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ABSTRACTGenetic variants are traditionally known to shape the susceptibility to neuropsychiatric disorders. An increasing number of studies indicate that remodeling of the gut microbiome by genetic variance serves as a versatile regulator of gut-brain crosstalk and behavior. Evidence also emerges that certain behavioral symptoms are specifically attributed to gut microbial remodeling and gut-to-brain signals, which necessitates rethinking of neuropsychiatric disease etiology and treatment from a systems perspective of reciprocal gene-microbe interactions. Here, we present an emerging picture of how gut microbes and host genetics interactively shape complex psychiatric phenotypes. We illustrate the growing understanding of how the gut microbiome is shaped by genetic changes and its connection to behavioral outcome. We also discuss working strategies and open questions in translating associative gene-microbiome-behavior findings into causal links and novel targets for neurobehavioral disorders. Dual targeting of the genetic and microbial factors may expand the space of drug discovery for neuropsychiatric diseases.

Anatomical studies and magnetic resonance imaging studies indicated that there are differences in the degenerative changes that occur in the corpus callosum - which play arole in interhemispheric transfer information - in healthy and elderly people with neurocognitive disorders.The current study aims to investigate whether these anatomical differences result in functional differences in Tactile interhemispheric transfer in people with neurocognitive disorders and in healthy Aging. The main problem of the study was: Are there differences between healthy Aging and with neurocognitive disorders in Tactile interhemispheric transfer? The study assumed that there are differences between the three study groups. The study was conducted on a sample of (45) elderly people, divided into three groups: healthy Aging (n = 15), mild cognitive disorder (n = 15), severe cognitive disorder (n = 15). Participants Performed on interhemispheric transfer of sterognostic information. using nonparametric statistical methods. The results revealed that there were differences between healthy Aging, with mild cognitive disorder, and with severe cognitive disorder. The results were discussed in the light of the anatomical abnormalities in the corpus callosum, and the interpretation of the contradictions between the results and each other and between the heritage. [ABSTRACT FROM AUTHOR]

To investigate if patients with neuropsychological disorders (neglect, aphasia, or cognitive dysfunction measured with the Mini-mental state examination) short after stroke have different functional outcome at follow-up compared to patients without these disorders. Embase, Medline-Ovid, PsycINFO, Cochrane CENTRAL, Web of Science and Google Scholar were systematically searched for cohort studies up to 3 March 2019. PRISMA guidelines were followed. Functional outcome had to be measured with the Barthel Index or the Functional Independence Measure. If at least three studies studying the same neuropsychological disorder reported functional outcome at comparable follow-up, meta-analysis were performed and the quality of evidence was assessed using GRADE. The search resulted in 5398 unique articles and finally 27 articles were included. Pooled results show a standardized mean difference of −0.93 (95% confidence interval [−1.27 to −0.59]), indicating that the group with neglect short after stroke has significant lower functional outcome at follow-up. Regarding aphasia, the standardized mean difference was −0.50 (95% confidence interval [−0.72 to −0.28]). It appears in the limited articles available that patients with cognitive dysfunction have lower scores for functional outcome. Patients with neglect or aphasia, especially aphasia with comprehension deficits, short after stroke have significant worse functional outcome. Clinicians should perform an extensive screening for neglect, aphasia, and cognitive disorders to make sure to diagnose the different neuropsychological disorders correctly. When patients with neuropsychological disorders are referred for rehabilitation, it can be expected that they need a longer rehabilitation period or may never reach the same level of functioning. Clinicians should pay attention to instructions of training moments outside therapy and involve caregivers and patients family making these training moments more effective. [ABSTRACT FROM AUTHOR]

Neonatal Diabetes (ND) mellitus is a rare genetic disease (1 in 90,000 live births). It is defined by the presence of severe hyperglycaemia associated with insufficient or no circulating insulin, occurring mainly before 6 months of age and rarely between 6 months and 1 year. Such hyperglycaemia requires either transient treatment with insulin in about half of cases, or permanent insulin treatment. The disease is explained by two major groups of mechanism: malformation of the pancreas with altered insulin-secreting cells development/survival or abnormal function of the existing pancreatic β cell. The most frequent genetic causes of neonatal diabetes mellitus with abnormal β cell function are abnormalities of the 6q24 locus and mutations of the ABCC8 or KCNJ11 genes coding for the potassium channel in the pancreatic β cell. Other genes are associated with pancreas malformation or insufficient β cells development or destruction of β cells. Clinically, compared to patients with an ABCC8 or KCNJ11 mutation, patients with a 6q24 abnormality have lower birth weight and height, are younger at diagnosis and remission, and have a higher malformation frequency. Patients with an ABCC8 or KCNJ11 mutation have neurological and neuropsychological disorders in all those tested carefully. Up to 86% of patients who go into remission have recurrent diabetes when they reach puberty, with no difference due to the genetic origin. All these results reinforce the importance of prolonged follow-up by a multidisciplinary pediatric team, and later doctors specializing in adult medicine. 90% of the patients with an ABCC8 or KCNJ11 mutation as well as those with 6q24 anomalies are amenable to a successful switch from insulin injection to oral sulfonylureas.

Whipple’s disease is a rare, chronic systemic infection caused by gram-positive Tropheryma whipplei actinobacterium. So far, the reasons for the Tropheryma whipplei infection have not been explained. Clinical symptoms are non-specific and may suggest other diseases, mainly gastrointestinal disease. Nervous system symptoms such as personality disorders, behavioral disorders, depressive symptoms and disturbances of consciousness are also observed.The aim of the study is to collect information on neuropsychological disorders found in Whipple’s disease.Central nervous system (CNS) involvement can take place in three cases: classic form, in the relapse of previously treated classic form (with changes in the digestive system) and in isolated CNS infection (without evidence of gastrointestinal involvement by T. whipplei). Neurological disorders resulting from CNS involvement are variable and may be similar to other diseases of the nervous system. Treatment is difficult due to the long-term course of the disease and non-specificity of its symptoms, which is why the problem is the selection of effective pharmacotherapy. Untreated disease results in worsening neuropsychological disorders. Pharmacotherapy involves the use of antibiotics. The use of antibacterial therapy reduces the risk of recurrence of clinical symptoms. [ABSTRACT FROM AUTHOR]

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Le syndrome des dysfonctions nonverbales (SDNV) est un trouble neurodéveloppemental n'appartenant à aucune classification officielle à ce jour. Il est caractérisé par trois déficits principaux : une perturbation des capacités visuospatiales, des déficits exécutifs et attentionnels ainsi que des difficultés socio-émotionnelles (jugement social, communication non verbale). Le cas de M. P. traite d'un syndrome rare, dont le diagnostic repose essentiellement sur le bilan neuropsychologique ainsi que sur un diagnostic différentiel avec le syndrome d'Asperger, le trouble déficitaire de l'attention, la déficience intellectuelle et la dyspraxie. Cette étude de cas interroge à la fois la difficulté à mettre en évidence un syndrome rare et peu étudié chez l'adulte, mais également la pertinence d'une prise en charge psychiatrique (e.g. habiletés sociales, suivi psychologique, accompagnement social permanent et rapproché, reconnaissance du handicap) pour un patient présentant un trouble des apprentissages d'origine neurologique. Dans le but de renforcer son autonomie et son insertion sociale, la réhabilitation psychosociale apparaît comme un acteur pertinent. Cet article présente l'intérêt de l'évaluation neuropsychologique pour le diagnostic différentiel et la nécessité d'une approche des soins axée sur le handicap psychique. Nonverbal learning disability is a neurodevelopmental disorder not belonging to any official classification to date. It is characterized by three core deficits: visuospatial impairments, executive and attentional deficits as well as socio-emotional disorders (social judgment, nonverbal communication). We describe a rare syndrome for which the diagnosis is essentially based on the neuropsychological assessment. Differential diagnoses are: Asperger syndrome, attention deficit hyperactivity disorder, intellectual disability and dyspraxia. This case study highlights the difficulty in identifying a rare and poorly studied syndrome in adults, but also the relevance of psychiatric care (e.g. social skills training, psychological counseling, continuous and close social support, recognition of disability) for a patient with a learning disability of neurological origin. In order to reinforce his autonomy and his social integration, psychosocial rehabilitation (development of resources necessary for proper functioning in the community) appears to be a relevant player. This article shows the interest of a neuropsychological assessment in the differential diagnosis and the need of care approach based on mental disability. [ABSTRACT FROM AUTHOR]

Among patients afflicted by congenital heart diseases (CHD) diverse, and complex neurological alterations are commonly observed. These have neither been completely identified nor understood. With the aim of identifying specific neurocognitive alterations among children and adolescents afflicted by CHD we investigated the possible presence of cognitive disorders related to the presence of cardiovascular disease with the aid of a sample of 20 patients (12 teenagers and 8 school-age children). Taken altogether, 9 of them were afflicted by simple and 11 by complex pathologies (respectively, CHDs/c). The Neuropsychological Test for Memory and Attention (Neuropsi), standardized for Mexico by Ostrosky et al. (2004), was individually applied to all participants. The information of cognitive performance was obtained in relation to the categories attention and memory, and the same areas allowed us to assess global performance. CHDc subjects performed significantly poorer compared to CHDs in i) attention and executive function, ii) memory and iii) attention and memory. Likewise, among CHDc subjects a significantly higher proportion of cases were diagnosed as abnormal in the same variables. Also a significant and negative correlation was determined between CHD severity and neuropsychological scoring. Children and adolescents afflicted by CHD are at high risk of developing cognitive function alterations including aspects of memory, attention and executive functions, alterations which are likely to be worst among those cases carrying CHDc conditions. [ABSTRACT FROM AUTHOR]

An assessment system for assessing the severity of neuropsychological disorders is presented in the following. In particular, it includes specific criteria for determining the severity of a disorder, which are in turn set in relation to the functionality and working ability of a patient or insured person. The assessment system is based on the criteria defined in Suva table 8 for assessing the psychological consequences of a brain injury. As a result, it is fundamentally consistent with it, but constitutes also a significant further development due to the inclusion of neuropsychological test results in the form of standard values as assessment criteria as well as combined with the explanations of their interpretation and application. In contrast to Suva table 8, the assessment system is independent of the insurance context defined in the Swiss Accident Insurance Law (UVG). It can therefore also be applied within the framework of the Swiss Invalidity Insurance Law (IVG) as well as the Swiss Health Insurance Law (KVG) and Swiss Law on Insurance Contracts (IVG). In this sense it is independent of the aetiology of the respective symptoms as well as independent of the artificial dichotomous difference between "organic" and "inorganic" mental disorders. The preparation and publication of this new criteria table shall provide a contribution towards further improvement of interrater reliability in the course of assessing the severity of neuropsychological disorders as well as assessing the functionality. Last but not least, the assessment system is also compatible with the criteria for assessing the severity of a neurocognitive disorder defined in the Diagnostic and Statistical Manual of Mental Disorders, fifth edition (DSM-5). [ABSTRACT FROM AUTHOR]

Genetic variants are traditionally known to shape the susceptibility to neuropsychiatric disorders. An increasing number of studies indicate that remodeling of the gut microbiome by genetic variance serves as a versatile regulator of gut-brain crosstalk and behavior. Evidence also emerges that certain behavioral symptoms are specifically attributed to gut microbial remodeling and gut-to-brain signals, which necessitates rethinking of neuropsychiatric disease etiology and treatment from a systems perspective of reciprocal gene-microbe interactions. Here, we present an emerging picture of how gut microbes and host genetics interactively shape complex psychiatric phenotypes. We illustrate the growing understanding of how the gut microbiome is shaped by genetic changes and its connection to behavioral outcome. We also discuss working strategies and open questions in translating associative gene-microbiome-behavior findings into causal links and novel targets for neurobehavioral disorders. Dual targeting of the genetic and microbial factors may expand the space of drug discovery for neuropsychiatric diseases.

The importance of including measures of emotion processing, such as tests of facial emotion recognition (FER), as part of a comprehensive neuropsychological assessment is being increasingly recognized. In clinical settings, FER tests need to be sensitive, short, and easy to administer, given the limited time available and patient limitations. Current tests, however, commonly use stimuli that either display prototypical emotions, bearing the risk of ceiling effects and unequal task difficulty, or are cognitively too demanding and time-consuming. To overcome these limitations in FER testing in patient populations, we aimed to define FER threshold levels for the six basic emotions in healthy individuals. Forty-nine healthy individuals between 52 and 79 years of age were asked to identify the six basic emotions at different intensity levels (25%, 50%, 75%, 100%, and 125% of the prototypical emotion). Analyses uncovered differing threshold levels across emotions and sex of facial stimuli, ranging from 50% up to 100% intensities. Using these findings as “healthy population benchmarks”, we propose to apply these threshold levels to clinical populations either as facial emotion recognition or intensity rating tasks. As part of any comprehensive social cognition test battery, this approach should allow for a rapid and sensitive assessment of potential FER deficits. (JINS, 2015, 21, 568–572) [ABSTRACT FROM PUBLISHER]

Résumé Malgré leur absence de spécificité diagnostique, les troubles cognitifs constituent l’une des caractéristiques centrales des troubles du spectre schizophrénique, du fait de leur fréquence et de leur retentissement. De ce fait, tout patient souffrant de tels troubles devrait pouvoir bénéficier d’une évaluation fonctionnelle pluridisciplinaire comprenant un bilan neuropsychologique. Ce bilan, réalisé en période de stabilité clinique et thérapeutique, permet de décrire le profil cognitif qui est propre à chaque patient et qui peut comprendre des atteintes de la neurocognition (fonctions exécutives, attentionnelles et mnésiques), de la cognition sociale et de la métacognition. Alors que les traitements médicamenteux et psychothérapiques influencent peu les troubles cognitifs primaires, la remédiation cognitive a montré, à travers de nombreux essais contrôlés et plusieurs méta-analyses, son efficacité dans la réduction de ceux-ci, ainsi que de leurs impacts. Différents programmes ciblant certains processus cognitifs spécifiques sont disponibles en langue française. Ces outils de soins non médicamenteux s’appuient sur des tâches rééducatives permettant de renforcer des capacités atteintes ou de compenser leurs altérations par le renforcement des capacités préservées, tout en visant l’impact fonctionnel des déficits cognitifs. La remédiation cognitive vient ainsi compléter l’action des médicaments et de la psychothérapie et apparaît comme un nouvel outil de soin permettant de favoriser le rétablissement des personnes. Cognitive impairments represent a core deficit of schizophrenia spectrum disorders. Cognition is severely impaired in patients with schizophrenia and compromises the recovery process. All patients should have an initial baseline assessment including neuropsychological and medical evaluation. After the initial treatment and stabilization of patients, neuropsychological profile of schizophrenia spectrum disorders regularly shows neurocognitive (attention, memory and cognitive function), social cognitive and metacognitive deficits. While antipsychotic medications and psychotherapy appear to have little effect on primary cognitive impairments, cognitive remediation has shown its effectiveness in reducing the cognitive deficits and their impacts in many controlled trials and meta-analyses. Many programs targeting specific components of cognition are available in French. These non-drug approaches are behavioral training based intervention that aims to improve cognitive processes and functional outcome. Cognitive remediation does not replace medical treatments or certain types of psychotherapy, but complements their effects for promoting people's recovery. [ABSTRACT FROM AUTHOR]

Résumé: L’évaluation et la prise en charge de la douleur chronique nécessitent de se référer au modèle bio-psychosocial. Ce modèle prend en compte la diversité du patient et permet de proposer une stratégie globale de traitement. Les Thérapies Comportementales et Cognitives (TCC) s’inscrivent dans cette démarche pluridisciplinaire qui prend en compte les facteurs somatiques mais aussi les aspects psychosocioprofessionnels. Elles s’intègrent dans le cadre d’une démarche scientifique expérimentale, basée sur les théories de l’apprentissage. La douleur chronique est considérée comme un comportement conditionné et le travail thérapeutique se centre sur le « comment faire face » au comportement actuel qui pose problème. Ces thérapies s’aident de plusieurs stratégies de traitement de manière concomitante et présentent moins de clivage entre le modèle médical et le modèle « psy ». De ce fait, elles sont bien acceptées par les patients. Cette approche a montré son efficacité et est bien documentée dans la littérature. Les Anglo-Saxons utilisent le terme de « psychoeducation ». [ABSTRACT FROM AUTHOR]

Neonatal Diabetes (ND) mellitus is a rare genetic disease (1 in 90,000 live births). It is defined by the presence of severe hyperglycaemia associated with insufficient or no circulating insulin, occurring mainly before 6 months of age and rarely between 6 months and 1 year. Such hyperglycaemia requires either transient treatment with insulin in about half of cases, or permanent insulin treatment. The disease is explained by two major groups of mechanism: malformation of the pancreas with altered insulin-secreting cells development/survival or abnormal function of the existing pancreatic β cell. The most frequent genetic causes of neonatal diabetes mellitus with abnormal β cell function are abnormalities of the 6q24 locus and mutations of the ABCC8 or KCNJ11 genes coding for the potassium channel in the pancreatic β cell. Other genes are associated with pancreas malformation or insufficient β cells development or destruction of β cells. Clinically, compared to patients with an ABCC8 or KCNJ11 mutation, patients with a 6q24 abnormality have lower birth weight and height, are younger at diagnosis and remission, and have a higher malformation frequency. Patients with an ABCC8 or KCNJ11 mutation have neurological and neuropsychological disorders in all those tested carefully. Up to 86% of patients who go into remission have recurrent diabetes when they reach puberty, with no difference due to the genetic origin. All these results reinforce the importance of prolonged follow-up by a multidisciplinary pediatric team, and later doctors specializing in adult medicine. 90% of the patients with an ABCC8 or KCNJ11 mutation as well as those with 6q24 anomalies are amenable to a successful switch from insulin injection to oral sulfonylureas., (Copyright © 2020 Beltrand, Busiah, Vaivre-Douret, Fauret, Berdugo, Cavé and Polak.)

Non-pharmacological therapies are now used in many nursing homes often with residents presenting a risk of behavioural disorders. They include music therapy, animal-assisted therapy, physical activity as well as other approaches such as light therapy or aromatherapy. It requires rigorous assessment, the permanent involvement and engagement of residents as well as the staff as part of a compassionate and participative approach., (Copyright © 2018 Elsevier Masson SAS. All rights reserved.)