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PubMedDate not supplied

[Cognitions in eating disorders and their assessment].

UNLABELLED: Cognitions are of crucial importance in the -aetiology and the maintenance of eating disorders. Dysfunctional cognitions in eating disorders are related to body image, self-esteem and feeding. The aim of this paper is to review the actual knowledge in this area. First, we will display -cognitive models in eating disorders. Cognitive factors in -eating disorders are logical errors, cognitive slippage and conceptual complexity. Eating disorder patients seem to have a deficient cognitive development. Some cognitive models stipulate that eating disorder patients may develop organised cognitive structures schemas concerning the issues of weight and its implications for the self. These schemas can account for the persistence and for the understanding the "choice of the eating disorder symptomatology. Cognitive pheno-mena of interest are self-schema, weight-related schema and weight-related self-schema. The maintenance model of ano-rexia nervosa argued that, initially there is an extreme need to control eating which is supported by low self-esteem. The maintenance of the disorder is reinforced by three mechanisms: dietary restriction enhances the sense of being in control; aspects of starvation encourage further dietary restriction; concerns about shape and weight encourage restriction. The development and maintenance of bulimic symptomatology are explained by placing a high value on attaining an idealised weight and body shape accompanied by inaccurate beliefs. The cognitive model of specific family of origin experiences puts forward the development of -maladaptative expectancies for eating and thinness. Second, we discuss distortions in information processing. a) In feeding laboratories, bulimics show a wide range of caloric intake and a disruption of circadian feeding patterns. In overeating bulimics, large meals occurred mainly during afternoon and evening with high fat and carbohydrate intake, but the majority of meals were of normal size and frequency. Responsivity to food cues indicates that bulimics were more responsive to sight, smell and taste of their favourite binge food, and a greater responsivity was associated with increasing -cue salience. Eating disorder patients appear to have internalised a mediated social rule concerning "good food" and make drastic selections thus removing the possibility of choice of foodstuffs. b) Experimental processes: temporal factors in the processing of threat seem to be of importance in patients with high levels of eating psychopathology. There is no evidence for preattentive processing biases among anorectics. Changes in information processing speed after treatment were not linked to treatment condition or treatment response. c) Judgement and emotions: in eating disorder patients, distortions of depressogenic nature are found that influence the cognitive style; thoughts about eating, weight and shape are characterised by negative affective tone; negative emotions could account for bulimic behaviour; anxiety and distress are correlated to thought control strategies. Information treating seems to be impaired in a non-homogeneous way. d) Cognitive schemas are seriously maladaptive and not well investigated. In eating disorder patients, core beliefs are absolute, unconditional and dichotomous cognitions about oneself and the world. There are only few studies in this field moreover showing controversial results. Core beliefs can explain links between personality disorders and eating psychopathology. Pathological core beliefs have to be taken in to account because they influence the outcome and the efficacy of cognitive behavioural therapy. Third, the last part of this paper summarises actually available rating scales eva-luating distorted cognitions in eating disorders. There are different methods for evaluation: specific and non-specific self-report questionnaires, thought-sampling procedures, -methods derived from cognitive psychology. The Mizes Anorectic Cognition questionnaire (MAC) is a well-known self-rating scale with good psychometric properties. The revised form of the MAC appears to be an improvement in the area of internal consistency, sensitivity, and reliability. It is obvious that there is no particular rating scale referring to specific cognitions on food. IN CONCLUSION: the main result of this literature review reflects that the cognitive treatment in eating disorders is altered in a specific way on an emotional basis and on self-representation.

Attitude to Health↗

PubMed2001

Time course of postoperative recovery of N-acetyl-aspartate in temporal lobe epilepsy.

PURPOSE: To assess the time course of increases in N-acetyl-aspartate/creatine (NAA/Cr), which can be measured using proton MR spectroscopic imaging (1H-MRSI), in patients with intractable nonlesional temporal lobe epilepsy (TLE) after successful epilepsy surgery. METHODS: We performed pre- and postoperative 1H-MRSI in 16 seizure-free (SF) patients and 16 not seizure-free (NSF) TLE patients. We calculated a mixed-design analysis of variance (ANOVA) between SF and NSF groups, ipsi- and contralateral to the side of operation, and pre- and postoperative NAA/Cr measurements. We applied nonlinear regression between pre- and postoperative NAA/Cr differences and the time interval between 1H-MRSI scans to fit a negative exponential model to NAA recovery. RESULTS: Mixed-design ANOVA revealed that (a) postoperative NAA/Cr was significantly higher in SF than in NSF patients (p = 0.02) and that (b) in the SF group, postoperative NAA/Cr values were significantly higher than preoperative values (p < 0.05) and returned to the normal range in most patients. According to our nonlinear regression model, in SF patients, there was a 50% increase relative to preoperative NAA/Cr values after 5.8 months, whereas an improvement of 95% was reached after 25 months. CONCLUSIONS: Our results extend preliminary observations of postoperative NAA recovery of SF patients by characterizing the time course of recovery as an exponential function with a half-time of approximately 6 months. The reversal of neuronal metabolic dysfunction remote from the epileptic focus may underlie the clinical observation of improvement of cognitive dysfunction after successful epilepsy surgery.

Adolescent↗

PubMed2006

Aberrant cortical synaptic plasticity and dopaminergic dysfunction in a mouse model of Huntington's disease.

Predictive genetic testing for Huntington's disease (HD) has revealed early cognitive deficits in asymptomatic gene carriers, such as altered working memory, executive function and impaired recognition memory. The perirhinal cortex processes aspects of recognition memory and the underlying mechanism is believed to be long-term depression (LTD) of excitatory neurotransmission, the converse of long-term potentiation (LTP). We have used the R6/1 mouse model of HD to assess synaptic plasticity in the perirhinal cortex. We report here a progressive derailment of both LTD and short-term plasticity at perirhinal synapses. Layer II/III neurones gradually lose their ability to support LTD, show early nuclear localization of mutant huntingtin and display a progressive loss of membrane integrity (depolarization and loss of cell capacitance) accompanied by a reduction in the expression of D1 and D2 dopamine receptors visualized in layer I of the perirhinal cortex. Importantly, abnormalities in both short-term and long-term plasticity can be reversed by the introduction of a D2 dopamine receptor agonist (Quinpirole), suggesting that alterations in dopaminergic signalling may underlie early cognitive dysfunction in HD.

Animals↗

PubMed1993

Cognitive screening in mild brain injury.

A study of patients with mild traumatic brain injuries was performed to determine if cognitive screening in the acute care setting can identify patients who will have cognitive dysfunction following discharge to home. While still hospitalized, 166 patients were assessed with a cognitive screening tool. After discharge, telephone follow-up contacts were made by a nurse to assess for subjective reports of cognitive difficulties. A subsample (N = 39) received additional comprehensive cognitive evaluation after discharge. Statistically significant results were noted between cognitive screen and cognitive evaluation results (chi-square = 24.28, p < .0000) and between cognitive screen results and follow-up findings (chi-square = 6.7, p = .0350). Study results support the use of cognitive screening in the acute care setting to identify patients with mild traumatic brain injury who are likely to experience residual cognitive deficits after discharge so appropriate intervention may be planned.

Adolescent↗

PubMed1998

Epidemiology of paranoid symptoms in an elderly population.

BACKGROUND: Elderly people with paranoid symptoms are a taxing group for medical and social services, but studies of the prevalence of these symptoms in the general elderly population are rare. This study aimed to estimate the community prevalence and to identify some associated variables. METHOD: A community samples of 1420 elderly people, was extensively examined by nurses and physicians. RESULTS: Paranoid ideation was found in 6.3% of the sample. The prevalence in people with cognitive dysfunction (n = 381, 12.1%) was higher than in those without (n = 1039, 2.6%). Once cognitive impairment had been controlled the associated variables were: being divorced, being female, having depressive symptoms, using psychotropic drugs, having no friends or visitors, using community care and being an immigrant. CONCLUSION: Paranoid symptoms in this elderly population were associated most strongly with cognitive impairment. Other associated variables pointed to a higher level of social isolation than others in the community.

Aged↗

PubMed2001

[Cerebral white matter lesions in the elderly: vascular risk factors and cognitive consequences].

With the advent of sensitive brain imaging techniques, white matter lesions are commonly observed in healthy as well as in demented elderly people. Primarily vascular risk factors have been related to the presence of white matter lesions, such as hypertension, atherosclerosis and atrial fibrillation. Subcortical white matter lesions are mainly associated with depression in the elderly, while periventricular lesions are clearly associated with cognitive dysfunction. Current evidence on the relation between vascular risk factors, white matter lesions and cognition is based on cross-sectional studies. Prospective studies are needed to confirm causality and to study the efficacy of treatment of vascular risk factors.

Aged↗

PubMedDate not supplied

Cognitive flexibility, reaction time, and attention in women with premenstrual dysphoric disorder.

OBJECTIVE: To evaluate cognitive functioning throughout the menstrual cycle in women who suffer from premenstrual dysphoric disorder (PDD) and controls. RESEARCH HYPOTHESIS: Measures of cognitive function will discriminate between women with prospectively documented PDD and women without PDD during the late-luteal phase of the menstrual cycle. PARTICIPANTS: The participants consisted of 37 women who met operationalized, prospectively documented criteria of premenstrual dysphoric disorder and 32 women without PDD who served as controls. DESIGN: A series of neurocognitive tasks were used to assess selective, sustained attention, reaction time, and cognitive flexibility in women with PDD and controls. Tests were administered on two occasions: once during the follicular phase of the menstrual cycle, and once during the late-luteal phase. RESULTS: Repeated measures and discriminant analyses failed to demonstrate significant group differences between women with PDD and controls in neurocognitive functioning. CONCLUSIONS: The findings indicated that cognitive functioning in the late-luteal phase was not compromised in either group, in spite of subjective reports from the PDD group. The findings suggest that complaints of cognitive dysfunction may be mediated by altered perceptions and sociocultural expectations rather than by identifiable cognitive deficits.

Adult↗

PubMedDate not supplied

[Dementia and cognitive impairment in Parkinson disease].

Changes in cognitive function and disturbances in behavior are commonly seen in parkinsonian patients and they are inherent features of the disease. Estimates on the prevalence of dementia in this disorder are quite variable, ranging from 15 to 25%. Advanced age, depression, severity of akinesia, and the presence of dopaminomimetic psychosis, are considered as risk factors in the development of cognitive deterioration within this patient population. Cognitive dysfunction may manifest as relatively circumscribed deficits or overt dementia. The finding of mild cognitive deficits is common in Parkinson's disease, such as reduced flexibility, psychomotor slowing, reduction in learning capacity and information retrieval, and disturbances in visuospatial tasks. The most prevalent cognitive disturbance is an impairment in visuospatial tasks, not necessarily related to the degree of motor disability. Dementia, when present early on in the course of the disease may suggest alternative diagnoses (Diffuse Lewy body dementia, Alzheimer's disease with extrapyramidal features, Fronto-temporal dementia, etc.), while in those cases in whom the dementing disorder develops at a later stage, it is assumed to be an integral part of the disease, albeit corresponding to variable pathogenetic mechanisms.

Cognition Disorders↗

PubMed2006

Racial analyses of longer-stay nursing home residents with multiple sclerosis.

OBJECTIVES: Compare profiles of African Americans with multiple sclerosis (MS) to White residents with MS one year after admission to a nursing facility. METHODS: We used all admission assessments recorded in the national Minimum Data Set (MDS) from 1999 to 2001 as well as all MDS annual assessments recorded from 2000 to 2002. We matched admission assessments with first annual assessment for 3632 White residents with MS and 461 African-American residents with MS. RESULTS: African Americans with MS were admitted at a significantly younger age and with more aid to daily living (ADL) dependence and cognitive dysfunction than Whites with MS one year after admission. Despite significantly poorer physical performance, cognitive function, and more medical comorbidities, African Americans with MS did not receive significantly more therapies or medications than White residents with MS after one year in the facility. CONCLUSIONS: Basic differences in MS expression and progression in African Americans appear to have to do with both genetic and environmental factors. Further study will help to clarify the reasons for these differences.

Adult↗

PubMed2006

Treatment of cognitive deficits in schizophrenia.

Cognitive deficits are a core feature of schizophrenia and are a major contributor to functional disability. These impairments persist even when patients are in remission of psychotic symptoms and have, to date, eluded treatment. While some improvement is noted with existing medications, current trends in this field include studying and searching for adjunctive treatments to truly remediate cognitive dysfunction in schizophrenia. Psychosocial treatments have demonstrated some success, but the use of existing cognitive enhancers in schizophrenia treatment has provided little cognitive improvement. This paper reviews the current status of cognitive deficit treatment in schizophrenia and offers suggestions for future work.

Antipsychotic Agents↗

PubMed1998

Postmortem studies in schizophrenia.

The past decade has seen renewed interest in the neuropathology of schizophrenia. The advent of new postmortem techniques and functional imaging, along with a greater understanding of the neuropsychology of schizophrenia, have provided many new clues to the nature of the underlying brain dysfunction in this disorder. There has also been a greater understanding of the presence of severe cognitive dysfunction among many elderly persons with schizophrenia. In this article, a series of investigations are described that seek to answer basic questions about the neuropathology of schizophrenia, in particular as it pertains to cognitive impairment. The first study describes neuropathological findings in 100 consecutively autopsied persons with schizophrenia, the majority of whom had had detailed antemortem assessments. Results from this first study prompted the conclusion that schizophrenia is not characterized by classical, histologically identifiable neuropathology. Moreover, most cases of dementia in schizophrenia are probably not the result of neuropathologically identifiable dementing illnesses. The next four studies examined chemical markers that are altered in Alzheimer's disease and some other dementing conditions and have also been suggested to be abnormal in schizophrenia: choline acetyltransferase, catecholamines and indolamines, neuropeptides, and synaptic proteins. Schizophrenia cases as a group did not show a cholinergic deficit; nor did they differ from elderly comparison cases with respect to cortical catecholamines and indolamines. Among the schizophrenia cases, however, cognitive impairment was negatively correlated with choline acetyltransferase activity. Those with cognitive impairment showed evidence of cortical noradrenergic and serotonergic deficits. Neuropeptide deficits were also present in schizophrenia, but their pattern differed from that seen in Alzheimer's disease. Increased synaptic protein activity was found in the cingulate cortex of persons with schizophrenia, and this activity was correlated with schizophrenia symptoms. From this second series of studies, it was concluded that some biological measures in schizophrenia may be related to cognitive impairment (e.g., cortical amines), whereas others may be related to diagnosis (e.g., neuropeptide deficits). In addition, synaptic organization may correlate with schizophrenia symptoms.

Aged↗

PubMed2001

Dysfunctional schemas and cognitive distortions in psychopathology: a test of the specificity hypothesis.

This study aimed at testing whether there were different types of dysfunctional schemas and cognitive distortions that could help to differentiate three emotional/behavioural problems, i.e., anxiety, depression, and aggression, from each other. Five hundred and eighty-one Chinese adolescents from five mainstream high schools in Hong Kong were recruited and completed several self-report questionnaires. Bivariate correlation showed an indiscriminate pattern of association between dysfunctional schemas, cognitive distortions, and the three emotional/behavioural problems. However, when the effects of the confounding correlated emotional/behavioural problems were controlled in regression analysis, different problems did show some specific association with different types of dysfunctional schemas and/or cognitive distortions. Despite some inconsistency, these findings generally supported a specificity hypothesis. Cognitive variables were thus not only relevant in understanding psychopathology, but their different patterns of association with anxiety, depression, and aggression also supported the separability of these three emotional/behavioural problems, despite their significant correlation.

Adolescent↗

PubMed1993

Cognitive processes in dieting disorders.

This study is an empirical investigation of the prevailing notion that dieting disorder patients have more dysfunctional cognitions and cognitive styles than the nonclinical population. Groups of anorexics, bulimics, normal restrainers, and normal nonrestrainers completed three questionnaires and two repertory grids. Overall, the data supported a cognitive model of dieting disorders. Patients exhibited a lack of awareness of the role played by inner sensations in regulating weight and eating behavior, and emphasized black and white rules instead. Anorexic patients tended to evaluate self-worth almost entirely in terms of self-control. Both patient groups evidenced extreme negativity in their views of themselves, but anorexics showed a particularly severe sense of self-isolation. Unlike bulimics, they extended a tendency to think in absolute terms from the area of eating to the rest of their lives. Thus, the psychopathology of the anorexic patient group appeared more severe than that of bulimics.

Adult↗

PubMed1992

Hippocampal formation volume, memory dysfunction, and cortisol levels in patients with Cushing's syndrome.

Patients with chronic hypercortisolemia due to Cushing's syndrome (CS) exhibit cognitive dysfunction. Because glucocorticoid excess is associated with hippocampal damage in animals, and the hippocampus participates in learning and memory, we explored the relationships between hippocampal formation (HF) volume, memory dysfunction, and cortisol levels in 12 patients with CS. After magnetic resonance imaging, HF volume was determined using digital sum of track ball traces of dentate gyrus, hippocampus proper and subiculum, correcting for total intracranial volume. For 27% of the patients, HF volume fell outside the 95% confidence intervals for normal subject volume given in the literature. In addition, there were significant and specific correlations between HF volume and scores for verbal paired associate learning, verbal recall, and verbal recall corrected for full-scale IQ (r = 0.57 to 0.70, p < 0.05). HF volume was negatively correlated with plasma cortisol levels (r = -0.73, p < 0.05). These studies suggest an association between reduced HF volume, memory dysfunction, and elevated cortisol in patients with CS.

Adolescent↗

PubMed2001

Frontal lobe hypometabolism predicts cognitive decline in patients with lacunar infarcts.

BACKGROUND: A proportion of patients with subcortical lacunes will suffer progressive cognitive dysfunction, but the basis for this decline is controversial and little is known about predicting cognitive decline in these patients. Studies of Alzheimer disease have shown that imaging measures of temporal and parietal metabolism and blood flow predict disease course. OBJECTIVE: To determine whether regional cerebral glucose metabolism predicts cognitive decline by testing 2 opposing hypotheses: (1) temporoparietal activity predicts decline (based on the idea that concomitant Alzheimer disease causes decline) vs (2) frontal hypometabolism predicts decline (based on evidence that subcortical frontal circuits are especially vulnerable to small vessel ischemia). DESIGN: Prospective cohort study. SETTING: University outpatient dementia center. PATIENTS: A convenience sample of 26 patients with radiologically defined lacunes and baseline cognitive function ranging from normal to moderately demented. MAIN OUTCOME MEASURES: Regional cerebral metabolism was quantitated in the form of atrophy-corrected positron emission tomographic activity ratios in cortical regions that were defined a priori. Patients were followed up at a mean of 1.8 years, and the dependent variable was rate of change in the Mini-Mental State Examination score. RESULTS: Bilateral and right hemisphere dorsolateral frontal metabolism significantly predicted cognitive decline, with right dorsolateral frontal metabolism explaining 19% of the variance. No other positron emission tomographic region was a significant predictor, nor were demographic variables or baseline Mini-Mental State Examination scores significant predictors. CONCLUSION: Cognitive decline in patients with lacunes may result in part from progressive vascular compromise in subcortical frontal circuits.

Aged↗

PubMed1990

Criterion-related validity of the Anorectic Cognitions Questionnaire.

Several authors have suggested core cognitive dysfunction as central to anorexia and bulimia nervosa. However, psychometrically sound assessment devices for these cognitions are notably lacking. Previous research with the Anorectic Cognitions Questionnaire (MAC) has suggested that it has good concurrent and criterion-related validity, and high internal consistency. As well, the factor structure has been supported. The purpose of this investigation was to further assess the criterion-related validity of the MAC. Male and female college students completed the MAC and a questionnaire about eating and weight-related behavior and attitudes in four areas: general emphasis on weight regulation, relative importance of specific benefits of losing or maintaining weight (i.e., psychological, appearance, and health benefits), use of calorie restriction strategies, and use of calorie burning strategies. In general, persons scoring above the mean on the MAC showed more evidence of pathological eating attitudes and behavior in all four areas.

Adult↗

PubMed1995

Cognitive deficits precede motor deficits in a slowly progressing model of parkinsonism in the monkey.

Five adult Macaca fascicularis monkeys were trained to perform tests of cognitive and motor functioning that included a complex visual pattern discrimination task, an object retrieval task, a test of task persistence, and a timed motor task. Once stable baseline performance was achieved, monkeys were administered 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) at doses of 0.05 to 0.075 mg/kg, 2 to 3 times per week for a total of 24 weeks. Animals were assessed weekly for performance on the previously learned tasks. All monkeys developed performance deficits in a predictable pattern with behavioural and cognitive deficits (i.e. deficits in task persistence and the cognitive component of object retrieval) appearing in advance of measurable motor deficits. Deficits in visual pattern discrimination never appeared. These results show that specific cognitive dysfunction pre-dates motor dysfunction in a chronic, slowly progressing parkinson model in monkeys and support the contention that cognitive deficits in Parkinson's disease may precede the motor signs of the disorder and may not be caused by them.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗

PubMed2005

Apolipoprotein E4 genotype is not associated with short-term cognition deficits during alcohol withdrawal.

Aim of this prospective study was to investigate a possible association between the apolipoprotein E4 (ApoE4) genotype and clinically well-known cognition deficits during alcohol withdrawal. We examined 172 patients with alcohol dependence (137 men, 35 women) during withdrawal treatment. The ApoE genotype was determined in all patients using polymerase chain reaction. Cognitive function was assessed applying the c.I.-Test on day 0 (admission) and on day 7 of withdrawal treatment. Using Pearson's chi2 test we found no significant association between the ApoE4 genotype and cognition deficits for both dates (day 0: p=.463; day 7: p=.760). Moreover, multivariate logistic regression analyses revealed no significant association between presence of the ApoE4 allele and cognitive dysfunction. Even though ApoE4 plays an important role in alcoholism-related brain atrophy and cognition deficits in demented as well as in nondemented healthy elderly people, this study provides no evidence for an association with short-term cognition deficits during alcohol withdrawal.

Adult↗