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PubMed1992

Recombinant erythropoietin improves cognitive function in chronic haemodialysis patients.

Psychometric performance was studied on two occasions in 18 chronic haemodialysis patients. Nine patients treated with rHuEpo performed a battery of psychometric tests before treatment, haemoglobin [mean (SD)] 5.8 (0.6) g/dl and after partial correction of anaemia, haemoglobin 9.3 (1.28) g/dl. The same battery of psychometric tests was administered on two occasions to nine patients (haemoglobin 7.3 (1.2) g/dl) matched with the treatment group for age, educational status and social class, who did not receive rHuEpo. In the rHuEpo-treated group, IQ, measured by the Wechsler Adult Intelligence Scale-Revised, improved by a mean of 8.7 points (P less than 0.01), while in the control group an improvement by a mean of 2.5 points was not significant. Comparison between the groups of the change in IQ score was significant (P = 0.04). There was no change in the mean scores obtained in either group for the other psychometric tests administered including the Paced Auditory Serial Addition Test, Rey auditory verbal learning, and Borkowski verbal fluency test. These results indicate that anaemia makes a reversible contribution to uraemic cognitive dysfunction.

Adult↗
PubMed2005

Cognitive strategies versus self-management skills as adjunct to vocational rehabilitation.

Cognitive dysfunctions and negative symptoms are "rate-limiting factors" for community outcome and response to psychosocial intervention in people with schizophrenia. Therefore, two cognitive-behavioral group therapies were developed-computer-assisted cognitive strategy training (CAST) and training of self-management skills for negative symptoms (TSSN)-to target these barriers to rehabilitation readiness. One hundred thirty-eight DSM-IV schizophrenia inpatients on a rehabilitation ward were randomly assigned to CAST plus vocational rehabilitation, TSSN plus vocational rehabilitation, or vocational rehabilitation alone. CAST included computer-based training in coping strategies focusing on deficits in attention, verbal memory, and planning. TSSN focused on social withdrawal/social anhedonia, lack of drive/volition, and affect flattening using techniques such as time scheduling, mastery, and pleasure techniques. Treatment outcome was assessed at intake and at discharge after 8 weeks. Analyses of covariance controlling for basis-level functioning demonstrated that patients receiving CAST plus vocational rehabilitation showed greater improvement on attention and verbal memory but not on planning ability. Patients receiving TSSN plus vocational rehabilitation failed to demonstrate improvement in negative symptoms. CAST plus vocational rehabilitation was found to be associated with a higher rate of successful job placement at the 12-month followup interval. Hierarchical logistic regression analyses demonstrated that improvement in short- and long-term verbal memory predicted a higher proportion of variance of successful job placement in the followup than pretreatment history of employment alone. Cognitive training as an adjunct to inpatient vocational rehabilitation demonstrated cognitive improvement, which was found to be associated with successful job placement in the followup. TSSN's efficacy was less clear; reasons for this uncertainty are provided.

Adult↗
PubMed1990

Information processing: a new model for understanding cognitive disturbances in psychiatric patients.

Information processing models are influenced by the information sciences and by computer technology, which progressed in the 1960s and 1970s. During the last decade these models have formed the theoretical basis for much of the experimental research on cognitive dysfunctions in psychiatric patients. An essential element in all of these models is that information is processed in several discrete stages. Different experimental paradigms have been developed in order to tap information about the processes taking place in each of these stages. Most of the research so far on pathological groups has been done on schizophrenic patients. Some deficits found in schizophrenics seem to be symptom-related. This is the case with performance deficits on the Continuous Performance Test with low processing load. Other dysfunctions might be vulnerability indicators, such as deficit performance on the forced choice Span of Apprehension task and the Continuous Performance Test with high momentary processing load, backward masking, serial recall for items that involve active rehearsal, and eye movement dysfunctions. However, information processing deficits do not seem to be specifically related to schizophrenia. Deficits can be found in other psychiatric syndromes too, especially in manic patients. Generally speaking, the dysfunctions emerge in a milder form in nonschizophrenic patients.

Attention↗
PubMed1998

Cognition and anxiety: the cognitive effects of anti-anxiety medication.

There does not appear to be a single hypothesis or theory which can adequately explain the aetiology of anxiety, although there is no short-age of contenders. Neurochemical, existential, sociogenic, familial, pathological, psychodynamic and behavioural explanations have all been offered as putative reasons for the psychological disorder, which in its various representations (panic disorder, obsessive-compulsive disorder, phobias, post-traumatic stress disorder, generalized anxiety disorders, etc.) can affect up to 20% of the population on a lifetime basis (1). Notwithstanding the variety of theories and the diversity of presentation of anxiety disorders, it would appear that cognitive dysfunction of one sort or another is a characteristic feature of anxiety in all its manifestations. Indeed, it is possible to argue that a cognitive impairment is the primary presenting feature of pathological anxiety, with the characteristic syndrome of somatic symptoms as secondary or necessary consequences of such cognitive disorder.

Anti-Anxiety Agents↗
PubMed2004

Correlation of entorhinal amyloid with memory in Alzheimer's and vascular but not Lewy body dementia.

OBJECTIVE: To examine the relationship of the anatomic distribution of amyloid deposition to focal and global cognitive dysfunction in different subtypes of dementia. METHODS: We quantified AB40 and AB42 in the temporal lobe and entorhinal cortex and examined their relationship to cognitive functions in Alzheimer's disease (AD), vascular dementia (VaD) and dementia with Lewy bodies (DLB). RESULTS: We found a correlation between memory impairment, but not global cognitive impairment, and amyloid load in these areas in AD and VaD but not in DLB. This relationship was stronger for AB42 and in the entorhinal cortex. CONCLUSION: The anatomic location of amyloid deposition is an important factor-specific factor in memory impairment in AD and VaD.

Aged↗
PubMed2002

Global and domain-specific cognitive impairment and outcome after subarachnoid hemorrhage.

BACKGROUND: Cognitive dysfunction is the most common form of neurologic impairment after subarachnoid hemorrhage (SAH). OBJECTIVE: To evaluate the impact of global and domain-specific cognitive impairment on functional recovery and quality of life (QOL) after SAH. METHODS: One hundred thirteen patients (mean age 49 years; 68% women) were evaluated 3 months after SAH. Three simple tests of global mental status and neuropsychological tests to assess seven specific cognitive domains were administered. Four aspects of outcome (global handicap, disability, emotional status, and QOL) were compared between cognitively impaired and unimpaired patients with analysis-of-covariance models controlling for age, race/ethnicity, and education. Multiple linear regression was used to evaluate the relative contribution of global and domain-specific cognitive status for predicting concurrent modified Rankin Scale (mRS) and Sickness Impact Profile (SIP) scores. RESULTS: Impairment of global mental status on the Telephone Interview of Cognitive Status (TICS) was associated with poor performance in all seven cognitive domains (all p < 0.0005) and was the only cognitive measure associated with poor recovery in all four aspects of outcome (all p < or = 0.005). Cognitive impairment in four specific domains was also associated with functional disability or reduced QOL. After accounting for global cognitive impairment with the TICS, however, neuropsychological testing did not contribute additional predictive value for concurrent mRS or SIP total scores. CONCLUSIONS: Cognitive impairment impacts broadly on functional status, emotional health, and QOL after SAH. The TICS may be a useful alternative to more detailed neuropsychological testing for detecting clinically relevant global cognitive impairment after SAH.

Adult↗
PubMed1997

GABAB receptor agonists and antagonists: pharmacological properties and therapeutic possibilities.

Gamma-aminobutyric acid (GABA), an inhibitory neurotransmitter, is widely distributed throughout the brain and spinal cord. Two major families of GABA receptors have been identified, GABAA and GABAB. While much is known about the pharmacological and molecular properties of GABAA receptors, it is only within the last few years that potent and selective antagonists have been developed for the GABAB site, and only within the past few months that this receptor has been cloned. Thus, tools are now available to define more fully the GABAB receptor in terms of its biology and the therapeutic potential of manipulating this site. Data suggest that, in addition to their established use as muscle relaxants, GABAB receptor agonists possess analgesic and antitussive properties, and may be useful for treating bladder dysfunction. While there is less clinical data on GABAB receptor antagonists, preclinical results indicate that they may be of value in treating absence epilepsy, cognitive dysfunction and, possibly, pulmonary and intestinal disorders. However, for this potential to be fully exploited, it is necessary to identify and characterise molecularly and pharmacologically distinct GABAB receptor subtypes.

Editorial↗
PubMedDate not supplied

Co-dergocrine mesylate. A review of its pharmacodynamic and pharmacokinetic properties and therapeutic use in age-related cognitive decline.

Co-dergocrine mesylate is a combination of the mesylated forms of dihydroergocornine, dihydroergocristine, dihydro-alpha-ergocryptine and dihydro-beta-ergocryptine. In animal models and healthy elderly volunteers the compound improves indices of cognitive function such as memory and learning. The mechanism(s) behind such action remains under investigation. Nonetheless, it has been proposed that co-dergocrine mesylate has a dual effect on central monoaminergic neurotransmitter systems, compensating for both hyperactivity and deficits of the adrenergic, serotoninergic and dopaminergic systems. The compound also appears to have a normalising effect on the power of electroencephalogram frequencies, and may improve cerebral metabolism. Results from controlled studies of elderly patients with age-related cognitive decline have established that co-dergocrine mesylate is well tolerated and, in some studies, had statistically significant positive effects on symptoms of cognitive dysfunction. However, there is considerable controversy over the clinical relevance of these results as there was wide variability in the number and type of cognitive and neuropsychological assessments used in individual studies and there may have been considerable overlap in diagnosis of patients with varying degrees of dementia. In addition, the drug has not been compared with most other, more recently developed, centrally active agents. Thus, the specific place of co-dergocrine mesylate in the treatment of age-related cognitive decline remains undetermined, despite many years of clinical use.

Aging↗
PubMed2000

Nicotinic modulation of mesoprefrontal dopamine neurons: pharmacologic and neuroanatomic characterization.

Schizophrenics have cortical dysfunction that may involve mesoprefrontal dopamine (DA) systems. Rates of nicotine dependence approach 90% in schizophrenia, and nicotine administration through cigarette smoking may ameliorate cognitive dysfunction, which may be related to cortical DA dysregulation. We have shown that repeated, but not acute, nicotine pretreatment (0.15 mg/kg daily s.c.) reduces footshock stress-induced mesoprefrontal DA metabolism and immobility responses. This effect of repeated nicotine is dependent on mecamylamine (MEC)-sensitive nicotinic acetylcholine receptor (nAChR) stimulation and endogenous opioid peptides. In the present study, we have further characterized these effects of repeated nicotine on the stress reactivity of mesoprefrontal DA neurons by using the following: 1) local infusion of MEC into cell bodies (ventral tegmental area) and terminal fields (medial prefrontal cortex) to determine the site of action of nicotine; and 2) systemic administration of selective nAChR antagonists. Results of bilateral local infusions of MEC (0.1-1.0 microgram/side) into ventral tegmental area or medial prefrontal cortex in saline- and nicotine-pretreated rats suggests a modulatory role for somatodendritic versus terminal field nAChRs on mesoprefrontal DA neurons under stress-induced states. Experiments with dihydro-beta-erythroidine (a beta2-subunit-selective blocker; 0.0-3.0 mg/kg) and methylycaconitine (an alpha7-subunit-selective blocker; 0.0-8.4 mg/kg) suggest that both alpha4beta2- and alpha7-containing nAChRs modulate mesoprefrontal DA neurons. Thus, complex regulation of mesoprefrontal DA neurons by nAChRs is suggested, which may have relevance to prefrontal cortical DA dysfunction and the high comorbid rates of nicotine dependence in schizophrenia.

Animals↗
PubMed2001

Neuropeptides in the therapy of Alzheimer's disease.

Owing to the heterogeneity of cognitive dysfunctions in patients with Alzheimer's disease (AD), a single drug may not suffice. Combination therapy may be the most appropriate solution, but the cognitive networks in the brain have yet to be unraveled. In the years ahead, more comprehensive and precise knowledge of neurological function will allow scientists to pinpoint ever more sophisticated and effective therapeutic options for AD patients. In this review, the author discusses the currently known advantages and disadvantages of neuropeptides and how they may provide yet another drug target for AD treatment.

Journal Article↗
PubMed2003

The influence of risperidone on cognitive functions in schizophrenia.

Introduction of the antipsychotics of the second generation (SGA) into the therapy of schizophrenia roused expectations that, finally, the cognitive dysfunction in schizophrenia could be eliminated by psychopharmacological therapy. The purpose of the study was to verify the effect of atypical antipsychotic risperidone on cognitive functions in schizophrenic patients. The study was carried out upon 48 male schizophrenic patients aged 21-47 years who were switched from the antipsychotics of the first generation (FGA) to the antipsychotic risperidone, due to intolerance, during the treatment. Intelligence, abstract and concrete thinking and mental speed, attention, and short-term non-verbal memory prior to the switch, one month after the switch, and three months after the switch to risperidone, were evaluated. One month after the switch the number of subjects with severe impairment of intellectual abilities decreased significantly from 62% to 15% and after three months the number was even lower-8%. The impairment of concrete and abstract thinking and mental speed also showed the same tendencies of decrease. The improvement of the cognitive functioning after the switch from the antipsychotics of the first generation to the antipsychotic risperidone is explained by removal of the antipsychotics of the first generation from the therapy and the consequential disinhibition of secondary cognitive impairments and by decreased average dose of anticholinergic and decreased number of patients who need anticholinergic therapy beside risperidone. The possibility of clear pro-cognitive effect of risperidone is suggested and its verification is proposed with strict control of other factors that improve cognitive functioning of schizophrenic patients during the treatment.

Adult↗
PubMed2005

[An impact of pronoran on cognitive and affective disorders in Parkinson's disease].

Sixty patients with different types of Parkinson's disease (PD), the disease stage 2.3 +/- 0.08 according to Hoehn&Yahr scale, were treated with Pronoran. Impact of the drug on movement, cognitive and affective disorders assessed by corresponding scales and psychological tests has been studied. Pronoran exerted a positive effect on all the disorders. It improved cognitive function, i.e. reasoning, memory and attention. A more pronounced influence on cognitive function was detected in earlier stages of the disease and for less severity cases of rigid-tremor PD type. A moderate antidepressive effect of Pronoran was found, being more pronounced in the severe PD stages. Emotional disorders were better treated, when Pronoran was used in combination with madopar, and cognitive dysfunction--in case of monotherapy.

Adult↗
PubMedDate not supplied

[Levodopa and cognitive disorders in Parkinson's disease].

AIMS: Most of the patients with Parkinson's disease evaluated in formal neuropsychological studies are found to have cognitive disorders similar to those of patients with lesions in the prefrontal cortex. A large number of anatomical, physiological, pharmacological and clinical data indicate that dopamine transmission plays an important role in frontal cortical functions. We review the main types of cognitive impairment in Parkinson's disease and their response to treatment with levodopa. DEVELOPMENT: In studies involving the acute administration of levodopa, the results obtained with regard to the cognitive functions have been heterogeneous, since improvements, exacerbations and the absence of any changes have all been observed. This heterogeneity is affected by methodological problems deriving from the disease itself, the treatment administered and the way evaluation is carried out. Longitudinal studies show a pattern of initial improvement, followed by stability, or maintenance, over a period of 2 or 3 years and then renewed exacerbation with no response to levodopa. On occasions, patients may only respond after a certain period of continued treatment. Generally speaking, the more severe the cognitive impairment is, the poorer the response to levodopa will be. CONCLUSIONS: Therapy with levodopa modifies, in one sense or another, the cognitive disorders in Parkinson's disease, which indicates that the dopaminergic deficit unquestionably plays a role in these disorders. The absence of response in some patients or in some cognitive functions or the fact that it 'wears off' in most patients suggests that the dopaminergic deficit is only one of the factors in the aetiopathogenesis of the cognitive dysfunction found in Parkinson's disease.

Antiparkinson Agents↗
PubMed2002

The impact of postoperative atrial fibrillation on neurocognitive outcome after coronary artery bypass graft surgery.

UNLABELLED: Neurocognitive decline is a continuing source of morbidity after cardiac surgery. Atrial fibrillation occurs often after cardiac surgery and has been linked to adverse neurologic events. We sought to determine whether postoperative atrial fibrillation was associated with postoperative cognitive dysfunction. Four-hundred-eleven patients were enrolled to receive a battery of neurocognitive tests both preoperatively and 6 wk after elective coronary artery bypass graft surgery. Neurocognitive test scores were separated into four cognitive domains, with a composite cognitive index (the mean of the four domain scores) determined for each patient at every testing period. Multivariable analysis controlling for age, years of education, diabetes mellitus, left ventricular ejection fraction, and preoperative atrial fibrillation compared the presence of postoperative atrial fibrillation with change in cognitive function. Three-hundred-eight patients completed both pre- and postoperative cognitive testing; 69 patients (22%) had postoperative atrial fibrillation. Those who developed atrial fibrillation showed more cognitive decline than those who did not develop postoperative atrial fibrillation (P = 0.036). Atrial fibrillation was associated with poorer cognitive function 6 wk after surgery. Although the mechanism of this association is yet to be determined, prevention of atrial fibrillation may result in improved neurocognitive function. IMPLICATIONS: Neurocognitive dysfunction is common after coronary artery bypass graft surgery. The relationship between atrial fibrillation and neurocognitive dysfunction has not been examined. Our study shows that postoperative atrial fibrillation is associated with neurocognitive decline.

Aged↗
PubMedDate not supplied

Short-term effects of improved glycemic control on cognitive function in patients with type 2 diabetes.

BACKGROUND: According to numerous studies, type 2 diabetes is associated with mild cognitive dysfunction, and there is some evidence suggesting favorable effects of improved metabolic control on the mental capability of elderly diabetic patients. OBJECTIVE: To compare patients with type 2 diabetes to normal controls with respect to cognitive performance and to investigate the consequences of glycemic adjustment. METHODS: 53 patients with type 2 diabetes, most of them in secondary failure on oral antidiabetic drugs, but free from conditions which may cause brain dysfunction, were included (mean age 58.8 +/- 6.1 years, duration of disease 12.0 +/- 6.4 years). They were examined prior to (t1), and following (t2) glycemic adjustment with a time interval of approximately 2 weeks. 29 non-diabetic controls, comparable with regard to age, gender, education and verbal intelligence were examined twice with a corresponding time interval. Cognitive performance was assessed by well-standardized tests with a focus on attention/concentration, psychomotor speed, verbal fluency and verbal memory; mood status by two self-rating scales. Restoration of glycemic control included insulin treatment in the majority of patients (46/53). RESULTS: Diabetic subjects scored significantly lower in all cognitive tests used, while they did not differ from controls in mood status. From t1 to t2 they improved in those tests measuring attention/concentration, and psychomotor speed. With regard to similar changes in controls, we interpret these improvements as practice effects rather than the consequence of altered metabolic control. CONCLUSION: In a sample of patients with long-standing type 2 diabetes we could not confirm previous reports of improved cognitive capacity with restoration of glycemic control. Further studies on the effects of changes in control of blood glucose on cognitive performance in type 2 diabetes should be conducted with special regard to drugs used to lower blood glucose.

Adult↗
PubMed1992

Individual differences in the cognitive and neurobiological consequences of normal aging.

Defining the neural basis of age-related cognitive dysfunction is a major goal of current research on aging. Compelling evidence from laboratory animals and humans indicates that aging does not inevitably lead to cognitive decline. Conducting neurobiological investigations in subjects that have previously undergone behavioral characterization has therefore emerged as a promising strategy for identifying those alterations in brain structure and function that are specifically associated with age-related cognitive impairment.

Aging↗
PubMed2005

Prenatal cocaine exposure specifically alters spontaneous alternation behavior.

Our laboratory has previously characterized a rabbit model of gestational cocaine exposure in which permanent alterations in neuronal morphology, cell signaling and psychostimulant-induced behavior are observed. The cellular and molecular neuroadaptations produced by prenatal cocaine occur in brain regions involved in executive function and attention, such as the anterior cingulate and medial prefrontal cortices. Therefore, in the present study, we have measured the effects of prenatal cocaine exposure on specific behavioral tasks in adult offspring whose mothers were treated with cocaine (3mg/kg, twice a day, E16-E25). We assessed non-spatial, short-term memory in a two-object recognition task and found no deficits in memory or exploratory behaviors in cocaine-exposed offspring in this paradigm. We also evaluated a different memory task with a more robust attentional component, using spontaneous alternation in a Y maze. In this task, young adult rabbits exposed to cocaine prenatally exhibited a significant deficit in performance. Deficits in spontaneous alternation can be induced by a wide variety of behavioral and cognitive dysfunctions, but taken together with previous findings in this and other animal models, we hypothesize that prenatal exposure to cocaine alters highly specific aspects of cognitive and emotional development.

Animals↗