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10 25th, 2008| 
Investing in normative, age-graded social roles has broad implications for both the individual and society. The current meta-analysis examines the way in which personality traits relate to four such investments—work, family, religion, and volunteerism. The present study uses meta-analytic techniques (K = 94) to identify the cross-sectional patterns of relationships between social investment in these four roles and the personality trait domains of agreeableness, conscientiousness, and emotional stability. Results show that the extent of investment in social roles across these domains is positively related to agreeableness, conscientiousness, emotional stability, and low psychoticism. These findings are more robust when individuals are psychologically
committed to rather than simply demographically associated with the investment role. Read the rest of this entry »
Abstract (Summary)
Taylor assesses the moral development in Japanese children. The data came from structured interviews with kindergarten children, their teachers, and their director. Social system morality, emotions, and responsibility were seemingly related to these children’s moral development.
Copyright World Organization for Early Childhood Education 2002
Abstract
This is a study of Japanese children ’s moral development. The data came from structured interviews with kindergarten children, their teachers, and their director. Social system morality, emotions, and responsibility were seemingly related to these children’s moral development. The results of this study’s implications for education were presented.
Resting her hand on Keiko ’s shoulder, Mild asked, “What ’s wrong?” Tearful Keiko was unable to respond. Miki took Keiko ’s hands, “It is going to be okay,” she said, ” I will play with you; remember, we are all friends at school. ” Miki took Keiko to a group of children on the playground and said, “Hey everybody, Keiko is crying; we have to play with her so she won’t be sad! My mom said we need to play with everybody at school”
Introduction
The incident described above is informative about how children make moral decisions based on their experiences and on information gained at school and at home. “From these sources spring the rules that are made to be golden” (Taylor, Wilson, Kaneda, & Ogawa, 2000). These intellectual patterns of thinking are a product of the activities practiced in the culture in which children are reared (Vygotsky, 1978), and cultural value systems shape their morality. At around age five, children are familiar with their cultural expectations and are able to make culturally appropriate moral decisions (Damon, 1988).
Researchers (Hamilton, Blumenfeld, & Akoh, 1989; Taylor, et al., 2000; Wainryb, 1993) have studied children’s moral development in relation to cultural differences, and Taylor et al. (2000) found that universal concepts, as well as cultural filters, influenced both American and Japanese first and second graders’ moral decisions. Japanese children made moral decisions through their cultural filters of sunao (cooperation), hansei (reflection), apology, and feelings, while American children made their decisions through such cultural filters as honesty, feelings, and a sense of right and wrong. Likewise, Hamilton et al. (1989) compared American and Japanese fifth graders’ reasons for achievement and moral conduct, finding that Japanese children tended to internalize their cultural norms in social procedure and morality. Read the rest of this entry »
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III. Structura si dinamica personalitatii
1). Conceptul de personalitate:
- Modele de abordare a personalitatii - modelul trasaturilor, modelul factorial,
modelul umanist s.a;
- Structura personalitatii - temperament, aptitudini, caracter. Unitatea si dinamica lor.
Perspective noi in abordarea structurii personalitatii.
2). Caracteristicile dezvoltarii psiho-fizice a scolarului mic si mijlociu.
3). Dimensiunea creativa a personalitatii. Formare, dezvoltare, exprimare, afirmare in plan individual si social.
4). Metode si tehnici de cunoastere a personalitatii copilului prescolar
Tags: aptitudini, Aptitudinile, atitudinile, autoeducatie, capacitatea, caracterul, Educatia, entuziasmBIBLIOGRAFIE
• Allport,G.,Structura si dezvoltarea personalitatii, Bucuresti, EDP, 1981.
* Badea A., Caracterizarea dinamica a copilului si adolesentului de la 3 la 18 ani, cu aplicatii la fisa scolara, Bucuresti, EDP, 1993
*Cosmovici,A.; Iacob,L., Psihologie scolara, Iasi, Editura Polirom, 1998.
• Cretu,C., Psihopedagogia succesului, Iasi, Editura Polirom,1997.
• Davitz,G.;Ball,S., Psihologia procesului educational, Bucuresti, EDP, 1978.
• Dragu Anca, Cristea Sorin, Psihologie si pedagogie scolara, Ovidius University Press, 2003
* Miclea M. Psihologie cognitiva. Modele teoretico-experimentale, Polirom, Iasi, 2003
* Mitrofan, N., Testarea psihologica a scolarului mic, Bucuresti, Editura Press Mihaela
SRL, 1997
• Oprescu,V., Fundamentele psihologice ale pregatirii si formarii didactice, Craiova,
Editura Universitaria,1996.
• Pavelcu,V., Cunoastera de sine si cunoasterea personalitatii, Bucuresti,EDP,1982.
• Popescu-Neveanu, P., Zlate, M.,Cretu,T.,(sub redactie) Psihologia scolara Bucuresti
Tipografia Universitatii Bucuresti, 1987.
* Raducu, A., Reprezentarile copiilor de 6-7 ani despre scoala, Bacau, Editura Tudor, 1998
• Schiopu,U., Verza,E.,Psihologia varstelor. Ciclurile vietii,Bucuresti,EDP,1995.
• Zlate,M., Fundamentele psihologiei, Bucuresti Editura XXI,1994.
• Zlate,M., Eul si personalitatea ,Bucuresti,Editura”Trei”,1997.
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Summary - Behavioral disturbances in Parkinson’s disease (PD) are a common sourceof disability to both patients and their families, but there is a considerable controversy regarding their frequency and their neuropathological and neurochemical bases.
Since they are so common, the disorders associated with PD should be well recognized, and proper management by neurologists is required. The most frequent behavioral disturbances encountered in patients with PD are depression, anxiety, cognitive impairment and dementia.
Also frequent are sleep disorders such as sleep fragmentation, REM sleep behavior disorder, insomnia and altered dreaming.
The most troublesome situations come from drug-induced psychiatric states, such as delusional states, hallucinations, paranoid ideation, delirium, and confusion.
The treatment of these behaviors is reviewed here.
In the general population, benzodiazepines are the most commonly used drugs to improve anxiety ymptoms. Lorazepam, a relatively short acting drug, is usually well tolerated in older patients. Diazepam or hlordiazepoxide have longer half lives, but they are poorly tolerated by older patients and patients with impaired renal function. When discontinuing their use, these drugs must be tapered over a two week period. Barbiturate drugs are not commonly used in PD patients because of their excessive sedative side effects. Drugs which are active in the autonomic nervous system, such as diphenhydramine or hydroxyzine, can be useful to treat symptoms of autonomic dysfunction such as wet and cold hands, tachycardia, tachypnea, dry mouth, diarrhea and parestesia in hands or feet.
Beta-blockers, which can be used for the treatment of postural tremor or dyskinesia in PD, have a mild effect over anxiety related tachycardia. They should not be prescribed in patients with a heart block or impaired respiratory function.
Depression is almost as frequent as anxiety in PD. Once detected, depression should be treated promptly by the physician because of its clinical implications and the repercussion in the quality of the patient’s life.
Furthermore, there is evidence for an association between depression and dementia in PD.
L-dopa treatment seems to have only a short positive effect on depression in PD, presumably due to the amelioration of motor symptoms. Most patients with depression continue to be depressed one to six years after starting L-dopa therapy.
Since the overall efficacy of most antidepressants is similar, the clinical utility of a given drug often depends on the presence or absence of particularly troublesome side effects. Serotonin re-uptake inhibitors, such as sertraline, fluoxetine, paroxetine and citalopram among others, have certain advantages over the classic tricyclic antidepressants with regard to their side effects spectrum. The anticholinergic features typically associated with tricyclics, such as dry mouth and constipation, are less frequent with these drugs. Postural hypotension and sedation are also infrequent, but other important side effects have been reported.
Most of the common side effects of serotonin reuptake inhibitors include anxiety (present in 10-15% of patients), insomnia (in 10-30% of patients), restlessness, weight loss, anorexia, somnolence, postural tremor, light-headedness, gastrointestinal disturbances, allergic reactions, and libido disturbances in men. In addition, the most common side effects of classical tricyclic antidepressants include anticholinergic effects (dry mouth, constipation, urinary retention, blurred vision), anti-histaminic effects, excessive sedation, and anti-adrenergic effects such as postural hypotension, tachycardia or anxiety. There have also been several reports concerning the use of serotonin re-uptake inhibitors in PD that have pointed out the possibility of a worsening of motor symptoms during treatment with fluoxetine and paroxetine.
However, these symptoms were found improve after withdrawal of the drug. Fluoxetine has also been associated with the induction of akathisia. However, no alteration of motor condition was found in 14 PD patients treated with a daily dose of 20 mg of fluoxetine. Another study with 23 PD patients treated with fluoxetine and deprenyl, showed no adverse effects.
In conclusion, there are very few single case reports that have suggested that serotonin re-uptake blockers worsen the motor condition in PD. Moreover, these drugs show less important side effects than tricyclic antidepressants, especially in the elderly population, and should therefore be regarded as the first choice drugs in the treatment of depression in PD. They should however be used cautiously until controlled studies have been carried out. Read the rest of this entry »
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Abstract
Negative symptoms generally refer to a reduction in normal functioning. In schizophrenia they encompass apathy, anhedonia, flat affect, avolition, social withdrawal and, on some accounts, psychomotor retardation.
Negative symptoms have been identified in other psychiatric disorders, including melancholic depression, and also in neurological disorders, such Parkinson’s disease. Achieving a better understanding of negative symptoms constitutes a priority in mental health. Primarily, negative symptoms represent an unrelenting, intractable and disabling feature for patients, often amounting to a severe burden on families, carers and the patients themselves. Identifying and understanding subgroups within disorders may also contribute to the clinical care and scientific understanding of the pathophysiology of these disorders. The purpose of this paper is to review the current literature on negative symptoms in schizophrenia and explore the idea that negative symptoms may play an important role not only in other psychiatric disorders such as melancholic depression, but also in neurological disorders, such as Parkinson’s disease. In each disorder negative symptoms manifest with similar motor and cognitive impairments and are associated with comparable neuropathological and biochemical findings, possibly reflecting analogous impairments in the functioning of frontostriatal-limbic circuits.
Negative symptoms are a cluster of symptoms generally characterised by the absence of normal levels of activation, initiative, and affect. They are a well established aspect of the symptomatology in schizophrenia. Unlike the episodic, treatment–responsive nature of positive symptoms, negative symptoms in schizophrenia tend to be enduring and less reactive to medication. They are perhaps the most unrelenting and disabling features , constituting a severe burden on relatives as well as on the patient themselves. Over the past decade there has been a resurgence of interest in negative symptoms, related partially to their significant prognostic value and additionally to the development and partial success of atypical antipsychotic medication in treating negative symptoms.
Although negative symptoms are considered an important feature of schizophrenia, they are not pathognomic of it.
Over recent years, the concept of negative symptoms has also been described as a prominent feature, distinct from depression, in other neurological and psychiatric disorders including melancholic depression ; Parkinson’s disease; Alzheimer’s disease; fronto-temporal dementia.
Recognising that negative symptoms are not limited to patients with schizophrenia is important, not only for clinical implications regarding potential treatment, but also to enhance the current understanding of the neurobiological substrate of an apparently homogeneous group of symptoms. To avoid variability within studies and consequent inconsistency between findings, it is essential for both research and clinical purposes to have an understanding of the existence of subgroups. The purpose of this paper is to review the current literature on negative symptoms in schizophrenia and explore the idea that negative symptoms play an important role in other neurological and psychiatric disorders, in particular melancholic depression and Parkinson’s disease. Clinical presentations and aetiological models will be considered. Read the rest of this entry »
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Abstract
Objectives: We investigated the role of stage of disease, motor status and dopaminergic treatment in cognitive impairment of Parkinson’s disease (PD) patients with visual hallucination (VH) and the presence of specific cognitive impairment patterns.
Method: We compared 33 PD patients with VH ( group 1 ) with 30 PD patients without VH (group 2) with regard to demographic characteristics and neuropsychological test scores.
Results: The group with VH demonstrated significantly worse Short Test of Mental Status scores; the cognitive impairment pattern presented in the form of frontal dysfunction and memory deterioration. There were significant differences in Stroop duration/error, verbal fluency, Wechsler Memory Scale and Sozel Bellek Surecleri Test (a Turkish verbal learning test) scores.
Conclusion: In PD patients with VH the main pattern of cognitive impairment is frontal dysfunction and memory deterioration. Because visual perceptive functions were not different between the two groups, such deterioration may not be a primary factor in the development of VH.
1. Introduction
Visual hallucinations ( VH ) may occur in up to 33% of patients undergoing long-term treatment for Parkinson’s disease (PD).1–3 Although VH had been reported in PD before the dopamine era,4,5 they were commonly reported as a side-effect of antiparkinsonian treatment.6,7 Goetz et al. reported in a prospective longitudinal study that the prevalence of VH reached 63% at the end of 48 months. The hallucinations in PD are a risk-factor for permanent nursing home placement with associated high mortality rate and control of hallucinations may be warranted.
However, the pathogenesis and pathophysiology of VH are not yet entirely understood. The effects of exogenous dopaminergic agents on the mesolimbic system have been implicated as the primary cause; however, recent data suggest that other factors such as stage and duration of disease, cognitive status and age, history of depression and sleep-wake cycle disturbances may contribute. Visual dysfunction may contribute to the development of VH.
While cognitive deterioration is one of the most common risk factors for the development of VH in PD, there is insufficient information on this cognitive impairment pattern. Understanding of the cognitive impairment patterns may aid in understanding of the nature of the VH.
This study aims to determine the role of duration of disease and stage, motor status and dopaminergic treatment on cognitive impairment of patients with VH and whether PD patients with VH present a specific cognitive impairment pattern.
2. Materials and methods
2.1. Subjects
After local ethics committee approval of the study, a total 63 PD patients were enrolled. Thirty-three of these with VH (group 1) were recruited consecutively from our out-patient clinic. These patients had experienced several episodes of definite VH in the past 3 months. VH were classified according to the Unified Parkinson’s disease rating scale (UPDRS) (0: none, 1: vivid dreams, 2: hallucinations with retained insight, 3: frequent hallucinations without retained insight, 4: psychotic process). The patients
with 2 and 3 points were assessed as the group with VH (n = 33) (group 1). A total of 30 patients with PD but without a history of VH were selected for the control group with similar demographic variables (group 2). Patients were evaluated while in the ‘on’ state but without hallucinations.
All patients were examined by a specialist in movement disorders and were diagnosed as PD according to the United Kingdom Parkinson’s Disease Society Brain Bank criteria.
Patients with dementia were not recruited into the study. Dementia was diagnosed according to the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) criteria. The use of DSM-IV criteria for dementia in patients with PD may be difficult, so not only patients with certain dementia, but also ones with suspected dementia and diffuse Lewy body disease were excluded.
Patients with pyramidal signs, cerebellar signs, clear gaze palsy or autonomic dysfunction or who had head trauma, encephalitis, cerebrovascular attacks or exposure to toxic agents were not included the study.
All patients were assessed according to clinical features, UPDRS total, motor and mental subscores and Hoehn-Yahr stages. They were also assessed according to dosage and duration of levodopa treatment.
Antiparkinsonian treatments were recorded and the total daily dose of levodopa was calculated for each patient.
For dopaminergic agonists we calculated the equivalent levodopa dosage as follows: 10 mg bromocriptine = 1 mg lisuride = 1 mg pergolide = 100 mg levodopa (with a dopa-decarboxylase inhibitor).
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Abstract
Behavioral and psychiatric problems associated with idiopathic Parkinson’s disease (PD) include cognitive dysfunction, drug-related psychosis, depression, anxiety, apathy, fatigue and sleep disturbance. These nonmotor symptoms are a significant cause of disability at all stages of illness. Cognitive dysfunction spans a continuum from circumscribed cognitive impairments to severe global dementia which can occur in up to 10±30% of advanced PD patients. Psychosis develops in 20±30% of PD patients receiving chronic antiparkinsonian therapy.
Visual hallucinations and paranoid delusions are the most frequent symptoms. The gradual elimination of drugs of lesser priority that may affect cognition and/or cloud the sensorium constitutes the first step in the management of cognitive and psychotic symptoms. Atypical neuroleptic agents are an invaluable tool in those cases in which maximum drug regimen simplification is not adequate or results in unacceptable immobility. Depression and anxiety often go unrecognized although they are eminently treatable and may be important contributors to the morbidity of PD. They are present in 30±40% of PD patients and frequently occur together in association with other nonmotor symptoms such as apathy, fatigue and sleep disturbance. A combination of early recognition, counseling, antidepressant therapy, antianxiety and well-balanced antiparkinsonian therapy sets the stage for improved quality of life for patients with PD.
1. Introduction
There are a wide range of behavioral disturbances associated with idiopathic Parkinson’s disease (PD) including depression [1], anxiety [2], fatigue [3], sleep disturbances [4], cognitive dysfunction [5,6] and drug-related psychosis [7]. Collectively these symptoms affect the majority of patients with PD [1-7]. While PD is traditionally described as a motor disorder, there is increasing awareness that the behavioral non-motor symptoms constitute an important source of disability. Early recognition and effective management of the non-motor symptoms of PD is integral to the quality of life of both patients and caregivers [8]. We will review the current knowledge in this expanding field, focusing on the practical issues involved in the delicate balance of managing both motor and non-motor symptoms in PD.
2. Cognitive dysfunction
Cognitive dysfunction in Parkinson’s disease (PD) spans a continuum that ranges from circumscribed cognitive impairments that may be observed relatively early in the disease process to global dementia in the late stages of the disease. Although estimates vary, dementia occurs in 10±30% of advanced PD patients [5,6,9], while more discrete cognitive impairments not only occur earlier, but also, affect the large majority of patients. These cognitive changes may not be fully appreciated if targeted testing with a broad neuropsychological battery is not performed [10].
The age standardized ratio of dementia in PD patients compared to controls was 4.6 in a recent study conducted in France [11]. Mayeux et al. [12] in a re-evaluation of the clinic-based sample 5 years after his prevalence analysis [10], indicated that the incidence of dementia was 69 per 1000 person years of observation, which was almost 6 times that expected in an aged-matched cohort.
Several risk factors have been associated with the development of dementia in PD including older age at the onset of PD [10,11,13], severity of extrapyramidal signs, especially bradykinesia [14,15], family history of dementia [16,17], depression [13,14,18], psychological stress [19] and low socioeconomic or educational attainment [20].
Cognitive dysfunction in PD is primarily attributed to defects of subcortical processing as opposed to cognitive impairment in Alzheimer’s disease (AD) which is attributed to cortical dysfunction [21]. The dementia associated with PD is characterized by impairment of executive functions (e.g. planning, sequencing, monitoring and shifting between responses), visuomotor skills, visuospatial skills, free recall of both verbal and nonverbal material and verbal fluency. Cortical functions such as praxis, calculations, orientation, cued recall, recognition memory and certain other aspects of language are relatively spared [22]. Perhaps the main distinguishing factor between patients with PD and those with AD is performance on delayed recall as compared to immediate recall. PD is characterized by relatively good retention of ewly acquired information following a delay, while patients with AD tend to rapidly forget it. This supports he belief that the memory impairment associated with PD is primarily a retrieval deficit as opposed to AD, which is characterized by deficient encoding or consolidation of information. The poor retrieval of new information by PD patients may be secondary to a form of executive dysfunction, consisting of the inability to initiate a systematic search of memory, reflecting a dysfunction of subcorticofrontal circuits [23].
The relatively circumscribed cognitive problems seen in many PD patients may or may not progress to global dementia [22]. Risk factors associated with the development of dementia were previously described. Additional neuropsychological predictors of later decline have also been identified including the individual’s performance on tests of letter, category and verbal fluency [24,25]. The progression of the milder and more circumscribed cognitive deficits seen in many PD patients towards more global impairments appears to represent not only a quantitative change but also, a qualitative shift in the pattern of cognitive domainsinvolved [26]. This concept is supported by neuropathological evidence of damage extending beyond the dopaminergic system in PD patients with advanced dementia [27,28].
3. Drug-related psychosis
Drug-related psychosis occurs in 20±30% of PD patients following chronic antiparkinsonian therapy [36]. The mechanisms responsible for its appearance are not well understood but dopaminergic (especially mesolimbic) and serotoninergic systems are likely to be involved [36].
Almost all of the drugs used to treat PD may induce psychosis although individual patients commonly demonstrate particular sensitivity to individual medications. The emergence of drug related psychotic ideation requires careful monitoring since this problem can be severely disabling and is more likely to lead to nursing home placement than either motor dysfunction or dementia [37]. In addition, there is a marked increase in the mortality rate of PD patients with drug-related psychosis [38].
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ANXIETY DISORDERS
IN PARKINSON’S DISEASE: INSIGHTS
INTO THE NEUROBIOLOGY OF NEUROSIS
It is within living professional memory that mental states in clinical medicine were understood as radically demarcated from their underlying neuroanatomy, neurochemistry, and neuropsychology.
The behavioral disorders were relegated to the realm of the “functional,” whereas all the rest of clinical medicine was navigated to the “organic” subcontinents of neurology, cardiology, and general medicine. The bridging insights of neuropsychiatry over the past 20 years have greatly improved our insights about the interactive nature of neurology and psychiatry [1]. First in the aphasias, then in the dementias, and later in the affective disorders, neuropsychiatry has helped us to understand how thought, feeling, and action can be directly influenced by the neurobiology of certain neurologic diseases.
The anxiety disorders may be the most common of the psychiatric disorders [2].
Lifetime prevalence rates for DSM-III-R-diagnosable anxiety disorders are as high as 30.5% for women and 19.2% for men [3]. These disorders occur across the lifespan, from childhood to later years. They include a variety of distressing symptoms including nervousness, sleeplessness, hypochondrias is, and many somatic symptoms.
They tend to persist, and they are difficult to diagnose and treat. One might wonder whether these disorders will become the mood disorders of the next century.
The observation that persons suffering from certain neurological diseases develop certain behavioral syndromes at incidence rates greater than expected has been a most useful insight for neuropsychiatry. Such observations have substantially shaped our theoretical understanding of the affective disorders [4], obsessive–compulsive disorder [5], and the psychoses [6].
The anxiety disorders, however, have not received analogous clinical neuropsychiatric investigation. We do have certain neurobiological insights concerning the neuroanatomy and neurochemistry which is of importance to the clinical expression of generalized or episodic anxiety [7]; however, these insights derive primarily from animal experiments, or from functional imaging in humans. Disease-based neuropsychiatry has yet to make its contributions to our understanding of the anxiety disorders.
Clinical reports are now becoming available which indicate that there might be an association between the anxiety disorders and idiopathic Parkinson’s disease (PD), or its treatments [8]. Both episodic and generalized anxiety syndromes have been reported to occur in PD populations at elevated rates compared with normal and disease controls [9–11]. Some of these patients clearly seem to have onset of the anxiety symptomatology prior to first motor symptoms of PD, suggesting some underlying, shared neurobiologic vulnerability to PD and anxiety [12]. It has been difficult to specify a relationship between episodic or generalized anxiety in PD patients and dopamine agonist pharmacotherapy. Some investigators have reported an association between the timing of levodopa dosing and panic attacks [13], but others have not [9]. In one study of levodopa infusions under controlled conditions anxiety was reduced in patients with advanced PD and motor fluctuations [14]. It is certainly the case, however, that older neurologists recall remarkable anxiety symptoms in PD patients prior to the advent of levodopa therapy, and that many PD patients demonstrate their anxiety symptoms prior to the initiation of levodopa [15].
Tags: ANXIETY, cardiology, childhood, diagnose, DISEASE, fear, incidence, investigation, levodopa, Lifetime, medicine, neuroanatomy, NEUROBIOLOGY, neurology, neuropsychiatry, psychiatry, vulnerability
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