The Neurobehavioral Evaluation System was designed for field studies of workers, but many NES tests can be performed satisfactorily by children as young as 7 or 8 years old and a few tests, such as simple reaction time, can be performed by preschool children. However, little comparative data from children of different ages or grade levels are available. Studies of school children in the Czech Republic indicate that 2nd-grade children could perform the following NES tests satisfactorily: Finger Tapping, Visual Digit Span. Continuous Performance, Symbol-Digit Substitution, Pattern Comparison, and simpler conditions of Switching Attention. Comparative scores of boys and girls from the 2nd, 4th, and 8th grades and power analyses to estimate appropriate sample size were presented. Performance varied systematically with grade level and gender. Larger samples were needed with younger children to achieve comparable levels of statistical power. Gender comparisons indicated that boys responded faster, but made more errors than girls.
- MeSH
- Diagnosis, Computer-Assisted instrumentation standards MeSH
- Child MeSH
- Cognition physiology MeSH
- Memory, Short-Term physiology MeSH
- Humans MeSH
- Adolescent MeSH
- Neuropsychological Tests standards MeSH
- Sex Characteristics MeSH
- Fingers physiology MeSH
- Psychomotor Performance physiology MeSH
- Aging psychology MeSH
- Verbal Learning physiology MeSH
- Check Tag
- Child MeSH
- Humans MeSH
- Adolescent MeSH
- Male MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Clinical Trial MeSH
- Research Support, Non-U.S. Gov't MeSH
- Research Support, U.S. Gov't, Non-P.H.S. MeSH
- Comparative Study MeSH
- Geographicals
- Czech Republic MeSH
Cyanobacteria are known for their ability to produce and release mixtures of up to thousands of compounds into the environment. Recently, the production of novel metabolites, retinoids, was reported for some cyanobacterial species along with teratogenic effects of samples containing these compounds. Retinoids are natural endogenous substances derived from vitamin A that play a crucial role in early vertebrate development. Disruption of retinoid signalling- especially during the early development of the nervous system- might lead to major malfunctions and malformations. In this study, the toxicity of cyanobacterial biomass samples from the field containing retinoids was characterized by in vivo and in vitro bioassays with a focus on the potential hazards towards nervous system development and function. Additionally, in order to identify the compounds responsible for the observed in vitro and in vivo effects the complex cyanobacterial extracts were fractionated (C18 column, water-methanol gradient) and the twelve obtained fractions were tested in bioassays. In all bioassays, all-trans retinoic acid (ATRA) was tested along with the environmental samples as a positive control. Retinoid-like activity (mediated via the retinoic acid receptor, RAR) was measured in the transgenic cell line p19/A15. The in vitro assay showed retinoid-like activity by specific interaction with RAR for the biomass samples. Neurotoxic effects of selected samples were studied on zebrafish (Danio rerio) embryos using the light/dark transition test (Viewpoint, ZebraLab system) with 120 hpf larvae. In the behavioural assay, the cyanobacterial extracts caused significant hyperactivity in zebrafish at 120 hpf after acute exposure (3 h prior to the measurement) at concentrations below the teratogenicity LOEC (0.2 g dw L-1). Similar effect was observed after exposure to fractions of the extracts with detected retinoid-like activity and additive effect was observed after combining the fractions. However, the effect on behaviour was not observed after exposure to ATRA only. To provide additional insight into the behavioural effects and describe the underlying mechanism gene expression of selected biomarkers was measured. We evaluated an array of 28 genes related to general toxicity, neurodevelopment, retinoid and thyroid signalling. We detected several affected genes, most notably, the Cyp26 enzymes that control endogenous ATRA concentration, which documents an effect on retinoid signalling.
- MeSH
- Biomass MeSH
- Biological Assay MeSH
- Water Pollutants, Chemical metabolism toxicity MeSH
- Behavior, Animal drug effects MeSH
- Zebrafish growth & development metabolism MeSH
- Embryo, Nonmammalian drug effects metabolism MeSH
- Gene Expression drug effects MeSH
- Mice MeSH
- Cell Line, Tumor MeSH
- Receptors, Retinoic Acid genetics metabolism MeSH
- Cyanobacteria growth & development metabolism MeSH
- Tretinoin metabolism toxicity MeSH
- Animals MeSH
- Check Tag
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
Cílem studie bylo ověření kvality českého překladu Addenbrookského kognitivního testu (Addenbrooke's Cognitive Examination, ACE). ACE je neuropsychologickou screeningovou testovou baterií, která slouží k zachycení demence a napomáhá k odlišení mezi demencí při Alzheimerově nemoci a frontotemporální demencí. Výzkumný soubor byl tvořen 60 pacienty s diagnostikovanou pravděpodobnou demencí Alzheimerova typu dle DSM IV a NINCDS-ADRDA kritérií. Všichni pacienti prošli vstupním neurologickým, základními biochemickými a morfologickými vyšetřeními. Administrovány byly též psychologické testy a škály, včetně ACE. Nejvýraznější kognitivní deficity v ACE byly zaznamenány v subtestech paměti a verbální fluence. Statistickým zpracováním byla zjištěna dobrá senzitivita českého překladu ACE testu: cut-off skór 88 vykazoval 100 senzitivitu a cut-off skór 83 vykazoval 96 senzitivitu pro zachycení demence. Položková reliabilita testu, hodnocená pomocí Cronbachova koeficientu alfa, dosahovala hodnoty 0,8. Lze konstatovat, že český překlad Addenbrookského kognitivního testu se jeví nejen jako nový užitečný test pro zhodnocení kognitivních deficitů, ale je i dostatečně kvalitním a senzitivním testem pro zachycení demence.
Velké množství pacientů s depresivní poruchou se potýká s narušením kognitivních a exekutivních funkcí, které má negativní psychosociální dopad a výrazně zhoršuje kvalitu života těchto nemocných. Tyto poruchy se v odborné literatuře označují souhrnným pojmem kognitivní deficit. Na jeho vzniku se podílí celá řada faktorů (působení dlouhodobého stresu narušující přirozenou plasticitu mozku, dysbalance neurotransmiterového systému atd.). Narušení mozkových funkcí má spíše globálně-difuzní charakter, nemá specifický profil a jeho průběh je ovlivňován mnoha klinickými faktory (např. subtypy a hloubka deprese, vliv medikace, hospitalizace atd.). Zdá se, že k tomuto poškození dochází ještě před rozvinutím plné depresivní symptomatologie a určitá míra narušení přetrvává i v období remise. Zhoršený výkon v neuropsychologických testech se dává do souvislosti s rozličnými strukturálními a funkčními změnami mozku (nejčastěji bývá poškozen hipokampus, amygdala a prefrontální kortex). Při diagnostice kognitivního deficitu je třeba vybírat vhodné, krátké a méně náročné neuropsychologické testy. Rehabilitační postupy vytvořené přímo pro depresivní pacienty s kognitivním deficitem zatím k dispozici nemáme, ale lze používat metody osvědčené u jiných poruch.
Number of patients sufferring from unipolar depression have problems with impairment of cognitive and executive functions which we marked as cognitive deficit. This deficit has a big influence on their quality of life, every day lifestyle, etc. Many different factors involve in formation of cognitive deficit like influence of longitudinal stress, imbalance of neurotransmitters, etc. Impairment of cognitive functions in depression has global diffused character, it does not has a specific profile and its course is influenced by many clinical factors (subtypes and severity of depression, medication, hospitalization…). Cognitive impairment is present in depression probably already before presence of symptomatology and also in remission of depression. We found different structural and functional brain abnormities in patients suffering from depression (especially hippocampus, amygdala, prefrontal cortex). During diagnostic process we should use short, unpretentious and adequate neuropsychological tests. Actually we have not rehabilitation procedures directly for patients with depression, so we use well tried methods from another disorders.
- MeSH
- Depressive Disorder complications physiopathology MeSH
- Humans MeSH
- Neurobehavioral Manifestations MeSH
- Neuropsychology MeSH
- Check Tag
- Humans MeSH
- Publication type
- Review MeSH
- MeSH
- Activities of Daily Living MeSH
- Dementia diagnosis classification physiopathology MeSH
- Cognition Disorders diagnosis MeSH
- Humans MeSH
- Neurobehavioral Manifestations MeSH
- Neurologic Examination methods standards MeSH
- Neuropsychological Tests MeSH
- Severity of Illness Index MeSH
- Check Tag
- Humans MeSH
Systémový lupus erytematodes (SLE) je chronické autoimunitní onemocnění se širokým spektrem klinických manifestací. Postižení nervového systému se objevuje až u 80 % pacientů se SLE. Diagnóza neuropsychiatrického postižení (NPSLE) je velmi obtížná vzhledem k rozmanitosti klinických projevů. Kognitivní dysfunkce (KD) je jednou z nejčastějších manifestací NPSLE. Příčina jejího vzniku není dosud zcela objasněna, uvažuje se o možné roli různých autoprotilátek, zánětlivých mediátorů, vaskulárních abnormalit a neuropeptidů. Diagnostika kognitivní dysfunkce je založena na testování všech podstatných oblastí kognitivních funkcí: hodnotí se percepce, pozornost, paměť, motorické a jazykové dovednosti, řešení problémů, exekutivní (řídící, též výkonové) funkce (schopnosti plánovat, účelně jednat a dosáhnout cíle).
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with a broad spectrum of manifestations. Involvement of the nervous system is present in up to 80% of patients with SLE. Diagnosis of neuropsychiatric involvement (NPSLE) is very difficult with regard to a variety of clinical symptoms. Cognitive dysfunction (CD) is one of the most common manifestations of NPSLE. Its cause has not yet been entirely elucidated; a possible role of various autoantibodies, inflammatory mediators, vascular abnormalities, and neuropeptides has been discussed. Diagnosis of cognitive dysfunction is based on the testing of all substantial areas of cognitive functions: perception, attention, memory, motoric and verbal abilities, problem solving, and executive (controlling, also performing) functions (abilities to plan, act effectively, and achieve a goal) are evaluated.
