automatic process. Time-based (non-'focal') prospective memory proved to be a more complex process, requiring active monitoring of the environment. Performance was predicted by speed of processing, attention/executive functioning and retrospective memory. Thirteen percent of the patients suffered from selective prospective memory impairment, which was associated with damage to the superior temporal gyrus. CONCLUSIONS: Impairment of prospective memory occurs frequently after stroke. Different cognitive operations are involved in distinct types of prospective memory. Results fit within the multi-process framework of prospective memory and help further specify its contents.

Ophthalmic impairment or higher-order visual deficit? Posterior cortical atrophy: a case report.

A 64-year-old man (GK) was referred to our memory clinic because of progressive memory and concentration problems. His symptoms had started 3 years earlier with gradually increasing visual problems for which no ophthalmologic explanations could be found. Neuropsychological assessment with detailed examination of the visuoperception revealed striking impairments in the higher-order visual functions, leading to a probable diagnosis of posterior cortical atrophy (PCA). The results of magnetic resonance imaging and cerebrospinal fluid examination supported the diagnosis. PCA is considered the posterior variant of Alzheimer's disease that typically presents with problems in visuoperception or, less frequent, apraxia. Despite its clear clinical features, the diagnosis of PCA is often delayed because of the focus on ophthalmologic examination. In this case report, the diagnosis of PCA in a 64-year-old man was not considered until further neuropsychological decay was evident. We argue that screening of higher-order visual functions can significantly contribute to an early diagnosis and treatment of PCA.

The effect of stimulus features on working memory of categorical and coordinate spatial relations in patients with unilateral brain damage.

Spatial relations are typically divided into categorical and coordinate spatial relations. Categorical relations are abstract and show a left hemisphere (LH) advantage, whereas coordinate relations are metric and related to a right hemisphere (RH) advantage. In the current study a working memory task was used to asses categorical and coordinate performance with two different stimulus sets. In this task, participants had to compare two sequentially presented stimuli, consisting of a dot and a cross. The cross size used in the stimuli was either large or small; a direct manipulation of the amount of information provided to determine a category, or to assess a distance. Patients with damage in the LH or the RH and highly comparable controls were tested. In control participants, categorical processing is faster with the use of a large cross, i.e., more visual information about category boundaries. In contrast, coordinate performance was more accurate with a small cross, i.e., presenting less unnecessary visual information. LH patients showed a specific defect in processing categorical stimuli with a small cross and coordinate stimuli with a large cross. The RH patients were impaired in all conditions except for the categorical small cross condition. We conclude that a larger amount of information present in stimuli increases categorical processing performance and decreases coordinate processing performance, while opposite effects are found for less stimulus information.