Specific Learning Deficits Research Articles

Approaches to medical student remediation after a comprehensive clinical skills examination

Most US medical schools conduct comprehensive clinical skills assessments during Years 3 and 4. This study explores strategies used to identify and remediate students who perform poorly on these assessments. In the academic year 2005-06, we conducted 33 semi-structured interviews with individuals responsible for standard setting in and remediation after their schools' comprehensive clinical skills assessments. We coded interviews to identify major themes. Prior to remediation, some schools employed a 'verification' step to ensure the accuracy of the failing score or need for remediation. Participants described a remediation process that included some or all of 3 steps. Firstly, students' specific learning deficits were diagnosed. Next, students participated in remedial activities such as performance review sessions or practice with standardised or actual patients. Lastly, students were re-tested, usually with a shorter, more formative examination. All participants reported using a diagnostic step, most offered or required remedial activities and many re-tested, although schools varied in the emphasis placed on each step. Many participants cited the individualised attention students received from remediation faculty staff as a strength of their approach, although they raised concerns about the substantial time demands placed on remediation faculty. Most respondents reported some dissatisfaction with their school's remediation process, particularly uncertainty about efficacy or rigour. Schools vary in the intensity and scope of remediation offered to students who perform poorly on clinical skills assessments. Although many schools invest significant resources in remediation, the effect of these efforts on students' subsequent clinical performance is unknown.

Cancer chemotherapy impairs contextual but not cue-specific fear memory

This study examined the effects of a standard breast cancer chemotherapeutic protocol on learning and memory in rats. Ovariectomized rats were treated once a week for 3 weeks with a combination of cyclophosphamide and doxorubicin prior to training in a classical fear conditioning task. Training took place 1 week after the final treatment. During the training session, an auditory stimulus (a tone) was paired with a mild foot-shock. The resulting conditioned fear to the tone (cue-specific fear) and to the training environment (contextual fear) was measured in subsequent test sessions. Chemotherapy did not affect the acquisition of the conditioned response (freezing) during the training session or the expression of fear during the tone test session. In contrast, rats treated with cyclophosphamide and doxorubicin exhibited decreased freezing during the context test session, suggestive of a specific deficit in hippocampal-related learning and memory. Together, these data indicate that administration of cyclophosphamide and doxorubicin may have toxic effects on the hippocampus and results in specific learning deficits shortly after treatment has ended.

Virus infection causes specific learning deficits in honeybee foragers

In both mammals and invertebrates, virus infections can impair a broad spectrum of physiological functions including learning and memory formation. In contrast to the knowledge on the conserved mechanisms underlying learning, the effects of virus infection on different aspects of learning are barely known. We use the honeybee (Apis mellifera), a well-established model system for studying learning, to investigate the impact of deformed wing virus (DWV) on learning. Injection of DWV into the haemolymph of forager leads to a RT-PCR detectable DWV signal after 3 days. The detailed behavioural analysis of DWV-infected honeybees shows an increased responsiveness to water and low sucrose concentrations, an impaired associative learning and memory formation, but intact non-associative learning like sensitization and habituation. This contradicts all present studies in non-infected bees, where increased sucrose responsiveness is linked to improved associative learning and to changes in non-associative learning. Thus, DWV seems to interfere with molecular mechanism of learning by yet unknown processes that may include viral effects on the immune system and on gene expression.

New potential leads in the biology and treatment of attention deficit-hyperactivity disorder

This review highlights recent neuroimaging and genetic studies of attention deficit-hyperactivity disorder that may inform biologically targeted interventions and treatments. The findings suggest that attention deficit-hyperactivity disorder is characterized by specific learning and cognitive deficits due to abnormalities in dopamine-rich prefrontal circuitry, of genetic or environmental origins. In addition to prefrontal cortical areas, the basal ganglia, cerebellum, and parietal cortex have been implicated in the condition. These regions are part of unique circuits that project both to and from the prefrontal cortex, thus providing a means for signaling prefrontal regions when top-down control of behavior needs to be imposed. Ineffective signaling of control systems by any one of these regions can lead to poor regulation of behavior. Likewise, intact signaling but inefficient top-down control could result in poor regulation of behavior. Identification of which cognitive and neural processes are altered in attention deficit-hyperactivity disorder and acknowledgement of different casuses of the condition will lead to more individualized, biologically targeted interventions and treatments. This new direction in research and treatment has occurred as the result of a shift from diagnosis as a phenotype, to refined phenotypes of core cognitive deficits that can be more easily tied to the underlying biology.

Learning Styles—Making Too Many “Wrong Mistakes”: A Response to Castro and Peck

The notion that attention to students' learning styles is useful for classroom teaching has been proposed by educators for more than 40 years (Willingham, 2005). The learning styles concept is based on the premise that in individual processing capabilities create significantly different requirements in learning environments. Once identified, advocates argue, it becomes possible to improve the academic achievement of each individual by matching instruction and the learning environment with their individual (Stahl & Kuhn, 1995, p. 396). Over the years, a number of learning styles models have been proposed but most hold that learners exhibit differences in information processing (e.g., visual vs. auditory or global vs. analytic learners), or vary in dimensions such as their environmental preferences, physiological characteristics, and sociological preferences (see reviews by Coffield, Moseley, Hall, & Ecclestone, 2004; Keefe & Farrell, 1990; O'Neil, 1990; Stahl, 1999).' Despite their differences, each of the models proposes the matching of instruction with a student's style (preference) for learning. In a recent article published in this journal, Castro and Peck (2005) examined whether a particular learning style is favored by students enrolled in regular and modified sections of foreign language classes. They administered the KoIb Learning Style Inventory (LSI) (1993) to students enrolled in modified Spanish classes who had encountered serious difficulties with foreign language learning and to students without a history of foreign language learning problems enrolled in regular sections of Spanish at a large university in the United States. The authors reported that regardless of any specific learning deficit, students' preferred styles either helped or hindered their performance in the foreign language classroom. Castro and Peck suggested that having knowledge of college foreign language learners' preferred styles is important for both the instructors and students. In my view, the emphasis on examining students' learning styles in relation to foreign language learning is unfounded. Using the example of Castro and Peck's article, I respond to styles advocates by illustrating the types of problems with the learning styles concept that they leave unstated in their work. Most notably, styles advocates fail to take into account: (a) the preponderance of empirical evidence since the 1970s which has shown that learning styles models have a host of conceptual and empirical problems and that matching students' preferred styles with a compatible teaching method does not improve academic achievement; (b) research studies which have found that learning styles instruments, including the LSI, lack appropriate psychometric properties; and (c) the evidence that shows that students' aptitude (ability) is confused with their style (preference).2 In their study, Castro and Peck also make unsupported assumptions about the use of the Modern Language Aptitude Test (MLAT) and about the importance of styles for foreign language learning. In my response, I focus on the aforementioned problems. Problems with the Learning Styles Concept and Styles Instruction In his review of learning styles models, Stahl (1999) acknowledged that the idea of all children learning differently seems intuitive and plausible. In his work, he found that the large majority of teachers believe it is appropriate to take learning styles into account and that tailoring instruction to individual styles enables students to learn more easily and effectively. However, a preponderance of evidence over time has found that the learning styles concept has numerous flaws. In retrospect, there were special education researchers who early on cited problems with the learning styles concept (e.g., see Hammill & Larsen, 1974; Mann, 1970; Mann & Goodman, 1975). Originally, the notion of learning styles was embraced by professionals in the learning disabilities (LD) field (see Mann, 1971). …

Differential effects of age on sequence learning and sensorimotor adaptation

Although many studies have documented declines in the ability of the elderly to learn new manual motor skills, studies have not directly compared the capacity of older adults to learn sequences versus adapt to sensorimotor perturbations within the context of the same task paradigm, despite differences in the underlying neural mechanisms and strategic processes supporting the two types of learning. The purpose of the current study was to exploit these task differences in an effort to determine whether aging results in a generalized or more specific skill learning deficit. Groups of young and older adult subjects learned to make a sequence of actions, adapted to one of two visuomotor rotations, or adapted to an altered gain of display, all while performing the same basic manual joystick aiming task. While the older adults exhibited normal sequence learning in comparison to the young adults, they exhibited impairments in all three of the adaptation tasks. These deficits in adaptation for the older adults were associated with hypometric movements and reduced velocity modulation in comparison to that seen in the younger adults. These data suggest that older adults may have greater difficulty with learning cerebellar-mediated motor skills.

Cognitive disruption and altered hippocampus synaptic function in Reelin haploinsufficient mice

The heterozygote reeler mouse (HRM) shows many neuroanatomical and biochemical features that are also present in some human cognitive disorders, such as schizophrenia. In the present study, hippocampal dependent plasticity and cognitive function of the HRM were characterized in detail in an attempt to reveal phenotypic functional differences that result from Reelin haploinsufficiency. The HRM and wild type mice show similar levels of overall activity, coordination, thermal nociception, startle responses, and anxiety-like behavior. In addition, both genotypes show similar shock threshold, identical cued freezing behavior and comparable spatial learning in Morris water maze tasks. However, a significant reduction in contextual fear conditioned learning was observed in the HRM. Electrophysiological studies in hippocampal CA1 synapses revealed a plethora of differences between genotypes. The HRM exhibits reduced field excitatory postsynaptic potentials in responses to similar synaptic inputs, lowered paired pulse facilitation ratio and impaired long-term depression and tetanus-induced long-term potentiation (LTP). Also, deficits were detected in LTP elicited by theta burst stimulation or by a whole cell pairing protocol. These physiologic differences could not be accounted for by changes in the overall amount of glutamate receptor subunits. In addition, it was determined that network-driven excitatory and inhibitory activities recorded in CA1 pyramidal neurons showed that the HRM had comparable amplitude and frequency of spontaneous excitatory postsynaptic currents, but a marked reduction in spontaneous inhibitory postsynaptic currents. Thus, the HRM exhibits a specific hippocampal-dependent learning deficit accompanied with a pronounced impairment of hippocampal plasticity and functional inhibitory innervation.

Glucocorticoids, 11beta-HSD1 and cognitive function with ageing

Cumulative exposure to high glucocorticoid levels is a major factor advanced to explain individual decline in cognitive function with ageing. Current manipulations to maintain low circulating glucocorticoid levels throughout life (adrenalectomy with low dose corticosterone replacement, neonatal handling), though effective in preventing the emergence of memory deficits with age in rodent models, are however not clinically applicable. 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) catalyses the intracellular regeneration of active glucocorticoids from circulating inert 11-keto steroids thus amplifying glucocorticoid levels within specific target cells. In primary hippocampal neurons in vitro, inhibition of 11beta-HSD1 attenuates glucocorticoid-associated neurotoxicity. To determine the importance of 11beta-HSD1 in the ageing brain in vivo, we examined the impact of enzyme loss on hippocampal function using transgenic mice lacking expression of 11beta-HSD1. Wildtype mice develop elevated plasma corticosterone levels with age that correlated with hippocampal specific learning deficits in the watermaze. In contrast, despite similar elevated plasma corticosterone levels, aged 11beta-HSD1 knockout mice show significantly better learning than age-matched wildtype controls; this implicates lower intracellular corticosterone levels through the lack of 11-dehydrocorticosterone re-activation. Consistent with this, aged 11beta-HSD1 knockout mice show lower hippocampal tissue corticosterone levels than in wildtype controls. At the cellular level, enhanced hippocampal long-term potentiation in the CA1 region of aged 11beta-HSD1 knockout mice may, in part, underlie the improved cognitive function.

Learning Styles and Foreign Language Learning Difficulties

Abstract: In order to identify what other elements besides linguistic deficits could be playing a role in foreign language learning difficulties, the Kolb Learning Styles Inventory was administered to students enrolled in regular and modified Spanish classes at a major U.S. university. Preliminary results gathered as part of a longitudinal study on learning styles and foreign language learning difficulties indicate that regardless of any specific language learning deficit or difficulty, a student's preferred learning style can hinder or help success in the foreign language classroom. Findings from this study also indicate that having access to information about the preferred learning styles of the majority of students enrolled in beginning foreign language classes at the college level will be of great importance for researchers, instructors, and students alike.

Organization of cortico-hippocampal networks in rats related to learning and memory

Declarative memory is largely mediated by neuronal networks in the medial temporal lobe/(para)hippocampal system, whereas executive functions and attention strongly depend on the circuitry of the prefrontal lobe. There is convincing evidence that the two cortical systems function as complementary systems in normal cognition, including learning and memory, and that disruption of the interplay between the two lead to profound deficits. On the basis of our own experimental anatomical data in the rat, we suggest that this interplay is mediated by at least three direct and indirect parallel pathways. The first one makes use of direct projections from the hippocampal formation to the prefrontal cortex (PFC), as well as parallel indirect routes through the parahippocampal region. The second pathway comprises the connections of both domains with intrinsically connected parts of the posterior and anterior cingular cortices. Finally, the strong and rather specific reciprocal connections with certain midline and intralaminar thalamic nuclei form a third pathway for hippocampal–prefrontal systems to interact. Lesions disrupting any of these three routes lead to specific learning and memory deficits both in experimental animals as well as in humans, supporting the functional relevance of each of these pathways.

Learning and Memory Deficits in Notch Mutant Mice

Notch is a critical component of evolutionarily conserved signaling mechanisms that regulate development [1] and may contribute to plasticity-related processes, including changes in neurite structure [2] and maintenance of neural stem cells [3]. Deficits in the Notch pathway are responsible for Alagille [4] and Cadasil syndromes [5], which are associated with mental retardation and dementia. Additionally, in postmitotic neurons, Notch proteins interact with presenilins [6-9] and with β-amyloid precursor protein [10] and could therefore have a role in the memory deficits associated with familial and sporadic Alzheimer's disease. To test if alterations in Notch signaling can lead to learning and memory deficits, we studied mice with mutations in this pathway. Here, we show that null heterozygous mutations in Notch1 result in deficits in spatial learning and memory without affecting other forms of learning, motor control, or exploratory activity. We also show that null heterozygous mutations in the downstream cofactor RBP-J result in similarly specific spatial learning and memory deficits. These data indicate that a constitutive decrease in Notch signaling can result in specific learning and memory deficits and suggest that abnormalities in Notch-dependent transcription may contribute to the cognitive deficits associated with Alzheimer's disease and Alagille and Cadasil syndromes.

Specific spatial learning deficits become severe with age in beta -amyloid precursor protein transgenic mice that harbor diffuse beta -amyloid deposits but do not form plaques.

Memory impairment progressing to dementia is the main clinical symptom of Alzheimer's disease (AD). AD is characterized histologically by the presence of beta-amyloid (Abeta) plaques and neurofibrillary tangles in specific brain regions. Although Abeta derived from the Abeta precursor protein (beta-APP) is believed to play a central etiological role in AD, it is not clear whether soluble and/or fibrillar forms are responsible for the memory deficit. We have generated and previously described mice expressing human wild-type beta-APP(751) isoform in neurons. These transgenic mice recapitulate early histopathological features of AD and form Abeta deposits but no plaques. Here we describe a specific and progressive learning and memory impairment in these animals. In the Morris water maze, a spatial memory task sensitive to hippocampal damage, one pedigree already showed significant differences in acquisition in 3-month-old mice that increased in severity with age and were expressed clearly in 6-month- and 2-year-old animals. The second transgenic pedigree displayed a milder impairment with a later age of onset. Performance deficits significantly decreased during the 6 days of training in young but not in aged transgenic animals. Both pedigrees of the transgenic mice differed from wild-type mice by less expressed increase of escape latencies after the platform position had been changed in the reversal experiment and by failure to prefer the goal quadrant in probe trials. Both pedigrees performed at wild-type level in a number of other tests (open field exploration and passive and active place avoidance). The results suggest that plaque formation is not a necessary condition for the neuronal beta-APP(751) transgene-induced memory impairment, which may be caused by beta-APP overexpression, isoform misexpression, or elevated soluble Abeta.

Prenatal phenytoin exposure and spatial navigation in offspring: effects on reference and working memory and on discrimination learning.

Previous research has shown that rats exposed to phenytoin (PHT) in utero demonstrate abnormal circling, decreased learning, hyperactivity, and delayed air righting reflex development. The effects of prenatal PHT on offspring learning have been found on multiple-T mazes (Biel and Cincinnati types) and on spatial navigation (Morris maze). However, the specificity of the latter effects is unknown. Herein, we tested the effects of prenatal PHT in a Morris maze using six different procedures: cued versus spatial reference memory-based learning, cued versus spatial working memory-based learning, and cued versus spatial discrimination learning. PHT-exposed offspring showed increased preweaning mortality, growth reduction, and abnormal circling as noted in previous studies. PHT offspring were separated into those exhibiting circling and those not. PHT noncircling offspring demonstrated impaired reference memory-based spatial learning (acquisition and reversal), but no other effects. By contrast, PHT circling offspring demonstrated not only impaired reference memory-based spatial learning, but also impaired cued platform learning, impaired spatial discrimination, and impaired working memory-based learning. These data confirm that prenatal PHT induces a specific reference memory-based spatial learning deficit even in asymptomatic (noncircling) offspring that is distinct from the impairment induced in littermates exhibiting the circling impairment.

Decreased Odor Avoidance after Electric Shock inDrosophilaMutants Biases Learning and Memory Tests

The Drosophila mutants amnesiac, dunce (dnc), and rutabaga were isolated after associative conditioning tests, during which animals were trained to associate the presence of an odor with that of electric shocks (ES). In the absence of conditioning, the odor avoidance (OA) of these mutants was shown to be normal, indicating that their poor associative conditioning performance was attributable to specific learning or memory deficits. However, I show that the OA of the mutants is greatly decreased after their exposure to ES. This effect can last for hours. These results strongly suggest that part of the defect displayed by these mutants in associative conditioning tests does not correspond to a learning or memory deficit but might arise from abnormal sensitivity to stressful stimuli. I looked at the OA after ES of two previously characterized dnc mutants. Df(1)N79f specifically decreases Dnc expression in the mushroom bodies, leading to a normal level of learning but decreased memory. Df(1)N79f mutants displayed a normal OA after ES. Df(1)N64j15 affects the entire brain expression of Dnc, leading to decreased learning and memory. Df(1)N64j15 animals showed a strong decrease of their OA after ES. Thus, the lack of Dnc "general" expression is most likely responsible for the OA defect, which would be responsible for the apparent learning defect after conditioning. In contrast, the Dnc phosphodiesterase accumulated in the mushroom bodies would be involved specifically in memory formation.

Primidone-induced embryolethality and DRL deficits in surviving offspring.

Pregnant Sprague-Dawley rats were administered primidone (PRM) by oral gavage on gestation days 8-20 in doses of 0 or 120 mg/kg. This dose did not produce body weight differences in the dams during the dosing period nor were there differences in the birth weights of the offspring. PRM was embryolethal with only 43% of drug-treated dams maintaining their pregnancies, whereas 100% of the pregnant controls produced offspring. An analysis of resorption sites in PRM-treated dams that did not deliver showed a nearly identical number of implantation sites (12.6) compared to the litter size of controls (12.8) that delivered pups. There were no overall differences in exploratory activity levels between PRM-treated and control animals. However, in the PRM-treated females there was an absence of the sexually dimorphic increase in activity seen in control females when compared to control males. The PRM-treated males showed an impairment in the acquisition of a DRL-20 (differential reinforcement of low rates) operant schedule over a 9-week acquisition period. There were no differences in the total response rates between the groups, suggesting that this is a specific learning deficit and not a performance deficit. The results of these experiments provide evidence that prenatal PRM exposure can be embryolethal and also impair behavior in the surviving rat offspring.

Effect of practice on performance of a skilled motor task in patients with Parkinson's disease.

Parkinson's disease leads to a breakdown in the execution of highly practised, skilled movements such as walking and handwriting. The improved execution of skilled movements with practice can be understood as a process of schema learning, the determining of the relevant parameters of the specific movement. The ability of patients with Parkinson's disease and age matched normal control subjects to improve their performance, with practice, on a skilled motor task, doing up buttons, was assessed. The task was assessed on its own and with simultaneous foot tapping. Both groups showed an initial improvement in the task on its own and deterioration in performance when buttoning with foot tapping. The amount of interference, however, decreased with practice, particularly in the patients with a 2 Hz tapping rate. The results suggest that patients with Parkinson's disease are capable of schema learning but require more practice than control subjects to achieve comparable levels of performance. This may be a reflection of the fundamental motor dysfunction of the disease rather than a specific learning deficit.

Long-Term Psychological Effects of Childhood Leukemia and its Treatment

We report the results of a 5-year follow-up of the cognitive development of 19 survivors of acute lymphoblastic leukemia, all of whom received 24 Gy cranial irradiation and a course of intrathecal methotrexate. Assessment was made before radiotherapy and annually thereafter. Cognitive impairment was found to be transient in children who did not manifest somnolence who were under 5 years at the time of treatment. Despite having normal IQs and normal CT scans, 9 of 18 survivors in continuous complete remission were having learning problems at school 5 years after diagnosis. Assessment of their intellectual and memory functions revealed that as compared with matched healthy children, patients had lowered IQs but also had a specific auditory learning deficit independent of IQ. Long-term memory was found to be impaired for verbal auditory but not for verbal visual material. Results are discussed in terms of possible remediation of the learning disability.

High proline levels in the brains of mice as related to specific learning deficits

Hyperprolinemic PRO/Re mice have been studied as potential models for hyperprolinemia in man. In addition to high proline levels, some heretofore unreported amino acid abnormalities in the brains of PRO/Re mice are described. The T-maze and shuttlebox learning abilities of PRO/Re mice were compared with those of CD-1 mice having normal proline levels. PRO/Re mice had a significant deficit for T-maze learning, but a significantly greater aptitude for shuttlebox learning when compared to CD-1 mice. By studying the F3 progency of the PRO/Re × CD-1 cross, these strain-specific differences in learning ability for different tasks were shown to be unrelated to the differences in brain proline levels. F3 mice could be subdivided into two distinct groups: those with high proline (HP+) and low proline (HP−) titers. Other amino acids in brain tissues were essentially identical in both groups. A comparison of learning abilities of these HP+ mice with their HP− littermates showed no meaningful differences. However, the slightly slower rate at which HP+ mice acquired shuttlebox learning was sufficiently consistent over the 8 day training period so that it became significant. These results do not support the hypothesis that high levels of proline in brain tissues and blood are necessarily accompanied by impaired learning and memory, but are in agreement with those studies of hyperprolinemia in man that suggest no consistent learning deficits in hyperprolinemic subjects. The results seem to validate the suitability of the PRO/Re mouse as a model for hyperprolinemia in man. The data suggest also that the altered amino acid pattern in brains of PRO/Re mice has multiple etiologies. The possibility remains that in PRO/Re mice, the differences in ability to learn the T-maze and shuttlebox are the result of the interaction of high proline levels with some of the other biochemical abnormalities in the brain tissues of this mouse strain.

Cognitive Profile: Basic Determinant of Academic Achievement

AbstractThe results of this study indicate that a cognitive profile (combination of seven cognitive dimensions) can 1) separate seventh and eighth grade subjects into significantly (p > .05 or better) different achievement level groups as measured by standardized tests; 2) account for as high as 87 percent of the variance in standardized test scores, and 3) predict those scores at a level of .05 or better. Results indicate that the cognitive profile is a basic determinant of an individual’s level of academic achievement and can accurately identify specific learning deficits significantly contributing to low academic achievement.

An intensive therapeutic program for learning disabled prepubertal children.

This article contends that intervention in learning problems should be twofold. First, the child's attitudes toward both himself and learning need to be reworked. Second, remediation to amehorate specific learning deficits is required. Traditionally, these two aspects have been carried out by two different professionals, the psychologist and the teacher. The present article describes a program that has attempted to synthesize these functions into one composite helping role. A case example is offered to illustrate the approach.