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 19 recordsLinked to original sources

PubMed1996

Central auditory dysfunction, cognitive dysfunction, and dementia in older people.

OBJECTIVES: To determine in older people the relation between auditory dysfunction and cognitive dysfunction, and if central auditory test abnormalities predict the onset of clinical dementia or cognitive decline. DESIGN: Prospective population-based cohort study. SETTING: Framingham Heart Study outpatient biennial examinations 18 and 21. PARTICIPANTS: Members of the Framingham Heart Study cohort with normal findings from cognitive screening tests at biennial examination 18. MEASUREMENTS: Peripheral audiometric thresholds and word recognition in quiet; Synthetic Sentence Identification with Ipsilateral Competing Message (SSI-ICM); Mini-Mental State Examination; and detailed neuropsychological testing of subjects with abnormal findings from the Mini-Mental State Examination. Relative risk of dementia was determined using age-adjusted Cox proportional hazards regression models. RESULTS: Hearing loss significantly lowered performance on the verbal parts of the Mini-Mental State Examination. The relative risk of subsequent clinical dementia or cognitive decline was 6 in subjects with very poor scores (< 50%) in one ear on the SSI-ICM (P = .02); the relative risk was 12.5 if the poor scores were present in both ears (P = .001). CONCLUSIONS: Central auditory dysfunction precedes senile dementia in a significant number of cases and may be an early marker for senile dementia. Hearing tests should be included in the evaluation of persons older than 60 years and in those suspected of having cognitive dysfunction.

Aged↗

PubMed2005

The natural history of cognitive dysfunction in late-onset GM2 gangliosidosis.

BACKGROUND: Late-onset GM2 gangliosidosis (LGG) is a rare disease that is often considered in the differential diagnosis of adolescents and young adults who present with multiple realms of neurologic dysfunction. Cognitive disturbances are common but have not been systematically studied. OBJECTIVE: To determine the natural history of cognitive dysfunction in patients with LGG. DESIGN: Case series and literature review. SETTING: Urban tertiary referral clinic. PATIENTS: Individuals with hexosaminidase A deficiency as the origin of LGG. MAIN OUTCOME MEASURES: Cognitive dysfunction, psychiatric symptoms, and cerebellar, upper motor neuron, lower motor neuron, or extrapyramidal symptoms and signs. RESULTS: Historical and examination data from 62 patients were found. Forty-four percent of LGG patients had some degree of cognitive dysfunction. Cognitive dysfunction was associated with a greater number of other elemental neurologic deficits. In 21 patients with acceptable longitudinal information, 8 (38%) had a static cognitive disorder, whereas progressive dementia was evident in 13 patients (62%), including 2 of our cases with serial neuropsychological testing. Neuroimaging often showed nonspecific cerebellar and/or cerebral atrophy. CONCLUSIONS: Cognitive dysfunction is a frequent manifestation of LGG. Patients who experience cognitive dysfunction are more likely to have a greater number of other neurologic manifestations of the disease. Cognitive dysfunction may take the form of static encephalopathy, but progressive dementia is more often encountered. The pathogenesis of cognitive dysfunction in this disease is unknown, highlighting the need for further study.

Adult↗

PubMed1997

Duration of cognitive dysfunction after concussion, and cognitive dysfunction as a risk factor: a population study of young men.

OBJECTIVES: To establish how long cognitive dysfunction lasts after concussion, and the extent to which it may be a predisposing risk factor for concussion, by examining the prevalence of cognitive dysfunction among young men who have sustained concussion. DESIGN: Observational study. SETTING: Denmark. SUBJECTS: 1220 young men who had been admitted to hospital for concussion between the ages of 16 and 24 (identified in a national register of admissions) and who had also been cognitively tested by the Danish conscription draft board. MAIN OUTCOME MEASURE: Score on the draft board's cognitive screening test, dichotomised as dysfunctional or non-dysfunctional (20.4% of the general population of Danish men appearing before the draft board had a dysfunctional score). RESULTS: 700 of the 1220 men had been tested after sustaining concussion; 520 had been tested before concussion. Four (50%) of the eight men who were tested less than seven days after the injury had a dysfunctional score. Among groups of the remaining 692 men who were tested at later time points after injury, the rates were only marginally raised (range 21.4% to 26.5%) above the population level. Among men tested before injury, the rate of dysfunctional scores was higher (30.4% (158/520)). Apart from suggesting cognitive dysfunction as a risk factor for concussion, this higher proportion seems to relate to the fact that they were typically injured as young adults, whereas those men who were tested after concussion had more often been injured as adolescents. The relative risk for concussion in the presence of cognitive dysfunction is estimated to be 1.57 (95% confidence interval 1.32 to 1.86). CONCLUSIONS: Cognitive dysfunction is not only a short term consequence of concussion but also a predisposing risk factor for concussion, more so for young adults than for adolescents.

Adolescent↗

PubMed2002

Breast cancer chemotherapy-related cognitive dysfunction.

Cognitive side effects of systemic chemotherapy have become an increasing concern among breast cancer survivors, their families, and health care professionals. A growing body of research supports the hypothesis that chemotherapy can produce long-term cognitive changes in at least a subgroup of cancer survivors. We review evidence implicating systemic chemotherapy as the cause of cognitive changes; describe the limitations due to lack of longitudinal studies and gaps in knowledge (ie, no clear mechanism by which chemotherapy can produce cognitive changes has been proposed); discuss possible factors like age, intelligence quotient/education, and psychological, genetic, and hormonal factors that might increase risk for chemotherapy-induced cognitive changes; and outline future directions for research. Such future research includes large-scale, longitudinal studies of pretreatment neuropsychological assessments, use of imaging techniques and the development of animal models to study the mechanisms of chemotherapy-induced changes in cognitive functioning, and the development of interventions to prevent or reduce the negative cognitive effects of chemotherapy

Antineoplastic Combined Chemotherapy Protocols↗

PubMed2005

Cognitive dysfunction precedes neuropathology and motor abnormalities in the YAC128 mouse model of Huntington's disease.

Huntington's disease (HD) is an adult-onset neurodegenerative disorder involving motor dysfunction, cognitive deficits, and psychiatric disturbances that result from underlying striatal and cortical dysfunction and neuropathology. The YAC128 mouse model of HD reproduces both the motor deficits and selective degeneration observed in the human disease. However, the presence of cognitive impairment in this model has not been determined. Here, we report mild cognitive deficits in YAC128 mice that precede motor onset and progressively worsen with age. Rotarod testing revealed a motor learning deficit at 2 months of age that progresses such that by 12 months of age, untrained YAC128 mice are unable to learn the rotarod task. Additional support for cognitive dysfunction is evident in a simple swimming test in which YAC128 mice take longer to find the platform than wild-type (WT) controls beginning at 8 months of age. YAC128 mice also have deficits in open-field habituation and in a swimming T-maze test at this age. Strikingly, in the reversal phase of the swimming T-maze test, YAC128 mice take twice as long as WT mice to locate the platform, indicating a difficulty in changing strategy. At 12 months of age, YAC128 mice show decreased prepulse inhibition and habituation to acoustic startle. The clear pattern of cognitive dysfunction in YAC128 mice is similar to the symptoms and progression of cognitive deficits in human HD and provides both the opportunity to examine the relationship between cognitive dysfunction, motor impairment, and neuropathology in HD and to assess whether potential therapies for HD can restore cognitive function.

Acoustic Stimulation↗

PubMed1999

Benzodiazepines and postoperative cognitive dysfunction in the elderly. ISPOCD Group. International Study of Postoperative Cognitive Dysfunction.

Postoperative cognitive dysfunction (POCD) has been attributed to long-acting sedatives. We hypothesized that diazepam and its active metabolites could be detected in blood after surgery and correlated with POCD, 1 week after surgery in elderly patients. We studied 35 patients, 60 yr or older, undergoing abdominal surgery with general anaesthesia, including diazepam. Neuropsychological tests were performed before surgery and at discharge, where blood concentrations (free fraction) of benzodiazepines were also measured. POCD was found in 17 patients (48.6%). Diazepam or desmethyldiazepam was detected in 34 patients; median postoperative blood concentrations were 0.06 and 0.10 mumol kg-1, respectively. In a multiple regression analysis considering age, duration of anaesthesia and blood concentrations of diazepam and desmethyldiazepam, only age was found to correlate with the composite z-score (F test, P < 0.01). The postoperative cognitive dysfunction we found in elderly patients after operation could not be explained by benzodiazepine concentrations detected in blood.

Abdomen↗

PubMed1992

Prevalence of olfactory dysfunction, hearing deficit, and cognitive dysfunction among elderly patients in a suburban family practice.

Olfactory and hearing senses diminish with age, and cognitive dysfunction increases. The association between sensory deficits and cognitive dysfunction has not been well studied. This paper presents the results of testing a group of 50 community-dwelling patients of a family physician who developed a computer-assisted comprehensive geriatric assessment program. Olfactory dysfunction was present in 39% of subjects, with 18% being unable to detect smoke. There was no correlation between olfactory dysfunction and cognitive dysfunction. Hearing deficit, however, was found in 10% of subjects, all of whom also had either an associated olfactory or cognitive dysfunction. This study demonstrates the high prevalence of olfactory and auditory dysfunction in an ambulatory geriatric population, with a possible association between hearing deficit and cognitive dysfunction. The problem of multiple sensory deficits should be addressed in any long-term management decisions regarding elderly patients.

Aged↗

PubMed2005

[Postoperative cognitive dysfunction].

Postoperative cognitive dysfunction is a severe and life-threatening complication after an operation. The mobilisation of the patient is difficult and, therefore, the stay of the patient in the hospital is extended and the resulting immobilisation is associated with further complications (e.g. decubitus, pneumonia, or thrombosis). The genesis of the postoperative cognitive dysfunction has different causes and the highest risk factors are the age of the patient and the character and the duration of the operation. Preexisting diseases, like diabetes mellitus, heart failure, depression or alcohol excess are high risk factors as well as the use of anticholinergic drugs. A specific therapy for this cognitive dysfunction is unknown and, therefore, preventive measures should be used in patients with a preexisting high risk.

Anesthesia↗

PubMed1998

Long-term postoperative cognitive dysfunction in the elderly ISPOCD1 study. ISPOCD investigators. International Study of Post-Operative Cognitive Dysfunction.

BACKGROUND: Long-term postoperative cognitive dysfunction may occur in the elderly. Age may be a risk factor and hypoxaemia and arterial hypotension causative factors. We investigated these hypotheses in an international multicentre study. METHODS: 1218 patients aged at least 60 years completed neuropsychological tests before and 1 week and 3 months after major non-cardiac surgery. We measured oxygen saturation by continuous pulse oximetry before surgery and throughout the day of and the first 3 nights after surgery. We recorded blood pressure every 3 min by oscillometry during the operation and every 15-30 min for the rest of that day and night. We identified postoperative cognitive dysfunction with neuropsychological tests compared with controls recruited from the UK (n=176) and the same countries as study centres (n=145). FINDINGS: Postoperative cognitive dysfunction was present in 266 (25.8% [95% CI 23.1-28.5]) of patients 1 week after surgery and in 94 (9.9% [8.1-12.0]) 3 months after surgery, compared with 3.4% and 2.8%, respectively, of UK controls (p<0.0001 and p=0.0037, respectively). Increasing age and duration of anaesthesia, little education, a second operation, postoperative infections, and respiratory complications were risk factors for early postoperative cognitive dysfunction, but only age was a risk factor for late postoperative cognitive dysfunction. Hypoxaemia and hypotension were not significant risk factors at any time. INTERPRETATION: Our findings have implications for studies of the causes of cognitive decline and, in clinical practice, for the information given to patients before surgery.

Abdomen↗

PubMed2000

Cognitive dysfunction 1-2 years after non-cardiac surgery in the elderly. ISPOCD group. International Study of Post-Operative Cognitive Dysfunction.

BACKGROUND: Postoperative cognitive dysfunction (POCD) is a well-recognised complication of cardiac surgery, but evidence of POCD after general surgery has been lacking. We recently showed that POCD was present in 9.9% of elderly patients 3 months after major non-cardiac surgery. The aim of the present study was to investigate whether POCD persists for 1-2 years after operation. METHODS: A total of 336 elderly patients (median age 69 years, range 60-86) was studied after major surgery under general anesthesia. Psychometric testing was performed before surgery and at a median of 7, 98 and 532 days postoperatively using a neuropsychological test battery with 7 subtests. A control group of 47 non-hospitalised volunteers of similar age were tested with the test battery at the same intervals. RESULTS: 1-2 years after surgery, 35 out of 336 patients (10.4%, CI: 7.2-13.7%) had cognitive dysfunction. Three patients had POCD at all three postoperative test sessions (0.9%). From our definition of POCD, there is only a 1:64000 likelihood that a single subject would have POCD at all three test points by chance. Logistic regression analysis identified age, early POCD, and infection within the first three postoperative months as significant risk factors for long-term cognitive dysfunction. Five of 47 normal controls fulfilled the criteria for cognitive dysfunction 1-2 years after initial testing (10.6%, CI: 1.8-19.4%), i.e. a similar incidence of age-related cognitive impairment as among patients. CONCLUSION: POCD is a reversible condition in the majority of cases but may persist in approximately 1% of patients.

Aged↗

PubMed1999

[Postoperative cognition disorders in elderly patients. The results of the "International Study of Postoperative Cognitive Dysfunction" ISPOCD 1)].

OBJECTIVE: Cognitive dysfunction is a known problem after operations and may be especially relevant in the elderly. The aim of this international multicentre study was to investigate short- and long-term cognitive dysfunction in elderly patients and to elucidate the relevance of hypoxaemia and hypotension as causative factors. METHODS: 1218 patients aged 60 years and older and scheduled for major non-cardiac surgery under general anaesthesia were investigated. Oxygen saturation was measured by continuous pulse oximetry before surgery and throughout the day of and the first 3 nights after surgery. Blood pressure was recorded every 3 minutes during the operation and every 15-30 min for the rest of that day and night. Cognitive testing was performed before and 1 week and 3 months after the operation. Cognitive dysfunction was identified with neuropsychological tests compared with controls recruited from the UK (n = 176) and the same countries as study centres (n = 145). RESULTS: Postoperative cognitive dysfunction was present in 25.8% of patients 1 week after surgery and in 9.9% 3 months after surgery, compared with 3.4% and 2.8%, respectively, of the UK controls. Increasing age and duration of anaesthesia, little education, a second operation, postoperative infections, and respiratory complications were the risk factors for early postoperative cognitive dysfunction, but only age was a risk factor for long-term postoperative cognitive dysfunction. Hypoxaemia and hypotension were not significant risk factors at any time. CONCLUSION: With this investigation long-term cognitive dysfunction could be proven definitively for elderly patients after major operations under general anaesthesia. No factors with prophylactic or therapeutic influence were detectable so that aetiology and pathophysiology of POCD could not be further determined.

Aged↗

PubMed2006

Pharmacological approaches to the management of cognitive dysfunction in schizophrenia.

Cognitive dysfunction is a core feature of schizophrenia as deficits that are present in the majority of patients with schizophrenia frequently precede the onset of other symptoms and persist even after other symptoms have been effectively treated. The use of atypical antipsychotics has produced some small improvements, although the need for adjunctive treatment specifically targeting cognitive dysfunction is gaining widespread acceptance. Animal models and some small clinical trials have yielded results that are promising but not definitive. Psychosocial interventions have also met with some success in ameliorating some cognitive limitations. The mixed results of pharmacological interventions are most likely to be as a result of a combination of methodological flaws of many studies, poor outcome measures, dose administration effects and problems with the agents themselves.

Antipsychotic Agents↗

PubMed2002

Predictors of cognitive dysfunction after subarachnoid hemorrhage.

BACKGROUND: Cognitive dysfunction is a common and disabling sequela of subarachnoid hemorrhage (SAH). Although several clinical and radiographic findings have been implicated in the pathogenesis of cognitive dysfunction after SAH, few prospective studies have comprehensively and simultaneously evaluated these risk factors. METHODS: Between July 1996 and March 2000, we prospectively evaluated 113 of 248 consecutively admitted nontraumatic SAH patients alive at 3 months with a comprehensive neuropsychological evaluation. Summary scores for 8 cognitive domains were calculated to express test performance relative to the entire study population. Clinical and radiographic variables associated with domain-specific cognitive dysfunction were identified with forward stepwise multiple regression, with control for the influence of demographic factors. RESULTS: The study participants were younger (P=0.005), less often white (P=0.006), and had better 3-month modified Rankin scores (P=0.001) than those who did not undergo neuropsychological testing. The proportion of subjects who scored in the impaired range (>2 SD below the normative mean) on each neuropsychological test ranged from 10% to 50%. Predictors of cognitive dysfunction in 2 or more domains in the multivariate analysis included global cerebral edema (4 domains), left-sided infarction (3 domains), and lack of a posterior circulation aneurysm (2 domains). Other variables consistently associated with cognitive dysfunction in the univariate analysis included admission Hunt-Hess grade >2 and thick SAH in the anterior interhemispheric and sylvian fissures. CONCLUSIONS: Global cerebral edema and left-sided infarction are important risk factors for cognitive dysfunction after SAH. Treatment strategies aimed at reducing neurological injury related to generalized brain swelling, infarction, and clot-related hemotoxicity hold the best promise for improving cognitive outcomes after SAH.

Acute Disease↗

PubMed2002

Cerebral blood flow and cognitive dysfunction after coronary surgery.

BACKGROUND: Postoperative cognitive dysfunction after cardiac surgery has been attributed both to embolic events and periods with reduced cerebral perfusion. We investigated whether cognitive dysfunction after coronary surgery is associated with changes in regional cerebral blood flow (CBF) using single photon emission computed tomography. METHODS: Before surgery and at discharge, 15 coronary surgery patients were studied. Global and regional CBF were measured using a brain-dedicated single photon emission computed tomography scanner, and neuropsychological testing with seven subtests was performed. Postoperative cognitive dysfunction was defined as a Z score above 2. Normative single photon emission computed tomography data were available from 26 healthy age-matched controls. RESULTS: Preoperative global CBF was significantly lower in patients compared with controls (53.7 versus 46.1 mL/100 g/min, p = 0.006). After surgery, global CBF significantly decreased in the patient group (46.1 versus 38.6 mL/100 g/min, p = 0.0001). No significant differences were detected in regional CBF. Cognitive dysfunction was identified in 4 of the 15 patients (26.7%, 95% CI 7.8% to 55.1%). No correlation was found between the neuropsychological Z score and global or regional CBF. CONCLUSIONS: The significant decrease in CBF after coronary surgery was uniformly distributed and was not correlated to postoperative cognitive dysfunction.

Aged↗

PubMed1999

Neuroleptic-induced extrapyramidal symptoms are accompanied by cognitive dysfunction in schizophrenia.

Cognitive impairments in schizophrenics have been found to precede tardive dyskinesia and to co-exist with other motor deficits. However, little is yet known about the prevalence of cognitive disturbances in patients with neuroleptic-induced parkinsonism. From the literature on idiopathic parkinson, it was inferred that extrapyramidal symptoms (EPS) are accompanied by cognitive dysfunction. 85 schizophrenic in-patients were divided into EPS high and low scorers according to an established criterion (Simpson Angus Scale, cut-off score: 0.4). Cognitive impairments were assessed using a self-rating instrument measuring disturbances of information processing. Patients with high EPS exhibited significantly elevated scores in six of ten cognitive and perceptual subscales (t = 2.1-3.1) as compared to low EPS patients. It is concluded that high EPS patients suffer from cognitive disturbances which are assumed to possess high relevance for both psycho-social and medical treatment. Cognitive problems may, when not considered, disturb compliance, insight of illness and transfer of learnt skills into everyday life.

Adult↗

PubMed2005

Treatment of cognitive dysfunction in schizophrenia.

BACKGROUND: Cognitive impairment has always been regarded as an important characteristic of schizophrenia. Many domains of cognition are disrupted with varying degrees of deficit: attention, executive functions, verbal and visuospatial working memory, learning, and memory. However, it is only recently that cognitive dysfunction has been recognized as a primary and enduring core deficit in schizophrenia (rather than the previous focus on positive and negative symptoms). OBJECTIVE: This article discusses cognitive impairment and the therapeutic effects of newer antipsychotic agents on cognitive functioning in patients with schizophrenia. CONCLUSIONS: Cognitive dysfunction occurs before the first psychotic episode and persists throughout the course of the illness. It involves every aspect of cognitive functioning and has an important impact on long-term social and occupational outcomes. Improvement of cognitive functioning by antipsychotic treatment can be due indirectly to the improvement of therapeutic profiles of the newer antipsychotic agents (eg, higher efficacy on positive and negative symptoms, fewer side effects, less anticholinergic effects) or directly to effects on cerebral functioning (eg, by restoring dopamine prefrontal activity). However, further research is needed regarding the therapeutic effects of the newer antipsychotic drugs on cognitive functioning and their impact on psychosocial outcome. Although newer medications may improve cognitive functioning, they do not normalize neurocognitive deficits in schizophrenia. In addition, various nonpharmacologic, psychological interventions have been used in the rehabilitation of patients with cognitive deficits.

Antipsychotic Agents↗

PubMed2005

[Cognitive dysfunction and its therapy].

In the first part the meaning of terms cognition and cognitive dysfunction is clarified. Cognitive dysfunction is found in many neuropsychiatric disorders. Majority of studies were done in patients with schizophrenia and dementia. For studying cognitive dysfunction, the most appropriate appear the initial phases of the disease. The next part of the study summarizes the treatment possibilities of cognitive dysfunction in schizophrenia. Atypical antipsychotics represent the basal treatment. The improvement of cognitive deficit by atypical antipsychotics is significant, but its importance in real life is small. The new add-on treatment has the potential for further improvement of cognitive dysfunction. This approach includes augmenting effects of neurotransmitters related to cognition (glutamate, noradrenalin, serotonin, acetylcholine). The improvement of cognitive dysfunction can improve the long-term outcome and functional prognosis in patients suffering from schizophrenic disorder.

Antipsychotic Agents↗

PubMed1997

Cardiac surgery in special populations, Part 3: Patients with cognitive dysfunction.

Patients with cognitive dysfunction, usually Down's syndrome, frequently require corrective cardiac surgery for congenital cardiac anomalies. The most common cardiac anomalies in Down's syndrome are patent ductus arteriosus, atrial septal defect, ventricular septal defect, atrioventricular canal defects, and Tetralogy of Fallot. This article, the third and last in a series, discusses the physiology of the defects and the nursing care required for comprehensive care of the patient with delayed development.

Cardiac Surgical Procedures↗