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PubMed2005

[Cognitive dysfunctions in multiple sclerosis patients].

Cognitive dysfunctions are frequent symptoms of multiple sclerosis (MS) and occur in up to 65% of patients. Especially memory, attention, executive and visual constructive functions are impaired. These problems strongly affect patients' ability to work, social relationships, and quality of life. Symptoms of physical disabilities can arise independently. Cognitive dysfunctions are clear indicators of MS progression, since they represent highly complex functions depending on the integrity of neuronal networks. Once manifested after a relapse, they remain stable. Given a differentiating diagnosis, it is possible to treat these dysfunctions by cognitive training and pharmacologically for example by immunomodulating drugs. However, treatment options are limited at present. This report provides a detailed description of cognitive functions and performance in MS patients, their comorbidities such as fatigue and depression, currently available diagnostic tools, and therapeutic options.

Cognition Disorders↗

PubMed1991

Cognitive therapy with depressed inpatients: specific effects on dysfunctional cognitions.

Specificity of cognitive change following cognitive therapy for depression was assessed in 39 depressed inpatients who completed either a standard inpatient treatment (pharmacotherapy and milieu management) or the standard treatment plus cognitive therapy. Following treatment, patients in both groups endorsed fewer dysfunctional cognitions on 2 of 4 measures of cognitive distortion. Compared with patients receiving only the standard treatment, patients also receiving cognitive therapy reported less hopelessness and fewer cognitive biases at posttreatment and 6- and 12-month follow-up assessments and fewer dysfunctional attitudes at the 6-month follow-up. Treatment effects for dysfunctional cognitions were found even though the treatment groups did not differ in depression severity, suggesting that results did not reflect state-dependent differences between treatments secondary to difference in depression.

Adaptation, Psychological↗

PubMed2002

Cognitive dysfunction in multiple sclerosis: natural history, pathophysiology and management.

Cognitive dysfunction is a major cause of disability in patients with multiple sclerosis (MS). The prevalence of cognitive dysfunction is estimated at 45 to 65%. Natural history studies suggest that once cognitive dysfunction develops in a patient with MS, it is not likely to remit. Unlike physical disability in MS, cognitive disability correlates weakly with T2 lesion burden on brain magnetic resonance imaging (MRI). More robust correlations exist with magnetisation transfer imaging and MRI measures of brain atrophy. Patients with MS who have cognitive impairment most commonly display deficits in the cognitive domains of memory, learning, attention and information processing. In diagnosing cognitive dysfunction in a patient with MS, it is important first to recognise and treat the common comorbidities of fatigue and depression. The first step in the treatment of cognitive dysfunction is to delay disease progression, and there are currently five such disease-modifying agents approved for the treatment of MS (two preparations of interferon-beta-1a, interferon-beta-1b, glatiramer acetate and mitoxantrone). Nonpharmacological measures, such as cognitive rehabilitation, occupational therapy and psychotherapy, are the mainstays of symptomatic treatment. Pharmacological symptomatic therapy centres on the treatment of comorbid fatigue and depression. There are currently no effective pharmacological agents approved as symptomatic therapy of cognitive dysfunction in MS.

Adjuvants, Immunologic↗

PubMed2004

Odour identification as a marker for postoperative cognitive dysfunction: a pilot study.

The onset of postoperative cognitive dysfunction is delayed in some elderly surgical patients and the condition may persist. Increasing age is a risk factor for both postoperative cognitive dysfunction and dementia. Major surgery may unmask an underlying dementia; we report findings of a pilot study designed to inform this hypothesis. Impaired odour identification ability is a characteristic of the preclinical phase of some neuro-degenerative diseases. This pilot study was designed to establish whether odour identification deficit is a marker for postoperative cognitive dysfunction, particularly in elderly patients genetically predisposed to develop late-onset Alzheimer's disease. We found no association between odour identification ability and postoperative cognitive dysfunction in 53 patients aged 62-86, undergoing major non-cardiac surgery under general anaesthesia. Our pilot study showed that a high number of patients genetically predisposed to develop Alzheimer's disease is required to test the utility of odour identification as a marker for postoperative cognitive dysfunction.

Aged↗

PubMed2006

Heritability of an age-dependent categorical phenotype: cognitive dysfunction.

We investigated the extent to which cognitive dysfunction is shaped by genetic or environmental influences, and whether these factors differ in women and men. All members of the Swedish Twin Registry aged 65 and older were screened by telephone using the TELE, a brief cognitive assessment instrument (Gatz et al., 2002), and the Blessed Dementia Rating Scale (Blessed et al., 1968) from relatives of those who scored poorly on the TELE. Data were available for 4308 pairs where both members responded and 5070 pairs where only one member was alive and participated. To analyze all available data, we used a raw data method extended to ordinal data. As the prevalence of cognitive dysfunction increases with age, we incorporated age-adjusted thresholds. The best fitting model from biometric analyses indicated 35% of the variation in liability to cognitive dysfunction could be explained by heritable influences and the remaining 65% by nonfamilial environmental influences. Differences by gender were not significant. As this is a normative population including cognitively intact individuals, preclinical dementia cases and demented individuals, the relative magnitude of genetic and environmental effects is of particular interest in light of high heritabilities found for dementias such as Alzheimer's disease. The findings emphasize the extent to which research is needed to uncover nonfamilial environmental influences on cognitive dysfunction in later life.

Age of Onset↗

PubMed2004

Critical evaluation of cognitive dysfunctions as endophenotypes of schizophrenia.

OBJECTIVE: Cognitive dysfunctions are potential endophenotypes of schizophrenia. The aim of this study was to investigate whether recent evidence indeed suggests that cognitive dysfunctions are potent indicators of specific genetic traits that represent susceptibility for schizophrenia. METHOD: Studies including large, well-defined samples and controlled cognitive assessment have been reviewed. RESULTS: Evidence suggests that schizophrenia patients and their unaffected biological relatives are impaired in several cognitive domains, including working memory, executive functions, sustained attention, verbal episodic memory, processing of visual and auditory stimuli, and smooth pursuit eye movements. However, these impairments are present only in a limited proportion of subjects, showing low specificity and sensitivity and high variability. Linkage with specific genes is weak. CONCLUSION: Although some results are promising, at present cognitive dysfunctions cannot be considered as highly sensitive and specific endophenotypes of schizophrenia.

Case-Control Studies↗

PubMedDate not supplied

Cognitive dysfunction following adjuvant chemotherapy for breast cancer: two case studies.

PURPOSE/OBJECTIVES: To describe the cognitive dysfunction experienced by two women after they received adjuvant chemotherapy for breast cancer and to discuss the potential role of changes in reproductive status and depression in the development of cognitive dysfunction. DATA SOURCES: Journal articles, research data, and clinical experience. DATA SYNTHESIS: Following chemotherapy, 17%-50% of women with breast cancer experience cognitive dysfunction that may include decrements in memory, attention, and psychomotor efficiency. One mechanism that may contribute to cognitive dysfunction involves changes in reproductive status resulting from chemotherapy. Additionally, the presence of depression may confound the experience of cognitive dysfunction. CONCLUSIONS: A comprehensive description of cognitive dysfunction and improved understanding of the interrelationships among cognitive dysfunction, reproductive hormone levels, and depression in women with breast cancer receiving adjuvant chemotherapy may hasten the development of interventions for the management of cognitive dysfunction. IMPLICATIONS FOR NURSING: Nurses should teach women with breast cancer and their families about the potential for cognitive dysfunction after chemotherapy so the problem can be recognized and interventions can be implemented to help women compensate for the dysfunction.

Adult↗

PubMed2001

Cerebral white matter lesions and subjective cognitive dysfunction: the Rotterdam Scan Study.

OBJECTIVE: To determine the relationship between cerebral white matter lesions (WML) and subjective cognitive dysfunction. BACKGROUND: Subjective cognitive dysfunction is present when a person perceives failures of cognitive function. When annoying enough, these failures will be expressed as complaints. Subjective cognitive dysfunction may be a prelude to or coincide with objective cognitive impairment. WML have been related to objective cognitive impairment and dementia, but their relationship with subjective cognitive dysfunction is not clear. Previous population-based studies on the latter relationship have been limited in sample size, recording of subjective cognitive function, and assessment of WML severity. METHODS: We randomly sampled 1,049 elderly nondemented participants from the general population. Data on subjective cognitive dysfunction and its progression were derived from a 15-item questionnaire. Objective cognitive performance was assessed using a series of neuropsychological tests. WML were scored on MRI for periventricular and subcortical regions separately. RESULTS: WML were associated with more subjective cognitive failures. WML were more severe for participants reporting progression of these failures compared with participants without these failures, especially within participants with better than average cognitive performance (p = 0.008, for periventricular WML). Participants with severe WML reported progression of cognitive failures more than twice as often than did those with little or no WML. The relationship between the severity of WML and subjective cognitive failures was present for periventricular and subcortical WML. CONCLUSIONS: WML are associated with subjective cognitive failures and in particular with reporting progression of these failures, even in the absence of objective cognitive impairment.

Aged↗

PubMed2006

Bench-to-bedside review: critical illness-associated cognitive dysfunction--mechanisms, markers, and emerging therapeutics.

Cognitive dysfunction is common in critically ill patients, not only during the acute illness but also long after its resolution. A large number of pathophysiologic mechanisms are thought to underlie critical illness-associated cognitive dysfunction, including neuro-transmitter abnormalities and occult diffuse brain injury. Markers that could be used to evaluate the influence of specific mechanisms in individual patients include serum anticholinergic activity, certain brain proteins, and tissue sodium concentration determination via high-resolution three-dimensional magnetic resonance imaging. Although recent therapeutic advances in this area are exciting, they are still too immature to influence patient care. Additional research is needed if we are to understand better the relative contributions of specific mechanisms to the development of critical illness-associated cognitive dysfunction and to determine whether these mechanisms might be amenable to treatment or prevention.

Biomarkers↗

PubMed2002

The relationship between cognitive dysfunction and coping abilities in schizophrenia.

Cognitive dysfunction is a core feature of schizophrenia [Psychiatr. Clin. North Am., 16 (1993) 295; Psychopharmacology: The fourth generation of progress, Raven Press, New York (1995) 1171; Clinical Neuropsychology, Oxford University Press, New York (1993) 449] and is related to psychosocial functioning in this population [Am. J. Psychiatry, 153 (1996) 321]. It is unclear whether cognitive dysfunction is related to specific areas of functioning in schizophrenia, such as coping abilities. Individuals with schizophrenia have deficient coping skills, which may contribute to their difficulties dealing with stressors [Am. J. Orthopsychiatry, 62 (1992) 117; J. Abnorm. Psychol., 82 (1986) 189]. The current study examined the relationship between coping abilities and cognitive dysfunction in a community sample of individuals with schizophrenia. It was hypothesized that executive dysfunction and mnemonic impairments would be positively related to deficiencies in active coping efforts involving problem solving and self-initiation (e.g. advocating for oneself and others with mental illness and becoming involved in meaningful activities, such as work), independent of the contributions of the general intellectual deficits associated with the disorder and psychiatric symptoms. The results indicated that both executive dysfunction and mnemonic impairments were related to decreased usage of active coping mechanisms after controlling for general intellectual deficits. Further, recognition memory made independent contributions to the prediction of coping involving action and help seeking after controlling for the effects of negative symptoms. These findings suggest that individuals with schizophrenia may be less flexible in their use of coping strategies, which may in turn contribute to their difficulties in coping with mental illness and its consequences.

Adaptation, Psychological↗

PubMed1994

Effect of aging on cerebral autoregulation during cardiopulmonary bypass. Association with postoperative cognitive dysfunction.

BACKGROUND: Age is a predictor of cognitive dysfunction after cardiac surgery, but the mechanism is unknown. The purpose of our study was to determine whether age-related decrements in cognition are associated with cerebral blood flow (CBF) autoregulation during cardiopulmonary bypass (CPB). METHODS AND RESULTS: Cognitive function testing was completed before surgery and before hospital discharge in 215 patients undergoing elective coronary artery bypass grafting (CABG) surgery. The battery consisted of seven tests with nine measures designed to evaluate memory, mood changes, and visuomotor speed and function. Pressure-flow and metabolic-flow cerebral autoregulation during hypothermic cardiopulmonary bypass were determined using the 133Xe clearance CBF method and radial artery and jugular bulb effluent to calculate cerebral metabolic rate (CMRO2) and cerebral AV difference (C[AV]O2). Pressure-flow autoregulation was tested by using two CBF measurements at stable hypothermia: one at stable mean arterial pressure (MAP) and the second 15 minutes later when MAP had increased or decreased > or = 20%. Metabolism-flow autoregulation was tested by varying the temperature (CMRO2) and measuring the coupling of CBF and CMRO2. Individual patient autoregulation was correlated with changes in cognitive measures. Cognitive performance declined in 6 of 9 measures after CABG surgery. Age predicted cognitive decline in 7 of 9 measures; short-term memory showed the greatest effect of age. Pressure-flow autoregulation during hypothermic CPB showed a small but significant (P < .0001) effect of pressure on CBF. There was no effect of age on the slope of CBF response to changes in MAP (pressure-flow autoregulation). There was a major effect of temperature on CBF during CPB (P < .0001). Coupling CBF and CMRO2 with changing temperature was unaffected by age. Changes in cognition were not associated with measures of cerebral autoregulation. However, increasing C(AV)O2 is associated with cognitive deficits in 5 of 9 measures; these associations were independent of age. CONCLUSIONS: Increased age predisposes to impaired cognition after cardiac surgery. This decline in cognitive function in the elderly is not associated with age-related changes in cerebral blood flow autoregulation. The association of increased oxygen extraction with decline in some measures of cognitive function suggests that an imbalance in cerebral tissue oxygen supply, which is unrelated to age, contributes to acute cognitive dysfunction after cardiac surgery. Cognitive dysfunction after CPB in the elderly cannot be explained by impaired CBF autoregulation.

Aging↗

PubMed2000

Treating cognitive dysfunction in patients with schizophrenia.

Cognitive dysfunction is a common, chronically disabling component of schizophrenia. It has been proposed that many of the symptoms of schizophrenia can be understood as a result of disruption of fundamental cognitive processes. This paper reviews treatment strategies aimed at improving cognitive function in patients with schizophrenia. Nonpharmacologic interventions include instruction in the performance of tasks such as the Wisconsin Card Sorting Test. Mixed results have been achieved, but it appears that instruction methods involving reinforcement of information held in working memory are more successful. Computer-aided remediation has also been used with variable success. Novel antipsychotic drugs appear to have an advantage over conventional antipsychotic drugs in terms of their effect on cognitive function. The development of more precisely tailored methods of remedial teaching, along with optimal pharmacologic treatment, may lead to more effective treatment of cognitive dysfunction in patients with schizophrenia.

Cognition Disorders↗

PubMed2002

The influence of successful prophylactic drug treatment on cognitive dysfunction in bipolar disorders.

BACKGROUND: Cognitive variables such as negative self-evaluations have been discussed as vulnerability factors for depressive syndromes. In the context of bipolar disorders dysfunctional cognitive structures have received little interest as these patients seem to be less disturbed during the euthymic interval than patients with major depression. METHODS: In the present study, the self-esteem of remitted patients with DSM-III-R diagnosis of major depression (n=20), bipolar disorder (n=20) and healthy controls (n=20) was measured with the Frankfurt Self-concept Scale (FSKN). RESULTS: 1) Statistical analysis by analysis of variance (ANOVA) showed no significant differences as to age, sex, etc. between the psychiatric groups. The clinical groups showed lower self-esteem ratings in comparison to healthy controls. 2) Four groups (T1-T4) of remitted patients with bipolar disorders (20 in each group) were successfully maintained on mood stabilizers (lithium or carbamazepine) and classified by the duration of their episode-free period. T1 included those who were episode-free for only the week before discharge from hospital. T2 were symptom-free for <30 months. T3 were episode-free for >30 months and <60 months. T4 were episode-free for >60 months. The comparison of their FSKN self-esteem ratings by ANOVA suggests that self-esteem improves during successful prophylactic treatment. A posteriori contrasts indicate a normalized self-esteem after a bipolar episode-free period of at least 47 months. CONCLUSIONS: Dysfunctional cognitions can be demonstrated in unipolar as well as in bipolar patients. Successful episode-preventive medication with mood stabilizers seems to counteract lowered self-esteem. Adjunctive cognitive therapy might help to optimize the long-term course of bipolar disorder.

Adult↗

PubMed2003

Reversal of aging and chronic ethanol-induced cognitive dysfunction by quercetin a bioflavonoid.

Cognitive dysfunction, one of the most striking age-related impairments seen in human beings, has been correlated to the vulnerability of the brain to increased oxidative stress during aging process. Quercetin is a bioflavonoid with strong antioxidant properties. Experiments were performed to study the possible effects of quercetin on cognitive performance of young, aged or ethanol-intoxicated mice (an animal model for cognition dysfunction) using one trail step down type of passive avoidance and elevated plus maze tasks, respectively. Aged or chronic ethanol-treated mice showed poor retention of memory in step-down passive avoidance and in elevated plus-maze task. Chronic administration of quercetin (10, 25 and 50 mg/kg) for 30 days or its co-administration with ethanol (15% w/v, 2g/kg per orally) for 24 days significantly reversed the age-related or chronic ethanol-induced retention deficits in both the test paradigms. However, in both memory paradigms chronic administration of quercetin failed to modulate the retention performance of young mice. Chronic quercetin administration for 30 days also reversed age associated increase in TBARS levels and decline in forebrain total glutathione (GSH), SOD and catalase levels. Chronic ethanol administration to young mice produced an increase in lipid peroxidation, and a decline in forebrain total glutathione (GSH), SOD and catalase levels, which was significantly reversed by the co-administration of quercetin (10, 25 and 50 mg/kg). The results of the present study showed that chronic quercetin treatment reverses cognitive deficits in aged and ethanol-intoxicated mice, which is associated with its antioxidant property.

Aging↗

PubMed1999

A review of nutrients and botanicals in the integrative management of cognitive dysfunction.

Dementias and other severe cognitive dysfunction states pose a daunting challenge to existing medical management strategies. An integrative, early intervention approach seems warranted. Whereas, allopathic treatment options are highly limited, nutritional and botanical therapies are available which have proven degrees of efficacy and generally favorable benefit-to-risk profiles. This review covers five such therapies: phosphatidylserine (PS), acetyl-l-carnitine (ALC), vinpocetine, Ginkgo biloba extract (GbE), and Bacopa monniera (Bacopa). PS is a phospholipid enriched in the brain, validated through double-blind trials for improving memory, learning, concentration, word recall, and mood in middle-aged and elderly subjects with dementia or age-related cognitive decline. PS has an excellent benefit-to-risk profile. ALC is an energizer and metabolic cofactor which also benefits various cognitive functions in the middle-aged and elderly, but with a slightly less favorable benefit-to-risk profile. Vinpocetine, found in the lesser periwinkle Vinca minor, is an excellent vasodilator and cerebral metabolic enhancer with proven benefits for vascular-based cognitive dysfunction. Two meta-analyses of GbE demonstrate the best preparations offer limited benefits for vascular insufficiencies and even more limited benefits for Alzheimer's, while "commodity" GbE products offer little benefit, if any at all. GbE (and probably also vinpocetine) is incompatible with blood-thinning drugs. Bacopa is an Ayurvedic botanical with apparent anti-anxiety, anti-fatigue, and memory-strengthening effects. These five substances offer interesting contributions to a personalized approach for restoring cognitive function, perhaps eventually in conjunction with the judicious application of growth factors.

Acetylcarnitine↗

PubMed2003

Chemotherapy-induced cognitive dysfunction: a clearer picture.

Chemotherapy-associated cognitive dysfunction occurs in a subset of patients treated with adjuvant chemotherapy. Recent data suggest that development of chemotherapy-related anemia predisposes patients to cognitive dysfunction. Endogenous erythropoietin (EPO) is well recognized for its central role in erythropoiesis, and recombinant human EPO (epoetin alfa) is established as a safe and effective treatment for chemotherapy-related anemia. Treatment with epoetin alfa also improved health-related quality of life in anemic cancer patients undergoing chemotherapy, and several controlled studies have documented increases in quality-of-life scores correlated with increases in hemoglobin. Erythropoietin also plays a role in neuroprotection, presumably by activation of antiapoptotic genes. Erythropoietin and its receptor are expressed in neural cells of the human brain, and their expression is upregulated after hypoxic or ischemic injury. In animal models, systemic administration of epoetin alfa protects against such neural injury. Ongoing and future studies will determine whether epoetin alfa can provide neuroprotection with respect to the development of cognitive dysfunction in patients undergoing adjuvant chemotherapy treatment for breast cancer.

Anemia↗

PubMed1997

Response to cognitive-behavioral therapy in depression: effects of pretreatment cognitive dysfunction and life stress.

Response to cognitive-behavioral therapy (CBT) for depression is variable and the factors that account for differences in response are not yet well established. Level of cognitive dysfunction and the occurrence of negative life stress have been theorized as patient variables, which may account for differences in response to CBT. The relationship between response to CBT and the interaction of cognitive dysfunction with negative life events was examined in a sample of 53 depressed outpatients. Overall, there was little support for the prediction of a difference in acute outcome between patients with or without pretreatment cognitive dysfunction and negative stressors.

Adult↗

PubMed2005

Examination of the use of cognitive domains in postoperative cognitive dysfunction after coronary artery bypass graft surgery.

BACKGROUND: Cognitive domain summary scores have been used to examine postoperative cognitive dysfunction in a number of influential studies. To successfully examine cognitive dysfunction in this way, the domains need to be consistent during the assessment time points or the results are distorted. The current study examines two methods of determining cognitive domains and examines their temporal stability during serial cognitive assessments after coronary artery bypass graft surgery. METHODS: Two hundred and four coronary artery bypass graft patients and 80 matched healthy control subjects 55 years or older completed a battery of neuropsychological assessments at baseline and at 7 days and 3 months. Domains were determined in two ways. The first was based on precedence, and neuropsychological tests were allocated to commonly attributed cognitive domains. The second method was to conduct principal components analysis to statistically determine the domains at each time. The stability of these factors was then assessed over time by conducting repeated analysis. RESULTS: There were discrepancies between the two methods used to determine decline, and among the factors in the control and surgical groups. Stability with time was not evident as the factors varied within the groups. CONCLUSIONS: The assessment of postoperative cognitive dysfunction would be best served by the use of individual test results with efforts made to minimize false-positive classification as the extracted cognitive domains do not appear to be temporally consistent, and were sample specific.

Aged↗