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Neuropsychiatric Disorders (neuropsychiatric + disorders)
Selected AbstractsExamining the Intersection of Sex and Stress in Modelling Neuropsychiatric DisordersJOURNAL OF NEUROENDOCRINOLOGY, Issue 4 2009N. Goel Sex-biased neuropsychiatric disorders, including major depressive disorder and schizophrenia, are the major cause of disability in the developed world. Elevated stress sensitivity has been proposed as a key underlying factor in disease onset. Sex differences in stress sensitivity are associated with corticotrophin-releasing factor (CRF) and serotonin neurotransmission, which are important central regulators of mood and coping responses. To elucidate the underlying neurobiology of stress-related disease predisposition, it is critical to develop appropriate animal models of stress pathway dysregulation. Furthermore, the inclusion of sex difference comparisons in stress responsive behaviours, physiology and central stress pathway maturation in these models is essential. Recent studies by our laboratory and others have begun to investigate the intersection of stress and sex where the development of mouse models of stress pathway dysregulation via prenatal stress experience or early-life manipulations has provided insight into points of developmental vulnerability. In addition, examination of the maturation of these pathways, including the functional importance of the organisational and activational effects of gonadal hormones on stress responsivity, is essential for determination of when sex differences in stress sensitivity may begin. In such studies, we have detected distinct sex differences in stress coping strategies where activational effects of testosterone produced females that displayed male-like strategies in tests of passive coping, but were similar to females in tests of active coping. In a second model of elevated stress sensitivity, male mice experiencing prenatal stress early in gestation showed feminised physiological and behavioural stress responses, and were highly sensitive to a low dose of selective serotonin reuptake inhibitors. Analyses of expression and epigenetic patterns revealed changes in CRF and glucocorticoid receptor genes in these mice. Mechanistically, stress early in pregnancy produced a significant sex-dependent effect on placental gene expression that was supportive of altered foetal transport of key growth factors and nutrients. These mouse models examining alterations and hormonal effects on development of stress pathways provide necessary insight into how specific stress responses can be reprogrammed early in development resulting in sex differences in stress sensitivity and neuropsychiatric disease vulnerability. [source] Traditional Healing and Its Discontents: Efficacy and Traditional Therapies of Neuropsychiatric Disorders in BaliMEDICAL ANTHROPOLOGY QUARTERLY, Issue 1 2004Robert Bush Lemelson In a discussion of patients suffering from obsessive-compulsive disorder (OCD) and/or Tourettes's Syndrome (TS), in Bali, Indonesia, traditional healing and psychiatric perspectives are used to highlight the power and weakness of each to treat these conditions. Given they are drawn from the same culture, should not indigenous explanatory models provide meaning and be more efficacious at relieving the suffering of people with OCD and TS-like symptoms? What if they provide an understandable meaning for patients but these meanings have no efficacy? Ethnographic data on Balinese models for illness are presented. Multiple data sources were used to frame the complex Balinese traditional healing systems. Forty patients were interviewed regarding their utilization of traditional healers, and healers were observed treating patients and interviewed regarding their treatment regimens and explanatory models. Traditional explanatory models for illness provide an understandable and integrated system of meaning for these disorders but are not successful in relieving symptomatology. Neurobiological approaches, traditional healing, and ethnographic methods are compared and contrasted to highlight the strengths and weaknesses of each in relation to issues of exegesis and efficacy, [obsessive-compulsive disorder, Tourette's Syndrome, traditional healing, Indonesia] [source] Annotation: PANDAS: a model for human autoimmune diseaseTHE JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES, Issue 3 2005Susan E. Swedo Background:, Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus infections (PANDAS) is a recently recognized syndrome in which pre-adolescent children have abrupt onsets of tics and/or obsessive-compulsive symptoms, a recurring and remitting course of illness temporally related to streptococcal infections, and associated neurologic findings including adventitious movements, hyperactivity and emotional lability. Methods:, Inspired by observations of similar symptoms in children with Sydenham's chorea, a search was undertaken for clinical and laboratory evidence in support of the new syndrome. Results:, Consistent and predictable clinical findings have been described in a large case series. Magnetic resonance imaging has supported the postulated pathobiology of the syndrome with evidence of inflammatory changes in basal ganglia. Antibasal ganglia antibodies have been found in some acute cases, mimicking streptococcal antigen epitopes. Conclusions:, While PANDAS remains a controversial diagnostic concept, it has stimulated new research endeavors into the possible links between bacterial pathogens, autoimmune reactions, and neuropsychiatric symptoms. [source] Neuropsychiatric disorders presenting with antisocial behaviourINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 7 2006Basant K. Puri No abstract is available for this article. [source] Ataxia, autism, and the cerebellum: a clinical study of 32 individuals with congenital ataxiaDEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 3 2005Ingegerd Åhsgren MD The suggested link between autism and cerebellar dysfunction formed the background for a Swedish clinical study in 2001. Thirty-two children (17 females, 15 males; mean age 12y, SD 3y 10mo; range 6 to 21y) with a clinical suspicion of non-progressive congenital ataxia were examined, and parents were interviewed about the presence of neuropsychiatric problems in the child. Twelve children had simple ataxia, eight had ataxic diplegia, and 12 had,borderline'ataxia. All but one of the 32 children had a mild to moderate gross motor disability according to Gross Motor Function Classification System (15 were categorized as level I,16 as level II, and one child as level IV). Neuroimaging and neuropsychological testing were achieved in most cases. There was a strong association between learning disability* and autism spectrum disorder (often combined with hyperactivity disorder) on the one hand, and both simple and borderline,ataxia'on the other, but a weaker link between ataxic diplegia and neuropsychiatric disorders. A correlation between cerebellar macropathology on neuroimaging and neuropsychiatric disorders was not supported. Congenital ataxia might not be a clear-cut syndrome of cerebellar disease, but one of many signs of prenatal events or syndromes, leading to a complex neurodevelopmental disorder including autism and learning disability. [source] The application of transcranial magnetic stimulation in psychiatry and neurosciences researchACTA PSYCHIATRICA SCANDINAVICA, Issue 5 2002P. B. Fitzgerald Objective:,Over recent years transcranial magnetic stimulation (TMS) has become widely applied in the study of neuropsychiatric disorders. The aim of this article is to review the application of TMS as an investigative tool and as a potential therapeutic modality in psychiatric disorders. Method:,A comprehensive literature review. Results:,When applied as an investigative tool, TMS provides innovative ways to directly study the excitability of the cortex, cortical regional connectivity, the plasticity of brain responses and cognitive functioning in illness and disease states. A number of studies suggest the potential of treatment with TMS in disease states, especially in patients with depression, although difficulties exist with the interpretation of the published literature. Conclusion:,TMS has a considerable role in neuropsychiatric research. It appears to have considerable potential as a therapeutic tool in depression, and perhaps a role in several other disorders, although widespread application requires larger trials and establishment of sustained response. [source] Cannabinoid modulation of limbic forebrain noradrenergic circuitryEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 2 2010Ana F. Carvalho Abstract Both the endocannabinoid and noradrenergic systems have been implicated in neuropsychiatric disorders. Importantly, low levels of norepinephrine are seen in patients with depression, and antagonism of the cannabinoid receptor type 1 (CB1R) is able to induce depressive symptoms in rodents and humans. Whether the interaction between the two systems is important for the regulation of these behaviors is not known. In the present study, adult male Sprague,Dawley rats were acutely or chronically administered the CB1R synthetic agonist WIN 55,212-2, and ,2A and ,1 adrenergic receptors (AR) were quantified by Western blot. These AR have been shown to be altered in a number of psychiatric disorders and following antidepressant treatment. CB1R agonist treatment induced a differential decrease in ,2A- and ,1-ARs in the nucleus accumbens (Acb). Moreover, to assess long-lasting changes induced by CB1R activation, some of the chronically treated rats were killed 7 days following the last injection. This revealed a persistent effect on ,2A-AR levels. Furthermore, the localization of CB1R with respect to noradrenergic profiles was assessed in the Acb and in the nucleus of the solitary tract (NTS). Our results show a significant topographic distribution of CB1R and dopamine beta hydroxylase immunoreactivities (ir) in the Acb, with higher co-localization observed in the NTS. In the Acb, CB1R-ir was found in terminals forming either symmetric or asymmetric synapses. These results suggest that cannabinoids may modulate noradrenergic signaling in the Acb, directly by acting on noradrenergic neurons in the NTS or indirectly by modulating inhibitory and excitatory input in the Acb. [source] Research Submission: Mixture Analysis of Age at Onset in Migraine Without Aura: Evidence for Three SubgroupsHEADACHE, Issue 8 2010Carlo Asuni MD (Headache 2010;50:1313-1319) Objective. , To verify the presence of different age at onset (AAO) subgroups of patients in a sample of patients with migraine without aura (MWA) and compare clinical correlates among them. Background., MWA is a long-lasting disease whose prognosis has not yet been fully investigated. Patients may present complete remission, partial clinical remission, persistence and progression (migraine attack frequency and disability may increase over time leading to chronic migraine). Limited evidence exists regarding the identification of risk factors or predictors which might influence migraine prognosis. AAO has been proven a useful tool in the investigation of the clinical, biological, and genetic characteristics able to influence the prognosis of a number of neuropsychiatric disorders. AAO distribution was studied using mixture analysis, a statistical approach that breaks down the empirical AAO distribution observed into a mixture of normal components. Methods., A sample of 334 outpatients affected by MWA, recruited in a clinical genetic study at our Headache Center from 2004 to 2008, was enrolled for this study. Diagnosis was made according to International Headache Society criteria 2004. AAO distribution in patients was studied using mixture analysis. Chi-square test was used to compare clinical correlates among identified subgroups. Logistic regression was performed in order to correct for effect of possible confounders. Results., Mixture analysis broke up the observed distribution of AAO into 3 normal theoretical distributions. Informational criteria clearly showed a better 3-component model rather than the 2-component one. An early-onset (,7 years of age), an intermediate-onset (,8 and ,22), and a late-onset group (,23) were identified. Comparison of clinical correlates among subgroups by means of chi-square test showed a statistically significant result for migraine frequency (,2 = 7.41, P = .02). Considering the frequency of migraine attacks as a main outcome, the regression model showed a higher AAO is associated with low frequency (odds ratio = 0.95; P = .02). Conclusions., The significant association between AAO and attack frequency found in our study supports the hypothesis that AAO could act as a predictor factor able to influence prognosis. AAO could represent a phenotype suitable for identifying MWA susceptibility genes. [source] The human hippocampus at 7 T,In vivo MRIHIPPOCAMPUS, Issue 1 2009Jens M. Theysohn Abstract The human hippocampus plays a central role in various neuropsychiatric disorders, such as temporal lobe epilepsy (TLE), Alzheimer's dementia, mild cognitive impairment, and schizophrenia. Its volume, morphology, inner structure, and function are of scientific and clinical interest. Magnetic resonance (MR) imaging is a widely employed tool in neuroradiological workup regarding changes in brain anatomy, (sub-) volumes, and cerebral function including the hippocampus. Gain in intrinsic MR signal provided by higher field strength scanners and concomitant improvements in spatial resolution seem highly valuable. An examination protocol permitting complete, high-resolution imaging of the human hippocampus at 7 T was implemented. Coronal proton density, T2, T2*, and fluid-attenuated inversion recovery contrasts were acquired as well as an isotropic 3D magnetization-prepared rapid acquisition gradient-echo (500 ,m isotropic voxel dimension, noninterpolated). Observance of energy deposition restrictions within acceptable scan times remained challenging in the acquisition of thin, spin-echo-based sections. At the higher resolution enabled by 7 T, demarcation of the hippocampus and some internal features including gray/white matter differentiation and depiction of the hippocampal mantle becomes much more viable when compared with 1.5 T; thus, in the future, this imaging technology might help in the diagnosis of subtle hippocampal changes. © 2008 Wiley-Liss, Inc. [source] Detection of endogenous lithium in neuropsychiatric disorders,a model for biological transmutationHUMAN PSYCHOPHARMACOLOGY: CLINICAL AND EXPERIMENTAL, Issue 1 2002Ravi Kumar Kurup Abstract The human hypothalmus produces an endogenous membrane Na+ -K+ ATPase inhibitor, digoxin. A digoxin induced model of cellular/neuronal quantal state and perception has been described by the authors. Biological transmutation has been described in microbial systems in the quantal state. The study focuses on the plasma levels of digoxin, RBC membrane Na+ -K+ ATPase activity, plasma levels of magnesium and lithium in neuropsychiatric and systemic disorders. Inhibition of RBC membrane Na+ -K+ ATPase activity was observed in most cases along with an increase in the levels of serum digoxin and lithium and a decrease in the level of serum Mg++. The generation of endogenous lithium would obviously occur due to biological transmutation from magnesium. Digoxin and lithium together can produce added membrane Na+ -K+ ATPase inhibition. The role of membrane Na+ -K+ ATPase inhibition in the pathogenesis of neuropsychiatric and systemic disorders is discussed. The inhibition of membrane Na+ -K+ ATPase can contribute to an increase in intracellular calcium and a decrease in magnesium, which can result in a defective neurotransmitter transport mechanism, mitochondrial dysfunction and apoptosis, defective golgi body function and protein processing dysfunction, immune dysfunction and oncogenesis. Copyright © 2002 John Wiley & Sons, Ltd. [source] PANDAS anorexia nervosa,Endangered, extinct or nonexistent?INTERNATIONAL JOURNAL OF EATING DISORDERS, Issue 1 2008Frances Puxley BSc Abstract Objective: Substantial evidence exists for the concept of pediatric autoimmune neuropsychiatric disorders associated with streptoccoccal infection (PANDAS) such as some cases of obsessive-compulsive disorder and tics/Tourette's syndrome. More recently PANDAS-AN has been described. The aim of this article is to provide a critical review of this concept. Method: The literature was searched using Medline, Psychinfo, and Google. Results: There is some evidence for the entity of PANDAS-AN but this is considerably limited by a wide range of methodological problems, including the seemingly low prevalence, the lack of clarity in diagnostic criteria, and the lack of specificity in the diagnostic tests. Innovative treatment approaches hold promise but require further evaluation. Conclusion: Further research into PANDAS-AN, using more clearly defined and consistent diagnostic criteria is needed, given the potential for enhancing the understanding of the pathogenesis of AN and for more effective treatments. © 2007 by Wiley Periodicals, Inc. Int J Eat Disord 2008 [source] A modified Mini Nutritional Assessment without BMI can effectively assess the nutritional status of neuropsychiatric patientsJOURNAL OF CLINICAL NURSING, Issue 13 2009Alan C Tsai Aim and objectives., To determine whether a modified version of the Mini Nutritional Assessment (MNA) without body mass index (BMI) can effectively identify individuals at risk of malnutrition among patients with neuropsychiatric disorders. Background., Neuropsychiatric patients have an additional risk of nutritional disorder due to functional impairments and drug effects. However, their nutritional status is generally neglected. It is important to find a tool that is simple, easy to use and non-invasive. Design., The study involved 105 patients in the acute phase of confirmed neuropsychiatric disorders in an area hospital. All subjects were cognitively able to have effective verbal communication. Method., The study included serum biochemical and anthropometric measurements and an on-site, in-person interview using a structured questionnaire to elicit personal data, health condition and answers to questions in the MNA. Subjects' nutritional statuses were graded with a MNA that adopted population-specific anthropometric cut-off points or one further with the BMI question removed and its assigned score redistributed to other anthropometric questions. Results., Both versions of the modified MNA effectively graded the nutritional status of neuropsychiatric patients and showed good correlations with the major nutritional indicators such as BMI, calf circumference and the length of hospital stay. Conclusions., The MNA can effectively assess the nutritional status of neuropsychiatric patients and enhance timely detection and intervention of their nutritional disorders. A modified MNA without the BMI question can maintain the full functionality of the tool. The version does not require weight and height measurements and thus will enhance the usefulness of the instrument. Relevance to clinical practice., Neuropsychiatric patients are a high-risk group of nutritional disorders. The MNA, especially the one without BMI, has the potential to improve professional efficiency of the primary care workers. [source] Pre-synaptic BK channels selectively control glutamate versus GABA release from cortical and hippocampal nerve terminalsJOURNAL OF NEUROCHEMISTRY, Issue 2 2010Maria Martire J. Neurochem. (2010) 115, 411,422. Abstract In the present study, by means of genetic, biochemical, morphological, and electrophysiological approaches, the role of large-conductance voltage- and Ca2+ -dependent K+ channels (BK channels) in the release of excitatory and non-excitatory neurotransmitters at hippocampal and non-hippocampal sites has been investigated. The results obtained show that the pharmacological modulation of pre-synaptic BK channels selectively regulates [3H]d -aspartate release from cortical and hippocampal rat synaptosomes, but it fails to influence the release of excitatory neurotransmitters from cerebellar nerve endings or that of [3H]GABA, [3H]Noradrenaline, or [3H]Dopamine from any of the brain regions investigated. Confocal immunofluorescence experiments in hippocampal or cerebrocortical nerve terminals revealed that the main pore-forming BK , subunit was more abundantly expressed in glutamatergic (vGLUT1+) versus GABAergic (GAD65-67+) nerve terminals. Double patch recordings in monosynaptically connected hippocampal neurons in culture confirmed a preferential control exerted by BK channels on glutamate over GABA release. Altogether, the present results highlight a high degree of specificity in the regulation of the release of various neurotransmitters from distinct brain regions by BK channels, supporting the concept that BK channel modulators can be used to selectively limit excessive excitatory amino acid release, a major pathogenetic mechanism in several neuropsychiatric disorders. [source] Metabotropic glutamate type 5, dopamine D2 and adenosine A2a receptors form higher-order oligomers in living cellsJOURNAL OF NEUROCHEMISTRY, Issue 5 2009Nuria Cabello Abstract G protein-coupled receptors are known to form homo- and heteromers at the plasma membrane, but the stoichiometry of these receptor oligomers are relatively unknown. Here, by using bimolecular fluorescence complementation, we visualized for the first time the occurrence of heterodimers of metabotropic glutamate mGlu5 receptors (mGlu5R) and dopamine D2 receptors (D2R) in living cells. Furthermore, the combination of bimolecular fluorescence complementation and bioluminescence resonance energy transfer techniques, as well as the sequential resonance energy transfer technique, allowed us to detect the occurrence receptor oligomers containing more than two protomers, mGlu5R, D2R and adenosine A2A receptor (A2AR). Interestingly, by using high-resolution immunoelectron microscopy we could confirm that the three receptors co-distribute within the extrasynaptic plasma membrane of the same dendritic spines of asymmetrical, putative glutamatergic, striatal synapses. Also, co-immunoprecipitation experiments in native tissue demonstrated the existence of an association of mGlu5R, D2R and A2AR in rat striatum homogenates. Overall, these results provide new insights into the molecular composition of G protein-coupled receptor oligomers in general and the mGlu5R/D2R/A2AR oligomer in particular, a receptor oligomer that might constitute an important target for the treatment of some neuropsychiatric disorders. [source] Multifunctional drugs with different CNS targets for neuropsychiatric disordersJOURNAL OF NEUROCHEMISTRY, Issue 4 2006Cornelis J. Van der Schyf Abstract The multiple disease etiologies that lead to neuropsychiatric disorders, such as Parkinson's and Alzheimer's disease, amyotrophic lateral sclerosis, Huntington disease, schizophrenia, depressive illness and stroke, offer significant challenges to drug discovery efforts aimed at preventing or even reversing the progression of these disorders. Transcriptomic tools and proteomic profiling have clearly indicated that such diseases are multifactorial in origin. Further, they are thought to be initiated by a cascade of molecular events that involve several neurotransmitter systems. In response to this complexity, a new paradigm has recently emerged that challenges the widely held assumption that ,silver bullet' agents are superior to ,dirty drugs' in therapeutic approaches aimed at the prevention or treatment of neuropsychiatric diseases. A similar pattern of drug development has occurred in strategies for the treatment of cancer, AIDS and cardiovascular diseases. In this review, we offer an overview of therapeutic strategies and novel investigative drugs discovered or developed in our own and other laboratories, that address multiple CNS etiological targets associated with an array of neuropsychiatric disorders. [source] Examining the Intersection of Sex and Stress in Modelling Neuropsychiatric DisordersJOURNAL OF NEUROENDOCRINOLOGY, Issue 4 2009N. Goel Sex-biased neuropsychiatric disorders, including major depressive disorder and schizophrenia, are the major cause of disability in the developed world. Elevated stress sensitivity has been proposed as a key underlying factor in disease onset. Sex differences in stress sensitivity are associated with corticotrophin-releasing factor (CRF) and serotonin neurotransmission, which are important central regulators of mood and coping responses. To elucidate the underlying neurobiology of stress-related disease predisposition, it is critical to develop appropriate animal models of stress pathway dysregulation. Furthermore, the inclusion of sex difference comparisons in stress responsive behaviours, physiology and central stress pathway maturation in these models is essential. Recent studies by our laboratory and others have begun to investigate the intersection of stress and sex where the development of mouse models of stress pathway dysregulation via prenatal stress experience or early-life manipulations has provided insight into points of developmental vulnerability. In addition, examination of the maturation of these pathways, including the functional importance of the organisational and activational effects of gonadal hormones on stress responsivity, is essential for determination of when sex differences in stress sensitivity may begin. In such studies, we have detected distinct sex differences in stress coping strategies where activational effects of testosterone produced females that displayed male-like strategies in tests of passive coping, but were similar to females in tests of active coping. In a second model of elevated stress sensitivity, male mice experiencing prenatal stress early in gestation showed feminised physiological and behavioural stress responses, and were highly sensitive to a low dose of selective serotonin reuptake inhibitors. Analyses of expression and epigenetic patterns revealed changes in CRF and glucocorticoid receptor genes in these mice. Mechanistically, stress early in pregnancy produced a significant sex-dependent effect on placental gene expression that was supportive of altered foetal transport of key growth factors and nutrients. These mouse models examining alterations and hormonal effects on development of stress pathways provide necessary insight into how specific stress responses can be reprogrammed early in development resulting in sex differences in stress sensitivity and neuropsychiatric disease vulnerability. [source] Behavioural Assays to Model Cognitive and Affective Dimensions of Depression and Anxiety in RatsJOURNAL OF NEUROENDOCRINOLOGY, Issue 10 2008M. D. S. Lapiz-Bluhm Animal models have been used extensively to investigate neuropsychiatric disorders, such as depression, and their treatment. However, the aetiology and pathophysiology of many such disorders are largely unknown, which makes validation of animal models particularly challenging. Furthermore, many diagnostic symptoms are difficult to define, operationalise and quantify, especially in experimental animals such as rats. Thus, rather than attempting to model complex human syndromes such as depression in their entirety, it can be more productive to define and model components of the illness that may account for clusters of co-varying symptoms, and that may share common underlying neurobiological mechanisms. In preclinical investigations of the neural regulatory mechanisms linking stress to depression and anxiety disorders, as well as the mechanisms by which chronic treatment with antidepressant drugs may exert their beneficial effects in these conditions, we have employed a number of behavioural tests in rats to model specific cognitive and anxiety-like components of depression and anxiety disorders. In the present study, we review the procedures for conducting four such behavioural assays: the attentional set-shifting test, the elevated-plus maze, the social interaction test and the shock-probe defensive burying test. The purpose is to serve as a guide to the utility and limitations of these tools, and as an aid in optimising their use and productivity. [source] Factors Influencing Standard Pretravel Health Advice,A Study in BelgiumJOURNAL OF TRAVEL MEDICINE, Issue 5 2007Kristina Van De Winkel MD Background Travelers with risk factors, medical conditions such as immunosuppression, medication intake, pregnancy, or elderly age, need adaptation or reinforcement of pretravel health advice. The literature provides little data on the frequency of these risk groups in the travel population. This study intended to investigate whether risk factors influencing standard travel advice are common in the population attending our travel clinic. Methods A prospective survey was carried out over a 2-month period in 2004 at the travel clinic of the Institute for Tropical Medicine in Antwerp, Belgium. A list of risk factors focused on the following three important advice categories: malaria prophylaxis, yellow fever vaccination, and travelers' diarrhea or other enteric infections. We counted how frequently a risk factor was observed for each advice category (potential influence) and, after considering the travel characteristics, how often a real adaptation of advice was necessary (actual influence). Results Of 2,227 travelers, 276 were found to have a possible influencing factor (12.4%). The potential influence was 10.9% (243/2,227) for malaria prophylaxis advice, 6.1% (136/2,227) for yellow fever vaccination, and 1.9% (43/2,227) for travelers' diarrhea advice. The actual influence was lower 8% (184/2,227), 5% (109/2,227), and 1.2% (27/2,227), respectively. The main interfering factors were as follows: for influence on malaria advice, age ,60 years (44%) and neuropsychiatric disorders (15.6%); for yellow fever vaccination, age ,60 years (63.2%) and immunosuppression (10.3%); and for influence on travelers' diarrhea advice, decreased gastric acidity (44.2%) and immunosuppression (32.6%). Conclusion Travelers with risk factors are not infrequently seen at our travel clinic. Some groups are more prominently present and could be the focus of travel group,specific instructions. The study suggests that being informed about risk groups is essential for advising travelers. [source] Mefloquine prescriptions in the presence of contraindications: prevalence among US military personnel deployed to Afghanistan, 2007,,PHARMACOEPIDEMIOLOGY AND DRUG SAFETY, Issue 2 2010Remington L. Nevin MD Abstract Purpose Contraindications to mefloquine use include a history of certain prevalent neuropsychiatric disorders, which are thought to increase the risk of severe adverse events including anxiety, paranoia, depression, hallucinations, psychosis, and possibly suicide. Within the US military, the continued availability and use of mefloquine is subject to administrative policies dating to 2002 that require clinicians to exercise added caution during prescribing. This analysis was performed to quantify the effectiveness of these policies in ensuring health care provider compliance with package insert prescribing guidance. Methods A previously identified cohort consisting of 11,725 active duty US military personnel, among whom 1127 (9.6%) had contraindications to mefloquine use identified through medical surveillance and pharmaceutical databases, was examined to identify individuals receiving prescriptions for mefloquine in the 45 days prior to a combat deployment in 2007. Results Among the 11,725 cohort members, 4505 (38.4% of the cohort) received a prescription for mefloquine. Among the 1127 cohort members with contraindications, 155 (1.3% of the cohort) were prescribed mefloquine, comprising 13.8% of those with contraindications. Conclusions Despite the longstanding administrative policies meant to reduce such events, approximately one in seven individuals with neuropsychiatric contraindications received a prescription for mefloquine prior to a recent combat deployment, significantly increasing the risk of subsequent adverse events. Given the prevalence of neuropsychiatric disorders among US military personnel and the continued availability of mefloquine, additional study is recommended to describe and quantify the nature and extent of mefloquine-associated adverse events experienced among this group. Published in 2009 by John Wiley & Sons, Ltd. [source] Association study between two variants in the DOPA decarboxylase gene in bipolar and unipolar affective disorder,AMERICAN JOURNAL OF MEDICAL GENETICS, Issue 5 2002Esther Jahnes Abstract Irregularities of dopaminergic and serotonergic neurotransmission have been implicated in a variety of neuropsychiatric disorders. DOPA decarboxylase (DDC), also known as aromatic L -amino acid decarboxylase, is an enzyme involved directly in the synthesis of dopamine and serotonin and indirectly in the synthesis of noradrenaline. Therefore, the DDC gene can be considered as a candidate gene for affective disorders. Recently, two novel variants were reported in the DDC gene: a 1-bp deletion in the promoter and a 4-bp deletion in the untranslated exon 1. Subsequently, an association case,control study including 112 English patients and 80 Danish patients with bipolar affective disorder (BPAD) revealed a significant association with the 1-bp deletion. This finding prompted us to analyze whether this effect was also present in a larger and ethnically homogeneous sample of 228 unrelated German patients with BPAD (208 patients with BP I disorder, 20 patients with BP II disorder), 183 unrelated patients with unipolar affective disorder (UPAD), and 234 healthy control subjects. For both BPAD and UPAD we could not detect a genetic association with either variant. Thus, our results do not support an involvement of the 1-bp or 4-bp deletion within the DDC gene in the etiology of affective disorders. © 2002 Wiley-Liss, Inc. [source] Developmental vitamin D deficiency alters brain protein expression in the adult rat: Implications for neuropsychiatric disordersPROTEINS: STRUCTURE, FUNCTION AND BIOINFORMATICS, Issue 5 2007Lionel Almeras Abstract An increased risk for multiple sclerosis and schizophrenia is observed at increasing latitude and in patients born in winter or spring. To explore a possible link between maternal vitamin D deficiency and these brain disorders, we examined the impact of prenatal hypovitaminosis D on protein expression in the adult rat brain. Vitamin D-deficient female rats were mated with vitamin D normal males. Pregnant females were kept vitamin D-deficient until birth whereupon they were returned to a control diet. At week 10, protein expression in the progeny's prefrontal cortex and hippocampus was compared with control animals using silver staining 2-D gels associated with MS and newly devised data mining software. Developmental vitamin D (DVD) deficiency caused a dysregulation of 36 brain proteins involved in several biological pathways including oxidative phosphorylation, redox balance, cytoskeleton maintenance, calcium homeostasis, chaperoning, PTMs, synaptic plasticity and neurotransmission. A computational analysis of these data revealed that (i) nearly half of the molecules dysregulated in our animal model have also been shown to be misexpressed in either schizophrenia and/or multiple sclerosis and (ii) an impaired synaptic network may be a consequence of mitochondrial dysfunction. [source] Total antioxidant response in patients with schizophreniaPSYCHIATRY AND CLINICAL NEUROSCIENCES, Issue 4 2006BILAL USTUNDAG md Abstract, There is a large amount of convincing data demonstrating that reactive oxygen species (ROS) are involved in initiation and development of many different forms of neuropsychiatric disorders. The levels of oxidants and antioxidants in schizophrenia have been evaluated. However, measurements of total antioxidant response (TAR) were not evaluated up to now. Therefore, the objectives of this study are to investigate plasma TAR levels in schizophrenia subtypes. A total of 76 patients with schizophrenia and 25 healthy volunteers were included in the study. Positive and Negative Syndrome Scale (SANS and SAPS, respectively) were applied to patients. TAR values were determined in the plasma of normal healthy controls and patients with schizophrenia. Plasma TAR levels of each schizophrenia subtype were significantly lower than healthy controls (P < 0.01 for disorganized, residual and undifferentiated subtypes and P < 0.01 for paranoid subtype). When intragroup comparisons were performed, paranoid subtype had higher plasma TAR levels compared to other subtypes (P < 0.01). Accordingly, as a whole group, patients with schizophrenia had lower plasma TAR levels compared to controls. Plasma TAR levels were significantly and negatively correlated with SANS scores, and duration of illness was evaluated but not related to other parameters. Consequently, the present study further emphasizes the growing consideration that free radical damage may have an important etiopathogenetic role on the development of schizophrenia and suggests that decreased plasma total antioxidant levels may be related to the progression of illness. [source] Plasma nitrate values in patients with obsessive-compulsive disorderPSYCHIATRY AND CLINICAL NEUROSCIENCES, Issue 5 2005MURAD ATMACA md Abstract Recently there has been increasing evidence that free oxygen species may play an important role in the pathophysiology of various neuropsychiatric disorders. The present study was performed to assess the changes in plasma nitric oxide (NO) levels in patients with obsessive-compulsive disorder (OCD) compared to age- and sex-matched normal controls. Twenty-three patients with OCD and 23 healthy volunteers were included in the study. NO values were determined in the plasma of normal healthy controls and the OCD patients. Plasma nitrate levels in OCD patients were significantly higher than those in controls and were significantly and positively correlated with Yale-Brown Obsession Compulsion Scale scores but not related to age or to the duration of illness. These findings indicated a possible role of increased NO may be relevant to the pathophysiology of OCD. [source] Annotation: Neurofeedback , train your brain to train behaviourTHE JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES, Issue 1 2007Hartmut Heinrich Background:, Neurofeedback (NF) is a form of behavioural training aimed at developing skills for self-regulation of brain activity. Within the past decade, several NF studies have been published that tend to overcome the methodological shortcomings of earlier studies. This annotation describes the methodical basis of NF and reviews the evidence base for its clinical efficacy and effectiveness in neuropsychiatric disorders. Methods:, In NF training, self-regulation of specific aspects of electrical brain activity is acquired by means of immediate feedback and positive reinforcement. In frequency training, activity in different EEG frequency bands has to be decreased or increased. Training of slow cortical potentials (SCPs) addresses the regulation of cortical excitability. Results:, NF studies revealed paradigm-specific effects on, e.g., attention and memory processes and performance improvements in real-life conditions, in healthy subjects as well as in patients. In several studies it was shown that children with attention-deficit hyperactivity disorder (ADHD) improved behavioural and cognitive variables after frequency (e.g., theta/beta) training or SCP training. Neurophysiological effects could also be measured. However, specific and unspecific training effects could not be disentangled in these studies. For drug-resistant patients with epilepsy, significant and long-lasting decreases of seizure frequency and intensity through SCP training were documented in a series of studies. For other child psychiatric disorders (e.g., tic disorders, anxiety, and autism) only preliminary investigations are available. Conclusions:, There is growing evidence for NF as a valuable treatment module in neuropsychiatric disorders. Further, controlled studies are necessary to establish clinical efficacy and effectiveness and to learn more about the mechanisms underlying successful training. [source] An immunological marker (D8/17) associated with rheumatic fever as a predictor of childhood psychiatric disorders in a community sampleTHE JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES, Issue 5 2003Gale Inoff-Germain Background: Previous studies have documented that various behavioral disturbances accompany Sydenham's chorea, a neurologic variant of rheumatic fever. Further, an immunological marker associated with rheumatic fever (monoclonal antibody D8/17) has been reported to be elevated in several neuropsychiatric disorders, most frequently tics and obsessive-compulsive disorder. We examined this association in a community sample of children previously identified as being D8/17 positive or negative. It was hypothesized that D8/17 positivity would predict increased rates of tics and obsessive-compulsive disorder, even in the absence of Sydenham's chorea. Possible associations with other disorders accompanying Sydenham's chorea , hyperactivity, anxiety, and depression, also were explored. Method: From 1991 to 1995, 2631 children (mean age = 9.6 ± 1.6 years) from a low socioeconomic area of Mexico City were screened for the D8/17 marker. In a 2- to 5-year follow-up of 240 of these children (108 positive and 132 negative), structured psychiatric interviews and rating scales were administered to the child and main caretaker. Assessments were conducted and scored blind to the child's D8/17 status. Results: No association was seen between D8/17 positivity and tics or OCD. Conclusion: This study failed to provide support for the generalized use of D8/17 as a marker of susceptibility to tics and OCD in a community sample. [source] A Genome-wide Association Study of Autism Reveals a Common Novel Risk Locus at 5p14.1ANNALS OF HUMAN GENETICS, Issue 3 2009Deqiong Ma Summary Although autism is one of the most heritable neuropsychiatric disorders, its underlying genetic architecture has largely eluded description. To comprehensively examine the hypothesis that common variation is important in autism, we performed a genome-wide association study (GWAS) using a discovery dataset of 438 autistic Caucasian families and the Illumina Human 1M beadchip. 96 single nucleotide polymorphisms (SNPs) demonstrated strong association with autism risk (p-value < 0.0001). The validation of the top 96 SNPs was performed using an independent dataset of 487 Caucasian autism families genotyped on the 550K Illumina BeadChip. A novel region on chromosome 5p14.1 showed significance in both the discovery and validation datasets. Joint analysis of all SNPs in this region identified 8 SNPs having improved p-values (3.24E-04 to 3.40E-06) than in either dataset alone. Our findings demonstrate that in addition to multiple rare variations, part of the complex genetic architecture of autism involves common variation. [source] SNP Discovery and Haplotype Analysis in the Segmentally Duplicated DRD5 Coding RegionANNALS OF HUMAN GENETICS, Issue 3 2009Donna J. E. Housley Summary The dopamine receptor 5 gene (DRD5) holds much promise as a candidate locus for contributing to neuropsychiatric disorders and other diseases influenced by the dopaminergic system, as well as having potential to affect normal behavioral variation. However, detailed analyses of this gene have been complicated by its location within a segmentally duplicated chromosomal region. Microsatellites and SNPs upstream from the coding region have been used for association studies, but we find, using bioinformatics resources, that these markers all lie within a previously unrecognized second segmental duplication (SD). In order to accurately analyze the DRD5 locus for polymorphisms in the absence of contaminating pseudogene sequences, we developed a fast and reliable method for sequence analysis and genotyping within the DRD5 coding region. We employed restriction enzyme digestion of genomic DNA to eliminate the pseudogenes prior to PCR amplification of the functional gene. This approach allowed us to determine the DRD5 haplotype structure using 31 trios and to reveal additional rare variants in 171 unrelated individuals. We clarify the inconsistencies and errors of the recorded SNPs in dbSNP and HapMap and illustrate the importance of using caution when choosing SNPs in regions of suspected duplications. The simple and relatively inexpensive method presented herein allows for convenient analysis of sequence variation in DRD5 and can be easily adapted to other duplicated genomic regions in order to obtain good quality sequence data. [source] Darier's disease in SingaporeBRITISH JOURNAL OF DERMATOLOGY, Issue 2 2005B.K. Goh Summary Background, Darier's disease is a rare, dominantly inherited genodermatosis. Although it has been well studied in caucasians, very little is known about the clinical spectrum of this disorder among Asians. Objectives, To determine the demographic and clinical profile of Asian patients with Darier's disease. Methods, This is a retrospective study of all new cases of Darier's disease seen in our centre over a 20-year period (1982,2002). Results, Twenty-four nonrelated cases of Darier's disease were studied. The incidence rate was 3·1 per million per decade. The gender distribution was 19 males and five females, and the ethnic origin was 21 Chinese, two Malays and one Nepalese. The peak age of onset was between 11 and 20 years. Sun exposure exacerbated the disease in 13 of the patients, and three had neuropsychiatric disorders. The disease affected predominantly seborrhoeic areas in 19 patients, flexural in three, acral in one and was segmental in one patient. Hand involvement was common and included palmar pits in nine patients, acrokeratosis verruciformis in four and nail changes in 12 patients. Haemorrhagic macules were not seen. Rare features included oral mucosal lesions (two patients) and guttate leucoderma (three patients). Pathogens involved in cutaneous infections included herpes simplex virus, Staphylococcus aureus, Streptococcus species and Morganella morgani. All patients treated with oral retinoids had improvement of clinical signs. In contrast, the response to topical retinoids was poor. Conclusions, Compared with western studies, our results show a similar incidence rate, age of onset, distribution of disease patterns and association with neuropsychiatric disorders. Features that differ include co-occurrence of guttate leucoderma, rarity of acrokeratosis, absence of haemorrhagic macules and poor response to topical retinoids. [source] | |||||||||||||||||||||||||||||||