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Статті в журналах з теми "Underlying cognitive deficits"
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Stanford, George, and Thomas Oakland. "Cognitive Deficits Underlying Learning Disabilities." School Psychology International 21, no. 3 (August 2000): 306–21. http://dx.doi.org/10.1177/0143034300213007.
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Dodd, Barbara, Judi Leahy, and Gail Hambly. "Phonological disorders in children: Underlying cognitive deficits." British Journal of Developmental Psychology 7, no. 1 (March 1989): 55–71. http://dx.doi.org/10.1111/j.2044-835x.1989.tb00788.x.
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Loe, Irene M., Heidi M. Feldman, Enami Yasui, and Beatriz Luna. "Oculomotor Performance Identifies Underlying Cognitive Deficits in Attention-Deficit/Hyperactivity Disorder." Journal of the American Academy of Child & Adolescent Psychiatry 48, no. 4 (April 2009): 431–40. http://dx.doi.org/10.1097/chi.0b013e31819996da.
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Wilmer, Jeremy B., Alexandra J. Richardson, Yue Chen, and John F. Stein. "Two Visual Motion Processing Deficits in Developmental Dyslexia Associated with Different Reading Skills Deficits." Journal of Cognitive Neuroscience 16, no. 4 (May 2004): 528–40. http://dx.doi.org/10.1162/089892904323057272.
Повний текст джерелаАнотація:
Developmental dyslexia is associated with deficits in the processing of visual motion stimuli, and some evidence suggests that these motion processing deficits are related to various reading subskills deficits. However, little is known about the mechanisms underlying such associations. This study lays a richer groundwork for exploration of such mechanisms by more comprehensively and rigorously characterizing the relationship between motion processing deficits and reading subskills deficits. Thirty-six adult participants, 19 of whom had a history of developmental dyslexia, completed a battery of visual, cognitive, and reading tests. This battery combined motion processing and reading subskills measures used across previous studies and added carefully matched visual processing control tasks. Results suggest that there are in fact two distinct motion processing deficits in developmental dyslexia, rather than one as assumed by previous research, and that each of these deficits is associated with a different type of reading subskills deficit. A deficit in detecting coherent motion is selectively associated with low accuracy on reading subskills tests, and a deficit in discriminating velocities is selectively associated with slow performance on these same tests. In addition, evidence from visual processing control tasks as well as self-reports of ADHD symptoms suggests that these motion processing deficits are specific to the domain of visual motion, and result neither from a broader visual deficit, nor from the sort of generalized attention deficit commonly comorbid with developmental dyslexia. Finally, dissociation between these two motion processing deficits suggests that they may have distinct neural and functional underpinnings. The two distinct patterns of motion processing and reading deficits demonstrated by this study may reflect separable underlying neurocognitive mechanisms of developmental dyslexia.
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Sagar, H. J. "Specificity of Cognitive Impairment in Neurological Disease: A Methodological Critique of Parkinson’s Disease." Behavioural Neurology 4, no. 2 (1991): 89–102. http://dx.doi.org/10.1155/1991/625647.
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Multiple cognitive deficits have been recognized in many neurological disorders but the specificity of the findings and the relationship to the underlying neuropathology remain obscure. Definitions of dementia have been proposed based on symptom profiles of the cognitive disorder and qualitative differences have been claimed between dementias of different aetiology. Some conditions have been claimed to show patterns of cognitive deficit that are distinguished from dementia and related to specific neuropathology or psychological processes, e.g. frontal lobe deficits in Parkinson's disease. Sometimes, a relationship has been established between certain cognitive deficits and particular neurochemical deficits which has led to the notion of specific drug treatment, e.g. cholinergic deficits and memory failure in Alzheimer's disease. However, these conclusions are often potentially flawed by methodological inadequacies. This critique presents some methodological issues relevant to the study of brain-behaviour and drug-behaviour relationships in syndromes of multiple cognitive deficit, using Parkinson's disease as the model. The following recommendations are made: rigid diagnostic criteria; representative patient groups; avoidance of arbitrary quantitative criteria to limit definitions of dementia; matching of groups for overall level of cognitive impairment in the search for qualitative cognitive differences related to neuropathology or effects of particular drugs; the use of suitable controls in patient groups, neuropsychological tests and treatment regimes; the use of specific quantitative tests of cognition, affect and motor disability; and longitudinal, compared with cross-sectional, study design.
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Cory-Slechta, Deborah. "Delineating behavioral domains underlying lead-induced cognitive deficits." Neurotoxicology and Teratology 32, no. 4 (July 2010): 497. http://dx.doi.org/10.1016/j.ntt.2010.04.005.
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McPhilemy, Genevieve, Leila Nabulsi, Liam Kilmartin, Denis O’Hora, Stefani O’Donoghue, Giulia Tronchin, Laura Costello, et al. "Neuroanatomical Dysconnectivity Underlying Cognitive Deficits in Bipolar Disorder." Biological Psychiatry: Cognitive Neuroscience and Neuroimaging 5, no. 2 (February 2020): 152–62. http://dx.doi.org/10.1016/j.bpsc.2019.09.004.
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Kalezic, Nevena, Ivan Dimitrijevic, Ljubica Leposavic, Mladen Kocica, Vesna Bumbasirevic, Cedomir Vucetic, Ivan Paunovic, Nemanja Slavkovic, and Jelena Filimonovic. "Postoperative cognitive deficits." Srpski arhiv za celokupno lekarstvo 134, no. 7-8 (2006): 331–38. http://dx.doi.org/10.2298/sarh0608331k.
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Cognitive dysfunctions are relatively common in postoperative and critically ill patients. This complication not only compromises recovery after surgery, but, if persistent, it minimizes and compromises surgery itself. Risk factors of postoperative cognitive disorders can be divided into age and comorbidity dependent, and those related to anesthesia and surgery. Cardiovascular, orthopedic and urologic surgery carries high risk of postoperative cognitive dysfunction. It can also occur in other types of surgical treatment, especially in elderly. Among risk factors of cognitive disorders, associated with comorbidity, underlying psychiatric and neurological disorders, substance abuse and conditions with elevation of intracranial pressure are in the first place in postoperative patients. Preoperative and perioperative predisposing conditions for cognitive dysfunction and their incidence were described in our paper. These are: geriatric patients, patients with substance abuse, preexisting psychiatric or cognitive disorders, neurologic disease with high intracranial pressure, cerebrovascular insufficiency, epilepsia, preeclampsia, acute intermittent porphyria, operation type, brain hypoxia, changes in blood glucose level, electrolyte imbalance, anesthetic agents, adjuvant medication and intraoperative awareness. For each of these factors, evaluation, prevention and treatment strategies were suggested, with special regard on anesthetic technique.
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Nieto, Rodrigo R., Hernán Silva, Alejandra Armijo, Rubén Nachar, Alfonso González, Carmen Paz Castañeda, Cristián Montes, and Manuel Kukuljan. "BDNF and Cognitive Function in Chilean Schizophrenic Patients." International Journal of Molecular Sciences 24, no. 13 (June 24, 2023): 10569. http://dx.doi.org/10.3390/ijms241310569.
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Despite cognitive symptoms being very important in schizophrenia, not every schizophrenic patient has a significant cognitive deficit. The molecular mechanisms underlying the different degrees of cognitive functioning in schizophrenic patients are not sufficiently understood. We studied the relation between brain-derived neurotrophic factor (BDNF) and cognitive functioning in two groups of schizophrenic patients with different cognitive statuses. According to the Montreal Cognitive Assessment (MoCA) results, the schizophrenic patients were classified into two subgroups: normal cognition (26 or more) and cognitive deficit (25 or less). We measured their plasma BDNF levels using ELISAs. The statistical analyses were performed using Spearman’s Rho and Kruskal–Wallis tests. We found a statistically significant positive correlation between the plasma BDNF levels and MoCA score (p = 0.04) in the subgroup of schizophrenic patients with a cognitive deficit (n = 29). However, this correlation was not observed in the patients with normal cognition (n = 11) and was not observed in the total patient group (n = 40). These results support a significant role for BDNF in the cognitive functioning of schizophrenics with some degree of cognitive deficit, but suggest that BDNF may not be crucial in patients with a normal cognitive status. These findings provide information about the molecular basis underlying cognitive deficits in this illness.
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Zulkifli, Nathratul Ayeshah, JesJeet Singh Gill Jeswant Singh, and Ng Chong Guan. "Sudden Cognitive Decline in Bipolar Mood Disorder Patient with Underlying Severe Tardive Dyskinesia After the Failure of His Deep Brain Stimulation Device Battery." Malaysian Journal of Science Health & Technology 7, no. 3 (September 1, 2021): 79–81. http://dx.doi.org/10.33102/mjosht.v7i3.163.
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Bipolar disorder (BD) is a chronic mood disorder associated with multiple comorbidities. Structural and functional abnormalities in these subjects’ brains have been related to cognitive deficits correlated with the severity of the mood symptoms. These deficits are also present in euthymic states, indicating a trait characteristic. Bipolar subjects would risk developing tardive dyskinesia due to being exposed to long periods of antipsychotic treatment. Unfortunately, the presence of tardive dyskinesia is also associated with worsening cognition. One treatment option for severe tardive dyskinesia is deep brain stimulation that has also been implicated with cognitive decline. We present a case of Bipolar disorder with underlying cognitive impairment, who had a deep brain stimulation device inserted for severe tardive dyskinesia. He was admitted to a depressive phase and was noted to have a sudden worsening of cognitive impairment following his deep brain stimulation device battery running low. Possible explanations discussed for this unexpected observation are attributed to a further deterioration of his tardive dyskinesia following the device failure and depressive episode, which causes added pseudo-cognitive deficit signs.
Дисертації з теми "Underlying cognitive deficits"
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Bull, Rebecca. "Cognitive deficits underlying children's mathematical difficulties." Thesis, University of St Andrews, 1998. http://hdl.handle.net/10023/15456.
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Many children have difficulties learning mathematics, and the consequences of poor mathematical skills are very far reaching. Studies examining the reasons why children struggle to learn mathematics are scarce, particularly in comparison to studies examining reading difficulties. The studies reported in this thesis attempted to provide insights into the cognitive limitations that may lead some children to have difficulties learning mathematics, re-examining some of the cognitive deficits already thought to be associated with mathematical difficulties, as well as providing the starting point for new lines of enquiry. Five main studies are reported. Four of these studies examined a range of cognitive skills and identify a number of fundamental cognitive mechanisms as playing a role in children's mathematical skills, these being a slowness in the speed of processing information, poor control of executive functioning, evidenced through difficulty switching strategies and poor self-regulation of actions, and a delay in the automatization of basic arithmetic facts. The final study aimed to investigate the implications of these recognised cognitive difficulties in the teaching of mathematics, and explored the use of two different teaching strategies, rote learning of basic arithmetic facts and a discussion method to allow alternative methods of solution to be learned, both of which attempted to overcome some of these cognitive limitations. Rote learning was found to be an effective device to improve performance in different areas of mathematical skill. The implications of this research and the foundations for future research are also discussed.
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Waters, Flavie. "Cognitive dysfunction underlying auditory hallucinations in schizophrenia : a combined-deficits model." University of Western Australia. School of Psychiatry and Clinical Neurosciences, 2005. http://theses.library.uwa.edu.au/adt-WU2005.0047.
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[Truncated abstract] Auditory hallucinations are some of the most distressing and disabling symptoms of schizophrenia. However very little is known about the exact processes responsible for auditory hallucinations. The aim of this thesis is to provide a new perspective on the nature of the cognitive deficits underlying auditory hallucinations in schizophrenia. As a preliminary study to the investigation of auditory hallucinations in schizophrenia, a factor analysis of a measure of hallucinatory predisposition, the Launay- Slade Hallucination Scale-Revised (Bentall & Slade, 1985), was carried out on data from a large sample of undergraduate students (N = 562). An overlap in characteristics between hallucinatory-like experiences in normal individuals and auditory hallucinations in schizophrenia should draw attention to factors that are important to the hallucinatory experience in general. One of the findings from this study was that intrusiveness is a commonly reported characteristic of hallucinatory-like experiences in normal individuals. Intrusiveness is also one of the defining features of auditory hallucinations in schizophrenia. Since the process of inhibition is essential for suppressing unwanted thoughts, the first set of two studies using patients with schizophrenia (N = 43) investigated the presence of an (intentional) inhibition failure in auditory hallucinations using the Hayling Sentence Completion Test (HSCT; Burgess & Shallice, 1996) and the Inhibition of Currently Irrelevant Memories Task (ICIM; Schnider & Ptak, 1999). It was found that auditory hallucinations were linked to a deficit in intentional inhibition as measured by these tasks. The process of inhibition was further investigated using the Affective Shifting task, but auditory hallucinations were not associated with a deficit on this task. Possible differences in the inhibitory demands of the HSCT, ICIM and Affective Shifting tasks are discussed.
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Wong, Hon-kwan, and 黃漢鈞. "Cognitive factors underlying pragmatic deficits in children with autism spectrum disorder." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/209676.
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Pragmatic language impairments have been found in children with high-functioning Autism (HFA). Limited studies have investigated the contributing factors. This study compared 23 children with HFA with 28 typically-developing children on pragmatic language measures, with their age, cognitive ability and language ability matched or controlled. Deficit of children with HFA was found in making inferences in comprehension but not in narrative ability, and abilities to make inferences in narrative and about psychological state. Theory of mind was an impairment for children with HFA and correlated with inferences about psychological state. In the measure of executive functioning at visual-perceptual level, better performance was found in children with HFA. This cognitive factor did not correlate with any pragmatic language measure.published_or_final_version
Educational Psychology
Master
Master of Social Sciences
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Knapman, Alana. "Cognitive Deficits and their Underlying Structural and Functional Alterations in Mice Selectively Bred for High Stress Reactivity." Diss., lmu, 2010. http://nbn-resolving.de/urn:nbn:de:bvb:19-125411.
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Morgan, Amanda. "Developmental Dyslexia and/or co-occurring Attention Deficit: Investigation of prevalence, underlying cognitive deficits, and family risk in a self-selected sample of parents and children." Thesis, Griffith University, 2017. http://hdl.handle.net/10072/376518.
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Reading acquisition is a major developmental achievement and plays a critical role in determining academic achievement. Developmental dyslexia is a heritable disorder with up to 66% of at-risk children later diagnosed with the disorder. Children with dyslexia represent a vulnerable group at high risk of underachievement at school, as well as for poorer socio-emotional outcomes. Dyslexia and Attention Deficit Hyperactivity Disorder (ADHD) commonly co-occur, and recent theories hypothesise that it is the inattentive (AD) symptom domain that is most closely associated with literacy problems. Despite an extensive overlap in symptoms, and a close genetic association, they have primarily been investigated as distinct disorders. However, recent theoretical models propose a multiple deficit framework to examine shared cognitive deficits as an explanation for their co-occurrence.
This research had seven aims: (1) investigate the prevalence of single and multiple developmental disorders, in a sample of children with a previous diagnosis of dyslexia or attention deficit, with or without hyperactivity disorder (ADHD, AD), or who had been identified by parents as underachieving in school; (2) determine whether the severity of the deficits found would be greater in children with more than one disorder compared to a single disorder; (3) validate an adult self-report protocol used to screen for dyslexia and ADHD, and use this measure to estimate family risk of each disorder; (4) determine the prevalence of symptoms of dyslexia, ADHD or AD in children with and without a family risk of dyslexia, ADHD or AD; (5) determine whether a single, double, multiple, or an intergenerational multiple deficit model is the best predictor of reading fluency; (6) examine the extent that difficulties with phonological awareness and rapid automatic naming differentiate dyslexia, and difficulties with interference control differentiate ADHD and AD; and (7) examine the Multiple Deficit Model as an explanation of the co-occurrence between dyslexia + ADHD, and dyslexia + AD using cognitive variables identified in the literature as common to both disorders. Seventy-two children aged 9 to 11 years of age, were assessed on a broad range of cognitive, reading, language, motor and attention measures. In Study 1 (Chapter 3), prevalence rates were estimated for the single and multiple developmental disorders using the clinical and subclinical scores from the reading, attention, language and motor measures. The hypothesis that most children would show evidence of more than one developmental disorder was not met using clinical criteria, as the overall prevalence rates for single and multiple disorders were similar. However, when subclinical symptoms were included, most children diagnosed with one disorder had subclinical symptoms of at least one other disorder. Results from one-way ANOVAs showed the groups with co-occurring dyslexia + AD, or dyslexia + ADHD were not more impaired than the single disorder groups, indicating that the severity of each disorder was not influenced by the number of disorders experienced by each child.
The Adult Reading Questionnaire (ARQ) and Adult ADHD Self-Report Scale (ASRS) are self-report protocols designed to evaluate reading, writing and spelling proficiency, expressive language difficulties (word finding), as well as problems of organization, attention and hyperactivity in adults. One hundred and seventeen parents (64 mothers and 53 fathers) completed the self-report questionnaire and the data was used to replicate the factor structures of the ARQ and ASRS separately (Study 2, Chapter 4). The parent data was then used to estimate family risk of dyslexia and ADHD or AD in the child sample, and the results supported the hypothesis that children from a family with parent-reported reading difficulties were significantly more likely to have clinical symptoms of dyslexia than children without family risk. Similarly, children whose parents reported symptoms of ADHD were more likely to have clinical and subclinical symptoms of ADHD, than children coming from a family without parental report of these disorders. Correlation, regression, logistic regression analyses, and odds ratios indicated a strong influence of parent-reported reading difficulties on child reading difficulties, as 70.4% of children at family risk of dyslexia had scores in the clinical range on the reading measure. The association between parent-reported symptoms and a child diagnosis was weaker for ADHD, as less than half (42.9%) the children at family risk met criteria for a clinical diagnosis, however, when subclinical symptoms were included, the children of parents with self-rated symptoms of ADHD were more likely to have clinical or subclinical symptoms than children from no-risk families. No significant association was found between parent-reported symptoms and a child diagnosis of AD.
In Study 3 (Chapter 5), correlation and multiple regression analyses were used to evaluate a number of cognitive variables (phonological awareness, rapid naming, and expressive language) identified in the research literature to be impaired in individuals with dyslexia. Single, double, and multiple deficit frameworks were used to determine which model best predicted reading fluency, with the results showing that children presented with a combination of deficits, indicating various pathways to dyslexia. Using the intergenerational multiple deficit model to examine the association between parent-reported reading difficulties and children’s reading fluency, it was shown that parent self-reported difficulties accounted for a substantial proportion (18.6%) of the variance in children’s reading fluency scores. After controlling for parent self-reported reading skills, phonological awareness and rapid letter naming each made additional contributions to the explanation of children’s reading fluency.
Finally, a multiple deficit model was used to achieve the final research aim (Study 4, Chapter 6). Mixed factorial ANOVAs, and moderated regression analyses were conducted to determine if impairments in phonological awareness and rapid automatic naming were unique to dyslexia, and if impairments in interference control were unique to ADHD and AD. The contribution of working memory and reading comprehension were examined as explanations of the co-occurrence between dyslexia and ADHD or AD. The ability to inhibit distractors (interference control) was found to be impaired in each of the three groups, however some differences were noted. The group with dyslexia responded more slowly on the incongruent Flanker condition, and the ADHD group was less accurate on both the congruent and incongruent conditions, while the AD group were found to be both slower and less accurate on each of the conditions. Phonological awareness and reading comprehension were found to be unique predictors of dyslexia. The relationship between reading fluency and working memory was moderated by AD and ADHD. When symptoms of AD and ADHD were low, working memory improved as reading fluency improved, however this was not the case when symptoms of AD and ADHD were high, where an increase in reading fluency was not accompanied by increases in working memory capacity. Although weaker, reading fluency and rapid naming was moderated by AD, however no association was found for ADHD.
From a theoretical perspective, this research advances our understanding of the co-occurrence between dyslexia, ADHD and AD in school age children, as well as the associations between some of the cognitive variables associated with the disorders. This research highlights the high prevalence of dyslexia among children at family risk, and the important contribution of parent-reported difficulties to the explanation of their children’s reading fluency. At a practical level this research is expected to contribute to the better identification of children with reading and attention difficulties. The findings demonstrate the substantial overlap between the symptoms of dyslexia and inattention, and the importance of assessing for both disorders. The success of reading interventions has been found to be limited, and this may be due to the high prevalence of attention deficits which co-occur with dyslexia and that may interfere with remediation. When underlying attentional difficulties are identified, appropriate cognitive training programs can be implemented in conjunction with reading remediation to improve academic performance in school.Thesis (Professional Doctorate)
Doctor of Philosophy in Clinical Psychology (PhD ClinPsych)
School of Applied Psychology
Griffith Health
Full Text
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Harrar-Eskinazi, Karine. "Dyslexie développementale et méthodes de remédiation : Conception et évaluation d'un programme d'intervention multimodale et multi-componentielle fondé sur les approches phonologique, visuo-attentionnelle et intermodalitaire." Electronic Thesis or Diss., Université Côte d'Azur, 2023. http://www.theses.fr/2023COAZ2025.
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Parmi les troubles du langage écrit, la dyslexie développementale est définie comme un trouble spécifique de l'apprentissage du langage écrit dont les répercussions sur les apprentissages scolaires, durables et délétères, nécessitent des réponses thérapeutiques efficaces. Les études sur la remédiation de la dyslexie développementale sont généralement fondées sur l'hypothèse causale d'une altération plus ou moins exclusive d'un processus cognitif sous-jacent. Or, chez la majorité des lecteurs dyslexiques, de multiples déficits cognitifs sous-jacents, variables selon les individus, seraient simultanément responsables des troubles comportementaux de la lecture et de l'orthographe. Ainsi, une multifactorialité étiologique de la dyslexie développementale entraîne une hétérogénéité sémiologique qui s'exprime dans une variabilité clinique très complexe dont les contours imprécis peuvent entraîner un diagnostic incertain, ce que nous avons nommé variabilité nosographique.Dans ce contexte théorique et à la lumière des modèles à déficits multiples de la dyslexie développementale, nous avons élaboré un protocole de remédiation multimodale et multi-componentielle ciblant à la fois les processus cognitifs sous-jacents audio-phonologiques, visuo-attentionnels et intermodalitaires et les troubles de la lecture et de l'orthographe, selon une approche qui combine plusieurs entrainements conçus en fonction du profil sémiologique individuel. Grâce à la participation de 94 orthophonistes, nous avons évalué les bénéfices de ce protocole à partir d'un essai clinique, multicentrique, longitudinal, randomisé, croisé, mené en trois phases sur une durée totale de 16 mois, auprès de 144 lecteurs dyslexiques âgés de 8 à 13 ans. Lors de la première phase, les participants répartis aléatoirement en deux groupes, ont bénéficié pendant 2 mois de consultations de rééducation orthophonique hebdomadaires sans entraînement intensif. Lors de la deuxième phase, les participants ont bénéficié, outre leur suivi hebdomadaire, de trois types d'interventions intensives informatisées d'une durée de deux mois chacune. Les deux premières interventions ciblent les processus audio-phonologiques et visuo-attentionnels (dont l'ordre est contrebalancé entre les deux groupes) puis sont suivies d'une intervention qui cible les processus intermodalitaires. La construction des trois programmes d'entraînement s'est appuyée sur la littérature scientifique, l'expertise des orthophonistes, la plainte du patient (décision partagée de soin) et sur le contexte environnemental. Lors de la troisième phase, les interventions intensives ont été interrompues et les consultations hebdomadaires de rééducation orthophonique maintenues pendant deux mois. A l'issue du protocole de remédiation, les effets de l'intervention multimodale et multi-componentielle intensive ont montré une amélioration significative de l'efficience en lecture (d de Cohen=2,3), de la compréhension en lecture (d de Cohen=0,9) et de l'orthographe (d de Cohen=0,78), comparée à une rééducation orthophonique hebdomadaire (première phase), et ce quel que soit l'ordre des interventions. L'analyse de cas multiples a révélé qu'à l'issue du protocole de remédiation 52 % des participants n'avaient plus de trouble de la lecture. En conclusion, nos résultats montrent l'efficacité d'une remédiation intensive multimodale et multi-componentielle dans le traitement de la dyslexie développementale. Ces résultats confirment le caractère davantage curatif que compensatoire de nos interventions et ouvrent une nouvelle piste pour la remédiation de la dyslexie développementaleDyslexia is a neurodevelopmental disorder that affects children's ability to read and spell words accurately and effectively. Most remediation studies are based on the hypothesis that the core deficit in dyslexic children is based on a single underlying cognitive deficit. However, a large number of studies suggest that most dyslexic children exhibit multiple underlying cognitive deficits that are simultaneously present to varying degrees, leading to a wide range of clinical disorders in reading and spelling. Thus, etiological multifactoriality in developmental dyslexia leads to semiological heterogeneity which explains clinical variability and leads to complex diagnosis, which we called nosographic variability. In line with multi-deficit models of developmental dyslexia, we designed and evaluated a remediation study with a multimodal and multi-componential protocol, which aimed at enhancing both underlying cognitive processes (audio-phonological, visual-attentional, and crossmodal) and reading and spelling procedures, using several training programs and taking into account the child's semiological profile.We assessed benefits of the protocol through a multicenter, longitudinal, randomized, crossover and clinical trial including 3 stages that lasted for a total duration of 16 months. An overall of 94 speech and language therapists and 144 dyslexic readers (aged around 8-13 years) participated in the study.In the first phase, participants were randomly assigned to 2 groups and received weekly speech and language therapy for 2 months without intensive training. In the second phase, in addition to weekly follow-up sessions with the speech therapist, participants received 3 types of intensive computer-based interventions for 2 months each. The first 2 interventions focused on audio-phonological and visual-attentional processes (the order of which was counterbalanced between the 2 groups) and were followed by a third intervention that focused on cross-modal integration processes. The construction of the 3 training programs was based on the scientific literature, the expertise of the speech and language therapists, the patient's complaint (shared care decision) and the environmental context. In the third phase, intensive interventions were discontinued and weekly speech therapy consultations were continued for two months. At the end of the remediation protocol, the multimodal and multi-componential intensive intervention lead to significant improvement in reading efficiency (Cohen's d=2.3), reading comprehension (Cohen's d=0.9), and spelling (Cohen's d=0.78), compared to the weekly speech and language therapy (first phase), and regardless of the order of the interventions. Multiple-case analysis revealed that 52 % of participants were reading disorder free.In conclusion, our results show that an intensive intervention based on a multi-componential and multimodal training program produces major benefits in the treatment of developmental dyslexia. These findings are consistent with a curative (rather than a compensatory) approach for remediation and open up a new avenue for developmental dyslexia treatment
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Thompson, Hannah Elizabeth. "Deficits of semantic cognition in stroke aphasia : underlying causes and ameliorating factors." Thesis, University of York, 2012. http://etheses.whiterose.ac.uk/3721/.
Повний текст джерелаАнотація:
Research suggests that semantic memory deficits can occur in at least three ways. Patients can (1) show amodal degradation of concepts within the semantic store itself, such as in semantic dementia (SD), (2) have an impairment of semantic control, leading to difficulty accessing appropriate knowledge in line with current goals or context, as in semantic aphasia (SA), and (3) experience a semantic deficit in only one modality following degraded input from sensory cortex. Patients with SA show damage to prefrontal cortex which extends posteriorly (PF+), or damage restricted to temporoparietal regions (TP-only), and have deficits of semantic control and ‘access’ across word and picture tasks, consistent with the view that their problems arise from impaired multimodal control processes. This thesis aims to explore the nature of these deficits, in four themes. (1) “Refractory effects” in SA patients are explored across modalities – i.e., these patients are shown to experience declining accuracy in cyclical matching tasks when semantically-related sets are presented rapidly and repeatedly. (2) We studied one case study with ‘verbal-only’ refractory effects, to investigate an apparent anomaly in the literature – the existence of patients who have ‘access’ deficits which are restricted to a single modality. These patients challenge the notion that semantic control processes are modality-general. We assessed the hypothesis that multimodal semantic control/ access impairments can follow a modality-specific pattern if paired with an input deficit of a single modality. (3) We explore the effect of lesion location on behavioural performance of semantic aphasia (SA) patients, who have PF+ or TP-only lesions by bringing together data published previously in different papers, together with some new SA cases. Past research suggests SA patients with these two lesions may show similar deficits of semantic control, yet the functional neuroimaging literature proposes a unique role for the prefrontal cortex. PF+ patients were less fluent, showed more associative picture naming errors, and overall somewhat stronger SA characteristics (e.g., they were more inconsistent, and less affected by frequency). (4) Semantic control recruits a wide cortical network, in both the left hemisphere (LH) and right hemisphere (RH). Semantic representations in the RH are partially distinct from the LH, including specialised knowledge of faces and metaphors. Our aim was to test whether damage to RH control regions would negatively affect performance on semantic control tasks which use items stored in the RH, in a similar way to our SA patients in the LH. Overall, the results suggest that semantic control operates in an amodal fashion, with deficits found across modalities. There was evidence to suggest a wide network involved in semantic control beyond the prefrontal cortex – including left posterior cortex and right hemisphere regions. However, these regions are subtly distinct in their role in semantic control.
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Cléry-Melin, Galichon Marie-Laure. "Étude des fonctions neurocognitives dans la dépression : caractérisation de déficits motivationnels et cognitifs, évaluation de leur valeur pronostique Why don't you try harder? An investigation of effort production in major depression Neural mechanisms underlying motivation of mental versus physical effort Psychomotor retardation is a scar of past depressive episodes, revealed by simple cognitive tests Are cognitive deficits in major depressive disorder progressive? A simple attention test in the acute phase of a major depressive episode is predictive of later functional remission Progress in elucidating biomarkers of antidepressant pharmacological treatment response: a systematic review and meta-analysis of the last 15 years Stability of the diagnosis of seasonal affective disorder in a long-term prospective study." Thesis, Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCB218.
Повний текст джерелаАнотація:
Les données issues de la recherche en neurosciences permettent de considérer la dépression comme une affection invalidante générale, caractérisée par des déficits neurocognitifs et comportementaux, au delà des symptômes dépressifs cliniques définis dans les classifications nosographiques. Ces déficits coexistent à la phase aiguë d’un épisode dépressif caractérisé (EDC) et interfèrent dans la prise de décision et réalisation d’un comportement orienté vers un but, et la sensation d’effort associée. Ils semblent persister en période de rémission clinique, altérant la qualité de la réponse thérapeutique et fonctionnelle et aggravant à terme le pronostic du trouble. L’objectif de ce travail est d’identifier des marqueurs neurocognitifs objectivement mesurables en pratique clinique, et d’étudier leur association au pronostic d’un EDC, afin de mieux prédire les probabilités de rémission et d’optimiser les stratégies de prescription thérapeutique des patients. L’altération des processus neurocognitifs liés à la récompense constitue un premier marqueur de vulnérabilité du trouble dépressif : dans une étude explorant la production d’un effort moteur dans le but d’obtenir une récompense, les patients déprimés présentaient un déficit de production d’effort, à la différence des sujets sains. Ce trouble de la motivation par incitation - processus sous tendu en imagerie fonctionnelle chez le sujet sain par l’activation de circuits cortico-striataux ventraux -pourrait constituer une dimension spécifique de la maladie dépressive. Participant à l’altération des processus de prise de décision et d’action, ce déficit motivationnel est associé, et possiblement secondaire, à des déficits plus spécifiquement cognitifs que nous avons ensuite étudiés. Dans une étude explorant plusieurs fonctions cognitives chez des patients déprimés au sein d’une large cohorte, la présence d’un ralentissement psychomoteur séquellaire après 6 à 8 semaines de traitement – chez des patients pourtant en rémission clinique -, était positivement et de manière indépendante, significativement corrélée au nombre d’épisodes dépressifs passés, constituant ainsi un marqueur d’une sévérité « cumulative » du trouble dépressif. Enfin, dans une revue de la littérature sur le caractère progressivement évolutif des déficits cognitifs dans le trouble dépressif unipolaire, nous avons discuté l’existence d’un effet « neurotoxique » cérébral de l’accumulation d’EDC, à l’origine de troubles neurocognitifs et de conséquences sur le cours évolutif de la maladie (risque majoré de rémission clinique et/ou fonctionnelle partielle, de récurrence, d’évolution démentielle). Un des principaux intérêts de l’identification de marqueurs de vulnérabilité cliniques et cognitifs est de mettre en évidence leur rôle prédictif du cours évolutif d’un épisode -ou d’un trouble- dépressif. Dans une étude menée sur une cohorte de plus de 500 patients déprimés, une variable attentionnelle (d2 test d’attention) était capable de prédire l’évolution ultérieure vers la rémission complète (clinique et fonctionnelle) de façon significative, linéaire, et indépendante des autres variables et de représenter un marqueur-trait de la dépression, aisément utilisable en pratique clinique. D’autres marqueurs cognitifs (tels que les fonctions exécutives) ont montré une valeur prédictive élevée de la réponse thérapeutique, avec une précision proche de celle de marqueurs d’imagerie ou électrophysiologie, selon les résultats d’une méta-analyse récente, justifiant leur emploi dans le suivi des patientsHese deficits coexist in the acute phase of a depressive episode and interfere with decision-making and goal-directed behaviors, and the associated feeling of effort. They appear to persist in periods of clinical remission, decreasing the quality of the therapeutic and functional response and lately worsening the prognosis of the disorder. The aim of this work is to identify objectively measurable neurocognitive markers in clinical practice, and to study their association with the prognosis of a depressive episode, in order to better predict remission and potentially to optimize therapeutic prescribing strategies for patients accordingly. The impairment of neurocognitive processes related to reward constitutes a first vulnerability marker for major depressive disorder (MDD): in a study assessing the production of motor effort in order to obtain a reward, depressed patients had a deficit in production of effort, unlike healthy subjects. Such deficit in incentive motivation - a process underpinned by the activation of ventral cortico-striatal circuits in healthy subjects - may constitute a specific dimension of MDD. It participates in the decision-making and action processes impairments and is associated with – and possibly a consequence of- more specifically cognitive deficits. In a study assessing several cognitive functions in a large cohort of depressed patients, the persistence of psychomotor retardation after 6 to 8 weeks of treatment - in patients considered as being in clinical remission - was positively and independently correlated with the number of past depressive episodes, thus constituting a marker of "cumulative" marker of past depressive episodes. Finally, in a literature review on the progressive evolution of cognitive deficits in MDD, we discussed the existence of a “neurotoxic” effect of the lifetime accumulation of depressive episodes on neurocognitive deficits and its consequences on disease prognosis (increased risk of incomplete functional/clinical remission, relapses, evolution towards dementia). One of the main interest in identifying clinical and cognitive markers of vulnerability is to highlight their capacity to predict the course of a depressive episode-or disorder. In a study based on a cohort of more than 500 depressed patients, a measurement of attention (d2 attention test) was able to significantly and independently predict the subsequent course towards complete remission (clinical and functional) and to constitute a trait -marker of depression, easy to use in clinical practice. Other cognitive markers (such as executive functions) have shown high predictive values for therapeutic response, comparable to those provided by imaging or electrophysiology markers, according to the results of a recent meta-analysis, that emphasizes the interest of using them in patient’s follow-up. Finally, in order to better assess the prognosis of depressive disorder, we have shown that Seasonal Affective Disorder (SAD) diagnosis criteria - which nevertheless represents a specific depressive disorder with well-known physiopathology substrates (construction validity) - had a low predictive validity, prompting to consider this disorder as a temporary expression of a mood disorder, rather than a specific disorder. The identification of clinical tools measuring motivational and cognitive deficits in clinical routine and predicting the course of a depressive episode or disorder represents a major challenge in the improvement of personalized therapeutic management and the long-term prognosis in depressed patients
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Araújo, Susana. "Cognitive processes underlying reading and naming deficits in dyslexic readers." Doctoral thesis, 2011. http://hdl.handle.net/10400.1/5580.
Повний текст джерелаАнотація:
In addition to phonological deficits, difficulties at the level of the visual recognition system (i. e. , the mechanisms that could affect the induction of orthographic representations or the connection of visual to lexical codes) constitute potential sources of the poor reading and visual naming that characterize dyslexia.Os estudos apresentados nesta tese sugerem que um défice no sistema de processamento fonológico por si só não é suficiente para explicar o padrão de resultados que caracterizam os leitores disléxicos, pelo menos no contexto de uma ortografia intermédia como o português. É sugerido que, nestes leitores, a existência de problemas ao nível do reconhecimento visual possa contribuir adicionalmente para os seus défices de leitura e de nomeação visual. Estes problemas parecem situar-se não apenas ao nível do processamento lexical das representações ortográficas (por exemplo, uma pobre representação ortográfica dos estímulos linguísticos) mas também nas etapas mais precoces de processamento visual, pré-lexical.
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Sanchez, Bezanilla Sonia. "Functional deficits after stroke: the key underlying mechanisms and the therapeutic potential of growth hormone." Thesis, 2020. http://hdl.handle.net/1959.13/1424038.
Повний текст джерелаАнотація:
Research Doctorate - Doctor of Philosophy (PhD)Background and aims: Stroke is currently the leading cause of long-term disability worldwide. Despite the efforts to minimise these negative outcomes, few treatments have been approved and have been mainly focused on the acute phase. This has led to a challenging situation where more than 90% of stroke survivors will experience long-lasting impairments in motor function and/or cognition. Therefore, clinical and pre-clinical research should focus on improving the understanding of underlying mechanisms contributing to neurological damage and functional impairment in later stages after stroke. One of the possible mechanisms that could explain these impairments is the development of secondary neurodegeneration (SND) in remote brain areas synaptically connected to the primary infarct site, such as the thalamus and hippocampus. This process is especially interesting because it occurs over a timescale of weeks to years after the primary infarct, providing a very interesting therapeutic target for chronic stroke treatment. This thesis focused on investigating the evolution of the functional outcomes after stroke and the mechanisms associated with these deficits (Chapter 3 and 4). Additionally, I was interested in studying a potential therapeutic intervention such as growth hormone (GH) to promote brain plasticity and alleviate motor and cognitive impairment (Chapter 5 and 6). Methods: The photothrombotic stroke model targeting the motor and sensory cortex was used to induce ischemia in mice. A touchscreen platform was used to analyse cognitive performance, and the grid walk and cylinder test were used to assess motor function. I also analysed the changes occurring after stroke in different brain areas (peri-infarct, thalamus and hippocampus) combining various molecular biology techniques such as Western Blot, immunohistochemistry, immunofluorescence and various histological stainings. In chapters 5 and 6, I used recombinant human GH (rhGH) delivered subcutaneously via a mini-osmotic pump for 28 days. Results: Stroke significantly impairs multiple cognitive domains and these deficits last for months after the primary infarction. Motor impairments were also long-lasting but a modest spontaneous recovery was observed over time. These deficits were associated with SND processes such as neuronal death, neuroinflammation (astrogliosis and microglia activation) and accumulation of neurotoxic proteins (amyloid-β and α-synuclein) in the thalamus and hippocampus (Chapters 3 and 4). Additionally, motor and cognitive impairment could be reversed by using GH as a therapeutic intervention. GH enhanced functional outcomes through a series of neurorestorative mechanisms including neurogenesis, synaptic plasticity and cerebrovascular remodelling (Chapters 5 and 6). Conclusion: Overall, in this thesis, I have deepened our understanding regarding cognitive and motor impairment after stroke and the mechanisms associated with these impairments. These important findings provide potential targets for translational medical research in the future. Finally, I have demonstrated that GH is an effective treatment following experimental stroke to promote brain plasticity and functional performance in the recovery phase after stroke. My results are encouraging and support the idea that GH represents a promising therapeutic intervention, which should be considered for clinical studies.
Книги з теми "Underlying cognitive deficits"
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Leeman-Markowski, Beth A., and Kimford J. Meador. Cognitive Enhancement in Epilepsy. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190214401.003.0007.
Повний текст джерелаАнотація:
Cognitive deficits, including attention, language, and memory dysfunction, are common in the setting of epilepsy and can greatly impair quality of life. Cognitive dysfunction in epilepsy is often multifactorial and may relate to the underlying etiology or epilepsy syndrome, comorbid psychiatric disease, interictal epileptiform discharges, effects of seizures, antiepileptic drugs, and surgical interventions. Studies have addressed the prevention of impairment and, less commonly, methods for cognitive enhancement. This chapter examines the possible underlying mechanisms of cognitive deficits in epilepsy, methods for prevention of dysfunction, issues in study design, and data regarding cognitive enhancement.
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Wilson, Maximiliano A., Bernadette Ska, and Yves Joanette. Discourse and Social Cognition Disorders Affecting Communication Abilities. Edited by Anastasia M. Raymer and Leslie J. Gonzalez Rothi. Oxford University Press, 2015. http://dx.doi.org/10.1093/oxfordhb/9780199772391.013.14.
Повний текст джерелаАнотація:
This chapter offers an overview of the pragmatic and social communication disorders that can occur after an alteration of the brain, as best exemplified by individuals with right hemisphere damage. It also discusses the theoretical approaches developed to explain indirect speech act comprehension and inference impairments affecting conversational and narrative comprehension. Similar deficits have been described in other brain-damaged populations such as individuals with traumatic brain injuries, early dementia, and some forms of aphasia. Taken together, deficits of discourse and social aspects of communication abilities show they depend upon the integrity of brain networks that are widely distributed over the brain. These deficits need to be better recognized and described with reference to the underlying cognitive processes involved in order to move toward a more efficient way of helping these individuals participate in society again.
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Maren, Stephen. Neural Circuits for Context Processing in Aversive Learning and Memory. Edited by Israel Liberzon and Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0005.
Повний текст джерелаАнотація:
The nature and properties of emotional expression depend importantly on not only the stimuli that elicit emotional responses, but also the context in which those stimuli are experienced. Deficits in context processing have been associated with a variety of cognitive-emotional disorders, including post-traumatic stress disorder (PTSD). These deficits can be localized to specific neural circuits underlying context processing in the mammalian brain. In particular, the hippocampus has been implicated through numerous animal and human studies to be involved both in normal contextual memory formation, but also in discrimination of trauma-related cues. Decreased hippocampal functioning, as is observed in PTSD, is associated with increased generalization of fear and threat responses as well as deficits in extinction of fear. Understanding context processing offers the opportunity to further understand the biology of PTSD and to target new approaches to therapeutics.
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Frost, Randy O., and Jessica L. Rasmussen. Phenomenology and Characteristics of Compulsive Hoarding. Edited by Gail Steketee. Oxford University Press, 2012. http://dx.doi.org/10.1093/oxfordhb/9780195376210.013.0020.
Повний текст джерелаАнотація:
This chapter discusses current understanding of the phenomenology and characteristics of compulsive hoarding. The disorder is conceptualized within a cognitive-behavioral framework that includes excessive acquisition, difficulties with discarding, and clutter/disorganization. Information-processing deficits, emotional attachments, beliefs about possessions, and perfectionism are examined as underlying etiological factors. Characteristics of the disorder such as prevalence, onset and course, demographics and comorbidity are discussed. It is suggested that the distinctive features of compulsive hoarding, including unique neural and genetic substrates, warrant diagnostic classification as a separate disorder. Methodological problems with existing research are identified.
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Manohar, Sanjay, Valerie Bonnelle, and Masud Husain. Neurological Disorders of Attention. Edited by Anna C. (Kia) Nobre and Sabine Kastner. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199675111.013.027.
Повний текст джерелаАнотація:
Attention deficits are a frequent and particularly disabling consequence of many neurological disorders, from patients with focal brain lesions through to individuals with traumatic brain injury or neurodegenerative conditions, such as Parkinson’s disease. They are often associated with apparent confusion, fatigue, irritability, and increased time and effort to perform even simple everyday tasks, and constitute a real challenge for rehabilitation. In many cases, attention deficits may be crucial factors underlying failures of memory and higher cognitive functions, contributing to difficulties in resuming previous activities and independent daily living. Here the authors first consider four aspects of attention—selective, sustained, executive, and divided—together with brain regions and networks considered to underpin normal attention and disorders of attention. The authors focus on focal brain lesions, traumatic brain injury and Parkinson’s disease as important examples illustrating the effects of different brain pathologies on attention function.
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Yoris, Adrián, Adolfo M. García, Paula Celeste Salamone, Lucas Sedeño, Indira García-Cordero, and Agustín Ibáñez. Cardiac interoception in neurological conditions and its relevance for dimensional approaches. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198811930.003.0010.
Повний текст джерелаАнотація:
Dimensional and transdiagnostic approaches have revealed multiple cognitive/emotional alterations shared by several neuropsychiatric conditions. While this has been shown for externally triggered neurocognitive processes, the disruption of interoception across neurological disorders remains poorly understood. This chapter aims to fill this gap while proposing cardiac interoception as a potential common biomarker across disorders. It focuses on key aspects of interoception, such as the mechanisms underlying different interoceptive dimensions; the relationship among interoception, emotion, and social cognition; and the roles of different interoceptive pathways. It considers behavioral and brain evidence in the context of an experimental and clinical agenda to evaluate the potential role of interoception as a predictor of clinical outcomes, a marker of neurocognitive deficits across diseases, and a general source of insights for breakthroughs in the treatment and prevention of multiple disorders. Finally, future directions to improve the dimensional and transdiagnostic assessment of interoception are outlined.
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Naninck, E. F. G., P. J. Lucassen, and Aniko Korosi. Consequences of Early-Life Experiences on Cognition and Emotion. Edited by Turhan Canli. Oxford University Press, 2013. http://dx.doi.org/10.1093/oxfordhb/9780199753888.013.003.
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Perinatal experiences during a critical developmental period program brain structure and function “for life,” thereby determining vulnerability to psychopathology and cognition in adulthood. Although these functional consequences are associated with alterations in HPA-axis activity and hippocampal structure and function, the underlying mechanisms remain unclear. The parent-offspring relationship (i.e., sensory and nutritional inputs by the mother) is key in mediating these lasting effects. This chapter discusses how early-life events, for example, the amount of maternal care, stress, and nutrition, can affect emotional and cognitive functions later in life. Interestingly, effects of perinatal malnutrition resemble the perinatal stress-induced long-term deficits. Because stress and nutrition are closely interrelated, it proposes that altered stress hormones and changes in specific key nutrients during critical developmental periods act synergistically to program brain structure and function, possibly via epigenetic mechanisms. Understanding how the adult brain is shaped by early experiences is essential to develop behavioural and nutritional preventive therapy.
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O’Neill, Sarah, Jeffrey M. Halperin, and David Coghill. Neuropsychological functioning and ADHD. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198739258.003.0012.
Повний текст джерелаАнотація:
The high prevalence of ADHD and its associated difficulties in adaptive functioning have led to significant efforts to better understand the underlying pathophysiology of the disorder. Prominent models of ADHD have suggested that neurocognitive deficits—particularly executive dysfunction—is directly related to ADHD symptomatology. Data suggests, however, that significant heterogeneity is observed in both the cognitive and adaptive functioning of individuals with ADHD, raising questions about current theoretical models. Furthermore, many of our current models do not explain the developmental trajectory of ADHD symptoms and impairment. This chapter will explore the state of the literature and remaining questions that are driving research on the role of neuropsychological functioning in ADHD, approaching the topic from a developmental perspective. We will conclude by considering implications of this knowledge for the development of effective and long-lasting interventions for individuals with ADHD.
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McCauley, Robert N., and George Graham. Hearing Voices and Other Matters of the Mind. Oxford University Press, 2020. http://dx.doi.org/10.1093/oso/9780190091149.001.0001.
Повний текст джерелаАнотація:
This book endorses an ecumenical naturalism toward all cognition, which will illuminate the long-recognized and striking similarities between features of mental disorders and features of religions. The authors emphasize underlying cognitive continuities between familiar features of religiosity, of mental disorders, and of everyday thinking and action. They contend that much religious thought and behavior can be explained in terms of the cultural activation of maturationally natural cognitive systems, which address fundamental problems of human survival, encompassing such capacities as hazard precautions, agency detection, language processing, and theory of mind. The associated skills are not taught and appear independent of general intelligence. Religions’ representations cue such systems’ operations. The authors hypothesize that in doing so they sometimes elicit responses that mimic features of cognition and conduct associated with mental disorders. Both in schizophrenia and in religions some people hear alien voices. The inability of depressed participants to communicate with or sense their religions’ powerful, caring gods can exacerbate their depression. Often religions can domesticate the concerns and compulsions of people with OCD. Religions’ rituals and pronouncements about moral thought-action fusion can temporarily evoke similar obsessions and compulsions in the general population. A chapter is devoted to each of these and to the exception that proves the rule. The authors argue that if autistic spectrum disorder involves theory-of mind-deficits, then people with ASD will lack intuitive insight and find inferences with many religious representations challenging. Ecumenical naturalism’s approach to mental abnormalities and religiosity promises both explanatory and therapeutic understanding.
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Cummings, Jeffrey L., and Jagan A. Pillai. Neurodegenerative Diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0001.
Повний текст джерелаАнотація:
Neurodegenerative diseases (NDDs) are growing in frequency and represent a major threat to public health. Advances in scientific progress have made it clear that NDDs share many underlying processes, including shared intracellular mechanisms such as protein misfolding and aggregation, cell-to-cell prion-like spread, growth factor signaling abnormalities, RNA and DNA disturbances, glial cell changes, and neuronal loss. Transmitter deficits are shared across many types of disorders. Means of studying NDDs with human iPS cells and transgenic models are similar. The progression of NDDs through asymptomatic, prodromal, and manifest stages is shared across disorders. Clinical features of NDDs, including cognitive impairment, disease progression, age-related effects, terminal stages, neuropsychiatric manifestations, and functional disorders and disability, have many common elements. Clinical trials, biomarkers, brain imaging, and regulatory aspects of NDD can share information across NDDs. Disease-modifying and transmitter-based therapeutic interventions, clinical trials, and regulatory approaches to treatments for NDDs are also similar.
Частини книг з теми "Underlying cognitive deficits"
1
Kucinski, Aaron, and Martin Sarter. "Cortico-Striatal, Cognitive-Motor Interactions Underlying Complex Movement Control Deficits." In Innovations in Cognitive Neuroscience, 117–34. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-42743-0_6.
Повний текст джерела
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Calabria, Marco. "Chapter 4. Bilingualism and language control." In Bilingual Processing and Acquisition, 130–58. Amsterdam: John Benjamins Publishing Company, 2023. http://dx.doi.org/10.1075/bpa.17.04cal.
Повний текст джерелаАнотація:
The field of neuropsychology can contribute to bilingualism research from a multidisciplinary perspective that ranges from psycholinguistics and brain imaging studies. While the psycholinguistic approach provides the outlook on linguistic processes in experimental study of patients with brain damage, neural models define the underlying brain areas of such processes and help to predict language deficits in said patients. Current neural models of bilingualism do not provide accurate predictions of deficits in bilinguals with brain damage since they have not been tested in a systematic way. However, they do offer a roadmap for the underlying cognitive and linguistic processes of bilingual language control and speech production. In this chapter, I propose how a neurolinguistic approach to bilingualism might be implemented in neuropsychology by including: (a) the application of traditional methods of cognitive (neuro)psychology to the field of bilingualism, such as dissociations, (b) the use of psycholinguistic methods, and (c) how neurodegenerative diseases may be a neuropsychological paradigm in which one can study bilingual language processes.
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Cho, Yoon H., and Yannick Jeantet. "Altered Neural Synchronies Underlying Cognitive Deficits in a Transgenic Mouse Model of Huntington’s Disease." In The Neurobiological Basis of Memory, 321–35. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-15759-7_14.
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Baune, Bernhard T. "Interventions for social cognitive deficits." In Cognitive Dimensions of Major Depressive Disorder, 83–88. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198835554.003.0010.
Повний текст джерелаАнотація:
Interventions for social cognitive deficits establishes the large impact these deficits exert on psychosocial functioning in major depressive disorder. The chapter reviews a variety of impairments of social cognition and how these may influence psychosocial functioning in the key domains of social performance, emotional/empathic performance, general cognitive functioning, and quality of life. It introduces multiple treatment modalities including antidepressant medication, psychotherapeutic approaches, and procedural interventions with potential treatment efficacy on facial affect recognition, interpretation of affective pictures, theory of mind performance, and prosody. It reviews evidence indicating that many current therapies are shown to have a normalizing effect on the accuracy of interpretation and the reduction of underlying negative interpretative bias. It concludes from evaluating the literature that certain antidepressants seem to correct facial affect recognition deficits, and several psychotherapeutic approaches appear well-suited for addressing impaired theory of mind or mood-congruent interpretive biases.
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Halder, Susmita, and Akash Mahato. "Cognitive Remediation Therapy in Chronic Schizophrenia." In Advances in Psychology, Mental Health, and Behavioral Studies, 292–307. IGI Global, 2017. http://dx.doi.org/10.4018/978-1-5225-0519-8.ch016.
Повний текст джерелаАнотація:
Cognitive impairments are now recognized as one of the most ubiquitous features of schizophrenia. Cognitive deficits appear to play a large role in how patients with schizophrenia function in their everyday lives. The role of cognitive deficits in schizophrenia may be gauged by the fact that even when patients with schizophrenia are relatively free of psychotic symptoms, many still have extraordinary difficulty with communication, motivation, self-care, and establishing and maintaining relationships with others. Patients with schizophrenia are often additionally treated with supportive psychotherapy, behavioral management, or social skills training as required. However, the efficacy of these adjunct therapies could be limited in presence of marked cognitive deficits. Thus it becomes crucial to have specific intervention for the underlying cognitive deficits that appear detrimental to improvement of functioning of patients with schizophrenia. The present chapter focuses on cognitive training based intervention program for schizophrenia patients and its efficacy.
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Halder, Susmita, and Akash Mahato. "Cognitive Remediation Therapy in Chronic Schizophrenia." In Research Anthology on Rehabilitation Practices and Therapy, 1337–53. IGI Global, 2021. http://dx.doi.org/10.4018/978-1-7998-3432-8.ch067.
Повний текст джерелаАнотація:
Cognitive impairments are now recognized as one of the most ubiquitous features of schizophrenia. Cognitive deficits appear to play a large role in how patients with schizophrenia function in their everyday lives. The role of cognitive deficits in schizophrenia may be gauged by the fact that even when patients with schizophrenia are relatively free of psychotic symptoms, many still have extraordinary difficulty with communication, motivation, self-care, and establishing and maintaining relationships with others. Patients with schizophrenia are often additionally treated with supportive psychotherapy, behavioral management, or social skills training as required. However, the efficacy of these adjunct therapies could be limited in presence of marked cognitive deficits. Thus it becomes crucial to have specific intervention for the underlying cognitive deficits that appear detrimental to improvement of functioning of patients with schizophrenia. The present chapter focuses on cognitive training based intervention program for schizophrenia patients and its efficacy.
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Meghana, S., and Sakshi Shishir. "Social Cognitive Rehabilitation for Neurodegenerative Disorders." In Principles and Clinical Interventions in Social Cognition, 269–87. IGI Global, 2024. http://dx.doi.org/10.4018/979-8-3693-1265-0.ch016.
Повний текст джерелаАнотація:
In this chapter, an initial exploration of the definition and symptoms of neurodegenerative disorders will be conducted along with an in-depth analysis of their underlying neurobiological basis, shedding light on their manifestation in the brain. The central focus will then shift towards comprehending and addressing the specific social cognitive deficits associated with different types of NDs and examining the challenges posed in the realm of social cognition. Strategies and interventions specifically designed for social cognitive rehabilitation will be investigated. The chapter will encompass a discussion on the caregiver burden and effective coping strategies to alleviate the stresses faced. The primary objective of this chapter is to provide readers with a comprehensive understanding of the intricate nature of social cognitive deficits in neurodegenerative disorders and equip them with practical tools aimed at enhancing social cognition and improving the quality of life for individuals affected by these complex conditions.
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Lee, Chuly, and Richard Brown. "Use of advance information in Parkinson’s disease." In Neuropsychological Disorders Associated with Subcortical Lesions, 190–203. Oxford University PressOxford, 1992. http://dx.doi.org/10.1093/oso/9780198546771.003.0008.
Повний текст джерелаАнотація:
Abstract In recent years, the question of cognitive function in patients with Parkinson’s disease (PD) has attracted a growing amount of attention from neuropsychologists. From this empirical research base it has become clear that patients with PD are impaired on some aspects of cognitive function while they are unimpaired on others. There has been considerable interest in the apparent similarities between the pattern of cognitive deficits shown by patients with PD and those with damage to the prefrontal cortex (see Brown and Marsden 1990). However, while it may be a convenient ‘shorthand’ description, to talk of the ‘frontal’ deficit of PD, it tells us little of the processes that are actually going wrong. The situation is further complicated by the fact that the role of the frontal lobes themselves is far from clear. It is perhaps better, at this stage, to think in terms of the task conditions under which patients show normal and impaired performance. This may provide an essential first step in understanding the cognitive processes underlying the deficits.
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Humphreys, Glyn W., and M. Jane Riddoch. "Fractionating the Intentional Control of Behaviour: A Neuropsychological Analysis." In Agency and Self-Awareness, 201–17. Oxford University PressOxford, 1992. http://dx.doi.org/10.1093/oso/9780199245611.003.0009.
Повний текст джерелаАнотація:
Abstract Neuropsychological studies have played an important role in guiding our understanding of cognitive function. For example, studies of selective deficits in particular tasks, following brain lesions, provide constraints on models of cognition, demonstrating functional modularity between processes underlying the tasks. In many instances, the deficits reflect impairments to specific forms of stored representation or in gaining access to those stored representations-even when the representations are normally accessed automatically (examples here would include deficits in object recognition and in the recognition of printed and auditory words; see Humphreys, 1999; Coltheart et al., 1980; Hall and Riddoch, 1997). In other cases, though, the deficits do not reside in automatic processes but rather in control processes that either modulate access to stored representations or that modulate the consequences of the access process. A classic illustration of this is so called ‘utilization behaviour’, following damage to the frontal lobes.
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Wasserman, Victor, Sheina Emrani, Emily Matusz, Catherine C. Price, Melissa Lamar, Rodney A. Swenson, Kenneth M. Heilman, and David J. Libon. "Vascular Cognitive Impairment." In Vascular Disease, Alzheimer's Disease, and Mild Cognitive Impairment, 83–101. Oxford University Press, 2020. http://dx.doi.org/10.1093/oso/9780190634230.003.0005.
Повний текст джерелаАнотація:
The term vascular cognitive impairment (VCI) was introduced and designed to encompass the broad spectrum of neurocognitive deficits attributable to cerebrovascular disease, including cerebral infarctions and ischemia, that may involve the cerebral cortex, subcortical nuclei, and subcortical white matter, including lacunes (small infarcts that are 3 to 15 mm cerebrospinal fluid–filled cavities in the basal ganglia or white matter) leukoaraiosis (subcortical white matter), and other vascular-related lesions. The resulting impairment can vary, including the signs-symptoms, the clinical course, and disease severity. Whereas there is now agreement that cerebrovascular disease can be a major contributing factor underlying dementia, there is limited agreement about diagnostic criteria and clinical presentations. This chapter seeks to review pertinent literature on VCI as well as to investigate the construct of mild vascular cognitive impairment. This chapter will also briefly review the history of VCI, epidemiological research, neuropsychological signs and symptoms, and recent research regarding biomarkers, as well as public health and treatment issues.
Тези доповідей конференцій з теми "Underlying cognitive deficits"
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Pinheiro, Mariana Maciel, Victor Albuquerque, Pedro Albuquerque, Eduardo Maranhão, Jonathan Diniz, and Breno Barbosa. "CORTICOBASAL SYNDROME DUE TO ALZHEIMER’S DISEASE." In XIII Meeting of Researchers on Alzheimer's Disease and Related Disorders. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1980-5764.rpda055.
Повний текст джерелаАнотація:
Background: Corticobasal Syndrome (CBS) is a neurodegenerative syndrome that combines cortical and cognitive deficits secondary to different underlying pathological entities. Objectives: to report an early onset dementia case fulfilling criteria of probable CBS due to Alzheimer’s Disease (AD) based on biomarkers and neuroimaging. Methods: case report. Results: a 57-yearsold woman with college-level education and 18 months of cognitive decline. The first symptom was progressive inability to change gears in her car, followed by difficulties to get dressed, cognitive and motor complaints. Neurological examination revealed marked limb bilateral ideomotor apraxia and mild asymetric parkinsonism. Cognitive tests showed mild visuospatial and language impairments, scoring 18/30 in the MoCA. Brain MRI and FDG PET showed bilateral posterior atrophy and hypometabolism worse to the left. CSF biomarkers revealed decreased amyloid and increased tau and p-tau levels, a pattern suggestive of CBS due to AD. Conclusions: this case illustrates recent evidence that suggests when AD presents as CBS (CBS-AD), limb apraxia and language impairment are more prevalent. CBS patients with underlying AD pathology and tauopathies correctly diagnosed in the future may benefit from symptomatic therapies and future disease-modifying agents.
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Dahmen-Zimmer, Katharina, and Alf C. Zimmer. "Maneuvering in Intersections – What Is the Specific Challenge for Elderly Drivers?Underlying Causes for Violations and a Design for an Assistive System." In Applied Human Factors and Ergonomics Conference (2022). AHFE International, 2022. http://dx.doi.org/10.54941/ahfe1001232.
Повний текст джерелаАнотація:
Statistics of traffic accidents in relation to specific situations and maneuvers show that in intersections elderly drivers have a significantly increased risk, especially when turning left. In cooperation with Ruhr University, Bochum, an extensive analysis of real maneuvers in various intersections has been undertaken by multiple-view video observations. The age of the drivers has been determined by rating the age as observable in the faces. It has turned out that this higher risk cannot be contributed to any distinctive constructive element in road. A subsequent experiment in a driving simulator has led to similar results. It is therefore plausible to assume that increased risk is related to already known age-related deficits in cognitive functions. These are of special importance for the dynamic and situational factors when maneuvering in an intersection, in contrast to the static factors as e.g. road design. In order to assist drivers in intersections when turning left, a Left-Turn- Assistant has been developed and evaluated in a driving simulator. It turns out that with the Intersection Assistant elderly drivers improve the quality of their decisions for their maneuvers significantly and no longer show an increased risk in comparison to experienced drivers in the medium-age category.