Статті в журналах: "Underlying cognitive deficits"

1

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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2

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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3

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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4

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.

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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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5

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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6

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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7

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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8

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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9

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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10

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.

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11

Trompeta, Clara, Beatriz Fernández Rodríguez, and Carmen Gasca-Salas. "What Do We Know about Theory of Mind Impairment in Parkinson’s Disease?" Behavioral Sciences 11, no. 10 (September 24, 2021): 130. http://dx.doi.org/10.3390/bs11100130.

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Theory of mind (ToM) is a social cognitive skill that involves the ability to attribute mental states to self and others (what they think (cognitive ToM) and feel (affective ToM)). We aim to provide an overview of previous knowledge of ToM in Parkinson’s disease (PD). In the last few years more attention has been paid to the study of this construct as a non-motor manifestation of PD. In advanced stages, both components of ToM (cognitive and affective) are commonly impaired, although in early PD results remain controversial. Executive dysfunction correlates with ToM deficits and other cognitive domains such as language and visuospatial function have also been related to ToM. Recent studies have demonstrated that PD patients with mild cognitive impairment show ToM deficits more frequently in comparison with cognitively normal PD patients. In addition to the heterogeneity of ToM tests administered in different studies, depression and dopaminergic medication may also be acting as confounding factors, but there are still insufficient data to support this. Neuroimaging studies conducted to understand the underlying networks of cognitive and affective ToM deficits in PD are lacking. The study of ToM deficit in PD continues to be important, as this may worsen quality of life and favor social stigma. Future studies should be considered, including assessment of the patients’ cognitive state, associated mood disorders, and the role of dopaminergic deficit.

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12

Rosenberg-Lee, M., L. Kondos, M. Barth, D. Geary, and V. Menon. "Neural deficits underlying Mathematical Disability in Children." NeuroImage 47 (July 2009): S110. http://dx.doi.org/10.1016/s1053-8119(09)70986-3.

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13

Bishop, D. V. M. "Cognitive Neuropsychology and Developmental Disorders: Uncomfortable Bedfellows." Quarterly Journal of Experimental Psychology Section A 50, no. 4 (November 1997): 899–923. http://dx.doi.org/10.1080/713755740.

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Cognitive neuropsychology provides a theoretical framework and methods that can be of value in the study of developmental disorders, but the “dissociation” logic at the centre of this approach is not well suited to the developmental context. This is illustrated with examples from specific language impairment. Within the developing language system there is ample evidence for interaction between levels of representation, with modularity emerging in the course of development. This means that one typically is seeking to explain a complex pattern of associated impairments, rather than highly selective deficits. For instance, a selective impairment in auditory processing can have repercussions through the language system and may lead to distinctive syntactic deficits that are seen in written as well as spoken language. Changes in the nature of representations and in the relationships between components of a developing system mean that cross-sectional data at a single point in development may be misleading indicators of the primary deficit. Furthermore, traditional cognitive neuropsychology places a disproportionate emphasis on representational (competence) deficits, with processing (performance) deficits being relatively neglected. Methods for distinguishing these two kinds of impairment are discussed, as well as other approaches for elucidating the underlying nature of developmental disorders.

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14

Chaudhary, Shefali, Simon Zhornitsky, Herta H. Chao, Christopher H. van Dyck, and Chiang-Shan R. Li. "Emotion Processing Dysfunction in Alzheimer’s Disease: An Overview of Behavioral Findings, Systems Neural Correlates, and Underlying Neural Biology." American Journal of Alzheimer's Disease & Other Dementias® 37 (January 2022): 153331752210828. http://dx.doi.org/10.1177/15333175221082834.

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We described behavioral studies to highlight emotional processing deficits in Alzheimer’s disease (AD). The findings suggest prominent deficit in recognizing negative emotions, pronounced effect of positive emotion on enhancing memory, and a critical role of cognitive deficits in manifesting emotional processing dysfunction in AD. We reviewed imaging studies to highlight morphometric and functional markers of hippocampal circuit dysfunction in emotional processing deficits. Despite amygdala reactivity to emotional stimuli, hippocampal dysfunction conduces to deficits in emotional memory. Finally, the reviewed studies implicating major neurotransmitter systems in anxiety and depression in AD supported altered cholinergic and noradrenergic signaling in AD emotional disorders. Overall, the studies showed altered emotions early in the course of illness and suggest the need of multimodal imaging for further investigations. Particularly, longitudinal studies with multiple behavioral paradigms translatable between preclinical and clinical models would provide data to elucidate the time course and underlying neurobiology of emotion processing dysfunction in AD.

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15

Liu, Teresa C., Sun M. Yoo, Myung S. Sim, Yash Motwani, Nisha Viswanathan, and Neil S. Wenger. "Perceived Cognitive Deficits in Patients With Symptomatic SARS-CoV-2 and Their Association With Post–COVID-19 Condition." JAMA Network Open 6, no. 5 (May 5, 2023): e2311974. http://dx.doi.org/10.1001/jamanetworkopen.2023.11974.

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ImportanceNeuropsychiatric symptoms are common in acute SARS-CoV-2 infection and in post–COVID-19 condition (PCC; colloquially known as long COVID), but the association between early presenting neuropsychiatric symptoms and PCC is unknown.ObjectiveTo describe the characteristics of patients with perceived cognitive deficits within the first 4 weeks of SARS-CoV-2 infection and the association of those deficits with PCC symptoms.Design, Setting, and ParticipantsThis prospective cohort study was conducted from April 2020 to February 2021, with follow-up of 60 to 90 days. The cohort consisted of adults enrolled in the University of California, Los Angeles, SARS-CoV-2 Ambulatory Program who had a laboratory-confirmed symptomatic SARS-CoV-2 infection and were either hospitalized in a University of California, Los Angeles, hospital or one of 20 local health care facilities, or were outpatients referred by a primary care clinician. Data analysis was performed from March 2022 to February 2023.ExposureLaboratory-confirmed SARS-CoV-2 infection.Main Outcomes and MeasuresPatients responded to surveys that included questions about perceived cognitive deficits modified from the Perceived Deficits Questionnaire, Fifth Edition, (ie, trouble being organized, trouble concentrating, and forgetfulness) and symptoms of PCC at 30, 60, and 90 days after hospital discharge or initial laboratory-confirmed infection of SARS-CoV-2. Perceived cognitive deficits were scored on a scale from 0 to 4. Development of PCC was determined by patient self-report of persistent symptoms 60 or 90 days after initial SARS-CoV-2 infection or hospital discharge.ResultsOf 1296 patients enrolled in the program, 766 (59.1%) (mean [SD] age, 60.0 [16.7] years; 399 men [52.1%]; 317 Hispanic/Latinx patients [41.4%]) completed the perceived cognitive deficit items at 30 days after hospital discharge or outpatient diagnosis. Of the 766 patients, 276 (36.1%) perceived a cognitive deficit, with 164 (21.4%) having a mean score of greater than 0 to 1.5 and 112 patients (14.6 %) having a mean score greater than 1.5. Prior cognitive difficulties (odds ratio [OR], 1.46; 95% CI, 1.16-1.83) and diagnosis of depressive disorder (OR, 1.51; 95% CI, 1.23-1.86) were associated with report of a perceived cognitive deficit. Patients reporting perceived cognitive deficits in the first 4 weeks of SARS-CoV-2 infection were more likely to report symptoms of PCC than those without perceived cognitive deficits (118 of 276 patients [42.8%] vs 105 of 490 patients [21.4%]; χ21, 38.9; P &lt; .001). Adjusting for demographic and clinical factors, perceived cognitive deficits in the first 4 weeks of SARS-CoV-2 were associated with PCC symptoms (patients with a cognitive deficit score of &gt;0 to 1.5: OR, 2.42; 95% CI, 1.62-3.60; patients with cognitive deficit score &gt;1.5: OR, 2.97; 95% CI, 1.86-4.75) compared to patients who reported no perceived cognitive deficits.Conclusions and RelevanceThese findings suggest that patient-reported perceived cognitive deficits in the first 4 weeks of SARS-CoV-2 infection are associated with PCC symptoms and that there may be an affective component to PCC in some patients. The underlying reasons for PCC merit additional exploration.

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Margolin, David I., Debra Sue Pate, Frances J. Friedrich, and Elizabeth Elia. "Dysnomia in dementia and in stroke patients: Different underlying cognitive deficits." Journal of Clinical and Experimental Neuropsychology 12, no. 4 (August 1990): 597–612. http://dx.doi.org/10.1080/01688639008401004.

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17

Geary, David C., Mary K. Hoard, Jennifer Byrd-Craven, Lara Nugent, and Chattavee Numtee. "Cognitive Mechanisms Underlying Achievement Deficits in Children With Mathematical Learning Disability." Child Development 78, no. 4 (July 2007): 1343–59. http://dx.doi.org/10.1111/j.1467-8624.2007.01069.x.

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18

Yurgelun-Todd, D. A., and C. S. Waternaux. "Cognitive deficits underlying verbal memory function in schizophrenic patients and controls." Schizophrenia Research 4, no. 3 (May 1991): 396–97. http://dx.doi.org/10.1016/0920-9964(91)90343-p.

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19

Young, JW, and MA Geyer. "Developing treatments for cognitive deficits in schizophrenia: The challenge of translation." Journal of Psychopharmacology 29, no. 2 (December 16, 2014): 178–96. http://dx.doi.org/10.1177/0269881114555252.

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Schizophrenia is a life-long debilitating mental disorder affecting tens of millions of people worldwide. The serendipitous discovery of antipsychotics focused pharmaceutical research on developing a better antipsychotic. Our understanding of the disorder has advanced however, with the knowledge that cognitive enhancers are required for patients in order to improve their everyday lives. While antipsychotics treat psychosis, they do not enhance cognition and hence are not antischizophrenics. Developing pro-cognitive therapeutics has been extremely difficult, however, especially when no approved treatment exists. In lieu of stumbling on an efficacious treatment, developing targeted compounds can be facilitated by understanding the neural mechanisms underlying altered cognitive functioning in patients. Equally importantly, these cognitive domains will need to be measured similarly in animals and humans so that novel targets can be tested prior to conducting expensive clinical trials. To date, the limited similarity of testing across species has resulted in a translational bottleneck. In this review, we emphasize that schizophrenia is a disorder characterized by abnormal cognitive behavior. Quantifying these abnormalities using tasks having cross-species validity would enable the quantification of comparable processes in rodents. This approach would increase the likelihood that the neural substrates underlying relevant behaviors will be conserved across species. Hence, we detail cross-species tasks which can be used to test the effects of manipulations relevant to schizophrenia and putative therapeutics. Such tasks offer the hope of providing a bridge between non-clinical and clinical testing that will eventually lead to treatments developed specifically for patients with deficient cognition.

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20

Fang, Congcong, Longqin Lv, Shanping Mao, Huimin Dong, and Baohui Liu. "Cognition Deficits in Parkinson’s Disease: Mechanisms and Treatment." Parkinson's Disease 2020 (March 24, 2020): 1–11. http://dx.doi.org/10.1155/2020/2076942.

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Parkinson’s disease (PD) is the second most common progressive neurodegenerative disorder mainly in middle-elderly population, which represents diverse nonmotor symptoms (NMS) besides such well-documented motor symptoms as bradykinesia, resting tremor, rigidity, and postural instability. With the advancement of aging trend worldwide, the global prevalence of PD is mounting up year after year. Nowadays, accumulating lines of studies have given a comprehensive and thorough coverage of motor symptoms in PD. Yet much less attention as compared has been paid to the nonmotor symptoms of PD, such as cognition deficits. Of note, a patient with PD who suffers from cognitive impairment may harbour a statistically significantly higher risk of progressing toward dementia, which negatively affects their life expectancy and daily functioning and overall lowers the global quality of life. Furthermore, it is a widely held view that cognitive dysfunction does not just occur in the late stage of PD. On the basis of numerous studies, mild cognitive impairment (MCI) is a harbinger of dementia in PD, which is observed as an intermediate state with considerable variability; some patients remain stable and some even revert to normal cognition. Considered that the timing, profile, and rate of cognitive impairment vary greatly among PD individuals, it is extremely urgent for researchers and clinicians alike to identify and predict future cognitive decline in this population. Simultaneously, early screening and canonical management of PD with cognitive deficits are very imperative to postpone the disease progression and improve the prognosis of patients. In our review, we focus on a description of cognitive decline in PD, expound emphatically the pathological mechanisms underlying cognition deficits in PD, then give a comprehensive overview of specific therapeutic strategies, and finally dissect what fresh insights may bring new exciting prospect for the subfield.

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Bocarsly, Miriam E., Maria Fasolino, Gary A. Kane, Elizabeth A. LaMarca, Gregory W. Kirschen, Ilia N. Karatsoreos, Bruce S. McEwen, and Elizabeth Gould. "Obesity diminishes synaptic markers, alters microglial morphology, and impairs cognitive function." Proceedings of the National Academy of Sciences 112, no. 51 (December 7, 2015): 15731–36. http://dx.doi.org/10.1073/pnas.1511593112.

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Obesity is a major public health problem affecting overall physical and emotional well-being. Despite compelling data suggesting an association between obesity and cognitive dysfunction, this phenomenon has received relatively little attention. Neuroimaging studies in obese humans report reduced size of brain regions involved in cognition, but few studies have investigated the cellular processes underlying cognitive decline in obesity or the influence of obesity on cognition in the absence of obesity-related illnesses. Here, a rat model of diet-induced obesity was used to explore changes in brain regions important for cognition. Obese rats showed deficits on cognitive tasks requiring the prefrontal and perirhinal cortex. Cognitive deficits were accompanied by decreased dendritic spine density and synaptic marker expression in both brain regions. Microglial morphology was also changed in the prefrontal cortex. Detrimental changes in the prefrontal cortex and perirhinal cortex occurred before metabolic syndrome or diabetes, suggesting that these brain regions may be particularly vulnerable to early stage obesity.

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Argenbright, Cassie M., Alysia M. Bertlesman, Izabella M. Russell, Tracy L. Greer, Yuan B. Peng, and Perry N. Fuchs. "The Fibromyalgia Pain Experience: A Scoping Review of the Preclinical Evidence for Replication and Treatment of the Affective and Cognitive Pain Dimensions." Biomedicines 12, no. 4 (April 2, 2024): 778. http://dx.doi.org/10.3390/biomedicines12040778.

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Fibromyalgia is a chronic, widespread pain disorder that is strongly represented across the affective and cognitive dimensions of pain, given that the underlying pathophysiology of the disorder is yet to be identified. These affective and cognitive deficits are crucial to understanding and treating the fibromyalgia pain experience as a whole but replicating this multidimensionality on a preclinical level is challenging. To understand the underlying mechanisms, animal models are used. In this scoping review, we evaluate the current primary animal models of fibromyalgia regarding their translational relevance within the affective and cognitive pain realms, as well as summarize treatments that have been identified preclinically for attenuating these deficits.

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Rodríguez-Sánchez, José Manuel, Benedicto Crespo-Facorro, Cesar González-Blanch, Rocío Pérez-Iglesias, and José Luis Vázquez-Barquero. "Cognitive dysfunction in first-episode psychosis: the processing speed hypothesis." British Journal of Psychiatry 191, S51 (December 2007): s107—s110. http://dx.doi.org/10.1192/bjp.191.51.s107.

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BackgroundSpeed of processing is a cognitive process underlying cognitive dysfunction in people with chronic schizophreniaAimsTo investigate the contribution of speed of processing to the cognitive deficits observed in a representative large sample with first-episode schizophreniaMethodPeople with a diagnosis of first-episode schizophrenia-spectrum disorders (n=26) and healthy controls (n=28) were compared on several cognitive measures before and after controlling for speed of processingResultsBefore controlling for speed of processing, patients and controls differed significantly on all cognitive measures. All significant differences in cognitive functioning disappeared when the result of the Digital Symbol Substitution Test was included as an additional covariateConclusionsSpeed of information processing may be considered a core cognitive deficit in schizophrenia and might be mediating a broader diversity of cognitive disturbances

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Onofri, Emanuela, Marco Mercuri, MariaLucia Salesi, Max Rapp Ricciardi, and Trevor Archer. "Cognitive Performance Deficits and Dysgraphia in Alzheimer’s Disease Patients." Open Medicine Journal 2, no. 1 (February 20, 2015): 6–16. http://dx.doi.org/10.2174/1874220301501010006.

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Introduction: Agraphia or dysgraphia, observed often in early AD, encompasses a progressive disorganization and degeneration of the various components of handwriting. Methods: Deficits in writing ability, dysgraphia, and the relationship with other measures of cognitive decline were studied in a group of 30 patients, originating from the Lazio region, Rome, Italy, presenting a moderate to relatively severe stage of Alzheimer’s disease (AD). Extent of dysgraphia and cognitive performance was compared with a matched group of healthy controls selected from the same region. Results: Several markedly strong relationships between dysgraphia and several measures of cognitive performance in AD patients were observed concomitant with consistent deficits by this patient sample in comparison with the matched group of healthy control subjects were obtained. Additionally, several measures of loss of functional integrity, MMSE, ADL and IADL, were found to be associated with both dysgraphia and impairments in cognitive performance. Conclusion: The present results are discussed from the notion of affected brain regions underlying functions in cognition, language and motor domains that are disturbed in AD.

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Tannock, Ian F., Tim A. Ahles, Patricia A. Ganz, and Frits S. van Dam. "Cognitive Impairment Associated With Chemotherapy for Cancer: Report of a Workshop." Journal of Clinical Oncology 22, no. 11 (June 1, 2004): 2233–39. http://dx.doi.org/10.1200/jco.2004.08.094.

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Cognitive dysfunction may occur in some patients who receive chemotherapy. We provide a summary of an April 2003 workshop on this topic, that included medical oncologists, radiologists, clinical and experimental psychologists, and patient advocates. Current studies indicate that cognitive deficits are often subtle, although they are observed consistently in a proportion of patients, may be durable, and can be disabling. Deficits have been observed in a range of cognitive functions. Underlying mechanisms are unknown, although preliminary studies suggest there may be genetic predisposition and that cognitive impairment may be accompanied by changes in the brain detectable by neuroimaging. The following priorities were established for future research: (1) large-scale clinical studies that use both a longitudinal design and concurrent evaluation of patients with cancer who do not receive chemotherapy—such studies should address the probability and magnitude of cognitive deficits, factors that predict them, and underlying mechanisms; (2) exploration of discrepancies between subjective reports of cognitive dysfunction and the objective results of cognitive testing; (3) studies of cognitive function in patients receiving treatment for diseases other than breast cancer, and in both men and women, to address the hypothesis that underlying mechanisms relate to changes in serum levels of sex hormones and/or to chemotherapy-induced menopause; (4) development of interventions to alleviate these problems; and (5) development of animal models and the use of imaging techniques to address mechanisms that might cause cognitive impairment associated with chemotherapy.

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Stradecki-Cohan, Holly M., Charles H. Cohan, Ami P. Raval, Kunjan R. Dave, Diego Reginensi, Rolando A. Gittens, Mehdi Youbi, and Miguel A. Perez-Pinzon. "Cognitive Deficits after Cerebral Ischemia and Underlying Dysfunctional Plasticity: Potential Targets for Recovery of Cognition." Journal of Alzheimer's Disease 60, s1 (September 15, 2017): S87—S105. http://dx.doi.org/10.3233/jad-170057.

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27

Russo, M., T. E. Van Rheenen, M. Shanahan, K. Mahon, M. M. Perez-Rodriguez, A. Cuesta-Diaz, E. Larsen, A. K. Malhotra, and K. E. Burdick. "Neurocognitive subtypes in patients with bipolar disorder and their unaffected siblings." Psychological Medicine 47, no. 16 (June 7, 2017): 2892–905. http://dx.doi.org/10.1017/s003329171700143x.

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BackgroundOur previous work revealed substantial heterogeneity in the cognitive profile of bipolar disorder (BD) due to the presence of three underlying cognitive subgroups characterized as: globally impaired, selectively impaired, or cognitively intact. In an effort to determine whether these subgroups are differentially related to genetic risk for the illness, we investigated whether cognitive deficits were more pronounced in unaffected siblings (UAS) of BD probands within identified clusters.MethodsCluster analysis was used to identify cognitive clusters in BD (N = 60). UAS (N = 49) were classified into groups according to their proband sibling's cluster assignment; comparisons were made across all clusters and healthy controls (HCs; N = 71).ResultsThree cognitive clusters in BD emerged: a globally impaired (36.7%), a selectively impaired (30%), and a cognitively intact cluster (33.3%). UAS showed a qualitatively similar pattern to their BD siblings; UAS of the globally impaired BD cluster showed verbal memory and general cognitive impairments relative to HCs. In contrast, UAS of the other two clusters did not differ from HCs.ConclusionsThis study corroborates findings from prior work regarding the presence of cognitive heterogeneity in BD. UAS of subjects in the globally impaired BD cluster presented with a qualitatively similar cognitive profile to their siblings and performed worse than all other BD clusters and UAS groups. This suggests that inherited risk factors may be contributing to cognitive deficits more notably in one subgroup of patients with BD, pointing toward differential causes of cognitive deficits in discrete subgroups of patients with the disorder.

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Gurd, J. M. "Verbal fluency deficits in Parkinson's disease: individual differences in underlying cognitive mechanisms." Journal of Neurolinguistics 13, no. 1 (January 2000): 47–55. http://dx.doi.org/10.1016/s0911-6044(99)00011-1.

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Palermo, Liana, Maria Cristina Cinelli, Laura Piccardi, Sara De Felice, Paola Ciurli, Chiara Incoccia, Laura Zompanti, and Cecilia Guariglia. "Cognitive functions underlying prospective memory deficits: A study on traumatic brain injury." Applied Neuropsychology: Adult 27, no. 2 (October 31, 2018): 158–72. http://dx.doi.org/10.1080/23279095.2018.1501374.

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McCarthy, Deirdre M., Genevieve A. Bell, Elisa N. Cannon, Kaly A. Mueller, Megan N. Huizenga, Ghazaleh Sadri-Vakili, Debra A. Fadool, and Pradeep G. Bhide. "Reversal Learning Deficits Associated with Increased Frontal Cortical Brain-Derived Neurotrophic Factor Tyrosine Kinase B Signaling in a Prenatal Cocaine Exposure Mouse Model." Developmental Neuroscience 38, no. 5 (2016): 354–64. http://dx.doi.org/10.1159/000452739.

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Prenatal cocaine exposure remains a major public health concern because of its adverse impact on cognitive function in children and adults. We report that prenatal cocaine exposure produces significant deficits in reversal learning, a key component of cognitive flexibility, in a mouse model. We used an olfactory reversal learning paradigm and found that the prenatally cocaine-exposed mice showed a marked failure to learn the reversed paradigm. Because brain-derived neurotrophic factor (BDNF) is a key regulator of cognitive functions, and because prenatal cocaine exposure increases the expression of BDNF and the phosphorylated form of its receptor, tyrosine kinase B (TrkB), we examined whether BDNF-TrkB signaling is involved in mediating the reversal learning deficit in prenatally cocaine-exposed mice. Systemic administration of a selective TrkB receptor antagonist restored normal reversal learning in prenatally cocaine-exposed mice, suggesting that increased BDNF-TrkB signaling may be an underlying mechanism of reversal learning deficits. Our findings provide novel mechanistic insights into the reversal learning phenomenon and may have significant translational implications because impaired cognitive flexibility is a key symptom in psychiatric conditions of developmental onset.

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Sun, Jiaming, Keli Jia, Mingtao Sun, Xianqiang Zhang, Jinhong Chen, Guohui Zhu, Changjiang Li, et al. "The GluA1-Related BDNF Pathway Is Involved in PTSD-Induced Cognitive Flexibility Deficit in Attentional Set-Shifting Tasks of Rats." Journal of Clinical Medicine 11, no. 22 (November 18, 2022): 6824. http://dx.doi.org/10.3390/jcm11226824.

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Background: Post-Traumatic Stress Disorder (PTSD) is a severe psychological disorder characterized by intrusive thoughts, heightened arousal, avoidance, and flashbacks. Cognitive flexibility dysfunction has been linked with the emergence of PTSD, including response inhibition deficits and impaired attentional switching, which results in difficulties for PTSD patients when disengaging attention from trauma-related stimuli. However, the molecular mechanisms of cognitive flexibility deficits remain unclear. Methods: The animals were exposed to a single prolonged stress and electric foot shock (SPS&S) procedure to induce PTSD-like features. Once the model was established, the changes in cognitive flexibility were assessed using an attentional set-shifting task (ASST) in order to investigate the effects of traumatic stress on cognitive flexibility. Additionally, the molecular alterations of certain proteins (AMPA Receptor 1 (GluA1), brain-derived neurotrophic factor (BDNF), and Postsynaptic density protein 95 (PSD95) in the medial prefrontal cortex (mPFC) were measured using Western blot and immunofluorescence. Results: The SPS&S model exhibited PTSD-like behaviors and induced reversal learning and set-shifting ability deficit in the ASST. These behavioral changes are accompanied by decreased GluA1, BDNF, and PSD95 protein expression in the mPFC. Further analysis showed a correlative relationship between the behavioral and molecular alterations. Conclusions: The SPS&S model induced cognitive flexibility deficits, and the potential underlying mechanism could be mediated by GluA1-related BDNF signaling in the mPFC.

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Ivanchak, N., E. L. Abner, S. A. Carr, S. J. Freeman, A. Seybert, J. Ranseen, and G. A. Jicha. "Attention-Deficit/Hyperactivity Disorder in Childhood Is Associated with Cognitive Test Profiles in the Geriatric Population but Not with Mild Cognitive Impairment or Alzheimer's Disease." Journal of Aging Research 2011 (2011): 1–7. http://dx.doi.org/10.4061/2011/729801.

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The frequency of ADHD in the aging population and its relationship to late-life cognitive decline has not been studied previously. To address this gap in our understanding, the Wender-Utah ADHD Rating scale (WURS) was administered to 310 geriatric subjects with cognitive status ranging from normal cognition to mild cognitive impairment to overt dementia. The frequency of WURS-positive ADHD in this sample was 4.4%. WURS scores were not related to cognitive diagnoses, but did show nonlinear associations with tasks requiring sustained attention. The frequency of ADHD appears stable across generations and does not appear to be associated with MCI or dementia diagnoses. The association of attentional processing deficits and WURS scores in geriatric subjects could suggest that such traits remain stable throughout life. Caution should be considered when interpreting cognitive test profiles in the aging population that exhibit signs and symptoms of ADHD, as attentional deficits may not necessarily imply the existence of an underlying neurodegenerative disease state.

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Vleugels, L., C. Lafosse, A. van Nunen, M. Charlier, P. Ketelaer, and E. Vandenbussche. "Visuoperceptual impairment in MS patients: nature and possible neural origins." Multiple Sclerosis Journal 7, no. 6 (December 2001): 389–401. http://dx.doi.org/10.1177/135245850100700608.

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Failures on visuoperceptual neuropsychological tasks (on neuropsychological tests of visuo-spatial perception or on tests concerning semantic properties of visual objects), may indicate focal deficits of visuoperceptual function, or could be the result of (an)other (peripheral) visual deficit(s), or be the effect of a more general cognitive decline. In multiple sclerosis (MS) patients exhibiting sufficient visual acuity and not showing severe cognitive deterioration, impairment on a comprehensive set of 31 visuoperceptual neuropsychological tasks was compared with spatial resolution deficits (SRD), temporal resolution deficits (TRD) for visual stimuli, abnormal pattern shift visual evoked potential (PSVEP) responses, and failing scores on neuropsychological tasks other than visuoperceptual tasks. Impairment on the visuoperceptual neuropsychological tasks was highly independent from the other abnormal visual and cognitive neurological impairments examined, suggesting that it mostly represented focal deficits. Only TRD in both eyes related to this impairment and this relationship was rather weak. Thus in some MS patients a slowed visual information processing may be one of the combined deficits underlying visuoperceptual neuropsychological task impairment. Given that SRD and TRD were not related to another stage of MS and reflect disturbances of a P (parvocellular channel and ventral stream projections) and M (magnocellular channel and dorsal stream projections) visual-system function respectively, demyelination of a certain M pathway may become a co-determinant of visuoperceptual neuropsychological task impairment more rapidly than damage to a certain P pathway.

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Kovac, Aleksandra, Vojislava Bugarski-Ignjatovic, Snezana Tovilovic, Jasmina Boban, and Dusko Kozic. "Neurocognitive changes in cancer patients as a current challenge in psycho-oncology." Medical review 73, no. 11-12 (2020): 357–63. http://dx.doi.org/10.2298/mpns2012357k.

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Introduction. Along with a high intensity emotional distress, cancer patients often face neurocognitive changes that are particularly pronounced after chemotherapy. Clinical features of neurocognitive deficits in non-central nervous system cancer patients. So far, studies have demonstrated that neurocognitive changes most often occur in domains of executive functions, attention and concentration, working memory, information processing speed and visuospatial abilities, but there is still no definite protocol for the diagnosis and management of this condition. Potential causal mechanisms and risk factors. Apart from chemotherapy, there are other factors associated with the development and manifestation of neurocognitive deficits in cancer patients: genetic, biological, psychological and socio-demographic. Assessment of cancer-related cognitive impairments. When assessing potential cognitive impairments, it is beneficial to combine neuropsychological test battery and self-report questionnaires for the assessment of cognitive and affective status, as well as modern neuroimaging methods that will indicate neural (structural and functional) changes underlying neurocognitive deficit. The role of psychosocial factors: implications for future research. In addition to cognitive reserve and emotional status, the patient?s personal characteristics may very likely play an important role in explaining neurocognitive functioning and neurocognitive adaptation of cancer patients upon completion of treatment. Conclusion. Further studies are needed to elucidate the mechanisms underlying neurocognitive changes in cancer patients, with special emphasis on the contribution of psychosocial factors. Based on the novel findings, adequate and timely cognitive rehabilitation treatment will be provided for patients suffering from malignant diseases.

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Hampson, R. E., R. A. España, G. A. Rogers, L. J. Porrino, and S. A. Deadwyler. "Mechanisms underlying cognitive enhancement and reversal of cognitive deficits in nonhuman primates by the ampakine CX717." Psychopharmacology 202, no. 1-3 (November 5, 2008): 355–69. http://dx.doi.org/10.1007/s00213-008-1360-z.

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LAU, MARK A., BRUCE K. CHRISTENSEN, LANCE L. HAWLEY, MICHAEL S. GEMAR, and ZINDEL V. SEGAL. "Inhibitory deficits for negative information in persons with major depressive disorder." Psychological Medicine 37, no. 9 (April 24, 2007): 1249–59. http://dx.doi.org/10.1017/s0033291707000530.

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ABSTRACTBackgroundWithin Beck's cognitive model of depression, little is known about the mechanism(s) by which activated self-schemas result in the production of negative thoughts. Recent research has demonstrated that inhibitory dysfunction is present in depression, and this deficit is likely valence-specific. However, whether valence-specific inhibitory deficits are associated with increased negative cognition and whether such deficits are specific to depression per se remains unexamined. The authors posit the theory that inhibitory dysfunction may influence the degree to which activated self-schemas result in the production of depressive cognition.MethodIndividuals with major depressive disorder (MDD, n=43) versus healthy (n=36) and non-depressed anxious (n=32) controls were assessed on the Prose Distraction Task (PDT), a measure of cognitive inhibition, and the Stop-Signal Task (SST), a measure of motor response inhibition. These two tasks were modified in order to present emotionally valenced semantic stimuli (i.e. negative, neutral, positive).ResultsParticipants with MDD demonstrated performance impairments on the PDT, which were most pronounced for negatively valenced adjectives, relative to both control groups. Moreover, these impairments correlated with self-report measures of negative thinking and rumination. Conversely, the performance of the MDD participants did not differ from either control group on the SST.ConclusionsImplications of these findings for understanding the mechanisms underlying the development and maintenance of depressive cognition are discussed.

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Wolfsgruber, Steffen, Luca Kleineidam, Jannis Guski, Alexandra Polcher, Ingo Frommann, Sandra Roeske, Eike Jakob Spruth, et al. "Minor neuropsychological deficits in patients with subjective cognitive decline." Neurology 95, no. 9 (July 7, 2020): e1134-e1143. http://dx.doi.org/10.1212/wnl.0000000000010142.

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ObjectiveTo determine the nature and extent of minor neuropsychological deficits in patients with subjective cognitive decline (SCD) and their association with CSF biomarkers of Alzheimer disease (AD).MethodWe analyzed data from n = 449 cognitively normal participants (n = 209 healthy controls, n = 240 patients with SCD) from an interim data release of the German Center for Neurodegenerative Diseases Longitudinal Cognitive Impairment and Dementia Study (DELCODE). An extensive neuropsychological test battery was applied at baseline for which we established a latent, 5 cognitive domain factor structure comprising learning and memory, executive functions, language abilities, working memory, and visuospatial functions. We compared groups in terms of global and domain-specific performance and correlated performance with different CSF markers of AD pathology.ResultsWe observed worse performance (Cohen d = ≈0.25–0.5, adjusted for age, sex differences with analysis of covariance) in global performance, memory, executive functions, and language abilities for the SCD group compared to healthy controls. In addition, worse performance in these domains was moderately (r = ≈0.3) associated with lower CSF β-amyloid42/40 and CSF β-amyloid42/phosphorylated tau181 in the whole sample and specifically in the SCD subgroup.ConclusionsWithin the spectrum of clinically unimpaired (i.e., before mild cognitive impairment) cognitive performance, SCD is associated with minor deficits in memory, executive function, and language abilities. The association of these subtle cognitive deficits with AD CSF biomarkers speaks to their validity and potential use for the early detection of underlying preclinical AD.

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Williams, Jonathan, and Eric Taylor. "Dopamine Appetite and Cognitive Impairment in Attention Deficit/Hyperactivity Disorder." Neural Plasticity 11, no. 1-2 (2004): 115–32. http://dx.doi.org/10.1155/np.2004.115.

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The underlying defects in ADHD (Attention Deficit/Hyperactivity Disorder) are not yet clear. The current paper tests three existing theories: State Regulation, Cognitive Deficit, and Temporal Difference (TD) learning. We present computational simulations of the Matching Familiar Figures Task and compare these with the experimental results reported by Sonuga- Barke (2002). The TD model contains four parameters: the learning rate, discounting for future rewards, brittleness (randomness) of behavior, and action bias. The results show that the basic TD model accounts well for control performance in trials of 5 sec, 10 sec, and 15 sec duration; but not for the deficits in ADHD performance at 5 sec and 15 sec. Extending the TD model to incorporate either a state regulation deficit, or working memory deficit and delay in starting trials, can provide a good account of both control and ADHD results, at all trial-lengths. We discuss the significance of the results for theories of ADHD and make suggestions for future experimentation.

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Kelly, Valerie E., Alexis J. Eusterbrock, and Anne Shumway-Cook. "A Review of Dual-Task Walking Deficits in People with Parkinson's Disease: Motor and Cognitive Contributions, Mechanisms, and Clinical Implications." Parkinson's Disease 2012 (2012): 1–14. http://dx.doi.org/10.1155/2012/918719.

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Gait impairments in Parkinson's disease (PD) are exacerbated under dual-task conditions requiring the simultaneous performance of cognitive or motor tasks. Dual-task walking deficits impact functional mobility, which often requires walking while performing concurrent tasks such as talking or carrying an object. The consequences of gait impairments in PD are significant and include increased disability, increased fall risk, and reduced quality of life. However, effective therapeutic interventions for dual-task walking deficits are limited. The goals of this narrative review are to describe dual-task walking deficits in people with PD, to discuss motor and cognitive factors that may contribute to these deficits, to review potential mechanisms underlying dual-task deficits, and to discuss the effect of therapeutic interventions on dual-task walking deficits in persons with PD.

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Kruiper, Caitlyn, Birgitte Fagerlund, Mette Ø. Nielsen, Signe Düring, Maria H. Jensen, Bjørn H. Ebdrup, Birte Y. Glenthøj, and Bob Oranje. "Associations between P3a and P3b amplitudes and cognition in antipsychotic-naïve first-episode schizophrenia patients." Psychological Medicine 49, no. 5 (June 19, 2018): 868–75. http://dx.doi.org/10.1017/s0033291718001575.

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AbstractBackgroundCognitive deficits are already present in early stages of schizophrenia. P3a and P3b event-related potentials (ERPs) are believed to underlie the processes of attention and working memory (WM), yet limited research has been performed on the associations between these parameters. Therefore, we explored possible associations between P3a/b amplitudes and cognition in a large cohort of antipsychotic-naïve, first-episode schizophrenia (AN-FES) patients and healthy controls (HC).MethodsSeventy-three AN-FES patients and 93 age- and gender-matched HC were assessed for their P3a/b amplitude with an auditory oddball paradigm. In addition, subjects performed several subtests from the Cambridge Neuropsychological Test Automated Battery (CANTAB).ResultsAN-FES patients had significantly reduced P3a/b amplitudes, as well as significantly lower scores on all cognitive tests compared with HC. Total group correlations revealed positive associations between P3b amplitude and WM and sustained attention and negative associations with all reaction time measures. These associations appeared mainly driven by AN-FES patients, where we found a similar pattern. No significant associations were found between P3b amplitude and cognitive measures in our HC. P3a amplitude did not correlate significantly with any cognitive measures in either group, nor when combined.ConclusionsOur results provide further evidence for P3a/b amplitude deficits and cognitive deficits in AN-FES patients, which are neither due to antipsychotics nor to disease progress. Furthermore, our data showed significant, yet weak associations between P3b and cognition. Therefore, our data do not supply evidence for deficient P3a/b amplitudes as direct underlying factors for cognitive deficits in schizophrenia.

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DeGregorio, Lisa Joanne, and Sara McLean. "The Cognitive Profiles of Maltreated Children in Care and Their Educational Needs: Supporting Good Outcomes." Children Australia 38, no. 1 (January 30, 2013): 28–35. http://dx.doi.org/10.1017/cha.2012.47.

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Children in care, who have been maltreated, consistently demonstrate poorer educational outcomes than their peers. A number of reasons have been suggested for this such as a lack of stability and opportunities, as compared to their peers. One possible contributor to the poorer educational attainment of children in care is their underlying cognitive vulnerabilities. Cognitive deficits in maltreated children are thought to arise as a result of the impact of trauma on the developing brain. These cognitive deficits include difficulties with executive functioning. Executive functioning abilities include the ability to inhibit behaviour, plan ahead and switch from task to task and are critical for navigating the day to day requirements of educational settings. This article summarises what we know about the cognitive vulnerabilities of maltreated children in care and outlines the implications of these cognitive deficits for supporting maltreated children.

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Dawe, Gavin S., Ern Huei Joel Hwang, and Chay Hoon Tan. "Pathophysiology and Animal Models of Schizophrenia." Annals of the Academy of Medicine, Singapore 38, no. 5 (May 15, 2009): 425–30. http://dx.doi.org/10.47102/annals-acadmedsg.v38n5p425.

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Animal models of schizophrenia are important for research aimed at developing improved pharmacotherapies. In particular, the cognitive deficits of schizophrenia remain largely refrac- tory to current medications and there is a need for improved medications. We discuss the pathophysiology of schizophrenia and in particular the possible mechanisms underlying the cognitive deficits. We review the current animal models of schizophrenia and discuss the extent to which they meet the need for models reflecting the various domains of the symptomatology of schizophrenia, including positive symptoms, negative symptoms and cognitive symptoms. Key words: Animal models, Pharmacotherapy, Schizophrenia

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Ragazzoni, Aldo, Francesco Pinto, Rosanna Taiuti, and Maria Caterina Silveri. "Myotonic Dystrophy: An Electrophysiological Study of Cognitive Deficits." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 18, no. 3 (August 1991): 300–306. http://dx.doi.org/10.1017/s0317167100031851.

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ABSTRACT:Patients with Myotonic Dystrophy (MyD) frequently suffer from a dysfunction of the primary sensory pathways, as documented by abnormalities of short-latency evoked potentials. Impairment of intellectual functions has been less extensively investigated. Short-latency brainstem auditory evoked potentials (BAEPs) as well as long-latency auditory event-related potentials (ERPs) were recorded from 5 female and 6 male patients affected by MyD. A simple discrimination (“oddball”) paradigm was used to record ERPs to tones from Fz, Cz, Pz. Both BAEPs and ERPs were significantly altered as compared to normals. BAEP abnormalities were detected in 9 patients and ERP components N2 and P3 were delayed or absent for all patients, who nonetheless correctly discriminated between tones. These data indicate that CNS dysfunction in MyD involves not only primary sensory systems but also neural mechanisms underlying cognitive events and ERP generation.

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Rounis, Elisabeth, Ajay Halai, Gloria Pizzamiglio, and Matthew A. Lambon Ralph. "Characterising factors underlying praxis deficits in chronic left hemisphere stroke patients." Cortex 142 (September 2021): 154–68. http://dx.doi.org/10.1016/j.cortex.2021.04.019.

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Mukku, Shiva Shanker Reddy, Ajit Bhalchandra Dahale, Nagalakshmi Rajavoor Muniswamy, Krishna Prasad Muliyala, Palanimuthu Thangaraju Sivakumar, and Mathew Varghese. "Geriatric Depression and Cognitive Impairment—An Update." Indian Journal of Psychological Medicine 43, no. 4 (January 21, 2021): 286–93. http://dx.doi.org/10.1177/0253717620981556.

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Background: Depression and cognitive impairment often coexist in older adults. The relation between depression and cognitive impairment is complex. The objective of this article is to review recent literature on cognitive impairment in older adults with depression and provide clinicians an update. Methods: We searched PubMed, Google Scholar, Science Direct, and Psych Info for the articles published in the English language related to late-life depression (LLD)/geriatric depression and cognitive impairment. We considered original research articles, relevant systematic reviews, chapters, and important conceptual articles published in the last 9 years (2011–2019). We selected relevant articles for this narrative review. Conclusion: The concept pseudodementia, indicating depression with cognitive impairment mimicking dementia, is now seen only as a historical concept. The current literature strongly agrees with fact that cognitive deficits often exist in LLD. The cognitive deficits in depression were initially seen as trait marker; however, some recent studies suggest that cognitive deficits persist even in the remission phase. There is heterogeneity among the studies in terms of the nature of the cognitive deficits, but higher number of studies reported impairment in attention and executive function. LLD with cognitive deficits is at a higher risk of progression to dementia. In older adults, depression with cognitive impairments requires a comprehensive evaluation. Electroencephalography, event-related potentials, fluorodeoxyglucose–positron emission tomography, amyloid positron emission tomography, and CSF amyloid will supplement clinical evaluation in differentiating functional depressive disorder with cognitive impairment from depression with an underlying degenerative condition.

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DIXON, T., E. KRAVARITI, C. FRITH, R. M. MURRAY, and P. K. McGUIRE. "Effect of symptoms on executive function in bipolar illness." Psychological Medicine 34, no. 5 (July 2004): 811–21. http://dx.doi.org/10.1017/s0033291703001570.

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Background. The relationship between cognitive function and symptomatology in bipolar disorder is unclear. This study assessed executive function during the manic, depressed and remitted stages of bipolar I disorder.Method. Tasks assessing phonological and semantic verbal fluency, the Hayling Sentence Completion Test, the Stroop Neuropsychological Screening Test and the Cognitive Estimates Test were administered to manic (n=15), depressed (n=15), and remitted (n=15) bipolar I patients, and to healthy controls (n=30). Multiple regression analyses and analyses of covariance were used to identify potential determinants of executive dysfunction in the three bipolar groups.Results. Executive function deficits were particularly associated with the manic state. In general, manic patients performed less accurately than the remitted and depressed groups, and their performance deficit was related to the severity of positive thought disorder. The depressed and remitted bipolar groups showed a less widespread pattern of impairment. Deficits in response initiation, strategic thinking and inhibitory control were evident in all the bipolar groups.Conclusions. Executive function deficits in bipolar I disorder are most evident during mania, and are particularly associated with formal thought disorder. However, deficits in response initiation, strategic thinking and inhibitory control may be more related to the underlying disorder than a particular symptom profile.

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Mondino, Marine, Clément Dondé, Layla Lavallé, Frédéric Haesebaert, and Jérôme Brunelin. "Reality-monitoring deficits and visual hallucinations in schizophrenia." European Psychiatry 62 (October 2019): 10–14. http://dx.doi.org/10.1016/j.eurpsy.2019.08.010.

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Abstract The presence of visual hallucinations in addition to auditory hallucinations (V + AH) is associated with poor prognosis in patients with schizophrenia. However, little consideration has been given to these symptoms and their underlying cognitive bases remain unclear. Based on cognitive models of hallucinations, we hypothesized that V + AH are underpinned by an impairment in reality-monitoring processes. The objective of the present study was to test whether reality-monitoring deficits were associated with V + AH in schizophrenia. This study examined reality-monitoring abilities in two groups of patients with schizophrenia: a group of patients with V + AH (n = 24) and a group of patients with AH only (n = 22). Patients with V + AH were significantly more likely to misremember imagined words as being perceived from an external source, compared to patients with AH only (p = 0.008, d = -0.82). In other words, V + AH patients display a larger externalization bias than patients with AH only. One explanation for these results could be that experiencing hallucinations in two sensory modalities may contribute to increased vividness of mental imagery and, in turn, lead to disruption in reality-monitoring processes. This study helps to refine our understanding of the cognitive processes underlying the presence of both auditory and visual hallucinations in patients with schizophrenia.

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Hill, Elisabeth L., and Uta Frith. "Understanding autism: insights from mind and brain." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 358, no. 1430 (February 28, 2003): 281–89. http://dx.doi.org/10.1098/rstb.2002.1209.

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Autism is a developmental disorder characterized by impaired social interaction and communication as well as repetitive behaviours and restricted interests. The consequences of this disorder for everyday life adaptation are extremely variable. The general public is now more aware of the high prevalence of this lifelong disorder, with ca . 0.6% of the population being affected. However, the signs and symptoms of autism are still puzzling. Since a biological basis of autism was accepted, approaches from developmental cognitive neuroscience have been applied to further our understanding of the autism spectrum. The study of the behavioural and underlying cognitive deficits in autism has advanced ahead of the study of the underlying brain abnormalities and of the putative genetic mechanisms. However, advances in these fields are expected as methodological difficulties are overcome. In this paper, recent developments in the field of autism are outlined. In particular, we review the findings of the three main neuro–cognitive theories of autism: theory–of–mind deficit, weak central coherence and executive dysfunction.

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Wang, Zan, Yonggui Yuan, Jiayong You, and Zhijun Zhang. "Disrupted structural brain connectome underlying the cognitive deficits in remitted late-onset depression." Brain Imaging and Behavior 14, no. 5 (April 11, 2019): 1600–1611. http://dx.doi.org/10.1007/s11682-019-00091-x.

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Baluchnejadmojarad, Tourandokht, Hossein Zeinali, and Mehrdad Roghani. "Scutellarin alleviates lipopolysaccharide-induced cognitive deficits in the rat: Insights into underlying mechanisms." International Immunopharmacology 54 (January 2018): 311–19. http://dx.doi.org/10.1016/j.intimp.2017.11.033.

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