Selective Deficit Research Articles

Mild Cognitive Impairment in de novo Parkinson's Disease: Selective Attention Deficit as Early Sign of Neurocognitive Decay.

Background: In the present study, we aimed to better investigate attention system profile of Parkinson's disease-Mild Cognitive Impairment (PD-MCI) patients and to determine if specific attentional deficits are associated with 123I-FP-CIT SPECT.Methods: A total of 44 de novo drug-naïve PD patients [(27) with normal cognition (PD-NC) and 17 with MCI (PD-MCI)], 23 MCI patients and 23 individuals with subjective cognitive impairment (SCI) were recruited at the Clinical Neurology Unit of Santa Chiara hospital (Pisa University Medical School, Italy). They were assessed by a wide neuropsychological battery, including Visual Search Test (VST) measuring selective attention. Performances among groups were compared by non-parametric tests (i.e., Kruskal-Wallis and Mann-Whitney, Bonferroni corrected). Further, Spearman's rank correlations were performed to explore the association between neuropsychological variables and 123I-FP-CIT SPECT data in PD subgroup.Results: PD-MCI patients performed worse on VST than patients with PD-NC (p = 0.002), patients with MCI and individuals with SCI (p < 0.001). The performance of PD-MCI patients on VST significantly correlated with caudate nucleus 123I-FP-CIT SPECT uptake (rho = 0.582, p < 0.05), whereas a negative correlation between such test and 123I-FP-CIT SPECT uptake in the left putamen (rho = −0.529, p < 0.05) was found in PD-NC patients.Conclusions: We suggest that selective attention deficit might be a trigger of cognitive decay in de novo PD-MCI patients. The VST should be routinely used to detect attentional deficits in hospital clinical practice, in the light of its closely association with dopamine depletion of basal ganglia in mildly impaired PD patients.

Manipulation of EGFR-Induced Signaling for the Recruitment of Quiescent Neural Stem Cells in the Adult Mouse Forebrain.

The ventricular-subventricular zone (V-SVZ) is the principal neurogenic niche in the adult mammalian forebrain. Neural stem/progenitor cell (NSPC) activity within the V-SVZ is controlled by numerous of extrinsic factors, whose downstream effects on NSPC proliferation, survival and differentiation are transduced via a limited number of intracellular signaling pathways. Here, we investigated the relationship between age-related changes in NSPC output and activity of signaling pathways downstream of the epidermal growth factor receptor (EGFR), a major regulator of NSPC activity. Biochemical experiments indicated that age-related decline of NSPC activity in vivo is accompanied by selective deficits amongst various EGFR-induced signal pathways within the V-SVZ niche. Pharmacological loss-of-function signaling experiments with cultured NSPCs revealed both overlap and selectivity in the biological functions modulated by the EGFR-induced PI3K/AKT, MEK/ERK and mTOR signaling modules. Specifically, while all three modules promoted EGFR-mediated NSPC proliferation, only mTOR contributed to NSPC survival and only MEK/ERK repressed NSPC differentiation. Using a gain-of-function in vivo genetic approach, we electroporated a constitutively active EGFR construct into a subpopulation of quiescent, EGFR-negative neural stem cells (qNSCs); this ectopic activation of EGFR signaling enabled qNSCs to divide in 3-month-old early adult mice, but not in mice at middle-age or carrying familial Alzheimer disease mutations. Thus, (i) individual EGFR-induced signaling pathways have dissociable effects on NSPC proliferation, survival, and differentiation, (ii) activation of EGFR signaling is sufficient to stimulate qNSC cell cycle entry during early adulthood, and (iii) the proliferative effects of EGFR-induced signaling are dominantly overridden by anti-proliferative signals associated with aging and Alzheimer’s disease.

Neuropsychological correlates of prospective memory: A comparison between tremor-dominant Parkinson’s disease and cervical dystonia

Cervical Dystonia (CD) and Parkinson’s disease, particularly tremor-dominant motor phenotype (TD-PD), showed a selective deficit of time-based prospective memory (TBPM). The two movement disorders are mainly characterized by dysfunctions of basal-ganglia and prefrontal cortex but it is reported that cerebellum also plays a key role in their pathogenesis. These cerebral structures are specifically involved in TBPM rather than in event-based PM (EBPM), but until now no study directly compared these two components of PM between CD and TD-PD patients. Therefore, the present study aimed at investigating if differences in PM functioning between CD and TD-PD patients might exist and if the type of movement disorder moderated the relationship between deficit of PM and deficit of executive functions and retrospective memory.Thirty TD-PD, 27CD patients and 29 healthy subjects (HCs), matched for demographic features, underwent neuropsychological tests for PM, executive functions, retrospective memory and self-rated questionnaires.The three groups did not differ on neuropsychological variables except for TBPM where TD-PD and CD patients performed worse than HCs; moreover, TD-PD performed worse than CD patients. Moderation analysis indicated that the type of movement disorder moderated the relationship between executive dysfunction and TBPM, but not EBPM.In conclusion, selective deficit of TBPM characterizes both CD and TD-PD but it is associated with executive dysfunction only in TD-PD. It might be possible to speculate that the involvement of the cerebellum, responsible for internal timing processes, could explain the impairment of TBPM in both movement disorders. This issue deserves to be explored in future neuroimaging studies.

The Therapeutic Potential of Carnosine/Anserine Supplementation against Cognitive Decline: A Systematic Review with Meta-Analysis.

Carnosine is a natural occurring endogenous dipeptide that was proposed as an anti-aging agent more than 20 years ago. Carnosine can be found at low millimolar concentrations at brain level and different preclinical studies have demonstrated its antioxidant, anti-inflammatory, and anti-aggregation activity with neuroprotective effects in animal models of Alzheimer’s disease (AD). A selective deficit of carnosine has also been linked to cognitive decline in AD. Different clinical studies have been conducted to evaluate the impact of carnosine supplementation against cognitive decline in elderly and AD subjects. We conducted a systematic review with meta-analysis, in accordance with the PRISMA guidelines coupled to the PICOS approach, to investigate the therapeutic potential of carnosine against cognitive decline and depressive symptoms in elderly subjects. We found five studies matching the selection criteria. Carnosine/anserine was administered for 12 weeks at a dose of 1 g/day and improved global cognitive function, whereas no effects were detected on depressive symptoms. These data suggest a preliminary evidence of clinical efficacy of carnosine against cognitive decline both in elderly subjects and mild cognitive impairment (MCI) patients, although larger and long-term clinical studies are needed in MCI patients (with or without depression) to confirm the therapeutic potential of carnosine.

Misplacement of something inside the refrigerator is not a sign of dementia, but a probable symptom of attention deficit due to depression

The objective of this study is to investigate the clinical significance of a specific behavior of misplacing items in a refrigerator (i.e., placing extremely unusual things such as remote control and/or cellular phone in a refrigerator) as a symptom of cognitive dysfunction. Patients with memory complaints were asked whether they ever experienced misplacing items in a refrigerator, such as placing a remote control, a cellular phone, or other extremely unusual things inside a refrigerator (referred to as the ‘fridge sign’). Among the 2172 individuals with memory complaints, 55 (2.5%) experienced symptoms of the ‘fridge sign’. We investigated the cognitive profiles of ‘fridge sign’-positive patients and performed follow-up evaluations with neuropsychological tests or telephone interviews. The ‘fridge sign’ was mostly found in individuals diagnosed as subjective cognitive decline (n = 33, 60%) or mild cognitive impairment (MCI, n = 20, 36.4%) with depressive mood and was relatively rare in dementia states (n = 2, 3.5%). Moreover, none of the ‘fridge sign’-positive patients showed significant cognitive decline over the follow-up period. We compared the cognitive profiles and the clinical progression of 20 ‘fridge sign’-positive MCI patients and 40 ‘fridge sign’-negative MCI patients. ‘Fridge sign’-positive MCI patients had worse scores on the Stroop test color reading and had higher scores on the geriatric depression scale than ‘fridge sign’-negative MCI patients, which indicates that the ‘fridge sign’ could be indicative of selective attention deficit in patients with depression rather than indicative of cognitive decline related to dementia.

Structural alterations in cortical and thalamocortical white matter tracts after recovery from prefrontal cortex lesions in macaques

Unilateral damage to the frontoparietal network typically impairs saccade target selection within the contralesional visual hemifield. Severity of deficits and the degree of recovery have been associated with widespread network dysfunction, yet it is not clear how these behavioural and functional brain changes relate with the underlying structural white matter tracts. Here, we investigated whether recovery after unilateral prefrontal cortex (PFC) lesions was associated with changes in white matter microstructure across large-scale frontoparietal cortical and thalamocortical networks. Diffusion-weighted imaging was acquired in four male rhesus macaques at pre-lesion, week 1, and week 8-16 post-lesion when target selection deficits largely recovered. Probabilistic tractography was used to reconstruct cortical frontoparietal fiber tracts, including the superior longitudinal fasciculus (SLF) and transcallosal fibers connecting the PFC or posterior parietal cortex (PPC), as well as thalamocortical fiber tracts connecting the PFC and PPC to thalamic nuclei. We found that the two animals with small PFC lesions showed increased fractional anisotropy in both cortical and thalamocortical fiber tracts when behaviour had recovered. However, we found that fractional anisotropy decreased in cortical frontoparietal tracts after larger PFC lesions yet increased in some thalamocortical tracts at the time of behavioural recovery. These findings indicate that behavioural recovery after small PFC lesions may be supported by both cortical and subcortical areas, whereas larger PFC lesions may have induced widespread structural damage and hindered compensatory remodeling in the cortical frontoparietal network.

Neurocognitive mechanisms of poor social connection in posttraumatic stress disorder: Evidence for abnormalities in social working memory.

Poor social connection is a central feature of posttraumatic stress disorder (PTSD), but little is known about the neurocognitive processes associated with social difficulties in this population. We examined recruitment of the default network and behavioral responses during social working memory (SWM; i.e., maintaining and manipulating social information on a moment-to-moment basis) in relation to PTSD and social connection. Participants with PTSD (n = 31) and a trauma-exposed control group (n = 21) underwent functional magnetic resonance imaging while completing a task in which they reasoned about two or four people's relationships in working memory (social condition) and alphabetized two or four people's names in working memory (nonsocial condition). Participants also completed measures of social connection (e.g., loneliness, social network size). Compared to trauma-exposed controls, individuals with PTSD reported smaller social networks (p = .032) and greater loneliness (p = .038). Individuals with PTSD showed a selective deficit in SWM accuracy (p = .029) and hyperactivation in the default network, particularly in the dorsomedial subsystem, on trials with four relationships to consider. Moreover, default network hyperactivation in the PTSD group (vs. trauma-exposed group) differentially related to social network size and loneliness (p's < .05). Participants with PTSD also showed less resting state functional connectivity within the dorsomedial subsystem than controls (p = .002), suggesting differences in the functional integrity of a subsystem key to SWM. SWM abnormalities in the default network may be a basic mechanism underlying poorer social connection in PTSD.

Category-selective deficits are the exception and not the rule: Evidence from a case-series of 64 patients with ventral occipito-temporal cortex damage

The organisational principles of the visual ventral stream are still highly debated, particularly the relative association/dissociation between word and face recognition and the degree of lateralisation of the underlying processes. Reports of dissociations between word and face recognition stem from single case-studies of category selective impairments, and neuroimaging investigations of healthy participants. Despite the historical reliance on single case-studies, more recent group studies have highlighted a greater commonality between word and face recognition. Studying individual patients with rare selective deficits misses (a) important variability between patients, (b) systematic associations between task performance, and (c) patients with mild, severe and/or non-selective impairments; meaning that the full spectrum of deficits is unknown. The Back of the Brain project assessed the range and specificity of visual perceptual impairment in 64 patients with posterior cerebral artery stroke recruited based on lesion localization and not behavioural performance. Word, object, and face processing were measured with comparable tests across different levels of processing to investigate associations and dissociations across domains. We present two complementary analyses of the extensive behavioural battery: (1) a data-driven analysis of the whole patient group, and (2) a single-subject case-series analysis testing for deficits and dissociations in each individual patient. In both analyses, the general organisational principle was of associations between words, objects, and faces even following unilateral lesions. The majority of patients either showed deficits across all domains or in no domain, suggesting a spectrum of visuo-perceptual deficits post stroke. Dissociations were observed, but they were the exception and not the rule: Category-selective impairments were found in only a minority of patients, all of whom showed disproportionate deficits for words. Interestingly, such selective word impairments were found following both left and right hemisphere lesions. This large-scale investigation of posterior cerebral artery stroke patients highlights the bilateral representation of visual perceptual function.

Cochlear neural degeneration disrupts hearing in background noise by increasing auditory cortex internal noise

Correlational evidence in humans suggests that selective difficulties hearing in noisy, social settings may reflect premature auditory nerve degeneration. Here, we induced primary cochlear neural degeneration (CND) in adult mice and found direct behavioral evidence for selective detection deficits in background noise. To identify central determinants for this perceptual disorder, we tracked daily changes in ensembles of layer 2/3 auditory cortex parvalbumin-expressing inhibitory neurons and excitatory pyramidal neurons with chronic two-photon calcium imaging. CND induced distinct forms of plasticity in cortical excitatory and inhibitory neurons that culminated in net hyperactivity, increased neural gain, and reduced adaptation to background noise. Ensemble activity measured while mice detected targets in noise could accurately decode whether individual behavioral trials were hits or misses. After CND, random surges of hypercorrelated cortical activity occurring just before target onset reliably predicted impending detection failures, revealing a source of internal cortical noise underlying perceptual difficulties in external noise.

Time or place? Dissociation between object-in-place and relative recency in young APPswe/PS1dE9 mice.

This study tests the predictions of a novel analysis of recognition memory based on a theory of associative learning, according to which recognition comprises two independent underlying processes, one relying on the to-be-recognized item having been experienced recently (self-generated priming), and the other on it being predicted by some other stimulus (retrieval-generated priming). A single experiment examined recognition performance in the amyloid precursor protein (APP)swe/PS1dE9 (APP/PS1) mouse, a double-transgenic model of Alzheimer's disease (AD), and wild type (WT) littermates. Performance on two variants of the spontaneous object recognition (SOR) was compared in 5-month-old APPswe/PS1dE9 (APP/PS1) mice, a double-transgenic model of AD, and their WT littermates, using junk objects. In the relative recency task animals were exposed to object A, and then object B, followed by a test with both A and B. In the object-in-place task the mice were exposed to both A and B, and then tested with two copies of A, occupying the same positions as the preeexposed objects. The WT mice showed a preference for exploring the first-presented object A in the relative recency task, and the copy of A in the "wrong" position (i.e., the one placed where B had been during the preexposure phase) in the object-in-place task. The APP/PS1 mice performed like the WT mice in the relative recency task, but showed a selective impairment in the object-in-place task. We interpret these findings in terms of-Wagner's (Information processing in animals: Memory Mechanisms, 1981, Erlbaum) theory of associative learning, sometimes opponent process (SOP), as a selective deficit in retrieval-generated priming. (PsycInfo Database Record (c) 2021 APA, all rights reserved).

Bilateral vestibulopathy causes selective deficits in recombining novel routes in real space

The differential impact of complete and incomplete bilateral vestibulopathy (BVP) on spatial orientation, visual exploration, and navigation-induced brain network activations is still under debate. In this study, 14 BVP patients (6 complete, 8 incomplete) and 14 age-matched healthy controls performed a navigation task requiring them to retrace familiar routes and recombine novel routes to find five items in real space. [18F]-fluorodeoxyglucose-PET was used to determine navigation-induced brain activations. Participants wore a gaze-controlled, head-fixed camera that recorded their visual exploration behaviour. Patients performed worse, when recombining novel routes (p < 0.001), whereas retracing of familiar routes was normal (p = 0.82). These deficits correlated with the severity of BVP. Patients exhibited higher gait fluctuations, spent less time at crossroads, and used a possible shortcut less often (p < 0.05). The right hippocampus and entorhinal cortex were less active and the bilateral parahippocampal place area more active during navigation in patients. Complete BVP showed reduced activations in the pontine brainstem, anterior thalamus, posterior insular, and retrosplenial cortex compared to incomplete BVP. The navigation-induced brain activation pattern in BVP is compatible with deficits in creating a mental representation of a novel environment. Residual vestibular function allows recruitment of brain areas involved in head direction signalling to support navigation.

Case study: A selective tactile naming deficit for letters and numbers due to interhemispheric disconnection

The role of white matter pathways in cognition is a topic of active investigation that is vital to both the fields of clinical neurology and cognitive neuroscience. White matter pathways provide critical connectivity amongst numerous specialized brain regions thereby enabling higher level cognition. While the effects of dissections and lesions of the corpus callosum have been reported, it is less understood how unilateral focal white matter lesions may impact cognitive processes. Here, we report a unique case study in which a small left lateralized stroke in the white matter adjacent to the body of the corpus callosum selectively impaired the ability to name letters and numbers presented to the ipsilesional, left hand. Naming of letters, numbers and objects was tested in both the visual and tactile modalities in both hands. Diffusion-weighted imaging showed a marked reduction in white matter pathway integrity through the body of the corpus callosum. Clinically, this case highlights the significant impact that a focal white matter lesion can have on higher-level cognition, specifically the integration of verbal and tactile information. Moreover, this case adds to prior reports on tactile agnosia by including DTI imaging data and emphasizing the role that white matter pathways through the body of the corpus callosum play in integrating tactile input from the right hemisphere with verbal naming capabilities of the left hemisphere. Finally, the findings also provoke fresh insight into alternative strategies for rehabilitating cognitive functioning when structural connectivity may be compromised.

Deletion of &lt;i&gt;Fmr1&lt;/i&gt; in Parvalbumin Inhibitory Neurons Leads to Dysregulated Translation and Selective Behavioral Deficits Associated with Fragile X Syndrome

Deletion of &lt;i&gt;Fmr1&lt;/i&gt; in Parvalbumin Inhibitory Neurons Leads to Dysregulated Translation and Selective Behavioral Deficits Associated with Fragile X Syndrome

Executive dysfunction profile in children and adolescents with fetal alcohol spectrum disorder – systematic review

The paper aims at reviewing data on the executive functioning in children and adolescents with fetal alcohol spectrum disorder (FASD) in the context of Suchy’s model of executive functioning. Suchy hypothesized that individuals with FASD would present with features of dysexecutive, disinhibited, apathetic and inappropriate, but not disorganized, syndromes. Eight papers satisfied the inclusion criteria for the review. In most respects, the performance of children with FASD was found to be lower than in the control group. According to Suchy’s model of executive functioning, children with FASD demonstrate features of dysexecutive syndrome (with deficits of executive cognitive functions) and of apathetic (deficit in initiation and maintenance) and disinhibited syndromes (deficit in response selection) as well as impaired social cognition that could correspond to socially inappropriate syndromes. None of the reviewed studies included measures of multi-tasking that would address features of disorganized syndrome. The results suggest a mixed pattern of executive deficits in FASD. Difficulties in delineating the executive functioning profile in children and adolescents with FASD may be related to heterogeneous patient populations (different clinical criteria, variable overall intellectual functioning and different living conditions) and also the complex nature of most of the executive measures that rarely tap one aspect of the executive functioning and typically engage a variety of cognitive processes.

Gender agreement in SLI: A study on production and inflection of articles in German

ABSTRACT This study addresses the question of whether gender agreement is impaired in SLI German. Article production and gender marking on articles were examined in three groups of German-speaking children: 10 children with Specific Language Impairment (SLI), 10 age-matched typically developing (TD) children, and 10 TD children who were on average two years younger. Gender marking on articles did not reveal any evidence of an agreement deficit in the SLI group. Nevertheless, the children of the SLI group had a selective deficit in assigning the correct gender to neuter nouns. Regarding article production, it was found that article omissions were more frequent in the SLI group than in the age-matched TD group. However, these omissions cannot be clearly attributed to a deficit in gender agreement. The data indicate that article omissions may also reflect an avoidance strategy due to a lack of gender information. These results provide evidence for the ability of SLI children to acquire and use rule-governed syntactic computations. This is incompatible with accounts of SLI that posit a broad syntactic deficit in these children.

Inhibitory control and impulsive responses in neurodevelopmental disorders.

The impairment of inhibitory control is often assumed to be the core deficit of several neurodevelopmental disorders characterized by poor impulse control. However, could the same deficit explain different clinical phenotypes? Evidence from behavioural studies is very mixed. This is partly because inhibition is a highly complex executive function. Thus, the different types of tasks that generically tap into inhibitory control are likely to provide different outcomes. Additionally, sample inhomogeneity in terms of age, comorbidity, and medical treatment are confounding factors. Therefore, to make a reliable assessment of the deficit of inhibitory control in a given disorder, the same task and samples with similar characteristics must be employed. This article reviews and discusses studies on five neurodevelopmental disorders with impaired impulse control where these criteria have been used: Tourette syndrome; obsessive-compulsive disorder; attention-deficit/hyperactivity disorder; primary motor stereotypies; and autism spectrum disorder. Overall, they suggest that the mechanisms underlying the inability to control urges are extremely heterogeneous and cannot be ascribed to a general impairment of inhibition. These findings do not support the hypothesis that inhibitory deficits represent a transdiagnostic feature of neurodevelopmental disorders with poor impulse control. WHAT THIS PAPER ADDS: The mechanisms underlying the inability to control urges in neurodevelopmental disorders are heterogeneous. Inhibition impairments cannot generally explain all neurodevelopmental disorders characterized by poor urge control.

Cognitive Profile and Its Evolution in a Cohort of Multiple System Atrophy Patients

Introduction: Cognitive decline is not a characteristic feature of multiple system atrophy (MSA), but recent evidence suggests cognitive impairment as an integral part of the disease. We aim to describe the cognitive profile and its progression in a cohort of patients with MSA.Methods: We retrospectively selected patients referred to our department with a clinical diagnosis of MSA who were evaluated at least once a year during the course of the disease and underwent a comprehensive neuropsychological evaluation.Results: At the first evaluation (T0), 37 out of 60 patients (62%) were cognitively impaired, mainly (76%) in attention and executive functioning. Thirteen patients were impaired in one cognitive domain and 24 in more than one cognitive domain. Six out of the 24 had dementia. Twenty patients underwent a follow-up evaluation (T1) after a mean of 16.6 ± 9.3 months from the first evaluation (T0). Eight out of 20 patients were cognitively normal at both T0 and T1. Seven out of 12 patients presented with stable cognitive impairment at T1, while cognitive decline progressed in five patients. Patients with progression in cognitive decline performed significantly worse at T0 than cognitively stable patients. Education was significantly different between patients with and without cognitive impairment. No other differences in demographic and clinical variables and autonomic or sleep disturbances were found. Patients with dementia were older at disease onset and at T0 and had lower education and disease duration at T0 compared to those in other groups.Conclusions: In patients with MSA, we observed three different cognitive profiles: normal cognition, stable selective attention-executive deficits, and progressive cognitive deficits evolving to dementia. The detection of cognitive impairment in patients with suspected MSA suggests the need for comprehensive and longitudinal neuropsychological evaluation.

Disrupted Anti-correlation Between the Default and Dorsal Attention Networks During Hyperthermia Exposure: An fMRI Study.

Environmental hyperthermia is a common risk factor for occupational safety in many situations due to decreased vigilance performances. Previously, we have reported that decreased resting-state functional connectivity within the default mode network (DMN) and decreased activations in dorsal attention network (DAN) such as dorsolateral prefrontal cortex (DLPFC) were correlated with selective attention deficits during hyperthermia. However, whether the inherent functionally organized anti-correlation between the DMN and DAN would contribute to the behavioral deficits remains unclear. In this study, we collected the resting-state fMRI data of 25 participants during two simulated thermal conditions: normothermic condition (25°C for 1 h) and hyperthermic condition (50°C for 1 h). Using group independent component analysis (ICA), we investigated the functional connectivity within the DMN and DAN, as well as the anti-correlations between both networks. Paired comparisons revealed that decreased intranetwork functional connectivity in the medial prefrontal cortex (mPFC)/anterior cingulate cortex (ACC) in the DMN contributed to executive control performance during hyperthermia using multivariate linear regression analysis. Paired comparison on the DAN showed that increased one in the posterior part of the middle and inferior temporal gyrus nearby the temporal–parietal junction area contributed to preserved alerting performance. Lastly but most importantly, we found that decreased correlation between mPFC in the DMN and intraparietal sulcus (IPS) area in the DAN contributed to the executive control deficit, suggesting a weaker intrinsic anti-correlation between DMN and DAN during hyperthermia. These findings indicated that a functional reorganized architecture of DMN and DAN might provide a potential neural basis of the selective deficits for different cognitive-demand attention tasks in high-temperature environments.

Role of cognitive reserve in cognitive variability in euthymic individuals with bipolar disorder: cross-sectional cluster analysis.

People with bipolar disorder have moderate cognitive difficulties that tend to be more pronounced during mood episodes but persist after clinical remission and affect recovery. Recent evidence suggests heterogeneity in these difficulties, but the factors underlying cognitive heterogeneity are unclear. To examine whether distinct cognitive profiles can be identified in a sample of euthymic individuals with bipolar disorder and examine potential differences between subgroups. Cognitive performance was assessed across four domains (i.e. processing speed, verbal learning/memory, working memory, executive functioning) in 80 participants. We conducted a hierarchical cluster analysis and a discriminant function analysis to identify cognitive profiles and considered differences in cognitive reserve, estimated cognitive decline from premorbid cognitive functioning, and clinical characteristics among subgroups. Four discrete cognitive profiles were identified: cognitively intact (n = 25; 31.3%); selective deficits in verbal learning and memory (n = 15; 18.8%); intermediate deficits across all cognitive domains (n = 30; 37.5%); and severe deficits across all domains (n = 10; 12.5%). Cognitive decline after illness onset was greater for the intermediate and severe subgroups. Cognitive reserve scores were increasingly lower for subgroups with greater impairments. A smaller proportion of cognitively intact participants were using antipsychotic medications compared with all other subgroups. Our findings suggest that individuals with cognitively impaired profiles demonstrate more cognitive decline after illness onset. Cognitive reserve may be one of the factors underlying cognitive variability across people with bipolar disorder. Patients in the intermediate and severe subgroups may be in greater need of interventions targeting cognitive difficulties.

Association of pediatric idiopathic intracranial hypertension with olfactory performance.

ObjectiveTo assess the association between pediatric Idiopathic intracranial hypertension (IIH) and olfactory performance.MethodsA cross-sectional comparative study was conducted including 17 patients under 18 years diagnosed with IIH at a tertiary hospital and 17 healthy age- and sex-matched subjects. All participants underwent the semi-objective chemosensory Sniffin’ Sticks test for evaluation of odor threshold (OT), indicative of peripheral olfactory function, and odor identification (OI), reflecting higher cognitive olfactory processing. Scores were compared and referred to the updated normative values. Demographic, clinical, and neuroimaging data were collected from the medical files. The patients with IIH were reassessed for olfactory function and clinical state at the subsequent follow-up, under treatment.ResultsCompared to controls, the IIH group had a significantly lower mean OT score (6.41 ± 3.43 vs 10.21 ± 2.79, p = 0.001) and higher rate of OT score below the 10th percentile for age and sex according to the normative values (47.1% vs 0%, p = 0.001). There was no significant between-group difference in mean OI scores (9.82 ± 1.63, vs 10.59 ± 1.84, p = 0.290). OT scores were not associated with sex, age, body mass index, neuroimaging abnormalities, or lumbar puncture opening pressure. At the follow-up assessment, the OT scores were improved (9.36 ± 4.17 vs 6.7 ± 3.32, p = 0.027) whereas the OI scores were unchanged (9.88 ± 2.5 vs 9.69 ± 1.58, p = 0.432).ConclusionsAs reported in adults, children and adolescents with IIH appear to have a selective reversible deficit in olfactory detection threshold, which may imply a reduction in peripheral olfactory perceptual ability. Future studies should examine the predictive value of olfactory function for IIH.