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Neurocognitive abilities were measured in 14 morbidly obese children, five of whom had obstructive sleep apnea as determined by polysomnography. As in adults, children with obstructive sleep apnea had deficits in learning, memory, and vocabulary. Moreover, apneic/hypopneic events were inversely related to memory and learning performance among the entire sample.
The possibility of a functional interaction between the amygdala and the ventral hippocampus on learning of a conditioned avoidance response when both brain structures are chemically stimulated with histamine was studied in rats. Adult male rats were stereotaxically implanted under ether anaesthesia with guide cannulae into the baso-lateral amygdala and the ventral hippocampus. Seventy-two hours after the implant, rats were microinjected with: 1 microl saline solution into both structures (SAL+SAL group); 9 or 90 nmol doses of histamine into both structures (HA+HA groups); 9 or 90 nmol histamine into the hippocampus and saline into the amygdala (HA+SAL groups); saline into the hippocampus and 9 or 90 nmol histamine into the amygdala (SAL+HA groups). Five minutes following the injection, rats were subjected to a learning task in eight consecutive trials, consisting of avoiding an electric shock applied to the feet of the animal when an ultrasonic tone of 40 kHz is on for 30 s. Results show that histamine applied in any dose into both amygdala and hippocampus was able to significantly increase the escape latency and impair the efficacy of learning. Chemical stimulation with histamine of only hippocampus or amygdala affected selectively the escape latency. Results suggest that there is a functional interaction between histamine-sensitive neurons of the amygdala and hippocampus during processing of a learning task.
Nurse educators must keep abreast of contemporary learning theory so that their teaching reflects current ideas of best practice. In view of this, it is important to report on recent developments in the field of learning. Of particular significance is the fact that behaviouristic explanations of learning have largely been replaced with cognitive perspectives which emphasise the complexity of the learning process. Memory, learning, problem solving and expertise have all been investigated from a cognitive stance. The highlights of this work include, firstly, the portrayal of learning as an active, constructivist, cumulative and self-regulated process leading to the development of understanding and complex, skilled performance. Secondly, the highly important role played by knowledge in learning has been identified and described. Lastly, novice-expert differences in problem solving and academic and practical performance more generally, are well understood as a result of investigations of expertise in many domains. In this paper, these three significant perspectives from cognitive psychology will be examined and their implications for the education of undergraduate nurses described. Developments in the field of nursing that reflect or challenge a cognitive outlook are also identified.
Cognitive impairment is common in multiple sclerosis (MS), yet patients seen in MS clinics and neurologic practices are not routinely assessed neuropsychologically. In part, poor utilization of NP services may be attributed to a lack of consensus among neuropsychologists regarding the optimal approach for evaluating MS patients. An expert panel composed of neuropsychologists and psychologists from the United States, Canada, United Kingdom, and Australia was convened by the Consortium of MS Centers (CMSC) in April, 2001. Our objectives were to: (a) propose a minimal neuropsychological (NP) examination for clinical monitoring of MS patients and research, and (b) identify strategies for improving NP assessment of MS patients in the future. The panel reviewed pertinent literature on MS-related cognitive dysfunction, considered psychometric factors relevant to NP assessment, defined the purpose and optimal characteristics of a minimal NP examination in MS, and rated the psychometric and practical properties of 36 candidate NP measures based on available literature. A 90-minute NP battery, the Minimal Assessment of Cognitive Function in MS (MACFIMS), emerged from this discussion. The MACFIMS is composed of seven neuropsychological tests, covering five cognitive domains commonly impaired in MS (processing speed/working memory, learning and memory, executive function, visual-spatial processing, and word retrieval). It is supplemented by a measure of estimated premorbid cognitive ability. Recommendations for assessing other factors that may potentially confound interpretation of NP data (e.g., visual/sensory/motor impairment, fatigue, and depression) are offered, as well as strategies for improving NP assessment of MS patients in the future.
Impairment of language function (aphasia) is one of the most common neurological symptoms after stroke. Approximately one in every three patients who have an acute stroke will suffer from aphasia. The estimated incidence and prevalence of stroke in Western Europe is 140 and 800 per 100,000 of the population. Aphasia often results in significant disability and handicap. It is a major obstacle for patients to live independently in the community. When recovery from aphasia occurs, it is usually incomplete and patients are rarely able to return to full employment and other social activities. Currently, the main treatment for aphasia is conventional speech and language therapy. However, the effectiveness of this intervention has not been conclusively demonstrated and empirical observations suggest that spontaneous biological recovery may explain most of the improvement in language function that occurs in aphasics. The generally poor prognosis of the severe forms of poststroke language impairment (Broca, Wernicke and global aphasia), coupled with the limited effectiveness of conventional speech and language therapy has stimulated the search for other treatments that may be used in conjunction with speech and language therapy, including the use of various drugs. Dopamine agonists, piracetam (Nootropil), amphetamines, and more recently donepezil (Aricept), have been used in the treatment of aphasia in both the acute and chronic phase. The justification for the use of drugs in the treatment of aphasia is based on two types of evidence. Some drugs, such as dextroamphetamine (Dexedrine), improve attention span and enhance learning and memory. Learning is an essential mechanism for the acquisition of new motor and cognitive skills, and hence, for recovery from aphasia. Second, laboratory and clinical data suggest that drug treatment may partially restore the metabolic function in the ischemic zone that surrounds the brain lesion and also has a neuroprotective effect following acute brain damage. An example of this is the nootropic agent piracetam. Extensive animal studies have demonstrated the beneficial effects of this and other drugs on neural plasticity, but data on humans are still sparse. This review provides a critical analysis of the current evidence of the effectiveness of these drugs in the treatment of acute and chronic aphasia.
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Connectionist modeling is one approach to understanding human intelligence using simulated networks of neuron-like processing units. In this article, we report on recent progress in connectionist models that simulate empirical data of higher-level cognitive processes, these being memory, learning, language, thinking, cognitive development, and social cognition. We also review and summarize the advantages and disadvantages of these connectionist models. The computational framework of connectionist modeling has the potential to integrate specialized psychological findings of different areas using the same architectures and local functions of units and connections, inspired from neuroscience. In particular, the problems of dealing with structured information in distributed form, and doing tasks that require variable binding in connectionist networks are discussed from several different perspectives. As one possible solution to treat systematic mental representations properly, the symbolic connectionist model, which is a hybrid approach using symbolic representations and connectionist architectures, is explained. We argue that connectionist computer simulation offers significant benefits for today's psychological researches, and that connectionist modeling is likely to have an important influence on future studies.
INTRODUCTION AND METHOD: The cellular mechanisms that regulate neuronal excitability and the propagation of electrical signals in the dendrites of pyramidal neurons are incompletely understood and of key functional and pathological importance. The capacity of dendrites to actively propagate action potentials is vital in processes related to memory and learning. The deregulation of dendritic excitability may also contribute to epilepsy. The contributions of ionic conductances that regulate neuronal excitability and dendritic signal propagation have been analyzed using the in vitro hippocampal slice technique and recordings of transmembrane voltage and current of CA1 pyramidal neurons. One of these ionic currents is the slow calcium activated potassium current that generates the slow spike after hyperpolarization. CONCLUSION: The dendritic localization of this current and its role in the control and propagation of electrical signals provide a key subcellular mechanisms for the control of the dendro somatic spread of synaptic signals and spike backpropagation, cellular processes closely linked with learning, memory and epilepsy.
Traumatic amnesia is a good index predictive of the disablement due sequelae of cranial injuries. The residual memory deficit, correlated with the return to work, mainly affects long-term memory, learning, verbal memory and sensitivity to interferences. The most relevant tests are Rey's 15 words--and particularly their retrieval at 30 minutes--and the verbal fluency test, but the changes in memory observed in the patient's daily life must also be evaluated. Rehabilitation tends to rely on the overall management of intellectual and behavioural disorders, as part of programmes that are specific to subjects with cranial injury.
Unmodified stroma-free hemoglobin has been found to produce neurotoxicity and behavioral impairment in rats. In contrast, a recent assessment of a modified (diaspirin alpha-alpha cross-linked) hemoglobin (HbXL) solution found normal memory, learning, and brain histology after infusion of a clinically relevant dose of a 14% HbXL solution. The current study examined this potential resuscitation fluid for evidence of neurobehavioral toxicity under clinical conditions. Rats were trained to complete a water alley maze, had 50% of their total blood volume (30 ml/kg) withdrawn, were resuscitated with 14% HbXL solution (45 ml/kg), Ringer's lactate (60 ml/kg), or autologous shed blood, and were subsequently retested in the water maze. Rats resuscitated with HbXL or autologous shed blood survived resuscitation, while 20% of those resuscitated with Ringer's lactate died during treatment. No significant performance degradation was observed in the HbXL rats following resuscitation, and no brain pathology was observed at necropsy 10 days after treatment. Ischemic brain lesions were observed in three (25%) of the surviving rats resuscitated with Ringer's lactate solution. Renal tubule regeneration indicative of an earlier insult was observed in animals from all three groups. A significant correlation between the total pathology in the five organs examined and maze errors was observed (p less than 0.001). The survival, maze performance, and histology results suggest that resuscitation with 14% HbXL solution does not cause neurotoxicity, as assessed in this lethal hemorrhage model.
Fifty-five studies of cognitive side effects of beta-blockers were reviewed. Many of the studies were limited by small sample size, use of drugs out of the range of normal administration, failure to control for known confounders for neuropsychological evaluation, or lack of a crossover design. As a result, one needs caution in drawing conclusions on this topic. Nevertheless, given the widespread use of beta-blockers and the frequent allegations about their relative side effect profiles, it is appropriate to summarize the results of these disparate studies. Across all beta-blockers and all cognitive domains, the drugs led to improved functioning in 16% of observations and worsened functioning in 17%, with no significant effect in the rest. Memory, learning, and abstraction have been studied less frequently. The perceptual motor cognitive domain was the most widely studied and was frequently affected by these drugs. There was no consistent evidence of a trend for lipophilic drugs to impair this domain more than lipophobic drugs. There is some evidence that these drugs have a positive effect on complex task performance. The drugs also seem to increase sedation; however, in these studies there was no evidence for a differential effect across lipophilic vs lipophobic drugs.
Physical and mental effects of a single oral dose of ephedrine (ephedrine HCl 30 or 40 mg), fenfluramine (fenfluramine HCl 15 or 20 mg), phentermine (7.5 or 11.25 mg) and prolintane (prolintane HCl 10 or 20 mg) were compared in a double-blind placebo-controlled study. Each group consisted of 16-43 healthy volunteer medical students. The subjects fasted for at least 3 hr before drug administration and further until the end of the experiment. All the parameters were measured just prior to giving the drug, and 1.5 hr and 2.5 hr afterwards. Ephedrine significantly increased systolic blood pressure (p less than 0.05) and heart rate (p less than 0.01), whereas the other sympathomimetics affected these parameters only slightly or negligibly. None of the drugs markedly changed the tapping rate of the dominant hand. Mental activity was evaluated with a self-rating check list consisting of various mental modalities. None of the sympathomimetics significantly modified the mental activity. Memory, learning and concentration ability were evaluated with sign recording and digit span tests. In the digit span test no changes were obtained. In the sign recording test (for 3 min), phentermine increased significantly the recording score at both 1.5 hr (p less than 0.05) and 2.5 hr (p less than 0.005), and prolintane at 2.5 hr (p less than 0.05) after drug administration. The results suggest that in the doses given, which are commonly used in medical practice, ephedrine has the most pronounced cardiovascular effects, while phentermine and prolintane seem to be most active in the performance of some mental tasks.
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In the present study, activity of salt soluble (SS) G1 and detergent soluble (DS) G4 molecular isoforms of acetylcholinesterase (AChE) has been investigated in rat brain areas in trained (learned), scopolamine (amnesic) and Tacrine (anti-dementic) treated rats to find out their role in learning and memory functions. AChE was estimated spectrophotometrically at 412 nm in rat brain areas. Isolation and partial purification of molecular isoforms G1 and G4 of AChE was done by gel filtration chromatography. Passive avoidance was used to test learning and memory functions. AChE activity was altered in both the fractions SS and DS of different brain areas following passive avoidance in control, scopolamine treated, tacrine treated and tacrine treatment in scopolamine pretreated rats. The peak AChE activity obtained in the DS (fraction 9) and the SS (fraction 13) fraction following gel filtration chromatography. On the basis of molecular weight fraction 9 (DS) and 13 (SS) represent the G4 and G1, respectively. The pattern of changes in the AChE activity of G1 isoform (fraction 13 of SS) and G4 isoform (fraction 9 of DS) in brain areas were similar to those of SS and DS fraction, respectively. In hippocampus, AChE activity in the fraction G1 isoform (fraction 13 of SS) was decreased only in tacrine treated rats but AChE activity in the G4 isoform (fraction 9 of DS) was decreased in both trained and tacrine treated rats. Changes in activity of G4 isoform of AChE in hippocampus could be correlated with passive avoidance learning, scopolamine induced deficit in passive avoidance and reversal of scopolamine deficit by tacrine.
This study examined intertask consistency on the Wide Range Assessment of Memory and Learning (WRAML), using two age cohorts of children. Eighty-one neurologically impaired children and 76 matched (i.e., age, gender, race) controls were separated into two age groups, 5- to 9- and 10- to 14-year-olds. Performance on four subtests from the WRAML Memory Screening Index were examined. For the older neurologic sample, all six intertask correlations were significant (mean r = .58) while only three of the six correlation coefficients were significant among the younger neurologic group (mean r = .26). In contrast, only three of the six intertask coefficients were statistically significant in both the younger and older controls. A possible explanation for these divergent findings and clinical implications of intertask variability on memory measures are discussed.
The present study aimed to examine whether the aged mice with naturally occurring cognitive deficits in learning and memory would benefit from supplementation of choline acetyltransferase (ChAT), the biosynthetic enzyme for neurotransmitter acetylcholine. Delivered by protein transduction domain (PTD), ChAT could pass through the blood-brain barrier, enter the neurons, interact with heat shock protein 70kDa, and retain enzyme activity. In behavior tests, PTD-ChAT given to the aged and memory-deficient mice almost completely reversed the behavioral changes, such as impairment of memory retention in the step-through test (an index of long-term memory) and prolonged swimming time in water maze test (an index of spatial recognition memory). The results suggest a novel and potential therapeutic use of PTD-ChAT in the age-related cognitive deficits.
The facilitative effects of early environmental enrichment and perinatal choline chloride dietary supplementation on adult rat spatial learning and memory were examined using delayed match-to-place (DMTP) and delayed spatial win-shift (DSWSh) discrimination tasks. Animals were either maintained in a standard lighted colony (LR) or were given supplementary exposure to a complex environment (CR) for 2-h daily from 20 to 90 days of age. In each case, half the animals were exposed to the choline supplementation both prenatally (through the diet of pregnant rats) and postnatally (subcutaneous injection) for 24 days. In the first experiment, all 90-day-old rats were given trials in which they first found a hidden platform in a Morris water maze (MWM) in a particular location (acquisition trial), and then were required to remember that position 10 min later (test trial). Both environmental enrichment and early diet had significant impacts on performance. CR animals, given neonatal choline pretreatment, found the platform on test trials significantly faster than any of the other groups. CR animals exposed to the control saline diet showed better retention than did the LR animals given the early choline diet, which in turn, were superior to animals given neither environmental enrichment nor choline. All animals were subsequently tested in the same paradigm immediately following atropine sulfate injections. The atropine eliminated the difference between the four groups of animals on test trials. In a second experiment, both CR, and neonatal choline treatment facilitated performance on a DSWSh radial arm maze (RAM) task previously found to be sensitive to hippocampal and/or medial prefrontal lesions. Performance differences between groups were facilitated by the anticholinesterase drug, tacrine and attenuated by the cholinergic antagonist, Atropine. The present study extends the descriptions of long-term functional enhancements produced by perinatal choline supplementation and environmental enrichment and to relate these effects to common modifications to targets of cholinergic basal forebrain systems.
Epigenetic modifications such as histone methylation permit change in chromatin structure without accompanying change in the underlying genomic sequence. A number of studies in animal models have shown that dysregulation of various components of the epigenetic machinery causes cognitive deficits at the behavioral level, suggesting that proper epigenetic control is necessary for the fundamental processes of learning and memory. Histone H3 lysine K4 (H3K4) methylation comprises one component of such epigenetic control, and global levels of this mark are increased in the hippocampus during memory formation. Modifiers of H3K4 methylation are needed for memory formation, shown through animal studies, and many of the same modifiers are mutated in human cognitive diseases. Indeed, all of the known H3K4 methyltransferases and four of the known six H3K4 demethylases have been associated with impaired cognition in a neurologic or psychiatric disorder. Cognitive impairment in such patients often manifests as intellectual disability, consistent with a role for H3K4 methylation in learning and memory. As a modification quintessentially, but not exclusively, associated with transcriptional activity, H3K4 methylation provides unique insights into the regulatory complexity of writing, reading, and erasing chromatin marks within an activated neuron. The following review will discuss H3K4 methylation and connect it to transcriptional events required for learning and memory within the developed nervous system. This will include an initial discussion of the most recent advances in the developing methodology to analyze H3K4 methylation, namely mass spectrometry and deep sequencing, as well as how these methods can be applied to more deeply understand the biology of this mark in the brain. We will then introduce the core enzymatic machinery mediating addition and removal of H3K4 methylation marks and the resulting epigenetic signatures of these marks throughout the neuronal genome. We next foray into the brain, discussing changes in H3K4 methylation marks within the hippocampus during memory formation and retrieval, as well as the behavioral correlates of H3K4 methyltransferase deficiency in this region. Finally, we discuss the human cognitive diseases connected to each H3K4 methylation modulator and summarize advances in developing drugs to target them.