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The prevalence of physical health disorders and measures of cognitive functioning were compared for 100 alcoholic and 100 nonalcoholic women matched on age and education. Alcoholic women were less healthy and more impaired on visual-spatial tasks than nonalcoholic women, and there were no relationships between health and cognitive functioning for either group.
Four studies examined impacts of iron supplementation on school children of various ages and both sexes. The first study investigated impact of iron-folic acid supplements for 60 d on cognition in 94 boys and girls aged 5-8 y. Improvement in total scores of the anemics was significantly higher than the nonanemics in 7-8-y-old children only. The second study assessed impacts of supplementation on cognition in 14 pairs of 5-6-y-old anemic boys, with clear beneficial effects on cognitive function. The third study investigated effects of varying dosages of elemental iron on cognitive function in 48 boys aged 8-15 y, with different levels of improvement. The fourth study investigated impacts of iron supplementation on 163 anemic girls aged 8-15 y with treatment and evaluations at 4 and 8 mo, with significantly improved scores in cognitive function after the eighth month.
OBJECTIVE: To establish whether initiation of treatment with diuretic or beta blocker is associated over 54 months with change in cognitive function. DESIGN: A cognitive substudy, nested within a randomised, placebo controlled, single blind trial. SETTING: 226 general practices from the Medical Research Council's general practice research framework. SUBJECTS: A subset of 2584 subjects sequentially recruited from among the 4396 participants aged 65-74 in the trial of treatment of hypertension in older adults. The 4396 subjects were randomised to receive diuretic, beta blocker, or placebo. Subjects had mean systolic pressures of 160-209 mm Hg and mean diastolic pressures <115 mm Hg during an eight week run in. OUTCOME MEASURES: The rate of change in paired associate learning test (PALT) and trail making test part A (TMT) scores (administered at entry and at 1, 9, 21, and 54 months) over time. RESULTS: There was no difference in the mean learning test coefficients (rate of change of score over time) between the three treatments: diuretic -0.31 (95% confidence interval -0.23 to -0.39), beta blocker -0.33 (-0.25 to -0.41), placebo -0.30, (-0.24 to -0.36). There was also no difference in the mean trail making coefficients (rate of change in time taken to complete over time) between the three groups: diuretic -2.73 (95% confidence interval -3.57 to -1.88), beta blocker -2.08 (-3.29 to -0.87), placebo -3.01, (-3.69 to -2.32). A less conservative protocol analysis confirmed this negative finding. CONCLUSION: Treating moderate hypertension in older people is unlikely to influence, for better or for worse, subsequent cognitive function.
Analysis of the scores of alcoholics on five tests of withdrawal, alcohol craving and cognitive function failed to support the hypothesis that the severity and frequency of alcohol withdrawal are related to impaired cognitive function.
We tested the cognitive function of elderly, community-dwelling residents in rural Newfoundland using the Canadian Mental Status Questionnaire. The prevalence of moderate and severe cognitive impairment was 9.3%. Physicians in the community had recognized those with severe impairment, but had not recognized any of those with moderate impairment. Cognitive function testing should be part of the periodic health examination of older patients.
In persons suffering from epilepsy, cognitive functioning may be compromised for various reasons, including--first and foremost--the learning and behavioral effects of the conditions causing the epilepsy. In addition, the epilepsy itself may cause changes in the nervous system through the metabolic and excitotoxic effects of the seizures and the neurotransmitter elements involved at the membrane level. The effect of the treatment modality, be it pharmacologic or surgical, may also play havoc with cognitive function. The neurobehavioral effects of antiepileptic drugs, although probably less important with the newer agents than in the past, must be considered, especially in polypharmacy, as recent reports have indicated. With increasing data, the effects of various surgical procedures on the cognitive elements of human behavior are becoming better recognized.
CONTEXT: Several studies have suggested that estrogen replacement therapy in postmenopausal women improves cognition, prevents development of dementia, and improves the severity of dementia, while other studies have not found a benefit of estrogen use. OBJECTIVE: To determine whether postmenopausal estrogen therapy improves cognition, prevents development of dementia, or improves dementia severity. DATA SOURCES: We performed a literature search of studies published from January 1966 through June 1997, using MEDLINE, manually searched bibliographies of articles identified, and consulted experts. STUDY SELECTION: Studies that evaluated biological mechanisms of estrogen's effect on the central nervous system and studies that addressed the effect of estrogen on cognitive function or on dementia. DATA EXTRACTION: We reviewed studies for methods, sources of bias, and outcomes and performed a meta-analysis of the 10 studies of postmenopausal estrogen use and risk of dementia using standard meta-analytic methods. DATA SYNTHESIS: Biochemical and neurophysiologic studies suggest several mechanisms by which estrogen may affect cognition: promotion of cholinergic and serotonergic activity in specific brain regions, maintenance of neural circuitry, favorable lipoprotein alterations, and prevention of cerebral ischemia. Five observational studies and 8 trials have addressed the effect of estrogen on cognitive function in nondemented postmenopausal women. Cognition seems to improve in perimenopausal women, possibly because menopausal symptoms improve, but there is no clear benefit in asymptomatic women. Ten observational studies have measured the effect of postmenopausal estrogen use on risk of developing dementia. Meta-analysis of these studies suggests a 29% decreased risk of developing dementia among estrogen users, but the findings of the studies are heterogeneous. Four trials of estrogen therapy in women with Alzheimer disease have been conducted and have had primarily positive results, but most have been small, of short duration, non-randomized, and uncontrolled. CONCLUSIONS: There are plausible biological mechanisms by which estrogen might lead to improved cognition, reduced risk for dementia, or improvement in the severity of dementia. Studies conducted in women, however, have substantial methodologic problems and have produced conflicting results. Large placebo-controlled trials are required to address estrogen's role in prevention and treatment of Alzheimer disease and other dementias. Given the known risks of estrogen therapy, we do not recommend estrogen for the prevention or treatment of Alzheimer disease or other dementias until adequate trials have been completed.
Most current and past research on the cerebral organization of cognitive functions has presupposed certain specialized hemisphere operations. At least for right handers, language and praxis are to be organized in the left hemisphere, while affective prosody, configurational spatial capacity, and global attention are lateralized in the right hemisphere. Deviations from these presuppositions, as in crossed aphasics and perhaps left handers, are generally considered to be 'exceptions' and either to disprove the rules or to be irrelevant to the rule. We report 4 very 'exceptional' cases, right handers with almost entirely reversed lateralization of functions. Analysis of the intrahemispheric relationships between functions suggests that there may be a specific neurobiology to the interrelationships between and among cognitive functions, handedness, and the intrahemisphere localization of the function.
In spite of the high prevalence of epilepsy and the importance of preserving cognitive function in people with learning disabilities, this population has received relatively little research attention. This study sets out systematically to investigate possible predictive factors of inter-ictal states of arousal and attention. The daytime function of 28 people with epilepsy and severe learning disabilities was assessed by performance on a two-choice reaction time vigilance task, behavioural analysis of time-sampled video recordings taken in naturalistic settings, and carer ratings on visual analogue scales. This methodology yielded eight discrete functional measures, from which two further index measures were derived after principal components analysis. A range of clinical and psychosocial assessments was completed and subjects had 36 hour ambulatory EEG and sleep EEG monitoring. Regression models identified significant predictors of cognitive function from a range of potential explanatory variables i.e. demographic, clinical, pharmacological, background EEG rhythms and sleep parameters. Results indicated that greater severity of learning disability, longer bedtime periods, poor sleep efficiency, frequent seizures and antiepileptic drug polytherapy were significant predictor variables. Explained variance (adjusted R2) was greater than 50% for six of 10 outcome variables (range up to 85%). Furthermore, significant regression equations (P < 0.05) were obtained for all but one variable. Thus, these results appear reasonably robust. Results support an interactional model of daytime arousal and attention in people with epilepsy plus severe learning disabilities. Inter-ictal cognitive function appears to be mediated by a combination of organic, circadian (sleep wake), clinical and pharmacological factors.
Stress affects cognition in a number of ways, acting rapidly via catecholamines and more slowly via glucocorticoids. Catecholamine actions involve beta adrenergic receptors and also availability of glucose, whereas glucocorticoids biphasically modulate synaptic plasticity over hours and also produce longer-term changes in dendritic structure that last for weeks. Prolonged exposure to stress leads to loss of neurons, particularly in the hippocampus. Recent evidence suggests that the glucocorticoid- and stress-related cognitive impairments involving declarative memory are probably related to the changes they effect in the hippocampus, whereas the stress-induced catecholamine effects on emotionally laden memories are postulated to involve structures such as the amgydala.
Sensory-motor and cognitive functioning was investigated in a group of 32 children treated with bone marrow transplantation (BMT), 1-6 years after treatment. Twenty-five of the patients had suffered from leukemia. The BMT procedure had involved a regimen of cytostatic drugs and, for leukemia patients, total body irradiation at a dose of 10 Gy, administered in one session. Cytostatic drugs and irradiation are known to be potentially neurotoxic, particularly when combined. The examination involved four neuropsychological tests of sensory-motor and cognitive functioning, as well as an age-appropriate intelligence test. For control the bone marrow donors (n = 32), siblings of the patients, were also investigated. A pronounced delay in motor development was found in four children, who had been treated with BMT including total body irradiation before 3 years of age. Patients between 3 and 11 years of age at BMT were at a slight disadvantage, compared to donors, on tasks involving perceptual and fine motor speed. In older patients no deficits were observed.
OBJECTIVE: To assess if and how demented patients' living conditions affect their level of functioning. DESIGN: A prospective concurrent control-study. SETTING: Sundsvall, an industrial community in the middle of Sweden. PARTICIPANTS: Forty-six demented patients in group-living (GL-group) and 62 controls (C-group). MAIN OUTCOME MEASURE: Cognitive function, ADL-capacity and behaviour were measured every third month during one year. RESULTS: Both groups deteriorated, but the decline was significantly slower in the GL-group regarding some ADL-functions, e.g. dressing and motor functions, whereas some behavioural disturbances were significantly more frequent in the GL-group. No differences were observed regarding the level of cognitive function. CONCLUSION: The living condition has small effects on cognitive function and ADL-capacity. The behavioural disturbances observed in GL should be the focus of future research.
The risk of hypoglycaemia and the resulting impairment in brain function are major factors preventing those with diabetes achieving normoglycaemia. The need to define these risks more precisely has prompted an increasing research effort to identify which aspects of cerebral function are particularly vulnerable and at which glucose level. Much of the evidence is inconsistent, reflecting not only the wide range of methods for measuring cognitive function and inducing hypoglycaemia, but also the inherent variability of the response. Nevertheless, the data suggest that those mental activities which are relatively undemanding are often unaffected at all levels of experimental hypoglycaemia while the performance of more complex tasks deteriorates at glucose concentrations of around 3 mmol l-1. The relative imprecision of cognitive testing is reflected in the debate which surrounds the pathogenesis of hypoglycaemia unawareness. There is some evidence that the glycaemic threshold for autonomic activation and symptoms can vary while the threshold for cognitive impairment is fixed. This has led to the hypothesis that hypoglycaemia unawareness arises when the autonomic response develops at a blood glucose below that for impaired cognition, thus preventing patients from recognizing or responding to their usual symptoms. However, contradictory data suggest that the threshold for cognitive impairment can alter in line with the autonomic response, a conclusion which falls to fit either the above hypothesis or the clinical description of hypoglycaemia unawareness. These differences may be methodological or relate to the relative imprecision of measurements of cognitive function. Resolution of these discrepancies may have to await the development of advanced technology such as high resolution MRI or PET scanning. In the meantime, progress could be made if all groups agreed on a limited range of cognitive function tests and used them in a standardized manner.
In recent years there has been an increased interest in understanding the role of somatostatin in the brain. This review summarizes the current knowledge of the anatomical distribution of somatostatin and its receptors, the receptor-coupling mechanisms and the somatostatinergic modulation of cognitive functions. Somatostatin is also highly concentrated in the extra-hypothalamic areas of the brain, including the frontal and parietal cortex and the hippocampus. At these locations somatostatin may play a fundamental role in the modulation of cognitive functions. Activation of somatostatin receptors in the brain results in an inhibition of adenylate cyclase enzyme activity, reduction in intracellular Ca2+ levels and hypopolarization of cells by inducing outward K+ currents. Biological studies on the effects of increased brain somatostatin showed a facilitation in learning behavioural tasks, while brain somatostatin depletion by cysteamine caused memory loss. These observations, along with the severe somatostatinergic neurotransmission impairment demonstrated in Alzheimer's patients, strongly suggest a fundamental role for somatostatin in the modulation of cognitive functions.
Event related P300 potentials as the electrophysiological substrate of cognitive functions, such as the stimulus processing time (P300 latencies) and visual attention capacity (P300 amplitudes) are suitable for the analysis of age-related changes in cognitive human brain functions. P300 investigations carried out in a total of 330 test subjects aged between 18 and 98 years, showed an overall slight prolongation of the P300 latencies by 10 ms for each decade, as well as a discrete reduction in the P300 amplitudes of 1 microV. To describe the relationship between the P300 parameters and chronological age, polynomial regression models are more suitable than linear functions. This means that in middle-age, P300 potentials change only slightly while, from about the age of 60 upwards, a noticeable acceleration in the P300 changes takes place. An interesting observation was the fact that the acceleration in the P300 latency increase occurred some 10 years earlier in women than in men, beginning in the early postmenopausal period. The polynomial course of the regression function for the age-dependence of P300 potentials might reflect the positive influence of socio-cultural factors on the aging of cognitive functions. The true extent of the age-related changes in cognitive functions, however, can be determined only with the aid of intra-individual longitudinal studies. This is of considerable importance for the early diagnosis of both metabolic and primarily degenerative encephalopathies.
The interactions among short stature, growth hormone (GH) and cognitive functions have been extensively studied so far. However, although it seems well established that short stature is associated with cognitive problems, little effort has been made to point out the presence of specific psychological effects related to the different forms of short stature. In 'short normal' children, the presence of a scholastic underachievement seems to suggest that short stature 'itself' might predispose these patients to some of their psychosocial difficulties. The higher incidence of academic failure, in presence of a normal intellectual functioning, has been attributed to environmental and psychosocial factors, including over-protective parents and low self-esteem resulting from the impact of short stature. These problems appear to be common also to other forms of short stature (such as Turner's syndrome) where, however, they are frequently associated with other specific deficits. The in vivo model which might allow, at least in part, better understanding of GH (per se)-dependent effects is represented by GH deficiency (GHD), in which, however, the specific role of GH on psychological functioning is frequently masked by the presence of associated hormonal deficiencies. Children with isolated GHD are reported to have specific educational deficits, in particular learning disability and attention-deficit disorders, which have been tentatively attributed to a compromised intellectual potential. The psychological effects of long-term GH treatment in children with GHD still remain controversial, with some retrospective studies describing a generally beneficial outcome. Since early experiences in school are closely related to success in adult life, the possible implications that GHD during childhood holds during adulthood have been recently considered. Although regional differences have been observed in subgroups of adults with GHD, it seems that these patients have normal cognitive functions and educational attainment, but are more likely to be unemployed (and unmarried) than members of the general population. In general, patients with GHD, who have been treated at centers where psychological counselling was an integral part of the treatment program, seem to be better adjusted in adult life. For these reasons, a multidisciplinary treatment approach could allow early detection of problems in academic achievement and psychosocial development in patients with short stature, being immediately able to provide the appropriate educational and counselling interventions.
To test the hypothesis that hypoglycemia unawareness is largely secondary to recurrent therapeutic hypoglycemia in IDDM, we assessed neuroendocrine and symptom responses and cognitive function in 8 patients with short-term IDDM (7 yr) and hypoglycemia unawareness. Patients were assessed during a stepped hypoglycemic clamp, before and after 2 wk and 3 mo of meticulous prevention of hypoglycemia, which resulted in a decreased frequency of hypoglycemia (0.49 +/- 0.05 to 0.045 +/- 0.03 episodes/patient-day) and an increase in HbA1c (5.8 +/- 0.3 to 6.9 +/- 0.2%) (P < 0.05). We also studied 12 nondiabetic volunteer subjects. At baseline, lower than normal symptom and neuroendocrine responses occurred at lower than normal plasma glucose, and cognitive function deteriorated only marginally during hypoglycemia. After 2 wk of hypoglycemia prevention, the magnitude of symptom and neuroendocrine responses (with the exception of glucagon and norepinephrine) nearly normalized, and cognitive function deteriorated at the same glycemic threshold and to the same extent as in nondiabetic volunteer subjects. At 3 mo, the glycemic thresholds of symptom and neuroendocrine responses normalized, and surprisingly, some of the responses of glucagon recovered. We concluded that hypoglycemia unawareness in IDDM is largely reversible and that intensive insulin therapy and a program of intensive education may substantially prevent hypoglycemia and at the same time maintain the glycemic targets of intensive insulin therapy, at least in patients with IDDM of short duration.
To enhance the awareness of physicians treating whiplash patients, findings from previous research regarding cognitive functioning of these patients are discussed and recommendations for assessment provided. Cognitive disturbances (i.e., deficient attentional functioning and impairment of memory) are frequent complaints in patients after whiplash injury. However, few prospective studies of nonselected patients have been performed. These studies indicate that impaired cognitive functioning relates either to trauma-induced somatic symptoms (i.e., pain) or psychologic symptoms resulting from problems adjusting to trauma-related somatic symptoms. Accordingly, cognitive disturbances after whiplash show a fair rate of recovery, which parallels recovery from trauma-related somatic symptoms. Current research does not indicate disturbances in higher cognitive functions after whiplash.