PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Cognitive Dysfunction”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 361 records · Page 20Linked to original sources

The Test for Severe Impairment: an instrument for the assessment of patients with severe cognitive dysfunction.

OBJECTIVE: To develop a reliable and valid test of cognitive function suitable for patients with severe cognitive impairment. DESIGN: Administration of a test; test-retest reliability; comparison to traditional test. SETTING: Chronic long-term-care facility. PATIENTS OR OTHER PARTICIPANTS: The participants were 40 elderly residents with severe cognitive impairment. MAIN OUTCOME MEASURES: Results of the Test for Severe Impairment (TSI) and its subsections (language, memory, executive function, and motor performance); correlation of test and retest scores; correlation of TSI with Mini-Mental State Exam. RESULTS: The TSI was significantly correlated with the Mini-Mental State Exam (r = 0.83, P less than or equal to 0.0001). Test-retest reliability was high (r = 0.96, P less than 0.0001). The internal reliability of the test was also good (alpha = 0.90). Preliminary result of a factor-analysis suggests that factor scores may be derived that relate to memory, language production, and knowledge of body parts. CONCLUSIONS: The TSI is a valid and reliable test of cognitive function in patients with severe cognitive impairment. It is appropriate to use it as a unified scale.

Aged↗

Age at onset of Alzheimer's disease: relation to pattern of cognitive dysfunction and rate of decline.

We examined the pattern of cognitive impairment and rate of cognitive and functional decline as a function of age at symptom onset in 127 patients with probable Alzheimer's disease (AD). At baseline, early-onset (before age 65) and late-onset groups were mildly and comparably impaired on the modified Mini-Mental State Examination (mMMS) and the Blessed Dementia Rating Scale-Part 1 (BDRS). Repeated-measures analysis of variance revealed significantly more rapid decline in early-onset subjects over a 2-year follow-up period. Multivariate linear regression analyses indicated that age at symptom onset strongly predicted rate of decline on the mMMS and the BDRS, even after controlling for symptom duration, gender, family history of dementia, and baseline mMMS and BDRS scores. Early- and late-onset AD subjects also differed in terms of pattern of performance on the mMMS. Early-onset subjects scored significantly lower than late-onset subjects on attentional items of the mMMS at baseline and follow-up. Conversely, late-onset subjects scored significantly lower than early-onset subjects on memory and naming items at baseline, and the two groups were comparable on these tasks at follow-up. Results provide longitudinal evidence of more rapid cognitive and functional decline in subjects with early-onset AD and suggest that early-onset AD may be characterized by predominant impairment of attentional skills.

Age of Onset↗

Cognitive dysfunction and recovery in alcoholics.

In summary, neuropsychological deficits (impaired cognitive and perceptual motor functioning) exist in many alcoholics. These deficits, are related to treatment benefit and outcome. In our male alcoholic population, the deficits seem remarkably resistent to attenuation even after 13 months in about 50% of the retested alcoholics, namely, those who resume drinking. The question of such alcoholics having pre-morbid cognitive deficits is an important problem to resolve. Studies of recovery heretofore have been based on the implicit assumption that the cognitive deficits are alcohol induced. From our data there is good reason now to suspect that certain cognitive deficits preceded the alcoholism especially those alcoholics who have a history of childhood hyperkinesis/minimal brain-damage syndrome or who have a history of familial alcoholism.

Adult↗

Relationship of APP mRNA transcripts and levels of NGF and low-affinity NGF receptors to behavioral measures of age-related cognitive dysfunction.

This study was designed to examine the relationship between cognitive function and endogenous levels of NGF, low-affinity NGF receptor (LNGFR), and amyloid precursor protein (APP) mRNAs. Using 3 month (n = 5), 18 month (n = 40), and 29 month (n = 17) Fischer-344 male rats, cognitive function was assessed with the Morris water maze, reverse transcription and polymerase chain reaction were used to quantify APP mRNAs, and NGF and LNGFR levels were determined with an ELISA. Cognitive function declined progressively with age from 3 months to 18 months, and from 18 months to 29 months, but only RNA content in the tissue declined significantly from 3 months to 18 months. Between 18 month and 29 month rats were small but statistically significant decreases only for Kunitz protease inhibitor (KPI)-inclusive mRNAs and cortical NGF levels. There was a small but statistically significant correlation between cognitive function and %KPI (the amount of KPI APP mRNAs relative to the total amount of APP mRNA), with lower %KPI related to more impaired spatial learning. No other statistically significant correlation or linear relationship could be detected between cognitive function and any of the other neurological measures or any combination of these measures (i.e., hippocampal levels of APP 695 mRNA, cortical and hippocampal levels of NGF, and cortical, hippocampal, and basal forebrain levels of LNGFR).(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

Addiction denial and cognitive dysfunction: a preliminary investigation.

This study explored the proposition that denial of addiction is often more a product of cognitive failure due to cerebral dysfunction than an emotion-driven rejection of the truth. Forty-four subjects were studied in an inpatient alcohol rehabilitation program. Denial was defined as the proportion of standardized denial-related treatment goals established at admission that remained unachieved at discharge. Cognitive deficiencies were identified through neuropsychological assessments. Persistent denial was significantly correlated with greater impairment of executive function, verbal memory, visual inference, and mental speed.

Adult↗

Resolution of left hemisphere cognitive dysfunction in multiple sclerosis with magnetic resonance correlates: a case report.

Cognitive impairment is common in multiple sclerosis and although deterioration has been observed in individual patients at the time of relapse, improvement in cognitive function in parallel with remission of neurological impairment has proved more difficult to document. We describe a 21-year-old women with a one-year history of relapsing remitting multiple sclerosis, who was admitted to hospital following a severe relapse which rendered her quadriplegic. Detailed psychometric assessment was carried out during relapse and on recovery of neurological function, eight weeks later. There were improvements in arithmetic, naming, and comprehension tasks. The patient had T2 weighted and gadolinium-enhanced magnetic resonance imaging and magnetic resonance spectroscopy. These showed a reduction in lesion size, lesion enhancement, and changes in brain chemistry which parallel the improvement in cognitive performance.

Journal Article↗

Morphological correlates to cognitive dysfunction in schizophrenia as studied with Bayesian regression.

BACKGROUND: Relationships between cognitive deficits and brain morphological changes observed in schizophrenia are alternately explained by less gray matter in the brain cerebral cortex, by alterations in neural circuitry involving the basal ganglia, and by alteration in cerebellar structures and related neural circuitry. This work explored a model encompassing all of these possibilities to identify the strongest morphological relationships to cognitive skill in schizophrenia. METHODS: Seventy-one patients with schizophrenia and sixty-five healthy control subjects were characterized by neuropsychological tests covering six functional domains. Measures of sixteen brain morphological structures were taken using semi-automatic and fully manual tracing of MRI images, with the full set of measures completed on thirty of the patients and twenty controls. Group differences were calculated. A Bayesian decision-theoretic method identified those morphological features, which best explained neuropsychological test scores in the context of a multivariate response linear model with interactions. RESULTS: Patients performed significantly worse on all neuropsychological tests except some regarding executive function. The most prominent morphological observations were enlarged ventricles, reduced posterior superior vermis gray matter volumes, and increased putamen gray matter volumes in the patients. The Bayesian method associated putamen volumes with verbal learning, vigilance, and (to a lesser extent) executive function, while caudate volumes were associated with working memory. Vermis regions were associated with vigilance, executive function, and, less strongly, visuo-motor speed. Ventricular volume was strongly associated with visuo-motor speed, vocabulary, and executive function. Those neuropsychological tests, which were strongly associated to ventricular volume, showed only weak association to diagnosis, possibly because ventricular volume was regarded a proxy for diagnosis. Diagnosis was strongly associated with the other neuropsychological tests, implying that the morphological associations for these tasks reflected morphological effects and not merely group volumetric differences. Interaction effects were rarely associated, indicating that volumetric relationships to neuropsychological performance were similar for both patients and controls. CONCLUSION: The association of subcortical and cerebellar structures to verbal learning, vigilance, and working memory supports the importance of neural connectivity to these functions. The finding that a morphological indicator of diagnosis (ventricular volume) provided more explanatory power than diagnosis itself for visuo-motor speed, vocabulary, and executive function suggests that volumetric abnormalities in the disease are more important for cognition than non-morphological features.

Adult↗

Cognitive dysfunction in congestive heart failure: transcranial Doppler evidence of microembolic etiology.

Cognitive symptoms are common in patients with congestive heart failure (CHF) and are usually attributed to low cerebral blood flow. In the present study, we aimed to evaluate global cognitive function (Mini Mental State Exam MMSE) in relation to both cardiac function (evaluated by echocardiogram) and cerebrovascular hemodynamics (evaluated by transcranial Doppler TCD) in CHF patients. In 83 patients studied, no correlation was found between echocardiographic parameters and MMSE scores. In contrast, a significant correlation was found between right middle cerebral artery (RMCA) mean flow velocity and MMSE score (r=0.231 p=0.039), as well as between RMCA pulsatility index and MMSE score (rs= -0.292 p=0.015). After excluding patients with a previous history of stroke, only RMCA pulsatility index correlated with MMSE score (rs=-0,314 p=0,007). The relationship between high cerebrovascular resistance and worse cognitive scores suggest that microembolism may be responsible for a significant proportion of cognitive symptoms in CHF patients.

Blood Flow Velocity↗

Cognitive dysfunction and chemotherapy: neuropsychological findings in perspective.

Currently, the interest in cognitive functioning following chemotherapy is rapidly expanding as is reflected in a growing number of published studies on this topic. Although most studies are indicative of cognitive deficits after chemotherapy, definite conclusions on the role of chemotherapy on cognitive function can often not be drawn due to methodological problems. On the basis of the studies on cognitive functioning after chemotherapy that are conducted in The Netherlands Cancer Institute, the current article describes a number of such methodological topics that obscure straightforward interpretation of neuropsychological findings in toxicity research. Measurement issues that diverge from usual assessment issues encountered in psychosocial oncology will be described, and factors that might play a role in the cause of cognitive impairment will be evaluated. Also, future developments necessary to gain more insight into the prevalence, the pattern, and the impact of cognitive problems following chemotherapy are discussed

Antineoplastic Combined Chemotherapy Protocols↗

Dysfunctional cognitions and adult psychological functioning in child sexual abuse survivors.

Two studies explored the relationship between cognitions and long-term symptoms in adult child sexual abuse (CSA) survivors. In Study 1, an American sample of 43 survivors completed questionnaires assessing attributional style and dysfunctional beliefs in cognitive themes affected by victimization, as well as measures of posttraumatic symptoms. Survivors' attributions of negative events were more internal, stable, and global than those of 29 comparison subjects without a history of CSA. However, only the globality scale was significantly related with severity of long-term symptoms. High correlations between dysfunctional beliefs concerning safety, trust, esteem, or intimacy, and posttrauma symptoms were found. The latter finding was replicated in Study 2 with a German sample of 35 CSA survivors, even when controlling for frequency of abuse.

Adult↗

The role of norepinephrine in the pathophysiology of cognitive disorders: potential applications to the treatment of cognitive dysfunction in schizophrenia and Alzheimer's disease.

The role of noradrenergic neurotransmission in normal cognitive functions has been extensively investigated, however, the involvement of noradrenergic functions in the cognitive impairment associated with schizophrenia and Alzheimer's disease has not been as intensively considered. The limited ability of atypical antipsychotics to treat the cognitive impairment of schizophrenia, and cholinomimetics to treat the cognitive impairment of Alzheimer's disease, may be related to the influence of a multiplicity of neurotransmitter abnormalities including noradrenergic dysfunction, which these treatments do not address. The evidence of noradrenergic dysfunction occurring concomitantly with dopamine dysfunction in schizophrenia and acetylcholine dysfunction in Alzheimer's disease supports therapeutic approaches using noradrenergic drugs in combination with neuroleptics and cholinesterase inhibitors, respectively, to enhance the treatment of cognitive impairment. Given the results of animal and human studies, it appears that alpha-2A agonists may be the optimal choice for this purpose.

Adrenergic alpha-2 Receptor Agonists↗

Animal models of working memory: insights for targeting cognitive dysfunction in schizophrenia.

BACKGROUND AND RATIONALE: Working memory performance is considered to be a core deficit in schizophrenia and the best predictor of social reintegration and propensity for relapse. This cardinal cognitive process is critical for human reasoning and judgment and depends upon the integrity of prefrontal function. Prefrontal dysfunction in schizophrenia has been linked to altered dopaminergic and glutamatergic transmission. However, to date, antipsychotics provide no substantial relief from the debilitating cognitive consequences of this disease. OBJECTIVES: This review examines the key rodent and non-human primate models for elucidating the neural mechanisms of working memory and their neuromodulation. We compare the physiology and pharmacology of working memory between the normal state and experimentally induced models of prefrontal dysfunction and evaluate their relevance for schizophrenia. RESULTS AND CONCLUSIONS: Rodent models have demonstrated the significance of aberrant dopaminergic and glutamatergic signaling in medial prefrontal cortex for working memory. However, there is some question as to the extent to which rodent tests of working memory tap into the same process that is compromised in schizophrenia. Non-human primates provide an unexcelled model for the study of influences on prefrontal function and working memory due to the high degree of homology between human and non-human primates in the relationship between prefrontal cortex and higher cognitive capacities. Moreover, non-human primate models of prefrontal dysfunction including amphetamine sensitization, subchronic phencyclidine, and neurodevelopmental insult are ideal for the analysis of novel compounds for the treatment of cognitive dysfunction in schizophrenia, thereby facilitating the translation between preclinical drug development and clinical trials.

Amphetamine↗

A multilevel analysis of cognitive dysfunction and psychopathology associated with chromosome 22q11.2 deletion syndrome in children.

We present a multilevel approach to developing potential explanations of cognitive impairments and psychopathologies common to individuals with chromosome 22q11.2 deletion syndrome. Results presented support our hypothesis of posterior parietal dysfunction as a central determinant of characteristic visuospatial and numerical cognitive impairments. Converging data suggest that brain development anomalies, primarily tissue reductions in the posterior brain and changes to the corpus callosum, may affect parietal connectivity. Further findings indicate that dysfunction in "frontal" attention systems may explain some executive cognition impairments observed in affected children, and that there may be links between these domains of cognitive function and some of the serious psychiatric conditions, such as attention-deficit/hyperactivity disorder, autism, and schizophrenia, that have elevated incidence rates in the syndrome. Linking the neural structure and the cognitive processing levels in this way enabled us to develop an elaborate structure/function mapping hypothesis for the impairments that are observed. We show also, that in the case of the catechol-O-methyltransferase gene, a fairly direct relationship between gene expression, cognitive function, and psychopathology exists in the affected population. Beyond that, we introduce the idea that variation in other genes may further explain the phenotypic variation in cognitive function and possibly the anomalies in brain development.

Attention↗

Donepezil in the treatment of cognitive dysfunction associated with traumatic brain injury.

Cholinesterase inhibitors are known to enhance cognitive function among patients with dementia of the Alzheimer's type. It is quite possible that this clinical benefit may extend to other patient groups, yet this issue awaits further exploration. This study examines the use of the cholinesterase inhibitor donepezil in the treatment of patients with a history of brain injury and subsequent cognitive impairment. The sample was comprised of 53 ambulatory psychiatric patients who were receiving care for psychiatric sequelae of brain injury. In this sample, residual cognitive impairment was treated with adjunctive donepezil. This study reports the clinical assessments of this patient sample in outpatient follow-up for up to two years duration. Assessments of cognition with the Wechsler Adult Intelligence Scale-Revised and the Hooper Visual Organization Test were obtained on a subset of this sample (N = 22). Clinician assessment ratings were analyzed for the entire sample. Results indicated an improvement in full-scale IQ (t = 2.5, p = 0.02) score as well as clinician-based ratings (t = 12.2, p < 0.0001). Further research will likely delineate whether specific types of brain injuries are most responsive to cholinesterase inhibitors. These findings suggest that donepezil may enhance clinical response by complementing the medication management of other concomitant psychiatric disturbances related to brain injury.

Adult↗