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 685 records · Page 38Linked to original sources

PubMed2006

The relationship between MRI and PET changes and cognitive disturbances in MS.

Cognitive dysfunction in multiple sclerosis (MS) is present in approximately 50% of the patients. Only moderate correlations have been found between cognitive dysfunction and T(2) lesion load, black holes or atrophy. Cognitive dysfunction in MS is probably related to the overall disease burden of the brain including abnormalities in normal appearing white matter (NAWM) and cortical grey matter, which is undetected with conventional magnetic resonance imaging (MRI). Hence, imaging techniques that embrace such abnormalities are needed to achieve better correlation with cognitive dysfunction. MR spectroscopy (MRS) performed with multi-slice echo planar spectroscopic imaging (EPSI) and PET measurements of brain metabolism as the cortical cerebral metabolic rate of glucose are imaging methods that are able to provide information on axonal loss or dysfunction in both MS lesions and in NAWM and cortical grey matter. Measurements of global NAA using multi-slice EPSI is a new promising method for measurement of the global neuron capacity and can be repeated with only little discomfort and without any risk for the patient.

Brain Mapping↗

PubMed2006

Long term morbidity and health related quality of life after multi-system Langerhans cell histiocytosis.

BACKGROUND: Langerhans' cell histiocytosis, a clonal multisystem disorder, can affect children or adults resulting in long term sequelae. However, the overall morbidity for survivors has not been formally determined. PATIENTS AND METHODS: We performed a cross-sectional study of 40 unselected long term survivors of childhood multisystem Langerhans cell histiocytosis, involving clinical examination, health-related quality of life assessment, brain imaging, neuropsychometry, endocrine assessment, respiratory function tests and audiometry. A specific 'morbidity score' was devised to measure outcome. RESULTS: Seventy-five percent of patients had detectable long term sequelae, hypothalamic-pituitary dysfunction (50%), cognitive dysfunction (20%) and cerebellar involvement (17.5%) being the most common. Half had moderate to severe morbidity, and the worst-affected patients were unable to lead an independent adult life. Health-related quality of life, which correlated well with the morbidity score (p<0.001), was adversely affected in >50% of patients. CONCLUSION: Organ damage from multisystem Langerhans cell histiocytosis causes long term morbidity extending into adult life. Carefully planned, multidisciplinary follow up is essential to ensure early recognition of problems with appropriate interventions to reduce the impact on patients' 'quality of life'.

Activities of Daily Living↗

PubMedDate not supplied

[Cognitive impairment in multiple sclerosis].

In this article we present a review of problems associated with cognitive dysfunctions in multiple sclerosis (MS). Neuropsychological investigations demonstrated that cognitive dysfunctions are common in MS patients and affect 40-65% of them. Cognitive deficits were found mainly on measures of memory, attention, information-processing speed, executive functions and abstract reasoning. The differences and degree of cognitive dysfunctions in MS are highlighted and usually related to different clinical appearance (clinical course, duration, disability level, treatment type). Furthermore, we have reviewed published correlations between psychopathological dysfunctions and neuroimaging results (mainly MRI techniques and functional imaging). The results of these correlations showed that an important role in cognitive impairment is related to the total lesion area, the severity of the pathological damage of the normal-appearing brain tissue (NABT), and brain atrophy.

Atrophy↗

PubMedDate not supplied

Beta-amyloid deposition and other measures of neuropathology predict cognitive status in Alzheimer's disease.

The relationship between progressive cognitive decline and underlying neuropathology associated with Alzheimer s disease (AD) is a key issue in defining the mechanisms responsible for functional loss. This has been a subject of much controversy, with separate studies comparing various clinical and neuropathological indices in AD. Further, it is difficult to compare studies with differences in histochemical staining protocols, brain regions examined, and data quantification criteria. There are many difficulties in designing a clinical-pathological correlative study involving AD patients. It is necessary to control for several key parameters. For example, a broad range of cognitively impaired subjects is needed, as well as short postmortem delays, brief intervals between cognitive testing and death, and the most sensitive detection and quantification techniques. In this study, we carefully controlled for each of these parameters to determine if there is a relationship between global cognitive dysfunction and multiple neuropathological indices. We selected 20 individuals representing a broad range of cognitive ability from normal to severely impaired based on the MMSE, Blessed IMC, and CDR. We counted plaque number, NFT number, dystrophic neurite number, and the relative extent of thioflavine positive plaques and neuritic involvement within plaques. We also quantified cortical area occupied by beta-amyloid immunoreactivity (A beta Load) and PHF-1 positive neuropil threads and tangles (PHF Load) using computer-based image analysis. Interestingly, we found that most pathologic measures correlated highly with the severity of dementia. However, the strongest predictor of premortem cognitive dysfunction on all three cognitive measures was the relative area of entorhinal cortex occupied by beta-amyloid deposition. In conclusion, our data show that in a carefully controlled correlative study, a variety of neuropathological variables are strongly correlated with cognitive impairment. Plaque related variables may be as strongly related to cognitive dysfunction as other established measures, including synapse loss, cell death and tau hyperphosphorylation, although no correlative study can demonstrate causality.

Aged↗

PubMed1999

Neurocognitive dysfunction in patients diagnosed with schizophrenia and alcoholism.

The authors administered the Halstead-Reitan Neuropsychological Test Battery to schizophrenic groups with (n = 54) and without (n = 217) coexisting alcoholism, nonschizophrenic groups with alcoholism (n = 231), and a patient comparison group (n = 145) to determine the extent of additive cognitive impairment in schizophrenia associated with alcoholism and to compare cognitive function in alcoholism and schizophrenia. The additive effects of alcoholism on cognitive dysfunction in schizophrenia were subtle but were consistently identifiable. Cognitive dysfunction in alcoholism was less severe than in schizophrenia with or without alcoholism. The magnitude of additive effects of alcoholism on cognitive dysfunction in schizophrenia was age related with a significant interaction between age and presence or absence of alcoholism on a global index of cognitive dysfunction.

Adult↗

PubMed1999

Beating heart surgery: why expect less central nervous system morbidity?

BACKGROUND: The incidence and etiology of brain dysfunction after conventional coronary artery bypass surgery using cardiopulmonary bypass (CPB) are reviewed. METHODS: Stroke rates and incidences of cognitive dysfunction from various studies are considered. Mechanisms of injury including cerebral embolization as detected by transcranial Doppler and retinal angiography, and imaging-based evidence for postoperative cerebral edema, are discussed. Preliminary results from a prospective clinical trial assessing cognitive dysfunction after beating heart versus conventional coronary artery bypass with CPB are discussed. RESULTS: Initial evidence for lower overall postoperative morbidity, and for a lower incidence of cognitive dysfunction specifically, after nonpump coronary revascularization is presented. CONCLUSIONS: Beating heart surgery results in less potential for generation of cerebral emboli and appears to produce a lower incidence of cognitive dysfunction in both short- and intermediate-term postoperative follow-up periods as compared with conventional coronary artery bypass surgery using CPB.

Cardiopulmonary Bypass↗

PubMed2004

[Disorders of neurocognitive function after coronary artery bypass grafting].

OBJECTIVE: Neurocognitive dysfunction still remains a frequent problem after heart surgery, complicating early recovery and strongly affecting postoperative quality of life. The aim of our study was to determine incidence of cognitive dysfunction after coronary artery bypass grafting for patients of low risk group and to find operative and postoperative factors associated with early cognitive impairment. MATERIAL AND METHODS: Using exclusion criteria, which are known as risk factors for postoperative neurological complications we selected a group of 30 coronary artery bypass grafting patients. The day before surgery and 7 to 8 days after operation we evaluated cognitive function of each patient using MMSE and standardized test battery of five neuropsychological tests. The incidence of cognitive decline was evaluated using composite z scores and 1 SD criteria. Preoperative ultrasound screening of asymptomatic carotid artery was performed for each patient. RESULTS: Early postoperative cognitive dysfunction was present in 13 (46.3%) of patients. Patients with cognitive decline more often had asymptomic, hemodynamicly significant carotid artery stenosis. Duration of operation and coronary artery bypass time was longer in cognitive dysfunction group. As well there were more grafts performed to this group of patients. We noticed a relationship between lower temperature during coronary artery bypass and cognitive impairment. CONCLUSIONS: Incidence of cognitive dysfunction for patients of low risk group was 46.3%. Cognitive decline was associated with prolonged coronary artery bypass, operation time and number of grafts.

Age Factors↗

PubMed2006

Anesthesia for the elderly: selected topics.

PURPOSE OF REVIEW: With the graying of the Western population, there is a continuous increase in the proportion of elderly patients undergoing surgical procedures. Geriatric anesthesia is emerging from a 'subspecialty' to the mainstream of today's anesthesia and perioperative care. Much has been written on anesthesia for the elderly, but this review will concentrate on selected topics related to elderly care that represent current unresolved and pertinent issues for the care of the elderly surgical patient. RECENT FINDINGS: Postoperative cognitive dysfunction, cardiac diastolic dysfunction and prophylactic perioperative beta-blockade in the process of major noncardiac surgery are three main topics that have recently attracted great interest in clinical practice and research, and have therefore been chosen as the selected topics for this current review. SUMMARY: Although age is a clear risk factor for postoperative cognitive dysfunction, the association of general anesthesia with cognitive dysfunction is less clear, as is the effect of anesthesia per se or surgery on long-term cognitive dysfunction. Cardiac diastolic dysfunction is a relatively new and evolving concept in anesthesia and perioperative medicine, yet clearly diastolic dysfunction even with a normal ejection fraction may have a significant effect on the perioperative outcome and management of elderly patients. Small, but powerful studies have shown significant outcome benefit with prophylactic perioperative beta-blockade in high-risk patients undergoing major noncardiac surgery. Data from other studies, however, are still conflicting and the final verdict awaits larger scale outcome studies.

Adrenergic beta-Antagonists↗

PubMed2006

The neurobiology of cognition in schizophrenia.

Cognitive dysfunction in schizophrenia differs from cognitive dysfunction in neurodegenerative illnesses because it is associated with neuronal dysfunction and not neurodegeneration. Pharmacologically, potential targets for developing treatments may differ from cognition in dementing disorders. Several putative molecular targets for treating cognition in schizophrenia show promise, such as treatments that act on the D(1) receptor of the dopamine system; the 5HT(1A), 5HT(2A), and 5HT(6), receptors of the serotonin system; and ampakines, Glycine/D-cycloserine, D-serine, and mGluR 2/3 agonists of the glutamatergic system. Other receptors associated with improvement in cognition include nicotinic and muscarinic receptors, and the alphalpha2 subunit receptor of the brain GABA system. Domain treatment of schizophrenia is a new method of treating schizophrenia that involves treating a single domain of dysfunction at a time.

Animals↗

PubMed1995

Pathophysiology of alcoholic brain damage: synergistic effects of ethanol, thiamine deficiency and alcoholic liver disease.

Chronic alcoholism results in brain damage and dysfunction leading to a constellation of neuropsychiatric symptoms including cognitive dysfunction, the Wernicke-Korsakoff Syndrome, alcoholic cerebellar degeneration and alcoholic dementia. That these clinically-defined entities result from independent pathophysiologic mechanisms is unlikely. Alcohol and its metabolite acetaldehyde are directly neurotoxic. Alcoholics are thiamine deficient as a result of poor diet, gastrointestinal disorders and liver disease. In addition, both alcohol and acetaldehyde have direct toxic effects on thiamine-related enzymes in liver and brain. Alcoholics frequently develop severe liver disease and liver disease per se results in altered thiamine homeostasis, in cognitive dysfunction and in neuropathologic damage to astrocytes. The latter may result in the loss of neuron-astrocytic trafficking of neuroactive amino acids and thiamine esters, essential to CNS function. The present review article proposes mechanisms whereby the effects of alcohol, thiamine deficiency and liver disease combine synergistically to contribute to the phenomena of cognitive dysfunction and "alcoholic brain damage".

Alcoholism↗

PubMed2000

[Dementia screening in psychiatric consultation for elderly patients in a general hospital].

BACKGROUND: Elderly patients on medical-surgical wards in general hospitals often suffer from cognitive dysfunction that hampers medical treatment of somatic diseases. Symptoms of cognitive dysfunction may not be recognized adequately by non-psychiatric physicians. PATIENTS AND METHOD: We studied the usefulness of a short screening instrument for cognitive dysfunctions (short mini mental state test) in a consecutive sample of 222 psychiatric consultation liaison patients older than 60 years of age. Normative data for the screening test from an epidemiological sample, the Berlin Aging Study, are given and compared with the consultation sample. RESULTS: Mild to moderate deficits in cognitive functions were found in 32% of patients, severe deficits indicating dementia- or delirium syndromes were found in 17.7%. Applying the cut off 4/5, 88.9% correct classifications of dementia patients were obtained. The item analysis demonstrates significant differences with respect to the age-matched population sample for the orientation items, the 2nd and subsequent subtractions of the serial seven task and, to a lesser degree, the memory items. CONCLUSION: A standardized assessment of the 15 items of the SMMS represents a practical, reliable and valid screening for relevant cognitive deficits, which may also serve as documentation of the time course especially in acute organic-psychiatric syndromes.

Aged↗

PubMed2002

Event-related potentials in different subtypes of multiple sclerosis--a cross-sectional study.

Impairment of cognitive skills is found in up to 65% of patients suffering from multiple sclerosis (MS). Little is known concerning the natural history or characteristics of progression of these cognitive dysfunctions. Furthermore, it has not been investigated to date whether there are differences in the course of cognitive impairment with respect to different diagnostic subgroups of MS. Event-related potentials (ERP) are an objective tool to evaluate cognitive processing. We performed a cross-sectional study on 179 consecutive patients suffering from MS (107 relapsing-remitting MS; 17 primary progressive MS; 50 secondary progressive MS; 5 undetermined). ERP were measured by a visual oddball paradigm, latencies of P3 components were correlated with demographic and clinical data. We found pathologically increased P3 latencies in 56% of all patients. Patients with secondary progressive MS showed significantly increased P3 latencies as compared to the other subgroups. There was a significant correlation between expanded disability status scale (EDSS) score and P3 latency (r=0.48; p<0.001). We conclude that ERP are an appropriate method to follow up cognitive dysfunction in MS and that cognitive dysfunction as measured by ERP is progressively impaired in the course of MS, in particular in the secondary progressive subtype.

Adult↗

PubMed1997

Improvement of cognitive function in schizophrenic patients receiving clozapine or zotepine: results from a double-blind study.

Clinical interest in the so-called atypical antipsychotics currently focuses on the possibility of improving the negative symptoms of schizophrenia and the cognitive dysfunction associated with the disease. While clozapine has been shown to be effective in this respect, no data are available on zotepine. We report on a double-blind randomized study designed to evaluate the impact of zotepine and clozapine on cognitive dysfunction in schizophrenia. Cognitive function was operationalized by a maze test in which patients traversed computer-displayed mazes of increasing complexity. Passage time, route, and motor errors were evaluated. 25 schizophrenic (DSM-IIIR) patients were included in each group. After washout, they were randomized on zotepine or clozapine and given up to 450 mg of substance each. Patients were followed for six weeks and evaluated weekly. We report on a subsample of 26 patients matched for baseline BPRS, SANS, and age. 13 matched healthy persons were recruited as controls. ANOVA with group and course over time as factors was used for analysis. Both clozapine and zotepine achieved a highly significant decrease in overall symptoms (BPRS) and negative symptoms (SANS). Zotepine and clozapine were equally effective. In the maze tests, motor errors in simple mazes were stable over time and differentiated schizophrenics from controls as a "trait" marker. In passage time and maze route, schizophrenics performed worse than controls. An improvement by medication was evident in both medication groups, but was more pronounced in the zotepine-treated group. The study confirms previous results on the efficacy of clozapine and zotepine in treating negative symptoms of schizophrenia. The data presented show for the first time that zotepine is efficacious in improving cognitive dysfunction, confirming this substance's value as an atypical antipsychotic.

Adult↗

PubMed2003

Cognitive functioning and psychiatric symptomatology in patients with chronic hepatitis C.

Hepatitis C virus (HCV) infection is a major public-health-care problem, with over 170 million infected worldwide. Patients with chronic HCV infection often complain of various cognitive problems as well as symptoms of depression, anxiety, and fatigue. Relatively little is known, however, about the specific cognitive deficits that are common among HCV patients, and the influence of psychiatric symptomatology on cognitive functioning. In the current study of 21 chronically infected HCV patients, we assessed subjective cognitive dysfunction, depression, anxiety, and fatigue and compared these symptom areas to cognitive tests assessing visuoconstruction, learning, memory, visual attention, psychomotor speed, and mental flexibility. Results revealed that cognitive impairment ranged from 9% of patients on a visuoconstruction task to 38% of patients on a measure of complex attention, visual scanning and tracking, and psychomotor speed, and greater HCV disease severity as indicated by liver fibrosis was associated with greater cognitive dysfunction. Objective cognitive impairment was not related to subjective cognitive complaints or psychiatric symptomatology. These findings suggest that a significant portion of patients with chronic HCV experience cognitive difficulties that may interfere with activities of daily living and quality of life. Future research using cognitive measures with HCV-infected patients may assist researchers in identifying if there is a direct effect of HCV infection on the brain and which patients may be more likely to progress to cirrhosis and hepatic encephalopathy.

Adult↗

PubMed1996

[Primary and secondary negative symptoms: a useful differentiation? An empirical study].

The concept of schizophrenic negative symptomatology consisting of primary, treatment-resistant negative symptoms associated with cognitive dysfunction and treatable secondary composite negative symptoms was tested by comparing a group with non-chronic schizophrenia and a neurotic group with negative symptoms before and 8 weeks after the start of treatment. Contrary to our hypothesis, we found no association between schizophrenic negative symptoms and cognitive dysfunction as measured by CPT and K-V-T either at the first or at the second assessment point, but did find a strong relation between depressive and negative symptomatology at both assessment points in both groups. Thus, we conclude that a chronic course, rather than primary negative symptomatology, may be associated with cognitive dysfunction. The concept of primary negative symptoms based on cognitive dysfunction versus secondary negative composite symptoms encompassing motivation and reactive attitudes is not supported by these results.

Adult↗

PubMed2006

Correlation of global N-acetyl aspartate with cognitive impairment in multiple sclerosis.

BACKGROUND: Whole-brain N-acetyl aspartate (NAA), a measure of neuronal function, can be assessed by multislice echo-planar spectroscopic imaging. OBJECTIVE: To test the hypothesis that the global brain NAA/creatine (Cr) ratio is a better predictor of cognitive dysfunction in multiple sclerosis than conventional magnetic resonance imaging measures. DESIGN: Survey. SETTING: Research-oriented hospitals. PATIENTS: Twenty patients, 16 women and 4 men (mean age, 36 years), with early relapsing-remitting multiple sclerosis (mean Expanded Disability Status Scale score, 2.5). MAIN OUTCOME MEASURES: Correlation between the global NAA/Cr ratio and a cognitive dysfunction factor comprising 16 measures from an extensive neuropsychological test battery that best distinguished patients with multiple sclerosis from healthy control subjects. RESULTS: A significant partial correlation between the global NAA/Cr ratio and the cognitive dysfunction factor was found (partial r = 0.62, P = .01), and 9 cognitively impaired patients had significantly lower global NAA/Cr ratios than 11 unimpaired patients (P = .04). No significant correlations were found between the cognitive dysfunction factor and conventional magnetic resonance imaging measures (ie, brain parenchymal fraction and lesion volume). CONCLUSIONS: Multislice echo-planar spectroscopic imaging provides global metabolic measures that distinguish between cognitively impaired and unimpaired patients with multiple sclerosis and correlate with a global cognitive measure. Standardization of the technique is needed, and larger-scale studies that include healthy controls are suggested.

Adult↗

PubMed2005

Cognition in liver disease.

BACKGROUND: Cognitive dysfunction has been observed in a range of liver diseases including chronic hepatitis C virus, alcoholic liver disease, primary biliary cirrhosis and Wilson's disease. Such dysfunction may range from mild cognitive changes to overt hepatic encephalopathy, and represents a significant complication of liver disease that may negatively impact the patient's quality of life, and normal activities of daily living (e.g., driving). METHOD: This article reviews the published evidence relating to cognitive dysfunction in liver disease. OUTCOME: Issues of definition, diagnosis, epidemiology, aetiology, treatment and outcome are discussed. Particular attention is devoted to identifying the mild cognitive changes that occur in liver diseases of different aetiology.

Activities of Daily Living↗

PubMed1994

Dynamics of cognitive brain dysfunction in patients with cirrhotic liver disease: an event-related P300 potential perspective.

The dynamics of cognitive brain functions of 104 patients with both chronic non-cirrhotic (NC) and cirrhotic liver disease (C: C1, non-encephalopathic; C2, encephalopathic) were investigated by means of visual P300 potentials elicited in both the paradigms of transient (PI) and selective attention (PII). Conventional PVEPs, psychometric tests and quantitative liver function tests were also performed. As compared to both an age-matched control group (N) and the non-cirrhotic patients (NC), the N250 and P300 latencies of the cirrhotics (C) were equally prolonged in both P300 paradigms (P = 0.0001). By contrast, the P300 amplitudes were not different between the patient groups in either P300 paradigm. In the cirrhotics, however, the P300 amplitude differences between PII and PI (+ 3.7 +/- 2.8 muV, mean +/- 1 S.D.) were significantly (P < 0.01) smaller than in the non-cirrhotics (+ 7.5 +/- 5.2 muV) reflecting disturbances in the dynamics of visual attention. Interestingly, these P300 amplitude differences between both paradigms were positively correlated (r = 0.35; P = 0.005) with hepatic metabolic capacity, but not with liver blood flow (r = 0.23; P > 0.05). The diagnostic efficacy of the visual P300 in PI (sensitivity, 48%; specificity, 100%) was lower than that of the visual P300 in PII (79%; 100%) and that of the psychometric tests (63%; 94%), but it remained superior to that of the PVEPs (29%; 97%). It is concluded that in patients with cirrhotic liver disease visual P300 potentials can even reveal the dynamics of minor cognitive brain dysfunction and may also provide interesting pathophysiological information.

Adult↗