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Cognitive Dysfunction (cognitive + dysfunction)
Kinds of Cognitive Dysfunction Selected AbstractsDonepezil Treatment of Topiramate-Related Cognitive DysfunctionHEADACHE, Issue 2 2006Steve D. Wheeler MD Six migraine patients experienced significant topiramate-related cognitive and language dysfunction that improved with donepezil treatment and allowed uninterrupted topiramate use. These patients represent the first report of topiramate-related cognitive and language dysfunction that improved with a cholinesterase inhibitor. Although, the mechanism responsible for this effect is uncertain, cholinesterase inhibition resulting in cholinergic augmentation and enhanced cognition probably account for some if not most of the improvement. [source] Diagnostic Accuracy of a New Instrument for Detecting Cognitive Dysfunction in an Emergent Psychiatric Population: The Brief Cognitive ScreenACADEMIC EMERGENCY MEDICINE, Issue 3 2010Steven P. Cercy PhD Abstract Objectives:, In certain clinical contexts, the sensitivity of the Mini-Mental State Examination (MMSE) is limited. The authors developed a new cognitive screening instrument, the Brief Cognitive Screen (BCS), with the aim of improving diagnostic accuracy for cognitive dysfunction in the psychiatric emergency department (ED) in a quick and convenient format. Methods:, The BCS, consisting of the Oral Trail Making Test (OTMT), animal fluency, the Clock Drawing Test (CDT), and the MMSE, was administered to 32 patients presenting with emergent psychiatric conditions. Comprehensive neuropsychological evaluation served as the criterion standard for determining cognitive dysfunction. Diagnostic accuracy of the MMSE was determined using the traditional clinical cutoff and receiver operating characteristic (ROC) curve analyses. Diagnostic accuracy of individual BCS components and BCS Summary Scores was determined by ROC analyses. Results:, At the traditional clinical cutoff, MMSE sensitivity (46.4%) and total diagnostic accuracy (53.1%) were inadequate. Under ROC analyses, the diagnostic accuracy of the full BCS Summary Score (area under the curve [AUC] = 0.857) was comparable to the MMSE (AUC = 0.828). However, a reduced BCS Summary Score consisting of OTMT Part B (OTMT,B), animal fluency, and the CDT yielded classification accuracy (AUC = 0.946) that was superior to the MMSE. Conclusions:, Preliminary findings suggest the BCS is an effective, convenient alternative cognitive screening instrument for use in emergent psychiatric populations. ACADEMIC EMERGENCY MEDICINE 2010; 17:307,315 © 2010 by the Society for Academic Emergency Medicine [source] Protective Effect of Sesamol against 3-Nitropropionic Acid-Induced Cognitive Dysfunction and Altered Glutathione Redox Balance in RatsBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 1 2010Puneet Kumar It is a well-known antioxidant, currently being tried against several neurological disorders. The present study was designed to evaluate the potential of sesamol treatment against 3-nitropropionic acid (3-NP)-induced cognitive impairment and oxidative damage in striatal, cortex and hippocampal regions of the rat. The memory performance was assessed by Morris water maze and elevated plus maze paradigms. The oxidative damage was assessed by estimating the total glutathione, reduced glutathione, oxidized glutathione levels and glutathione redox ratio. Glutathione- S -transferase and lactate dehydrogenase enzymes were also measured in different brain areas. 3-NP significantly impaired memory performance as assessed in Morris water maze and elevated plus maze, which was significantly attenuated by sesamol (5, 10 and 20 mg/kg) pre-treatment. On the other hand, 3-NP significantly induced oxidative stress and depleted total glutathione, reduced glutathione, glutathione- S -transferase, lactate dehydrogenase enzyme levels and redox ratio in the striatum, cortex and hippocampal regions as compared to the vehicle-treated group. Sesamol pre-treatment restored oxidative defence possibly by its free radical scavenging activity as compared to the 3NP-treated group. The present study suggests that sesamol could be used as an effective agent in the management of Huntington's disease. [source] Effect of N -Acetyl Cysteine against Aluminium-induced Cognitive Dysfunction and Oxidative Damage in RatsBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 2 2009Atish Prakash Chronic aluminium exposure induces oxidative stress and increases amyloid beta levels in vivo. The role of oxidative stress has been well-suggested in these cognitive problems. Therefore, the present study was designed to explore the possible role of N -acetyl cysteine against aluminium mediating cognitive dysfunction and oxidative stress in rats. Aluminium chloride (100 mg/kg, p.o.) was given to rats daily for 6 weeks. N -acetyl cysteine (per se; 50 and 100 mg/kg, i.p.) pre-treatment was given 30 min. before aluminium daily for 6 weeks. On the third (21st day) and sixth week (42nd day) of the study, various behavioural tests (Morris water maze and elevated plus maze task paradigms) and locomotion (photoactometer) were done to evaluate cognitive tasks. The rats were killed on the 43rd day following the last behavioural test, and various biochemical tests were performed to assess the extent of oxidative damage. Chronic aluminium chloride administration resulted in poor retention of memory in Morris water maze, elevated plus maze task paradigms and caused marked oxidative damage. It also caused a significant increase in the acetylcholinesterase activity. Chronic administration of N -acetyl cysteine significantly improved memory retention in tasks, attenuated oxidative damage and acetylcholinesterase activity in aluminium-treated rats. The study suggests a neuroprotective effect of N -acetyl cysteine against aluminium-induced cognitive dysfunction and oxidative damage. [source] Cognitive dysfunction in patients with type 2 diabetesDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 7 2010Yael D. Reijmer Abstract People with diabetes mellitus are at increased risk of cognitive dysfunction and dementia. This review explores the nature and severity of cognitive changes in patients with type 2 diabetes. Possible risk factors such as hypo- and hyperglycemia, vascular risk factors, micro- and macrovascular complications, depression and genetic factors will be examined, as well as findings from brain imaging and autopsy studies. We will show that type 2 diabetes is associated with modest cognitive decrements in non-demented patients that evolve only slowly over time, but also with an increased risk of more severe cognitive deficits and dementia. There is a dissociation between these two ,types' of cognitive dysfunction with regard to affected age groups and course of development. Therefore, we hypothesize that the mild and severe cognitive deficits observed in patients with type 2 diabetes reflect separate processes, possibly with different risk factors and aetiologies. Copyright © 2010 John Wiley & Sons, Ltd. [source] Cognitive dysfunction and health-related quality of life after a cardiac arrest and therapeutic hypothermiaACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 6 2010J. TORGERSEN Background: Evidence-based treatment protocols including therapeutic hypothermia have increased hospital survival to over 50% in unconscious out-of-hospital cardiac arrest survivors. In this study we estimated the incidence of cognitive dysfunctions in a group of cardiac arrest survivors with a high functional outcome treated with therapeutic hypothermia. Secondarily, we assessed the cardiac arrest group's level of cognitive performance in each tested cognitive domain and investigated the relationship between cognitive function and age, time since cardiac arrest and health-related quality of life (HRQOL). Methods: We included 26 patients 13,28 months after a cardiac arrest. All patients were scored using the Cerebral Performance Category scale (CPC) and Mini-Mental State Examination (MMSE). Twenty-five of the patients were tested for cognitive function using the Cambridge Neuropsychological Test Automated Battery (CANTAB). These patients were tested using four cognitive tests: Motor Screening Test, Delayed Matching to Sample, Stockings of Cambridge and Paired Associate Learning from CANTAB. All patients filled in the Short Form-36 for the assessment of HRQOL. Results: Thirteen of 25 (52%) patients were classified as having a cognitive dysfunction. Compared with the reference population, there was no difference in the performance in motor function and delayed memory but there were significant differences in executive function and episodic memory. We found no associations between cognitive function and age, time since cardiac arrest or HRQOL. Conclusion: Half of the patients had a cognitive dysfunction with reduced performance on executive function and episodic memory, indicating frontal and temporal lobe affection, respectively. Reduced performance did not affect HRQOL. [source] Cognitive dysfunction and the neurobiology of ageing in catsJOURNAL OF SMALL ANIMAL PRACTICE, Issue 10 2007D. Gunn-Moore With improvements in nutrition and veterinary medicine the life expectancy of pet cats is increasing. Accompanying this growing geriatric population there are increasing numbers of cats with signs of apparent senility. A recent study suggests that 28 per cent of pet cats aged 11 to 14 years develop at least one geriatric onset behavioural problem, and this increases to over 50 per cent for cats of 15 years of age or older. While behavioural changes may result from systemic illness, organic brain disease or true behavioural problems, the possibility of age-related cognitive dysfunction is often overlooked. Studies have revealed a number of changes in the brains of geriatric cats that showed signs of cognitive dysfunction, and potential causes include vascular insufficiency leading to hypoxia, increased free radical damage and the deposition of ,-amyloid plaques and/or the modification of other proteins. By recognising the importance of behavioural changes in old cats, investigating them fully for potentially treatable medical conditions, and instigating dietary and environmental modifications to meet their changing needs, we can make the lives of our geriatric cats much more comfortable and rewarding. [source] Cognition in liver diseaseLIVER INTERNATIONAL, Issue 1 2005Alexander Collie Abstract: 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. [source] The Montreal Cognitive Assessment as a screening tool for cognitive dysfunction in Huntington's disease,MOVEMENT DISORDERS, Issue 3 2010Aleksandar Videnovic MD Abstract Cognitive dysfunction is one of the hallmarks of Huntington's disease (HD) and may precede the onset of motor symptoms. The Montreal Cognitive Assessment (MoCA), a brief cognitive screening instrument with high specificity and sensitivity for detecting early cognitive impairments, has not been studied in the HD population. In this study, we compare the MoCA with the mini-mental state examination (MMSE) as a screening tool for cognitive dysfunction among 53 patients with HD. The mean MMSE score was 26 ± 2.4, and mean MoCA score was 21 ± 4.4. Twenty-one patients (81%) of those who scored ,26 on the MMSE had the MoCA score <26. Thirty-two patients (78%) of those who scored ,24 on the MMSE had the MoCA score <24. The MoCA may be a more sensitive screening tool for cognitive impairments in HD relative to the MMSE. © 2010 Movement Disorder Society [source] Cognitive dysfunction 1,2 years after non-cardiac surgery in the elderlyACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 10 2000H. Abildstrom 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 1:64 000 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. [source] Blood lead levels in Egyptian children from high and low lead-polluted areas: impact on cognitive functionACTA NEUROLOGICA SCANDINAVICA, Issue 1 2009G. A. Mostafa Objectives,,, Many children are harmed by low-level lead exposure which impairs cognitive development with subsequent poor scholastic achievement. We investigated blood lead levels in children in relation to cognitive function. Materials and methods,,, Blood lead levels were measured in 100 children recruited from high (n = 50) and low (n = 50) lead-polluted areas. Results,,, Blood lead levels ranged between 3 and 28 ,g/dl (median 9, interquartile range 6 ,g/dl). In addition, 43% of children had levels ,10 ,g/dl, of whom 90.1% were living in high-risk areas for lead pollution. Cognitive dysfunction was found in 37% of children. Children with cognitive dysfunction had significantly higher blood lead and lower hemoglobin than those without (P < 0.001). Conclusions,,, Increased blood lead level in many children is one of the health problems in Egypt which may be the reason, at least in part, for cognitive dysfunction with subsequent poor scholastic achievement. Thus, interventions to control lead exposure are mandatory. [source] Critical evaluation of cognitive dysfunctions as endophenotypes of schizophreniaACTA PSYCHIATRICA SCANDINAVICA, Issue 2 2004S. Kéri 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. [source] Advanced microscopic imaging methods to investigate cortical development and the etiology of mental retardationDEVELOPMENTAL DISABILITIES RESEARCH REVIEW, Issue 4 2005Tarik F. Haydar Abstract Studies on human patients and animal models of disease have shown that disruptions in prenatal and early postnatal brain development are a root cause of mental retardation. Since proper brain development is achieved by a strict spatiotemporal control of neurogenesis, cell migration, and patterning of synapses, abnormalities in one or more of these events during prenatal development can lead to cognitive dysfunction after birth. Many of underlying causes of mental retardation must therefore be studied in developing brains. To aid in this research, live imaging using laser scanning microscopy (LSM) has recently allowed neuroscientists to delve deeply into the complex three-dimensional environment of the living brain to record dynamic cellular events over time. This review will highlight recent examples of how LSM is being applied to elucidate both normal and abnormal cortical development. © 2005 Wiley-Liss, Inc. MRDD Research Reviews 2005;11:303,316. [source] Complex visual hallucination and mirror sign in posterior cortical atrophyACTA PSYCHIATRICA SCANDINAVICA, Issue 1 2006T. Yoshida Objective:, In posterior cortical atrophy (PCA), visual hallucinations are rare symptoms and mirror sign has not been described. Method:, Single case report. Results:, We reported a 60-year-old woman with PCA who reported complex visual hallucinations, such as a man walking in her room, and mirror sign, which was the perception of a stranger staring at her when she looked into a mirror. She could not recognize images of herself in the mirror correctly, although she could recognize that a person standing next to her and the images of that person reflected in the mirror were the same person. Conclusion:, Early complex visual hallucinations in this patient appeared to be more characteristic of dementia with Lewy body than Alzheimer's disease (AD). It is hard to explain mirror sign in this patient as being because of either prosopagnosia, Balint's syndrome or advanced AD. This patient may have other underlying cognitive dysfunction. [source] Cognitive dysfunction in patients with type 2 diabetesDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 7 2010Yael D. Reijmer Abstract People with diabetes mellitus are at increased risk of cognitive dysfunction and dementia. This review explores the nature and severity of cognitive changes in patients with type 2 diabetes. Possible risk factors such as hypo- and hyperglycemia, vascular risk factors, micro- and macrovascular complications, depression and genetic factors will be examined, as well as findings from brain imaging and autopsy studies. We will show that type 2 diabetes is associated with modest cognitive decrements in non-demented patients that evolve only slowly over time, but also with an increased risk of more severe cognitive deficits and dementia. There is a dissociation between these two ,types' of cognitive dysfunction with regard to affected age groups and course of development. Therefore, we hypothesize that the mild and severe cognitive deficits observed in patients with type 2 diabetes reflect separate processes, possibly with different risk factors and aetiologies. Copyright © 2010 John Wiley & Sons, Ltd. [source] How hypoglycaemia can affect the life of a person with diabetesDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 2 2008Brian M. Frier Abstract Hypoglycaemia is the commonest side-effect of insulin treatment for diabetes, and is the single greatest barrier to achieving and maintaining good glycaemic control. Severe hypoglycaemia (requiring assistance for recovery) is associated with significant morbidity and is feared by most people with type 1 diabetes and their families. It causes stress and anxiety and may influence self-management and glycaemic control. The annual prevalence of severe hypoglycaemia is around 30% in people with type 1 diabetes, and is higher in those with risk factors such as strict glycaemic control, impaired awareness of hypoglycaemia and increasing duration of diabetes. It is also common during sleep (nocturnal hypoglycaemia). Neurological manifestations include coma, convulsions, transient hemiparesis and stroke, while reduced consciousness and cognitive dysfunction may cause accidents and injuries. Cardiac events may be precipitated such as arrhythmias, myocardial ischaemia and cardiac failure. Hypoglycaemia can affect all aspects of life, including employment, driving, recreational activities involving exercise, and travel, and measures should be taken in all of these situations to avoid this potentially dangerous side-effect of insulin therapy. Copyright © 2007 John Wiley & Sons, Ltd. [source] Interactive effect of central obesity and hypertension on cognitive function in older out-patients with Type 2 diabetesDIABETIC MEDICINE, Issue 12 2008E. Kim Abstract Aim Central obesity, hypertension and diabetes mellitus have been related individually to cognitive dysfunction. We aimed to study the interactive effects of these co-occurring risk factors on cognitive decline, which remain unclear in older patients with diabetes. Methods We assessed metabolic profiles and neuropsychological functions in 60 older out-patients with Type 2 diabetes to examine the associations of central obesity with cognitive functions, while controlling for other confounding factors in these subjects. Results Waist circumference was associated with poor performance in digits forward (r2 = 0.11, P = 0.02), choice reaction time (r2 = 0.08, P = 0.04) and cognitive reaction time (r2 = 0.07, P < 0.05) even after adjustment for potential confounders including age, gender, education and HbA1c. There were also significant interactions between central obesity and hypertension with respect to performance of digits forward (P = 0.04) and delayed verbal cued recall (P = 0.03). Conclusion Our findings suggest that, in addition to glycaemic control, central obesity and hypertension influence cognitive functions, such as attention and psychomotor speed in older patients with Type 2 diabetes. [source] Cystatin C as an index of cerebral small vessel disease: results of a cross-sectional study in community-based Japanese elderlyEUROPEAN JOURNAL OF NEUROLOGY, Issue 3 2010M. Wada Background and purpose:, Recent studies have shown that kidney dysfunction is associated with cerebral small vessel disease (SVD). Although creatinine-based estimating equations have been used as the standard measure for the evaluation of kidney function, the accuracy of these is limited in the elderly because of muscle mass decrease with aging. Cystatin C is a more useful measurement than creatinine-based estimating equations for evaluating kidney function, however, the relationship amongst cystatin C, cognitive dysfunction, and cerebral SVD has not been fully examined in community-based elderly. Methods:, We performed a cross-sectional study using MRI to determine the relationship amongst cystatin C, cognitive function, and cerebral SVD in a total of 604 community-based Japanese elderly. Results:, In this study, subjects with higher cystatin C levels tended to have more lacunas and higher grades of white matter lesions. Although a decline of the Mini-Mental State Examination (MMSE) scores was associated with SVD-related lesions, the relationship between the tertiles of cystatin C and mean MMSE scores was not statistically significant. In the logistic regression analysis, the association between cystatin C and SVD-related lesions was statistically significant, even after adjustment for conventional risk factors and high-sensitivity C-reactive protein. Furthermore, subjects with higher cystatin C levels accompanied with albuminuria had a greater risk for the presence of subclinical cerebral SVD than those with lower cystatin C levels without albuminuria. Conclusions:, The present study suggests that there is a close relationship between cystatin C and subclinical cerebral SVD, independently of conventional risk factors, in community-based elderly. [source] Frontal-lobe mediated behavioral dysfunction in amyotrophic lateral sclerosisEUROPEAN JOURNAL OF NEUROLOGY, Issue 1 2010M. Witgert Background:, Cognitive impairment secondary to frontal lobe atrophy exists in 40,60% of Amyotrophic Lateral Sclerosis (ALS) cases. We aimed to determine the prevalence of frontal-lobe mediated behavioral impairment in (ALS) and to ascertain its relationship to cognitive impairment. Methods:, Two-hundred and twenty five patients diagnosed with sporadic ALS were evaluated for behavioral dysfunction using the Frontal Systems Behavior Scale (FrSBe), a validated measure used to examine frontal-lobe mediated behaviors, specifically apathy, executive dysfunction and disinhibition; a total behavior score is also provided. Additionally, a subset of patients also underwent a comprehensive neuropsychological evaluation. Results:, Changes in the total FrSBe scores were observed in 24.4% of the patients and 39.6% of the patients had impairment in at least one behavioral domain with symptoms of Apathy being the most common (31.1%). Cognitively impaired ALS patients had worse total (P = 0.05) and apathy scores (P < 0.01); however, behavioral dysfunction was also present in 16% of the cognitively intact patients. Half of the behaviorally intact patients exhibited cognitive impairment. Significant correlations were observed for performance on certain neuropsychological tests (Animal fluency, Block Design, Logical Memory I and Verbal Series Attention Test) and severity of behavioral dysfunction on certain FrSBe sub scores. Conclusions:, Frontal-lobe mediated behavioral dysfunction appears to be common in ALS. Cognitively impaired ALS patients had greater behavioral dysfunction. Recognition of behavioral and cognitive dysfunction may assist health-care providers and care-givers recognize changes in decision-making capacity and treatment compliance of patients with ALS. [source] ALS patients request more information about cognitive symptomsEUROPEAN JOURNAL OF NEUROLOGY, Issue 5 2008P. Wicks Background and purpose:, Once thought to impact only voluntary motor function, ALS/Motor neuron disease (MND) is now seen as a multi-system disorder in which a minority of patients experience mild cognitive dysfunction or frontotemporal dementia. Despite clinical guidelines advocating supplying complete information to patients, educational materials on ALS often state that the mind is unaffected. We sought to establish how much patients and caregivers understand about ALS, what they have been told to expect by their physician, and if they would have appreciated more complete information. Methods:, A two-part survey was administered online. An ,ALS quiz' gauged participants' knowledge of physical and psychological aspects of ALS. A second questionnaire assessed which symptoms patients had discussed with their clinician and explored patients' desire to receive information on psychological effects. Results:, A total of 247 ALS patients and 87 caregivers participated. Participants knew less about psychological symptoms than physical ones (72% correct responses versus 82%; paired t(333) = ,5.04, P < 0.001). Patients commonly reported being told by their doctor about physical symptoms such as problems walking (85%) or stiffness/cramps (74%) but not psychological issues like emotional lability (46%) or cognitive change (11%). The majority of patients (62%) and carers (71%) indicated a desire to be informed that cognitive change or dementia might occur. Conclusion:, ALS is a multi-system disorder. However, despite a desire for more information from patients and their carers, healthcare professionals continue to primarily address only the physical consequences of the disease. [source] Does motor subtype influence neurocognitive performance in Parkinson's disease without dementia?EUROPEAN JOURNAL OF NEUROLOGY, Issue 3 2008E. Lyros The postural instability and gait difficulty (PIGD) motor subtype has been shown to represent a risk factor for development of dementia in Parkinson's disease. Whether this relationship extends to a more subtle cognitive dysfunction in patients is less clear. Therefore, we administered a battery of selected neuropsychological tests to two groups of non-demented patients with mild to moderate disease classified either as PIGD or as non-PIGD subtype and to a group of healthy controls. Groups were matched on potential confounders of neuropsychological performance. No significant differences were revealed between the two groups of patients in the performance of any of the administered neuropsychological tests. However, relative to controls there was a tendency towards a differential pattern of cognitive dysfunction. The PIGD group had slower performance in a test of psychomotor speed and cognitive flexibility, whilst the non-PIGD group performed worse in measures of verbal learning and visuo-spatial perception. In conclusion, the PIGD subtype was not associated with more severe cognitive deficits and may to a certain extent share common mechanisms of cognitive dysfunction with non-PIGD subtypes. Diverse pathological processes however may develop to account for unequal rates of dementia amongst different motor subtypes. [source] CD4+CD25, effector T-cells inhibit hippocampal long-term potentiation in vitroEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 6 2007Gil M. Lewitus Abstract During neuroinflammation T-cells invade the CNS, and may lead to the development and progression of several pathologies, of which multiple sclerosis is the most common. In these pathologies neuroinflammation is often associated with cognitive dysfunction. Using mouse hippocampal slices, we show here that CD4+CD25, T-cells inhibit long-term potentiation (LTP) induced by high-frequency stimulation. The T-cell-mediated inhibition of LTP can be prevented by blockade of ,-aminobutyric acid (GABA)A receptors. These findings provide additional insight into the multiple functions of T-cells in CNS pathologies. [source] Characterization of a mouse model overexpressing beta-site APP-cleaving enzyme 2 reveals a new role for BACE2GENES, BRAIN AND BEHAVIOR, Issue 2 2010G. Azkona BACE2 is homologous to BACE1, a ,-secretase that is involved in the amyloidogenic pathway of amyloid precursor protein (APP), and maps to the Down syndrome critical region of chromosome 21. Alzheimer disease neuropathology is common in Down syndrome patients at relatively early ages, and it has thus been speculated that BACE2 co-overexpression with APP would promote the early neurodegenerative phenotype. However, the in vivo function of BACE2 has not yet been elucidated. The aim of the present work has been to analyse the impact of in vivo BACE2 overexpression using a transgenic mouse model. Our results suggest that BACE2 is not involved in the amyloidogenic pathway, cognitive dysfunction or cholinergic degeneration. However, TgBACE2 animals showed increased anxiety-like behaviour along with increased numbers of noradrenergic neurones in locus coeruleus, thus suggesting an unexpected role of BACE2 overexpression. [source] Optimal treatment of hypertension in the elderly: A Korean perspectiveGERIATRICS & GERONTOLOGY INTERNATIONAL, Issue 1 2008Kwang-Il Kim With the progression of the aging population, common diseases of the elderly have become the center of attention in most developed countries. Hypertension is one of the most common morbid conditions in the elderly and has a great impact on their health status because it is the main risk factor of cardiovascular and cerebrovascular diseases. However, a considerable amount of uncertainty remains regarding hypertension in the elderly, such as the benefits of hypertension control in oldest-old populations, the optimal level of blood pressure control, and the efficacy of antihypertensive drugs for the prevention of cognitive dysfunction. While there are many controversial issues concerning the optimal management of hypertension in the elderly, the number of elderly hypertensive patients that require treatment is expected to increase due to the aging population. As a result, knowledge regarding the mechanisms of hypertension in the elderly and specific consideration in managing hypertensive elderly patients are needed to improve the clinical outcome. Furthermore, new therapeutic interventions that are aimed at attenuating age-related vascular changes should be investigated, because hypertension in the elderly, especially isolated systolic hypertension has specific characteristics of increased arterial stiffness in most cases. [source] Comprehensive studies of cognitive impairment of the elderly with type 2 diabetesGERIATRICS & GERONTOLOGY INTERNATIONAL, Issue 3 2006Takashi Sakurai Type 2 diabetes mellitus is associated with cognitive dysfunction and increases the risk of dementia for the elderly. The aim of the study presented here was to provide a brief review of how disturbance of glucose and metabolic homeostasis may be implicated in the cognitive decline of patients with type 2 diabetes. Several risk factors such as nutrition, cerebrovascular disorders and the neurotoxic effects of hyperglycemia may combine for the formation of mechanisms of cognitive decline in the diabetic elderly. It should be noted that cognitive deficits of diabetes are accompanied by neuroradiological changes in the brain, so that cognitive dysfunction both with and without brain structural changes may overlap during cognitive decline of the diabetic elderly. Recently, we conducted two studies to explore, by means of brain imaging, hierarchical relationships among clinical profiles of diabetes, cognitive function, white matter hyperintensity and brain atrophy. The results suggested that subcortical brain atrophy and hyperintensity constitute predictors of the rate of progression of cognitive dysfunction in the diabetic elderly, while cortical atrophy is associated with high diastolic blood pressure and lower HbA1c. These hypotheses may explain in part the underlying mechanisms of cognitive impairment in the diabetic elderly. Prospective intervention studies are needed, however, to clarify the mechanism of cognitive dysfunction of the diabetic elderly and what the targets are for preventive measures. [source] Effect of improvement in anemia on electroneurophysiological markers (P300) of cognitive dysfunction in chronic kidney diseaseHEMODIALYSIS INTERNATIONAL, Issue 3 2006Narinder P. SINGH Abstract Our aim is to study the effect of improvement in anemia on event-related potentials (ERPs; P300) as markers of cognitive dysfunction in predialysis and dialysis patients of chronic kidney disease (CKD). Thirty anemic patients of CKD (hemoglobin [Hb]<9 g%), 15 in the predialysis group (Group A), and 15 patients on biweekly hemodialysis (Group B) were recruited for the study. Patients of uremic encephalopathy, dyselectrolytemia, and those with hearing problems were excluded. Both groups were given recombinant human erythropoietin (rhuEPO) 100 IU/kg biweekly for 6 weeks by the subcutaneous route. No intervention was performed in the third control group (Group C), which consisted of 30 normal healthy volunteers. The improvement in Hb was assessed every 2 weeks, and the amplitude and latency of the P300 component of the ERPs were studied before initiating treatment and after 6 weeks of rhuEPO administration. There was a significant increase in Hb in both the study groups without any significant alteration in kidney functions. A significant reduction in P300 latency was noted in both the study groups after intervention. Similarly, the amplitude of P300 also increased in both study groups, but attained statistical significance for the dialysis group only. No significant changes were observed in the control group. Administration of EPO in patients of anemia with CKD resulted in a significant improvement in the electrophysiological markers of cognitive function in the form of increased amplitudes and decreased latencies of P300 in both predialysis and dialysis patients. [source] Mutation frequencies of X-linked mental retardation genes in families from the EuroMRX consortium,,HUMAN MUTATION, Issue 2 2007Arjan P.M. de Brouwer Abstract The EuroMRX family cohort consists of about 400 families with non-syndromic and 200 families with syndromic X-linked mental retardation (XLMR). After exclusion of Fragile X (Fra X) syndrome, probands from these families were tested for mutations in the coding sequence of 90 known and candidate XLMR genes. In total, 73 causative mutations were identified in 21 genes. For 42% of the families with obligate female carriers, the mental retardation phenotype could be explained by a mutation. There was no difference between families with (lod score >2) or without (lod score <2) significant linkage to the X chromosome. For families with two to five affected brothers (brother pair=BP families) only 17% of the MR could be explained. This is significantly lower (P=0.0067) than in families with obligate carrier females and indicates that the MR in about 40% (17/42) of the BP families is due to a single genetic defect on the X chromosome. The mutation frequency of XLMR genes in BP families is lower than can be expected on basis of the male to female ratio of patients with MR or observed recurrence risks. This might be explained by genetic risk factors on the X chromosome, resulting in a more complex etiology in a substantial portion of XLMR patients. The EuroMRX effort is the first attempt to unravel the molecular basis of cognitive dysfunction by large-scale approaches in a large patient cohort. Our results show that it is now possible to identify 42% of the genetic defects in non-syndromic and syndromic XLMR families with obligate female carriers. © 2007 Wiley-Liss, Inc. [source] New insights into the pathophysiology of postoperative cognitive dysfunctionACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 8 2010L. KRENK There is evidence that postoperative cognitive dysfunction (POCD) is a significant problem after major surgery, but the pathophysiology has not been fully elucidated. The interpretation of available studies is difficult due to differences in neuropsychological test batteries as well as the lack of appropriate controls. Furthermore, there are no internationally accepted criteria for defining POCD. This article aims to provide an update of current knowledge of the pathogenesis of POCD with a focus on perioperative pathophysiology and possible benefits achieved from an enhanced postoperative recovery using a fast-track methodology. It is concluded that the pathogenesis of POCD is multifactorial and future studies should focus on evaluating the role of postoperative sleep disturbances, inflammatory stress responses, pain and environmental factors. Potential prophylactic intervention may include minimal invasive surgery, multi-modal non-opioid pain management and pharmacological manipulation of the inflammatory response and sleep architecture. [source] New once-daily formulation for trospium in overactive bladderINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 11 2010C. Chapple Summary Aims:, We examined the relative efficacy and safety of trospium 20 mg bid and 60 mg extended release formulations and position this drug against other antimuscarinic agents. Methods:, Data were identified on the pharmacology and pharmacokinetics of trospium chloride. Key publications on trospium 20-mg and 60-mg clinical studies in patients with overactive bladder (OAB) were identified and efficacy and safety compared between these formulations as well as other antimuscarinic agents. Results:, Trospium offers the principal advantage over other antimuscarinic agents that, as it is a quaternary amine, it does not cross the blood,brain barrier and is therefore less likely to cause central nervous system effects observed with several other agents. Moreover, with its minimal liver metabolisation, independent of the main cytochrome pathways, trospium has a low risk of drug,drug interaction in patients taking multiple pharmacological agents. Trospium 60 mg ER is as effective as trospium 20 mg bid in improving the key outcome parameters associated with OAB, but with a lower rate of dry mouth, the most common side effect of these agents. Trospium has comparable efficacy and safety to the other antimuscarinic agents currently marketed. Discussion:, Good patient persistence with treatment has been reported with trospium. There are currently a large number of antimuscarinic drugs on the market without clear evidence to distinguish one agent from another in terms of efficacy, provided that an adequate dose is used in the clinical setting. Conclusion:, The new formulation of trospium is certainly worth considering as a pharmacological treatment of patients with OAB, particularly in the elderly, in whom one wants to avoid the potential for cognitive dysfunction. [source] Measurement of post-operative cognitive dysfunction after cardiac surgery: a systematic reviewACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 6 2010J. L. RUDOLPH Post-operative cognitive dysfunction (POCD) is a decline in cognitive function from pre-operative levels, which has been frequently described after cardiac surgery. The purpose of this study was to examine the variability in the measurement and definitions for POCD using the framework of a 1995 Consensus Statement on measurement of POCD. Electronic medical literature databases were searched for the intersection of the search terms ,thoracic surgery' and ,cognition, dementia, and neuropsychological test.' Abstracts were reviewed independently by two reviewers. English articles with >50 participants published since 1995 that performed pre-operative and post-operative psychometric testing in patients undergoing cardiac surgery were reviewed. Data relevant to the measurement and definition of POCD were abstracted and compared with the recommendations of the Consensus Statement. Sixty-two studies of POCD in patients undergoing cardiac surgery were identified. Of these studies, the recommended neuropsychological tests were carried out in less than half of the studies. The cognitive domains measured most frequently were attention (n=56; 93%) and memory (n=57; 95%); motor skills were measured less frequently (n=36; 60%). Additionally, less than half of the studies examined anxiety and depression, performed neurological exam, or accounted for learning. Four definitions of POCD emerged: per cent decline (n=15), standard deviation decline (n=14), factor analysis (n=13), and analysis of performance on individual tests (n=12). There is marked variability in the measurement and definition of POCD. This heterogeneity may impede progress by reducing the ability to compare studies on the causes and treatment of POCD. [source] | ||||||||||||||||||||||||||||||||||||||||