Visuospatial Deficits Research Articles

Working memory impairment in aphasia: The issue of stimulus modality

Abstract The presence of short-term/working memory deficits in aphasia has been well-established in the relevant literature. Moreover, recent studies have demonstrated such deficits in both the verbal and visuospatial modalities in patients with aphasia following a left hemisphere stroke. The present study aims to investigate the prevalence and possible lesion correlates of modality-dependent and modality-independent short-term/working memory impairment in aphasia. For this purpose, 54 individuals with post-stroke aphasia were recruited. Aphasic disturbances were assessed with the Boston Diagnostic Aphasia Examination (BDAE) and memory deficits with the digit span and Corsi block-tapping tasks. Structural imaging data were obtained for each patient and lesion sites were identified and coded by two independent neuroradiologists for 16 predetermined left hemisphere areas. Results clearly showed that visuospatial deficits were relatively common, even though verbal deficits are more frequent, and further illustrate the existence of distinct performance patterns within each modality. Analyses revealed comparable lesion extent and locations between patients demonstrating modality-independent and patients demonstrating modality-dependent deficits. Hierarchical regression analyses indicated that deficient performance on digit span forward, indicating impaired verbal short-term memory, was associated with lesions encompassing the inferior frontal gyrus and the inferior parietal cortex. Similar analyses for digit span backward, and the two conditions of Corsi did not yield significant results. However, behavioral data indicate a dissociation between forward and backward visuospatial span, which could be explained by selectively impaired primacy and recency effects. The emergence of modality-dependent and modality-independent deficits is further discussed in relation to hemispheric lateralization during the course of human evolution.

Role of the left hemisphere in visuospatial working memory.

Visuospatial processing deficits are typically associated with damage to the right hemisphere. However, deficits on spatial working memory have been reported among some individuals with focal left hemisphere damage (LHD). It has been suggested that the left hemisphere may play a role in such non-verbal working memory tasks due to the use of subvocal, verbally-mediated strategies. The current study investigated the role of the left hemisphere in spatial working memory by testing spatial span performance, both forward and backward, in a large group of individuals with a history of left hemisphere stroke. Our first aim was to establish whether individuals with LHD are indeed impaired on spatial span tasks using standardized span tasks with published normative data. Our second aim was to identify the role that language plays in supporting spatial working memory by comparing LHD individuals with and without aphasia, and by relating spatial span performance to performance on a series of language measures. Our third aim was to identify left hemisphere brain regions that contribute to spatial working memory using voxel-based lesion symptom mapping (VLSM), a whole-brain statistical approach that identifies regions critical to a particular behavior on a voxel-by-voxel basis. We found that 28% of individuals with LHD performed in the clinically-impaired range on forward spatial span and 16% performed in the clinically-impaired range on backward spatial span. There were no significant differences in performance between individuals with and without aphasia, and there were no correlations between spatial span performance and language functions such as repetition and comprehension. The VLSM analysis showed that backward spatial span was associated with a left fronto-parietal network consisting of somatosensory cortex, the supramarginal gyrus, lateral prefrontal cortex, and the frontal eye fields. Regions identified in the VLSM analysis of forward spatial span did not reach the conservative statistical threshold for significance. Overall, these results suggest that spatial working memory, as measured by spatial span, can be significantly disrupted in a subset of individuals with LHD whose lesions infringe on a network of regions in the left hemisphere that have been implicated in domain-general working memory and attentional control mechanisms.

0679 Impaired Visual Processing In Rbd Patients: A Visual Search Task Study

Rapid Eye Movement (REM) sleep Behavior Disorder (RBD) is a REM sleep parasomnia known to be strongly associated with the development of neurodegenerative disorders. Cognitive deterioration has been shown to be a common issue in RBD patients, in particular impairments in visuo-spatial abilities. However, little is known about the effect of RBD on visual processing. The aim of this study was to evaluate the basic mechanisms of stimulus analysis in RBD patients by a visual search paradigm. 12 RBD patients (mean age: 68.25 ± 9.63, 9 males) and 12 age-matched healthy controls (HC) were enrolled in the study. After a nocturnal video-polysomnographic recording, patients performed a visual search task in which they had to detect the presence/absence of a target (letter T) embedded in the 50% of trials into a set of distractors (letters Os, Xs, or Ls). Target’s salience and distractors’ numerosity were manipulated as independent variables, whereas accuracy and reaction times (RT) were recorded as dependent variables. Typical effects of visual search were confirmed: RT increased with distractors’ number and decreased with targets’ salience. RBD patients showed significantly slower RT in comparison with HC. Furthermore, analyzing RT of stimuli containing the target in comparison to RT of stimuli in which the target was absent, patients differed from controls only in the condition of target absent. This result indicates a perceptual impairment specifically related to the exhaustive visual analysis, according to the Sternberg’s model. These results experimentally demonstrates a perceptual impairment revealed by the more demanding conditions of the visual search task. This impairment seems to be in line with previous neuropsychological researches that showed the presence of a visuo-spatial deficit in RBD patients. none.

New protocol for dissociating visuospatial working memory ability in reaching space and in navigational space.

Several studies have demonstrated that the processing of visuospatial memory for locations in reaching space and in navigational space is supported by independent systems, and that the coding of visuospatial information depends on the modality of the presentation (i.e., sequential or simultaneous). However, these lines of evidence and the most common neuropsychological tests used by clinicians to investigate visuospatial memory have several limitations (e.g., they are unable to analyze all the subcomponents of this function and are not directly comparable). Therefore, we developed a new battery of tests that is able to investigate these subcomponents. We recruited 71 healthy subjects who underwent sequential and simultaneous navigational tests by using an innovative sensorized platform, as well as comparable paper tests to evaluate the same components in reaching space (Exp. 1). Consistent with the literature, the principal-component method of analysis used in this study demonstrated the presence of distinct memory for sequences in different portions of space, but no distinction was found for simultaneous presentation, suggesting that different modalities of eye gaze exploration are used when subjects have to perform different types of tasks. For this purpose, an infrared Tobii Eye-Tracking X50 system was used in both spatial conditions (Exp. 2), showing that a clear effect of the presentation modality was due to the specific strategy used by subjects to explore the stimuli in space. Given these findings, the neuropsychological battery established in the present study allows us to show basic differences in the normal coding of stimuli, which can explain the specific visuospatial deficits found in various neurological conditions.

The nature of social cognitive deficits in children and adults with Klinefelter syndrome (47,XXY).

About 1 in 650 boys are born with an extra X chromosome (47,XXY or Klinefelter syndrome). 47,XXY is associated with vulnerabilities in socio-emotional development. This study was designed to assess types of cognitive deficits in individuals with 47,XXY that may contribute to social-emotional dysfunction, and to evaluate the nature of such deficits at various levels: ranging from basic visuospatial processing deficits, impairments in face recognition (FR), to emotion expression impairments. A total of 70 boys and men with 47,XXY, aged 8 to 60 years old, participated in the study. The subtests feature identification, FR and identification of facial emotions of the Amsterdam Neuropsychological Tasks were used. Level of intellectual functioning was assessed with the child and adult versions of the Wechsler Intelligence Scales. Reaction time data showed that in the 47,XXY group, 17% had difficulties in visuospatial processing (no social load), 26% had difficulties with FR (medium social load) and an even higher number of 33% had difficulties with facial expressions of emotions (high-social load). Information processing impairments increased as a function of "social load" of the stimuli, independent of intellectual functioning. Taken together, our data suggest that on average individuals with XXY may have more difficulties in information processing when "social load" increases, suggesting a specific difficulty in the higher-order labeling and interpretation of social cues, which cannot be explained by more basic visuospatial perceptual skills. Considering the increased risk for social cognitive impairments, routine assessment of social cognitive functioning as part of neuropsychological screening is warranted.

Spinocerebellar ataxia 17: full phenotype in a 41 CAG/CAA repeats carrier

BackgroundSpinocerebellar ataxia 17 (SCA17) is one of the most heterogeneous forms of autosomal dominant cerebellar ataxias with a large clinical spectrum which can mimic other movement disorders such as Huntington disease (HD), dystonia and parkinsonism. SCA17 is caused by an expansion of CAG/CAA repeat in the Tata binding protein (TBP) gene. Normal alleles contain 25 to 40 CAG/CAA repeats, alleles with 50 or greater CAG/CAA repeats are pathological with full penetrance. Alleles with 43 to 49 CAG/CAA repeats were also reported and their penetrance is estimated between 50 and 80%. Recently few symptomatic individuals having 41 and 42 repeats were reported but it is still unclear whether CAG/CAA repeats of 41 or 42 are low penetrance disease-causing alleles. Thus, phenotypic variability like the disease course in subject with SCA17 locus restricted expansions remains to be fully understood.Case presentationThe patients was a 63-year-old woman who, at 54 years, showed personality changes and increased frequency of falls. At 55 years of age neuropsychological tests showed executive attention and visuospatial deficit. At the age of 59 the patient developed dysarthria and a progressive cognitive deficit. The neurological examination showed moderate gait ataxia, dysdiadochokinesia and dysmetria, dysphagia, dysarthria and abnormal saccadic pursuit, severe axial asynergy during postural changes, choreiform dyskinesias. Molecular analysis of the TBP gene demonstrated an allele with 41 repeat suggesting that 41 CAG/CCG TBP repeats could be an allele associated with the full clinical spectrum of SCA17.ConclusionsThe described case with the other similar cases described in the literature suggests that 41 CAG/CAA trinucleotides should be considered as critical threshold in SCA17. We suggest that SCA17 diagnosis should be suspected in patients presenting with movement disorders associated with other neurodegenerative signs and symptoms.

Working-memory training following neonatal critical illness

__Objective__ To test the immediate and long-term effectiveness of Cogmed Working-Memory Training (CWMT) following ECMO and/or CDH. __Design__ A nationwide randomized controlled trial assessing neuropsychological outcome immediately and one year post-CWMT, conducted between October 2014-June 2017. Researchers involved in the follow-up assessments were blinded to group allocation. __Setting__ Erasmus MC-Sophia Children’s Hospital, Rotterdam and Radboud University Medical Center, Nijmegen, the Netherlands. __Patients__ Eligible participants were neonatal ECMO and/or CDH survivors (8-12 years) with an IQ ≥ 80 and a z-score ≤ -1.5 on at least one (working)memory test at first assessment. __Interventions__ CWMT, comprising 25 sessions of 45 minutes for five consecutive weeks at home. __Measurements and Main Results__ Participants were randomized to CWMT (n = 19) or no intervention (n = 24) (two dropped out after T0). Verbal working-memory (estimated coefficient = 0.87; p = .002) and visuospatial working-memory (estimated coefficient = 0.96, p = .003) had significantly improved in the CWMT group at T1, but was similar between groups at T2 (verbal, p = .902; visuospatial, p = .416). Improvements were found at T2 on long-term visuospatial memory following CWMT (estimated coefficient = 0.95, p = .003). Greater improvements in this domain at T2 following CWMT were associated with better self-rated school functioning (r = .541, p = .031) and parent-rated attention (r = .672, p = .006). __Conclusions__ Working-memory improvements after CWMT disappeared one year post-training in neonatal ECMO and/or CDH survivors. Gains in visuospatial memory persisted one year post-intervention. CWMT may be beneficial for survivors with visuospatial memory deficits.

Impaired spatial pattern separation performance in temporal lobe epilepsy is associated with visuospatial memory deficits and hippocampal volume loss

Individuals with chronic temporal lobe epilepsy (TLE) experience episodic memory deficits that may be progressive in nature. These memory decrements have been shown to increase with the extent of hippocampal damage, a hallmark feature of TLE. Pattern separation, a neural computational mechanism thought to play a role in episodic memory formation, has been shown to be negatively affected by aging and in individuals with known hippocampal dysfunction. Despite the link between poor pattern separation performance and episodic memory deficits, behavioral pattern separation has not been examined in patients with TLE. We examined pattern separation performance in a group of 22 patients with medically-refractory TLE and 20 healthy adults, using a task hypothesized to measure spatial pattern separation with graded levels of spatial interference. We found that individuals with TLE showed less efficient spatial pattern separation performance relative to healthy adults. Poorer spatial pattern separation performance in TLE was associated with poorer visuospatial memory, but only under high interference conditions. In addition, left hippocampal atrophy was associated with poor performance in the high interference condition in TLE. These data suggest that episodic memory impairments in patients with chronic, refractory TLE may be partially due to less efficient pattern separation, which likely reflects their underlying hippocampal dysfunction.

Memory for important item-location associations in younger and older adults.

Older adults typically experience memory impairments for verbal and visuospatial episodic information, which are most pronounced for associative information. Although some age-related verbal memory deficits may be reduced by selectively focusing on high-value item information, the binding of items to locations in visuospatial memory involves different processes that are impaired in older adults. In the current study, we examined whether age-related impairment in visuospatial binding could be alleviated by strategic focus on important information and whether varying study time and presentation formats would affect such selectivity. We also used novel spatial resolutions analysis to examine participants' gist-based visuospatial memory with respect to information importance. Younger and older adults were presented with items worth different point values in a visuospatial display, either sequentially (Experiment 1) or simultaneously (Experiment 2). When items were presented sequentially, participants became more selective with task experience, but when items were presented simultaneously, selectivity was maintained throughout the task. These patterns were also observed when encoding time was reduced for younger adults. Although older adults successfully engaged in value-based memory strategies, age-related visuospatial memory deficits were still present, even for high-value information, consistent with the associative deficit hypothesis. However, under some conditions, older adults showed reduced spatial relocation errors for high-value item-location associations. The results suggest that strategic control can be used when binding information in visuospatial memory, and that both younger and older adults can benefit by focusing on high-value items and their locations, despite associative memory deficits present in old age. (PsycINFO Database Record

Low performance on mathematical tasks in preschoolers: the importance of domain-general and domain-specific abilities.

Different domain-specific and domain-general cognitive precursors play a key role in the development of mathematical abilities. The contribution of these domains to mathematical ability changes during development. Primary school-aged children who show mathematical difficulties form a heterogeneous group, but it is not clear whether this also holds for preschool low achievers (LAs) and how domain-specific and domain-general abilities contribute to mathematical difficulties at a young age. The aim of this study was to explore the cognitive characteristics of a sample of preschool LAs and identify sub-types of LAs. 81 children were identified as LAs from 283 preschoolers aged 3 to 5years old and were assessed on a number of domain-general and domain-specific tasks. Cluster analysis revealed four subgroups of LAs in mathematics: (1) a weak processing sub-type; (2) a general mathematical LAs sub-type; (3) a mixed abilities sub-type; and (4) a visuo-spatial deficit sub-type. Whilst two of the groups showed specific domain-general difficulties, none showed only domain-specific difficulties. Current findings suggest that preschool LAs constitute a heterogeneous group and stress the importance of domain-general factors for the development of mathematical abilities during the preschool years.

Chapter 12 - Bilateral parietal dysfunctions and disconnections in simultanagnosia and Bálint syndrome

In 1909 Rezsö Bálint published an extraordinary case study of a man with complex visuospatial deficits resulting from bilateral parietal lesions. Despite some controversies over the nature of reported symptoms, in 1954 Hecaen and Ajuriaguerra conceived the term "Bálint syndrome," not only to honor Bálint's influential work but to firmly conceptualize this striking neurologic disorder. Nowadays it is largely agreed that, while Bálint syndrome may result from multiple etiologies, it is principally diagnosed based on the presence of three symptoms: simultanagnosia, optic ataxia, and ocular apraxia. One of the most striking characteristics of Bálint syndrome, perfectly capturing the nature of this remarkable disorder, is that affected patients cannot perceive more than one object at a time or comprehend multiobject visual scenes due to a lack of ability to detect several objects concurrently and to grasp the spatial relationships between them. This chapter gives an overview of the cognitive mechanisms and neuroanatomy underlying Bálint syndrome, which provides key insights into our understanding of the role of parietal cortex in human attention, visual perception, and visuomotor control. This chapter also pays homage to Glyn Humphreys (1954-2016), who pioneered contributions to the knowledge about complexity of visual and spatial deficits associated with Bálint syndrome.

Cognitive impairment in celiac disease and non-celiac gluten sensitivity: review of literature on the main cognitive impairments, the imaging and the effect of gluten free diet.

Celiac disease (CD) and non celiac gluten sensitivity (NCGS) can be responsible for neurological complications such as ataxia and peripheral neuropathies but also cognitive impairment. This cognitive involvement is variable in its expression, its duration and its prognosis ranging from transient and reversible subtle involvement to dementia itself. Through this article, we tried to achieve a review of the literature to better understand this topic. Several mechanisms were proposed to explain the deleterious influence of gluten-related pathologies on cognitive functions: nutritional deficiencies, elevation of circulating cytokine levels due to systemic inflammation, low brain serotonin levels… Several types of dementia such as Alzheimer dementia, vascular dementia, frontotemporal dementia were reported in association with CD. Memory disorder, acalculia, inattention, visuospatial deficits and executive dysfunction must be sought systematically by a neuropsychological assessment in patients with CD or NCGS. As far as the cognitive impairment is concerned, there is no pathognomonic radiological lesion. Concerning therapeutic management; although its effect is controversial, gluten free diet should be introduced, as early as possible, because of its potentially protective effect.

Does it fit? – Impaired affordance perception after stroke

Affordance perception comprises the evaluation of whether our given bodily capabilities and properties of the environment allow particular actions. Typical impairments after left brain damage in motor cognition as well as after right brain damage in visuo-spatial abilities may affect the evaluation of whether interactions with objects are possible. Further it is unclear whether deficient motor function is accounted for when deciding upon action opportunities. For these purposes we developed a paradigm with two tasks that differ in their type of demands on affordance perception and tested it in healthy young adults (Randerath and Frey, 2016). Here, we applied one of these two tasks in stroke patients and age matched healthy participants.A sample of 34 stroke patients with either left (LBD) or right brain damage (RBD) and 29 healthy controls made decisions about whether their hands would fit through a defined horizontal aperture presented in various sizes, while they remained still. Data was analyzed using a detection theory approach and included criterion, perceptual sensitivity and diagnostic accuracy as dependent variables. In addition we applied modern voxel based lesion analyses to explore neural correlates.Compared to controls, both patient groups demonstrated lower perceptual sensitivity. As predicted, increased motor cognitive deficiencies after left brain damage and visuo-spatial deficits after right brain damage were associated with worse performance. Preliminary lesion analyses demonstrated that next to lesions in ventro-dorsal regions, damage in the cortex-claustrum-cingulate pathway may affect perceptual sensitivity. Results were similar for left and right brain damage suggesting a bilateral network.Accordingly, we propose that perceptual sensitivity for affordance based judgments is a capability depending on motor-cognitive and visuo-spatial processing, which frequently is deficient after left or right brain damage, respectively. Further research on diagnostics and training in affordance perception after brain damage is needed.

Damage of the right dorsal superior longitudinal fascicle by awake surgery for glioma causes persistent visuospatial dysfunction

Patients with glioma frequently present with neuropsychological deficits preoperatively and/or postoperatively, and these deficits may remain after the chronic phase. However, little is known about postoperative recovery course of right hemispheric function. We therefore studied the characteristics and causes of persistent cognitive dysfunction in right cerebral hemispheric glioma. Eighteen patients who underwent awake surgery participated in this study. All patients who received preoperative neuropsychological examinations were assigned to two groups according to their test results: preoperative deficit and normal. They were reassessed 1 week and 3 months after surgery. The rates of remaining deficits in the deficit group at chronic phase were higher than those of the normal group for all functions. Despite preoperative normal function, the remaining rate for visuospatial cognitive deficits was the highest among all functions. The voxel-based lesion-symptom mapping analysis for visuospatial cognition revealed that a part of the medial superior and middle frontal gyri were resected with high probability in patients with low visuospatial cognitive accuracy. Our study indicates that in patients with preoperative neuropsychological deficits, these deficits tend to remain until the chronic phase. Visuospatial dysfunction frequently persists until the chronic phase, which might reflect damage to the superior longitudinal fasciclus I and II.

Set shifting and visuospatial organization deficits in body dysmorphic disorder

Individuals with body dysmorphic disorder (BDD) over-attend to perceived defect(s) in their physical appearance, often becoming “stuck” obsessing about perceived flaws and engaging in rituals to hide flaws. These symptoms suggest that individuals with BDD may experience deficits in underlying neurocognitive functions, such as set-shifting and visuospatial organization. These deficits have been implicated as risk and maintenance factors in disorders with similarities to BDD but have been minimally investigated in BDD. The present study examined differences in neurocognitive functions among BDD participants (n = 20) compared to healthy controls (HCs; n = 20). Participants completed neuropsychological assessments measuring set-shifting (Cambridge Neuropsychological Test Automated Battery Intra-Extra Dimensional Set Shift [IED] task) and visuospatial organization and memory (Rey-Osterrieth Complex Figure Test [ROCF]). Results revealed a set-shifting deficit among BDD participants compared to HCs on the IED. On the ROCF, BDD participants exhibited deficits in visuospatial organization compared to HCs, but they did not differ in visuospatial memory compared to HCs. Results did not change when accounting for depression severity. Findings highlight neurocognitive deficits as potential endophenotype markers of clinical features (i.e., delusionality). Understanding neuropsychological deficits may clarify similarities and differences between BDD and related disorders and may guide targets for BDD treatment.

Vulnerabilities in sequencing and task switching in healthy youth offspring of parents with mood disorders

ABSTRACTIntroduction: Visuospatial processing and task switching are impaired in individuals with mood disorders. It is unknown whether early deficits are present before mood symptom on set or are related to risk for a specific type of mood disorder. To investigate, we compared visual attention and task switching during sequencing among never-disordered youth with parental family histories of bipolar (BD) and major depressive disorders (MDD) and healthy controls (HC) with no personal or family history of psychopathology.Method: 8–17-year-old youth of parents with BD (n = 31, “BD-risk”), youth of parents with MDD (n = 49, “MDD-risk”), and demographically similar HC (n = 31, “HC”) were examined using the Delis–Kaplan Executive Functioning System Trail Making Test. Seed-based resting-state functional connectivity (RSFC) was collected from a subset of 88 participants (25 BD-risk, 37 MDD-risk, 26 HC) to investigate group differences in RSFC related to visuospatial processing.Results: BD-risk and MDD-risk offspring had impaired sequencing and task switching, demonstrated by reduced scores on visual scanning, F(2, 108) = 4.12, p = .02, number sequencing, F(2, 88) = 4.75, p = .01, letter sequencing, F(2, 108) = 4.24, p = .02, and number–letter sequencing, F(2, 108) = 4.66, p = .01, compared to scores in HC. RSFC between the posterior cingulate (PCC) and clusters in the subcallosal cortex, amygdala, and hippocampus significantly differed among HC, BD-risk, and MDD-risk groups. PCC-subcallosal/limbic RSFC was positively coupled in the MDD-risk and BD-risk groups and negatively coupled in HCs.Conclusions: Youth at familial risk for mood disorders demonstrate visuospatial deficits early in the processing stream. Improved methods for identifying at-risk children with the earliest possible neurocognitive impairments may inform remediation strategies that could prevent mood disorders.

Getting Lost Behavior in Patients with Mild Alzheimer's Disease: A Cognitive and Anatomical Model.

Getting lost behavior (GLB) in the elderly is believed to involve poor top-down modulation of visuospatial processing, by impaired executive functions. However, since healthy elderly and elderly with Alzheimer's disease (AD) experience a different pattern of cognitive decline, it remains unclear whether this hypothesis can explain GLB in dementia. We sought to identify whether poor executive functions and working memory modulate the relationship between visuospatial processing and prevalence of GLB in healthy elderly and patients with AD. Complementary to this, we explored whether brain regions critical for executive functions modulate the relationship between GLB and brain regions critical for visuospatial processing. Ninety-two participants with mild AD and 46 healthy age-matched controls underwent neuropsychological assessment and a structural MRI. GLB was assessed using a semistructured clinical interview. Path analysis was used to explore interactions between visuospatial deficits, executive dysfunction/working memory, and prevalence of GLB, in AD and controls independently. For both healthy controls and patients with mild AD, visuospatial processing deficits were associated with GLB only in the presence of poor working memory. Anatomically, GLB was associated with medial temporal atrophy in patients with mild AD, which was not strengthened by low frontal gray matter (GM) volume as predicted. Instead, medial temporal atrophy was more strongly related to GLB in patients with high frontal GM volumes. For controls, GLB was not associated with occipital, parietal, medial temporal, or frontal GM volume. Cognitively, a top-down modulation deficit may drive GLB in both healthy elderly and patients with mild AD. This modulation effect may be localized in the medial temporal lobe for patients with mild AD. Thus, anatomical substrates of GLB in mild AD may not follow the typical top-down modulation mechanisms often reported in the healthy aging population. Implications advance therapeutic practices by highlighting the need to target both working memory and visuospatial deficits simultaneously, and that anatomical substrates of GLB may be disease specific.

Neurocognitive performances of visuospatial attention and the correlations with metabolic and inflammatory biomarkers in adults with obesity.

What is the central question of this study? Obesity is linked to cognitive deficits, elevated energy metabolic indices and low-grade systemic inflammation. Do the relationships between neurocognitive performance and the biochemical markers (e.g. energy metabolic indices and inflammatory cytokines) occur independently of factors known to be associated with neurocognitive dysfunction (i.e. cardiorespiratory fitness) in young adults? What is the main finding and its importance? Young obese adults showed poorer neuropsychological performances, aberrant neural activity and higher C-reactive protein and energy metabolic indices. The higher leptin and C-reactive protein concentrations showed a significant negative association with lower P3 amplitudes. However, leptin was the sole predictive factor, implicating hyperleptinaemia in the altered neurocognitive function observed in obesity. The present study was designed to explore the neurophysiological mechanism of visuospatial attention deficits in obese adults and to examine the relationships between neurocognitive (neuropsychological and neurophysiological) performances and the biochemical markers. Thirty obese adults and 30 healthy-weight control subjects, categorized by body mass index and percentage fat as measured with dual-energy X-ray absorptiometry, provided a fasting blood sample and performed a visuospatial attention protocol with concomitant electrophysiological recording. The obese group showed slower reaction times and smaller P3 amplitudes when performing the cognitive task. Even when controlling for the covariable of cardiorespiratory fitness, the results remained. In addition, the serum concentrations of insulin, glucose, leptin and C-reactive protein were significantly higher in the obese group relative to the control group, but not those of interleukin-6, interleukin-1β and tumour necrosis factor-α. Partial correlations adjusting for cardiorespiratory fitness showed that leptin and C-reactive protein concentrations in the obese group were negatively associated with poorer neurophysiological (i.e. P3 amplitude) performance. However, the regression analysis showed that leptin was the sole predictor of P3 amplitude in the obese group. These findings indicate that the individuals with obesity exhibited neurocognitive deficits when performing the visuospatial attention task, and serum leptin concentrations could be one of the influential factors.

Neuro-ophthalmic manifestations of cerebrovascular accidents.

Ocular functions can be affected in almost any type of cerebrovascular accident (CVA) creating a burden on the patient and family and limiting functionality. The present review summarizes the different ocular outcomes after stroke, divided into three categories: vision, ocular motility, and visual perception. We also discuss interventions that have been proposed to help restore vision and perception after CVA. Interventions that might help expand or compensate for visual field loss and visuospatial neglect include explorative saccade training, prisms, visual restoration therapy (VRT), and transcranial direct current stimulation (tDCS). VRT makes use of neuroplasticity, which has shown efficacy in animal models but remains controversial in human studies. CVAs can lead to decreased visual acuity, visual field loss, ocular motility abnormalities, and visuospatial perception deficits. Although ocular motility problems can be corrected with surgery, vision, and perception deficits are more difficult to overcome. Interventions to restore or compensate for visual field deficits are controversial despite theoretical underpinnings, animal model evidence, and case reports of their efficacies.

P 164 Parietal stroke mimicking the Heidenhain variant of Creutzfeldt-Jakob Disease

The Heidenhain variant of Creutzfeldt-Jakob disease (CJD) is a rapidly progressive neurodegenerative disease with an occipito-parietal focus.It initially presents with visual disturbances such as visual agnosia or cortical blindness (Kropp et al., 1999).After presentation of early visual symptoms, rapid progression of dementia and death follows.While the Heidenhain variant matches neuropathological criteria of CJD, differential diagnosis from other neurological disorders using biomarkers from electroencephalography (EEG), magnetic resonance imaging (MRI), and cerebrospinal fluid (CSF) reveal low sensitivity and specificity.As a consequence, these tools may lead to an erroneous diagnosis of the Heidenhain variant. We report about a 81-year old female who was transferred to the intensive care unit due to a generalized tonic-clonic seizure followed by prolonged somnolence, additionally exhibiting myoclonic jerks of the distal legs, left horizontal gaze palsy and horizontal nystagmus to the right.A history of cognitive decline including short-term memory and word-finding difficulties as well as visuospatial and visuoconstructive deficits over the last few weeks was reported. Initial EEG revealed 1.5 Hz left lateralized periodic sharp-wave and polyspike-wave complexes of high amplitude and triphasic morphology suspicious for CJD. Brain MRI showed a hyperintense lesion in the left occipito-parietal lobe on diffusion-weighted and FLAIR sequences, respectively.Protein 14-3-3 was positive in CSF (ELISA). However, RT-QuIC confirmatory test was negative.Other serum and CSF parameters including anti-neuronal antibodies were negative.Given this information, is it reasonable to consider the Heidenhain variant of CJD? The patient suffered from a cardioembolic stroke due to atrial fibrillation affecting the parietal branches of the middle cerebral artery.Edoxaban had been removed three weeks previously because of repeated falls.During ICU treatment, the patient developed a prolonged nonconvulsive status epilepticus (NCSE) characterized by deep coma without significant motor phenomena.EEG was refractory to an initial antiepileptic drug treatment, but finally returned to normal with valproate monotherapy.The patient, however, remained comatose until transfer to rehabilitation, but she regained consciousness two weeks later. This case points out that a parietal stroke with complicating NCSE may mimic the Heidenhain variant of CJD, particularly by under-recognition of so-called CJD red flags: First, the occurrence of 14-3-3 proteins is known to be positive after either acute stroke or seizures.Secondly, though increased intensity on DWI in CJD is discussed as a noninvasive biomarker, such signal abnormalities – particularly if sparing the basal ganglia – are not specific to CJD. Thirdly, NCSE patients with altered consciousness often present with localized or lateralized sharp waves of triphasic configuration.These atypical triphasic waves are considered to be of epileptic origin if they disappear following antiepileptic drug treatment as in our case (Trinka and Leitinger, 2015).