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1
Mrowicki, Anna. "Disordered eating in gastrointestinal disorders." Thesis, University of Warwick, 2016. http://wrap.warwick.ac.uk/88064/.
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This thesis consists of three chapters, a literature review, an empirical paper, and a reflective paper. Chapter one is a critical review of case study research on Disordered Eating (DE) in Gastrointestinal disorders (GId). Following both database and manual searches, twelve case study reports, describing 29 cases, were included and reviewed. The case study data shows there be a relationship between DE and GId, though the nature and direction of this relationship remains unclear. Possible risk factors for the onset of DE behaviours in the GId population are identified and discussed, as are suggestions for future research. Chapter two is a quantitative research study looking at DE in people with Crohn’s Disease (CD), compared to the general population. Participants in both groups (CD and control) completed self-reported, standardised measures of eating attitudes/behaviours and mood. The prevalence of DE was shown to be higher for people with CD compared to the general population, with females with CD shown to be most at risk of developing DE behaviours. In addition, anxiety and depression in children is highlighted as a possible risk factor for the development of DE in CD, in children. Clinical implications and directions for future research are discussed. Chapter three is a reflective account exploring the researcher’s research journey, from beginning to end. In this paper the choice of thesis topic is discussed, as are the researcher’s associated thoughts and feelings. The researcher’s epistemological position in relation to the methodology and natural style is also explored.
2
Arnold, Marla N. "Validating a model of risk factors associated with eating disorder risk in adolescents." Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1148575712.
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Shaw, Allan. "Functional bowel disorders in anxiety disorder out patients." Thesis, London South Bank University, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.288174.
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MacCallam, Jackie. "Cognitive appraisals in obsessive-compulsive disorder & other anxiety disorders." Thesis, University of Plymouth, 1997. http://hdl.handle.net/10026.1/1138.
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This research applied ideas from the cognition-emotion literature to some of the theories in the OCD literature, and in so doing took'Va multi-dimensional approach to the understanding of OCD. The aim of the study was to explore the nature of 'emotionalcognitive profiles'^ of people with OCD,. and to compare these 'profiles' with those of people with other anxiety disorders and people from a non-clinical population. Participants from the three groups i.e. an OCD group, an anxiety group and a non-clinical group were asked to rate a number of appraisal dimensions, in response to four vignettes. There were 10 participants in each group (N=30). The vignettes were constructed to evoke feelings of anxiety, guilt, anger and pride. The responses of each group were then compared. The results showed that when anxiety is evoked, both people suffering with OCD and people suffering with other anxiety disorders, perceived more personal responsibility and more harm to self than the non-clinical group. The OCD group also seemed to perceive more personal responsiblity in the situation of guilt, which provoked discussion about the nature and role of guilt and responsibility in the aetiology and maintenance of this disorder. The results also led to some debate about the relationship between anxiety, depression and OCD and finally, a formulation of OCD was proposed. The formulation was an attempt to incorporate thinking from both cognitive and psychodynamic perspectives and to draw together some of the theories and models of OCD, which had been discussed in the study.
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Airaksinen, Eija. "Cognitive functions in depression and anxiety disorders : findings from a population-based study /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-954-8/.
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Butler, Emma. "The clinical relevance of personality disorder cognitions in the eating disorders." Thesis, University of East London, 2009. http://roar.uel.ac.uk/3729/.
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Although cognitive behavioural therapy (CBT) is recommended by the National Institute for Clinical Excellence (2004) as the treatment of choice for bulimia nervosa, it has only been found to be effective for 50-60% of individuals. In addition, the evidence base for the efficacy of CBT in the treatment of anorexia nervosa is weak. It is commonly recognised that there is a high comorbidity between personality disorders (and their associated traits) and eating disorders. The purpose of this study was therefore to examine the cognitions underpinning personality disorders in individuals with eating disorders, and to investigate whether those cognitions reduce the impact of CBT for eating disorders. Participants were 59 individuals with a diagnosed eating disorder presenting for CBT at a specialist eating disorder service. Each participant completed measures of personality disorder cognitions, eating disorder attitudes/dysfunctional assumptions and other psychological symptoms at session one of CBT. Participants were then asked to repeat the measures of eating disorder attitudes/dysfunctional assumptions at session six of CBT. Drop-out rates were recorded. Findings provided evidence of the rapid onset of action of CBT for eating disorders. There was a significant reduction in eating disorder attitudes over the first six sessions. Six personality disorder cognitions were significantly associated with eating disorder attitudes/dysfunctional assumptions and other psychological symptoms. These were avoidant, obsessive-compulsive, dependent, borderline, histrionic and paranoid personality disorder cognitions. Higher levels of dependent and narcissistic personality disorder cognitions were associated with dropping out of treatment before session seven of CBT, and higher levels of histrionic, avoidant and borderline personality disorder cognitions were associated with an improvement in eating disorder attitudes in the first six sessions of CBT. The limitations of the study and recommendations for future research are discussed. In addition, the clinical implications of the findings are considered.
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Stinson, Jill D., and Brittany V. Williams. "Redefining Borderline Personality Disorder: BPD, DSM-v, and Emotion Regulation Disorders." Digital Commons @ East Tennessee State University, 2013. https://dc.etsu.edu/etsu-works/7970.
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PISCIOTTA, LIVIA. "Autism Spectrum Disorder and other Neurodevelopmental Disorders: cytogenetic and genomic approaches." Doctoral thesis, Università degli studi di Genova, 2021. http://hdl.handle.net/11567/1057765.
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Introduction: Neurodevelopmental disorders (NDDs) are a heterogeneous class of conditions involving the brain, including intellectual disability (ID) and autism spectrum disorder (ASD), that affect about 1%-3% of children (Miller et al., 2010). The genetics of NDDs is complex and include copy number variations (CNVs), pathogenetic mutations in single genes. To date, more than 1000 genes have been implicated in the etiopathogenesis of NNDs. Preliminary investigations have suggested that the majority of Developmental Disorders, in particular ASD, are actually polygenic; in addition, the genetic and environmental interplay in defining the phenotype clearly classifies NDDs such as ID and ASD as complex disorders. In this dissertation, I sought to explore the contribution of rare de novo and inherited coding variation in neurodevelopmental disorders and use these genetic variations to identify neurodevelopmental disorder associated genes and new/unknown oligogenic mechanisms.
Methods: In a retrospective review of data, we re-evaluated all the results of diagnostic array-CGH tests on 700 cases with NDDs, focusing on variants previously interpreted as VOUS. Furthermore a series of 68 patients with autism spectrum disorder were recruited to perform whole exome sequencing and eventual whole genome sequencing. A deep analysis of VOUS, mainly consisting in a revision of gene expression/function annotation, and chromatine organization data, was performed. New candidate genes were analysed by GeneCodis4 to evidence enrichment for known NDD-associated GeneOntology terms and pathways. Whole exome sequencing was performed and potentially deleterious variants prioritized by custom filtering strategies including the use of ORVAL (Oligogenic Resource for Variant Analysis Platform) and enrichment analysis of candidate genes with GeneCodis4.
Results: In about 42% of cases pathogenic CNVs were found, while in 58% identified CNVs remained initially VOUS. New potential genes and mechanisms such as double-hit mechanisms were found in our patients. In our 34 analysed ASD patients 11 cases showed possible deleterious rare variants, in different and, in the majority of cases, in multiple genes. The role of X chromosome and neurotransmitter pathways appears important.
Conclusion: In our cohort of NDDs patients CNV-mediated double-hit mechanisms seem to play a relevant role in elucidate complex phenotypes. About 10% of patients from our ASD cohort also showed rare deleterious variants in multiple genes that seem to fully explain their complex phenotype.
9
Swinbourne, Jessica M. "The comorbidity between eating disorders and anxiety disorders." Thesis, The University of Sydney, 2008. http://hdl.handle.net/2123/4026.
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Research indicates that eating disorders and anxiety disorders frequently co-occur. The prevalence of anxiety disorders amongst anorexia nervosa and bulimia nervosa samples has been reported in a number of investigations. Despite the significant number of research papers investigating the comorbidity between eating disorders and anxiety disorders, many are plagued by methodological problems, limiting the usefulness of findings. Furthermore, there is a significant lack of research examining the prevalence of eating disorders among anxiety patients, and as a result, the frequency of eating disorder pathology among patients presenting to specialty anxiety clinics is unclear. The current research investigated the prevalence of comorbid eating and anxiety disorders amongst 152 women presenting for either eating disorder treatment or anxiety disorder treatment. The prevalence of anxiety disorders was determined from a sample of 100 women presenting for inpatient and outpatient eating disorder treatment. The prevalence of eating disorders was determined from a sample of 52 women presenting for outpatient treatment of an anxiety disorder. The current study found that 65% of women with eating disorders also met criteria for at least one comorbid anxiety disorder. Furthermore, 69% reported the onset of the anxiety disorder to precede the onset of the eating disorder. Of the anxiety disorders diagnosed, Social Phobia was most frequently diagnosed (42%) followed by PTSD (26%), GAD (23%), OCD (5%), Panic/Ag (3%) and Specific Phobia (2%). We also found that 13.5% of women presenting for anxiety treatment also met criteria for a comorbid eating disorder. The results of this study suggest that the prevalence of eating and anxiety disorder comorbidity is high. It is hoped that the present research will have significant etiological and therapeutic implications and further the understanding of the development and maintenance of eating disorder pathology.
10
Swinbourne, Jessica M. "The comorbidity between eating disorders and anxiety disorders." University of Sydney, 2008. http://hdl.handle.net/2123/4026.
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Doctor of Philosophy(PhD)Research indicates that eating disorders and anxiety disorders frequently co-occur. The prevalence of anxiety disorders amongst anorexia nervosa and bulimia nervosa samples has been reported in a number of investigations. Despite the significant number of research papers investigating the comorbidity between eating disorders and anxiety disorders, many are plagued by methodological problems, limiting the usefulness of findings. Furthermore, there is a significant lack of research examining the prevalence of eating disorders among anxiety patients, and as a result, the frequency of eating disorder pathology among patients presenting to specialty anxiety clinics is unclear. The current research investigated the prevalence of comorbid eating and anxiety disorders amongst 152 women presenting for either eating disorder treatment or anxiety disorder treatment. The prevalence of anxiety disorders was determined from a sample of 100 women presenting for inpatient and outpatient eating disorder treatment. The prevalence of eating disorders was determined from a sample of 52 women presenting for outpatient treatment of an anxiety disorder. The current study found that 65% of women with eating disorders also met criteria for at least one comorbid anxiety disorder. Furthermore, 69% reported the onset of the anxiety disorder to precede the onset of the eating disorder. Of the anxiety disorders diagnosed, Social Phobia was most frequently diagnosed (42%) followed by PTSD (26%), GAD (23%), OCD (5%), Panic/Ag (3%) and Specific Phobia (2%). We also found that 13.5% of women presenting for anxiety treatment also met criteria for a comorbid eating disorder. The results of this study suggest that the prevalence of eating and anxiety disorder comorbidity is high. It is hoped that the present research will have significant etiological and therapeutic implications and further the understanding of the development and maintenance of eating disorder pathology.
11
Fox, Andrew Paul. "Eating disorders." Thesis, University of Birmingham, 2009. http://etheses.bham.ac.uk//id/eprint/423/.
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Overview This thesis is submitted in partial fulfilment of the requirement for the degree of Doctor of Clinical Psychology at the School of Psychology, University of Birmingham. The thesis consists of two volumes. Volume I This volume comprises two parts. The first part is a review of the literature regarding the role of attachment processes in the eating disorders. The second part is a qualitative study that investigates the personal meaning of eating disorder symptoms. The literature review suggests that although attachment processes appear to play a role in the development and maintenance of eating disorders, the precise relationship is unclear. This paper has been prepared for submission to the British Journal of Clinical Psychology. The empirical study uses interpretative phenomenological analysis in an effort to understand the sense people make of their eating disorder experiences. This paper has been prepared for submission to the Journal of Health Psychology. The Executive Summary is also submitted in this volume. Volume II Five Clinical Practice Reports (CPR) are presented in this volume. The first report details the case of a young man experiencing panic attacks and anxiety, formulated from a cognitive-behavioural and psychodynamic perspective. The second report is an evaluation of a new assessment process within a Child and Adolescent Mental Health Service. The third report is a single-case experimental study of an older woman who was experiencing panic-attacks and separation anxiety. The fourth report is a case study of psychotic experiences in a middle-aged man with learning disabilities, formulated from a person-based cognitive therapy perspective. The fifth report is the abstract of an oral presentation of attachment-related considerations within work with a substance-misuse service. All names and identifying features have been changed to ensure confidentiality.
12
Vanhook, Patricia M. "Musculoskeletal Disorders." Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/etsu-works/7407.
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Vanhook, Patricia M., Lynne M. Dunphy, B. Porter, and C. Luskin. "Spinal Disorders." Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/etsu-works/7409.
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Book Summary: Serves the needs of advanced practice nurses because it’s written by nurse practitioners for nurse practitioners, in collaboration with a physician. Organizes content around the Circle of Caring framework for nursing-based knowledge and holistic care. Explores complementary and alternative treatments for each disorder. Covers the broadest range of human disease and disorders using a systems-based approach, presenting both common complaints and common problems to help students narrow down the possible differentials to the most likely diagnosis. Considers interactions of pharmaceuticals with alternative medications and nutraceuticals. Features coverage of pathophysiology and diagnostic reasoning as well as up-to-date guidance on laboratory and diagnostic tests. Emphasizes evidence-based practice with information on evidence levels and more references to primary studies. Integrates discussions of health policy and primary care throughout the text.
14
Rice, Judy A. "Dissociative Disorders." Digital Commons @ East Tennessee State University, 2014. https://dc.etsu.edu/etsu-works/7608.
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Book Summary:This is the only advanced practice guide to provide an overview of the major DSM-5 disorders across the lifespan and complete clinical guidelines for their psychopharmacologic management. It has been compiled by expert practitioners in psychiatric care and is designed for use by nurse practitioners and other primary caregivers in clinical practice.
The guide is organized in an easy-to-access format with disorders for which drugs can play a significant therapeutic role. The listing for each disorder includes clinical features and symptoms, as well as information about the most current and effective drugs for management. A clearly formatted table identifies the first and second lines of drug therapy along with adjunctive therapies for each disorder. Drugs are organized according to classification, and each listing provides the essential information needed to safely prescribe and monitor a patient's response to a particular drug. Brand and generic names, drug class, customary dosage, side effects, drug interactions, pharmacokinetics, precautions, and management of special populations are addressed. Convenient, practical, and portable, this guide will be a welcome and frequently used resource.
15
Rice, Judy A. "Dissociative Disorders." Digital Commons @ East Tennessee State University, 2011. https://dc.etsu.edu/etsu-works/7609.
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Book Summary: This quick reference serves as an authoritative clinical guide to diagnostic treatment and monitoring recommendations for patients with mental disorders in the primary care setting. It offers fast and efficient access to evidence-based diagnostic and therapeutic guidelines for managing psychiatric and mental health conditions. The book guides family and adult advanced practice nurses in making clinical decisions that are supported by the best available evidence, reflecting current research and expert consensus. Additionally, researchers may use this book to identify important clinical questions where more research could be conducted to improve treatment decision making.
This comprehensive text is organized by major diagnostic categories, such as anxiety disorders, with specific diagnoses organized alphabetically within each category. It supports informed practice, which increases confidence in differential diagnosis, safe and effective treatment decision making, reliable treatment monitoring and, ultimately, improved patient outcomes. Additionally, DSM-IV-TR diagnostic standard summaries and ICD-9 codes are incorporated for use in the clinical setting. It is an essential resource in everyday practice for all health care providers.
16
Tobiassen, Linn Graham. "Eating Disorders in Obsessive-Compulsive Disorder : Prevalence and Effect on Treatment Outcome." Thesis, Norges teknisk-naturvitenskapelige universitet, Psykologisk institutt, 2013. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-25188.
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The aim of the present study was to examine the prevalence of eating disorder symptoms in patients with obsessive-compulsive disorder (OCD). Additional aims were to assess whether having comorbid eating disorders could influence the treatment outcome for OCD, and if symptoms of eating disorders were reduced after treatment for OCD. The sample consisted of 93 patients with a primary diagnosis of OCD. The patients underwent assessment with the Yale-Brown Obsessive-Compulsive Scale, Beck Depression Inventory, and Eating Disorder Inventory both prior to and after treatment. First, the analysis showed that the sample of OCD patients had higher prevalence of eating disorders than a population of physically active students. Moreover, the women in the sample had significantly more symptoms of eating disorders than the men. Correlational analysis showed that eating disorders did not affect the treatment outcome for OCD; the patients generally had a significant improvement of OCD symptoms. On the other hand, symptoms of eating disorders were not significantly reduced after treatment. Summarized, this study concludes that there is a high prevalence of eating disorder symptoms among patients with OCD. It further shows that comorbid eating disorders does not hinder the effect of treatment for OCD. However, as the symptoms of eating disorders persist after such treatment, an implication of the present study is that these symptoms may need closer attention.
17
Päären, Aivar. "Long-Term Health Outcome of Adolescent Mood Disorders : Focus on Bipolar Disorder." Doctoral thesis, Uppsala universitet, Institutionen för neurovetenskap, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-239835.
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There has recently been an intense debate about the increased rate of bipolar disorders (BPD) in children and adolescents observed in clinical settings. Thus, there is great interest in child and adolescent symptoms of hypomania and whether these symptoms subsequently will develop into BPD. More knowledge about early signs could give insight into the development of the disorder. There are also concerns that hypomanic symptoms in adolescence indicate excess risk of other health conditions. It has been reported that patients with mood disorders have a high consumption of prescription drugs in different ATC classes. The primary objective of this thesis was to better understand the mental health outcome of adolescents with hypomania spectrum symptoms and to identify early risk factors for adult bipolar disorder among adolescents with mood disorders. In order to widen the scope and investigate health outcome of mood disorder in general psychopharmacological outcomes were included. A community sample of adolescents (N=2 300) in the town of Uppsala, Sweden, was screened for depressive symptoms. Both participants with positive screening and matched controls (in total 631) were diagnostically interviewed. Ninety participants reported hypomania spectrum episodes, while another 197 fulfilled the criteria for major depressive disorder (MDD) without a history of a hypomania spectrum episode. A follow-up after 15 years included a blinded diagnostic interview, a self-assessment of personality disorders, and national register data on prescription drugs and health services use. Adolescent mood symptoms, non-mood disorders, and family characteristics were assessed. Univariate and multivariate analyses were used. The results indicate that the phenomenology of the hypomania spectrum episodes during childhood and adolescence per se does not predict adult bipolar disorder. However, having both affective symptoms during adolescence and a family history of bipolar disorder increases the risk of developing bipolar disorders in adulthood. Disruptive disorder in childhood or adolescence as well as family histories of BPD emerged as significant risk factors that differentiated between the future development of BPD and MDD. Adolescents with hypomania spectrum episodes and adolescents with MDD do not differ substantially in health outcomes in adulthood. Both groups are at increased risk for subsequent mental health problems, high consumption of prescription drugs, and high health care use, compared with the control group. The high rates of prescription drugs in many ATC classes found among the former depressed females seem to indicate a series of co-morbid somatic illnesses. Thus, it is important to identify and treat children and adolescents with mood disorders, and carefully follow the continuing course. Characteristics such as disruptive disorders and family history warrant particular attention.
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Schweitzer, Jana. "Eating disorders : the correlation of family relationships with an eating disorder continuum." PDXScholar, 1988. https://pdxscholar.library.pdx.edu/open_access_etds/3844.
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For the purposes of this study, eating disturbances were placed on a continuum ranging from disordered to normal, and family factors were examined via this framework. Research on anorectics and bulimics indicates that a variety of family variables contribute to the etiology of eating disorders. Research suggests the presence of a subgroup of persons who experience some disturbance in their relationships with food but not to the severity observed among eating disordered individuals. This study examined the relationship between family factors and eating disturbances.
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Warner, Megan Beth. "Personality traits, traitedness, and disorders: towards an enhanced understanding of trait-disorder relationships." Texas A&M University, 2005. http://hdl.handle.net/1969.1/4238.
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Traitedness has been described as the âÂÂthe degree to which a particular trait
structure is approximated in a given personâ (Tellegen, p. 28, 1991) and has been
hypothesized as one explanation for findings of weak trait-behavior relationships. That
is, if traits are differentially applicable to different individuals, then trait-behavior
relationships may be moderated based on the strength with which an individual fits with
a given trait model. This study used moderated multiple regression to test the
moderating effects of four different traitedness indicators to increase the prediction of
diagnostic consistency in four personality disorders, and also tested the main effects of
traitedness estimates to predict cross-situational consistency of functional impairment.
Traitedness estimates performed better in the prediction of increased diagnostic
consistency, though there were some isolated findings of traitedness increasing crosssituational
consistency of functional impairment.
20
Rück, Christian. "Capsulotomy in anxiety disorders /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-769-3/.
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21
Thornton, Michelle J. St George Clinical School UNSW. "Benign anorectal disorders." Awarded by:University of New South Wales. St George Clinical School, 2005. http://handle.unsw.edu.au/1959.4/22466.
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Problem Investigated: A multitude of benign disorders affect the anorectal complex often resulting in significant morbidity. For many of these conditions the pathophysiology and clinical management continue to be debated. This is particularly so for anal fissures, anal incontinence and pelvic floor dysfunction. Procedures Followed: A series of clinical trials was performed. Anal Fissure: Two current management regimes for chronic anal fissure, Glyceryl Trinitrate and Botulinum Toxin, were prospectively assessed for manometric and clinical outcome. A new treatment regime, inducible nitric oxide, was prospectively assessed in an animal model and a new manometric observation in anal fissure patients, the Fast Wave, was validated. Anal Incontinence: The magnitude of the problem and the relative role of several previously identified risk factors was assessed from a manometric data-base. The impact of a standard treatment for Crohn???s disease, the seton, on anal continence was assessed via a retrospective cohort study. The long-term outcome of dynamic graciloplasty and re-do anal sphincter repair, two previously accepted treatments for anal incontinence, were also assessed retrospectively. A new intervention for treating anal incontinence, the magnetic ???Chair???, was prospectively trialed in incontinent patients. Pelvic Floor Dysfunction: A new treatment option for rectocoele, the laparoscopic repair, was compared with an accepted treatment option, the transanal repair via a matched cohort study. A further group of patients with multiple symptoms of pelvic floor dysfunction undergoing the same laparoscopic technique were then prospectively assessed for functional outcome across the pelvic floor compartments. General Results: Anal Fissure; The manometric effects of both glyceryl trinitrate and botulinum toxin, demonstrated in this thesis would imply that their mode of impact on the anal sphincter is other than that of anal pressure reduction. Fissure healing is dependent upon the pre-treatment anal resting pressure and fissure grade, not anal pressures following treatment. Inducible nitric oxide does not increase nitrate levels in the rat internal anal sphincter. A new manometric wave form in the hypertonic internal anal sphincter, the Fast Wave, has been validated. Faecal Incontinence; Faecal incontinence is multi-factorial. However, obstetric birth injuries are the most significant factor predisposing to faecal incontinence following age. Furthermore current government policies are failing to address the problem. The dynamic graciloplasty provides symptomatic long-term relief in only 16 percent of patients and results in significant co-morbidity in most patients. Re-do anal sphincter repair provides relief in 60 percent of patients without further side effects. The use of a seton in Crohn???s perianal disease prevents deterioration of patient continence. Extracorporeal magnetic stimulation, the Chair, may provide significant relief for patients with faecal incontinence. Pelvic Floor Dysfunction: The laparoscopic posterior compartment repair provides relief of bowel symptoms in 31 percent of patients. This does not compare favourably with the transanal long-term symptomatic improvement of 67 percent. The results of the laparoscopic pelvic floor repair in patients with multiple symptoms of pelvic floor dysfunction is disappointing, particularly for bowel and bladder symptom improvement. Major Conclusions: This thesis questions the accepted pathophysiology of anal fissure, highlights the long-term implications of obstetric childbirth injuries on faecal continence and raises concerns about current management strategies for faecal incontinence and pelvic floor dysfunction.
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Nicholson, Andrew Gordon. "Pulmonary lymphoproliferative disorders." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320619.
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Baxter-Versi, Doreen Mary. "Acquired spelling disorders." Thesis, University College London (University of London), 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.262683.
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Vanhook, Patricia M., Lynne M. Dunphy, M. Zycowizc, and C. Luskin. "Soft Tissue Disorders." Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/etsu-works/7410.
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Book Summary: Serves the needs of advanced practice nurses because it’s written by nurse practitioners for nurse practitioners, in collaboration with a physician. Organizes content around the Circle of Caring framework for nursing-based knowledge and holistic care. Explores complementary and alternative treatments for each disorder. Covers the broadest range of human disease and disorders using a systems-based approach, presenting both common complaints and common problems to help students narrow down the possible differentials to the most likely diagnosis. Considers interactions of pharmaceuticals with alternative medications and nutraceuticals. Features coverage of pathophysiology and diagnostic reasoning as well as up-to-date guidance on laboratory and diagnostic tests. Emphasizes evidence-based practice with information on evidence levels and more references to primary studies. Integrates discussions of health policy and primary care throughout the text.
25
Marks, Lori J. "Attention Deficit Disorders." Digital Commons @ East Tennessee State University, 1995. https://dc.etsu.edu/etsu-works/3575.
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Duffy, Colleen. "Prevalence of Undiagnosed Dissociative Disorders in an Inpatient Setting." Thesis, University of North Texas, 2000. https://digital.library.unt.edu/ark:/67531/metadc2578/.
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This study examined the prevalence of undiagnosed dissociative disorders in a sample of 201 adult patients admitted to a private psychiatric hospital in a major metropolitan city in the south-central United States, over an eight-month period. A screening measure, two blind structured interviews, and a blind clinical interview were employed. The lifetime prevalence of dissociate disorders among the interviewed subjects was 40.8%. More specifically, 7.5% were diagnosed with dissociative identity disorder, 15.4% with dissociative disorder not otherwise specified, 13.4% with dissociative amnesia, and 4.5% with depersonalization disorder. Dissociative fugue was not found in this sample. Cohen's kappa reliability coefficients were computed between the three interview measures, resulting in significant findings for the presence of dissociative identity disorder and dissociative disorder not otherwise specified versus no dissociative disorder. The Cohen's kappa reliability coefficients were as follows: DDIS-DES-T = 0.81; SCID-D-DES-T = 0.76; Clinician-DES-T = 0.74, DDIS-SCID-D = 0.74; DDIS-Clinician = 0.71, and SCID-D-Clinician = 0.56. A meeting was conducted at the end of all subject interviews to discuss discrepant findings between measures. Four additional sub-analyses were performed between dissociative and non-dissociative subjects on DSM-IV variables. Patients diagnosed with a dissociative disorder had higher rates of comorbid major depressive disorder, borderline personality disorder, somatization disorder, and childhood history of physical and/or sexual abuse. Theoretical and methodological issues were discussed as they relate to these findings.
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Cook, Laura Michele. "Elucidating the relation of hoarding to obsessive compulsive disorder and impulse control disorders." Diss., Online access via UMI:, 2007.
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28
Rall, Edrich. "Cluster analysis of disorders characterized by impulsivity in patients with methamphetamine use disorder." Master's thesis, Faculty of Health Sciences, 2019. http://hdl.handle.net/11427/31204.
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Background
Individuals with methamphetamine use disorder (MUD) frequently present with psychiatric comorbidities with impulsive features. Little research has been conducted on comorbidity with impulsive features in MUD. Therefore, this cross-sectional study aimed to delineate comorbid disorders with impulsivity in adult patients with a primary diagnosis of MUD.
Methods
Participants with lifetime MUD were included. Well established measures screened for comorbid psychiatric disorders with impulsive features. Illness severity was measured by the Yale Brown Obsessive-Compulsive Scale – adapted for drug use. The UPPS-P Impulsive Behavior Scale was used to assess impulsivity levels. A cluster analysis (CA) of lifetime comorbid disorders with impulsive features was performed. Demographic and clinical correlates of each identified cluster were identified.
Results
Sixty five (n = 65) adults with a primary diagnosis of MUD took part in the study. They were predominantly female (44 females; 21 males), with ages ranging between 18 and 44 years (mean = 30 years; SD = 6.53). The CA rendered 4 groups. Cases (n=12) in the “alcohol cluster” presented with AUD as their only impulsive disorder other than MUD. Cases (n=19) in the “healthy cluster” had no comorbidity. Cases (n=15) in the “antisocial cluster” all had comorbid antisocial personality disorder as well as polysubstance use disorders. Cases (n=19) in the “borderline cluster” had borderline personality disorder and polysubstance use disorders. Illness severity (Y-BOCS-du: p=0.03) and impulsivity levels (UPPS-P: p=0.01) differed significantly between the clusters. The “alcohol cluster” had the highest illness severity and the “antisocial cluster reported the highest levels of impulsivity.
Conclusion
The findings of this contribute to the paucity data on impulsivity in MUD and may have implications for treatment. Understanding how these conditions cluster in MUD, and remaining cognizant of the demographic and clinical correlates of each cluster in MUD, could potentially enable clinicians to identify patients who are at higher risk for engaging in risky behaviors rendering them more vulnerable to treatment non-adherence or relapse
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Wittchen, Hans-Ulrich, Katja Beesdo, and Andrew T. Gloster. "The Position of Anxiety Disorders in Structural Models of Mental Disorders." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2013. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-112646.
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„Comorbidity“ among mental disorders is commonly observed in both clinical and epidemiological samples. The robustness of this observation is rarely questioned; however, what is at issue is its meaning. Is comorbidity „noise“ – nuisance covariance that researchers should eliminate by seeking „pure“ cases for their studies – or a „signal“ – an indication that current diagnostic systems are lacking in parsimony and are not „carving nature at its joints?“ (Krueger, p. 921).
With these words, Krueger started a discussion on the structure of mental disorders, which suggested that a 3-factor model of common mental disorders existed in the community. These common factors were labeled „anxious-misery,“ „fear“ (constituting facets of a higher-order internalizing factor), and „externalizing.“ Along with similar evidence from personality research and psychometric explorations and selective evidence from genetic and psychopharmacologic studies, Krueger suggested that this model might not only be phenotypically relevant, but might actually improve our understanding of core processes underlying psychopathology. Since then, this suggestion has become an influential, yet also controversial topic in the scientific community, and has received attention particularly in the context of the current revision process of the Manual of Mental Disorders (Fifth Edition) (DSM-V) and the International Classification of Diseases, 11th Revision (ICD-11).
Focusing on anxiety disorders, this article critically discusses the methods and findings of this work, calls into question the model’s developmental stability and utility for clinical use and clinical research, and challenges the wide-ranging implications that have been linked to the findings of this type of exploration. This critical appraisal is intended to flag several significant concerns about the method. In particular, the concerns center around the tendency to attach wide-ranging implications (eg, in terms of clinical research, clinical practice, public health, diagnostic nomenclature) to the undoubtedly interesting statistical explorations.
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Sabo, Jason M. "Relative risk of comorbid disorders with childhood and adolescent depressive disorders." Virtual Press, 2007. http://liblink.bsu.edu/uhtbin/catkey/1379125.
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The purpose of this research was to examine the proportion of clients diagnosed with a depressive disorder who also exhibit one or more comorbid disorders. In addition, this study examined multiple aspects of age and gender associated with comorbid disorders in an attempt to better inform treatment and diagnosis of depressive disorders and associated disorders and to answer two questions: 1) What is the proportion of clients diagnosed with a depressive disorder who also exhibit one or more comorbid disorders; and 2) Are there significant differences in number of comorbid disorders among developmental stages and gender. The current study helps to shed light on the understanding of comorbid disorders related to childhood and adolescent depression. Previously, no other study had investigated the changes in comorbidity that take place across childhood development.The present study used an archival data set obtained from the Dean-Woodcock Neurological Battery. Participants included patients that had been referred for psychological and neuropsychological evaluation and treatment at a large outpatient Midwestern neurology practice. For the purpose of the present study, participants were selected from the data set for analysis if he or she were diagnosed with a depressive disorder and were than nineteen-years of age. The sample included 136 males and 74 females (n=210). The ages of the participants ranged from 4 year-old to 18 years-old. Results of an ordinal regression revealed that males were significantly more likely to have a greater number of comorbid diagnoses than females. Additionally, participants appeared to exhibit a greater number of comorbid disorders as the age of the participant increased.Department of Educational Psychology
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Wittchen, Hans-Ulrich, Katja Beesdo, and Andrew T. Gloster. "The Position of Anxiety Disorders in Structural Models of Mental Disorders." Technische Universität Dresden, 2009. https://tud.qucosa.de/id/qucosa%3A26858.
Full textAbstract:
„Comorbidity“ among mental disorders is commonly observed in both clinical and epidemiological samples. The robustness of this observation is rarely questioned; however, what is at issue is its meaning. Is comorbidity „noise“ – nuisance covariance that researchers should eliminate by seeking „pure“ cases for their studies – or a „signal“ – an indication that current diagnostic systems are lacking in parsimony and are not „carving nature at its joints?“ (Krueger, p. 921).
With these words, Krueger started a discussion on the structure of mental disorders, which suggested that a 3-factor model of common mental disorders existed in the community. These common factors were labeled „anxious-misery,“ „fear“ (constituting facets of a higher-order internalizing factor), and „externalizing.“ Along with similar evidence from personality research and psychometric explorations and selective evidence from genetic and psychopharmacologic studies, Krueger suggested that this model might not only be phenotypically relevant, but might actually improve our understanding of core processes underlying psychopathology. Since then, this suggestion has become an influential, yet also controversial topic in the scientific community, and has received attention particularly in the context of the current revision process of the Manual of Mental Disorders (Fifth Edition) (DSM-V) and the International Classification of Diseases, 11th Revision (ICD-11).
Focusing on anxiety disorders, this article critically discusses the methods and findings of this work, calls into question the model’s developmental stability and utility for clinical use and clinical research, and challenges the wide-ranging implications that have been linked to the findings of this type of exploration. This critical appraisal is intended to flag several significant concerns about the method. In particular, the concerns center around the tendency to attach wide-ranging implications (eg, in terms of clinical research, clinical practice, public health, diagnostic nomenclature) to the undoubtedly interesting statistical explorations.
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Fu, Pengfei. "Causes of neurological disorders : associations of pm2.5 exposure and intestinal disorders." HKBU Institutional Repository, 2020. https://repository.hkbu.edu.hk/etd_oa/742.
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Objective: The aims of this project were to (a) perform a systematic review and meta-analysis of the associations between multiple neurological disorders (or neurological diseases) and potential influencing factors, including the association between fine particulate matter (PM 2.5) and intestinal dysfunction, and (b) investigate the mechanisms and toxicological effects of PM 2.5 exposure in the brain and intestines using a mouse model of Alzheimer's disease (AD). Design: A systematic review and meta-analysis was conducted to assess the risks of PM 2.5 exposure, as manifested by the incidence of exposure-associate neurological disorders or intestinal dysfunction. An APP/PS1 transgenic mouse model for AD was used to study the brain damage resulting from PM 2.5 exposure, and the miRNA/mRNA regulatory mechanisms contributing to this damage. The inflammatory injuries and bacterial community changes in the intestines of AD mice exposed to PM 2.5 were also investigated. Data sources: Articles for systematic review and meta-analysis were obtained by searching PubMed and China National Knowledge Infrastructure (CNKI), which were published for more than ten years. Animal experiments were conducted at Shanxi University of Taiyuan in China, and toxicological tests were performed according to the stipulated methods and protocols. Review and experimental methods: Data on the risks of incidence of neurological disorders associated with the environmental factor (PM 2.5) and biological factors (intestinal disorders and bacteria) were obtained, and random- or fixed-effects models (depending on the I 2 value) were used to pool the odds ratios (OR) with the 95% confidence intervals (CI) from individual studies. In the animal experiments, mice were divided into four groups of five animals per group, as follows: normal control mice in filtered air, AD mice in filtered air, normal control mice in PM 2.5 air, and AD mice in PM 2.5 air. PM 2.5 mice were exposed to ambient PM 2.5 in a whole-body inhalation exposure device for 8 weeks in Taiyuan, China. Well-established methods were used to explore the toxicological mechanisms by which PM 2.5 exacerbated brain damage in AD mice, namely open-field testing, enzyme-linked immunosorbent assay (ELISA), real-time quantitative RT-PCR, hematoxylin-eosin (HE) staining, and transmission electron microscopy (TEM). Brain damage and related biomarkers in the brains were measured, and miRNA and mRNA profiles were detected using high-throughput sequencing methods. The signaling pathways of miRNAs or mRNAs were predicted and summarized, and specific miRNAs and mRNAs were screened to explore the possible regulatory mechanisms of PM 2.5 -induced brain damage in AD mice. Intestinal and fecal samples from these mice were also subjected to 16S rRNA gene sequencing. HE staining, ELISA, and metagenome bacterial diversity analyses were performed to investigate the effects of PM 2.5 inhalation on intestinal tissue damage, inflammatory responses, and changes of bacterial diversity and communities in AD mice. Results: Long-term PM 2.5 exposure has been associated with increased risks of stroke, dementia, AD, autism spectrum disorder (ASD), and Parkinson's disease (PD) in humans, with the risks of ischemic and hemorrhagic stroke being higher than that of stroke in general. Furthermore, a relatively higher risk of stroke has been observed in heavily polluted countries compared to less polluted countries. It is known that some intestinal disorders and related problems such as constipation, inflammatory bowel disease, irritable bowel syndrome, small intestinal bacterial overgrowth, and diarrhea significantly increase the risks of developing AD or PD. For example, the risk estimates of Helicobacter pylori infection were significantly associated with AD and PD. From another angle, preliminary animal experimental results showed that PM 2.5 promoted brain morphological damage and decreased spatial exploration ability in AD mice, and was concomitant with increases in the concentrations of amyloid-β-42, acetylcholinesterase, tumor necrosis factor-α, and interleukin-6 and decreases in the concentrations of choline acetyltransferase. High-throughput sequencing and bioinformatics analyses revealed that miRNAs and mRNA had differential expression profiles subsequent to PM 2.5 exposure, which suggested that these species are involved in the molecular regulatory mechanisms and possible signal pathways of PM 2.5 -aggravated brain injury in AD mice. These PM 2.5 -aggravated brain injuries were correlated with pathological intestinal injury, inflammatory responses, and changes in bacterial diversity in the intestines and feces of PM 2.5 -exposed AD mice, and decreases in predominant bacteria were identified. These data will assist in delineating the ability of PM 2.5 exposure to induce pathological changes in the brain and gut tissue via the brain-gut axis and thereby aggravate AD. Conclusions: A systematic review and meta-analysis showed that there is a significant association between PM 2.5 exposure and the occurrence of stroke, dementia, AD, ASD, and PD, and a strong association between intestinal disorders and the presence of certain bacteria and the development of AD and PD. PM 2.5 (environmental factors) and intestinal disorders accompanied by changes in bacterial diversity (internal biological factors) appeared to be the two most important factors that increase the risk of developing neurological disorders. Experimental animal data showed that PM 2.5 potently damaged the brain and intestines of AD mice, and that the toxicological mechanisms of this PM 2.5 -mediated brain injury led to morphological changes, inflammation, and perturbation of miRNA/mRNA regulation in the brain. These data suggest that PM 2.5 inhalation also have modulatory effects on the abundance and diversity of intestinal bacteria in AD mice. The findings of this study have clarified positive relationships between environmental and biological factors and neurological disorders and have elucidated the potential mechanisms by which PM 2.5 may mediate the initiation or exacerbation of AD
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Hommersen, Paul. "Separation Anxiety Disorder and Oppositional Defiant Disorder : perceived comorbidity between disorders resulting from ambiguous items and halo effects." Thesis, University of British Columbia, 2007. http://hdl.handle.net/2429/31331.
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Although theoretical arguments would suggest little comorbidity between Separation Anxiety Disorder (SAD) and Oppositional Defiant Disorder (ODD), epidemiological studies find otherwise. I examined whether ambiguous symptoms and negative halo effects contribute to this comorbidity. In Study 1, 72 mothers read scenarios of children displaying either SAD or ODD behaviors. The SAD scenarios included behaviors considered by judges to be pure exemplars of SAD, as well as behaviors considered to be ambiguous representations of the disorder. ODD scenarios also included both pure and ambiguous behaviors. After each scenario, mothers rated the child on the behaviors presented in the scenario, as well as behaviors of the alternate disorder, and somatic symptoms. Mothers endorsed the ambiguous behaviors presented in the scenarios significantly less than the pure behaviors; and rated the ambiguous behaviors of the non-presented disorder significantly more often than the pure behaviors of the non-presented disorder. This suggests that some comorbidity between SAD and ODD may be explained by the presence of ambiguous items representing the two disorders. For the SAD scenarios, mothers also endorsed non-presented somatic symptoms, suggesting a general negative halo bias in maternal ratings of anxious children. Study 2 used a clinical sample of parents (N = 201) and youth (N = 177) and examined whether using only nonambiguous, or pure, items from commonly used rating scales would decrease the degree of relatedness between SAD and ODD symptoms. Pure anxiety and oppositional scales were created from the Child Behavior Checklist (CBCL) and Youth Self-Report (YSR). In general, the relationship between these pure scales was compared to the relationship between the commonly used, empirically-derived and DSM-oriented scales assessing anxiety and oppositionality on the CBCL and YSR. The pure scales were significantly less related than the empirical or DSM-oriented scales. Thus, the relatedness of the disorders was decreased by assessing only pure exemplars. In sum, the results of these studies suggest that the comorbidity of SAD and ODD observed in epidemiological studies may be partially due to the inclusion of ambiguous items on commonly used rating scales. Implications for clinical assessment and theory are discussed.Arts, Faculty of
Psychology, Department of
Graduate
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Peter, Beate. "Multivariate characteristics and data-based disorder classification in children with speech disorders of unknown origin /." Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/8211.
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Jahng, Seungmin. "Analysis of affective instability on ecological momentary assessments data successive difference, variance decomposition, and mean comparison via multilevel modeling /." Diss., Columbia, Mo. : University of Missouri-Columbia, 2007. http://hdl.handle.net/10355/5077.
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Thesis (M.A.)--University of Missouri-Columbia, 2007.The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from title screen of research.pdf file (viewed on May 11, 2009) Includes bibliographical references.
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Green, Sophie. "The neural basis of disorders of social knowledge : Major Depressive Disorder and Frontotemporal Dementia." Thesis, University of Manchester, 2011. https://www.research.manchester.ac.uk/portal/en/theses/the-neural-basis-of-disorders-of-social-knowledge-major-depressive-disorder-and-frontotemporal-dementia(c5d16402-8a89-4143-b5fd-16c6fb386485).html.
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A fronto-temporo-mesolimbic integration model of moral cognition proposed that the experience of self- and other-blaming feelings is dependent upon integration of different forms of representations including: 1) differentiated conceptual representations about social behaviours served by the anterior temporal lobe, 2) sequential representations about the consequences of social actions in the ventral frontal lobes, and 3) motivational state representations in mesolimbic regions. Here, I use this model to investigate overgeneral forms of self-blaming feelings, such as self-contempt in remitted Major Depressive Disorder (MDD), and inappropriate social behaviour of patients with Frontotemporal Lobar Degeneration (FTLD). Individuals with remitted MDD demonstrated an increased proneness to experience overgeneral self-blaming feelings (self-contempt bias). This was associated with decreased conceptual differentiation when evaluating one's own social behaviour relative to that of others, combined with the tendency to find one's own behaviours more unpleasant than that of other people. An fMRI study revealed that compared to a control group, people with remitted MDD exhibited decreased functional connectivity across a fronto-temporo-limbic network that was selective for self-blaming relative to other-blaming feelings. These findings provide a neural mechanism for self-blaming biases, thereby helping to understand vulnerability to MDD. In the FTLD study, we demonstrated a double dissociation between deficits in conceptual and sequential social knowledge in patients with Semantic (SD) and Frontotemporal Dementia (FTD) respectively. This could partly explain the inappropriate social behaviours occurring in both of these groups. These results shed new light on the basis of self-blaming biases in MDD and inappropriate social behaviour in FTLD, and provide a platform for future investigations of these disorders from this perspective.
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Swetye, Michael Harrison. "Monitoring, identification, and intervention for metabolic disorders in veterans with psychotic disorders." [New Haven, Conn. : s.n.], 2008. http://ymtdl.med.yale.edu/theses/available/etd-12092008-164555/.
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Hill, Becky Carolynn. "Eating disorders during pregnancy." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq22744.pdf.
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Zetterberg, Eva. "Angiogenesis in myeloproliferative disorders /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-383-3/.
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Hoekstra, Rocco. "Pterins and affective disorders." [S.l.] : Rotterdam : [The Author] ; Erasmus University [Host], 2007. http://hdl.handle.net/1765/10522.
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Tomita, Yasushi, and Tamio Suzuki. "Genetics of pigmentary disorders." Wiley, 2004. http://hdl.handle.net/2237/8574.
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Mackay, Gillian Moira. "Kynurenines in neurological disorders." Thesis, University of Glasgow, 2007. http://theses.gla.ac.uk/39/.
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The kynurenine pathway is thought to be involved in neurological disorders but its precise role and the mechanisms involved have yet to be established. Tryptophan can be metabolised via this pathway to produce the neurotoxic N-methyl-D-aspartate (NMDA) receptor agonist, quinolinic acid (QUIN), and the direct generators of reactive oxygen species, 3-hydroxykynurenine (3HKYN) and 3-hydroxyanthranilic acid (3HANA), as well as the neuroprotective NMDA receptor antagonist, kynurenic acid (KYNA). High performance liquid chromatography (HPLC) methods were successfully developed and validated for measuring tryptophan, kynurenine, KYNA, 3HANA and anthranilic acid (ANA) in blood samples, using absorbance and fluorescence detection. The method for determining 3HKYN using electrochemical detection was more problematic and was only used for tryptophan loaded samples and their respective baseline samples. Using HPLC, the concentrations of tryptophan, kynurenine, KYNA, 3HKYN and 3HANA were measured in the blood of Huntington's disease (HD) patients and patients with chronic brain injury, where the injury had occurred at least one year previously. QUIN was also determined for these patients using gas chromatography-mass spectrometry (GC-MS). In addition, the dynamics of the kynurenine pathway were investigated following oral tryptophan depletion and loading. In contrast to these chronic conditions, patients with acute stroke were also studied. The concentrations of tryptophan, kynurenine, KYNA, ANA and 3HANA were determined in the blood of the stroke patients, examining any changes in these concentrations during the two weeks after the stroke. The extent of inflammation and oxidative stress were also assessed for all patients, by measuring the levels of neopterin and the lipid peroxidation products, malondialdehyde and 4-hydroxynonenal. Patients with late stage HD showed abnormal tryptophan metabolism via the kynurenine pathway, together with increased inflammation and oxidative stress. Increased levels of kynurenine together with increased kynurenine: tryptophan (K:T) ratios, indicating greater indoleamine 2,3-dioxygenase (IDO) activity, were observed in blood samples from HD patients in comparison with healthy control subjects. In conjunction with this increased IDO activity, there was a decrease in the ratios of KYNA: kynurenine, suggesting decreased kynurenine aminotransferase (KAT) activity. Inflammation, which may be stimulating IDO activity, could also be decreasing KAT activity, suggested by negativecorrelations between the KYNA: kynurenine ratios and the inflammatory marker, neopterin. The inactivity of KAT suggests a small deficiency in KYNA over a long period of time which could cause a reduction in NMDA receptor antagonism, resulting in slow progressive excitotoxicity contributing to the neurodegeneration in HD. Low KYNA: kynurenine ratios were observed in baseline and tryptophan depleted samples, but after tryptophan loading, HD patients showed similar ratios compared with control subjects. This suggests that loading may be beneficial for HD patients, as more of the neuroprotectant, KYNA can potentially be produced. However, the results suggest that concentrations of the neurotoxin, QUIN, may also be increasing after tryptophan loading. Low concentrations of 3HKYN and 3HANA, with no change in QUIN levels, were also observed in the blood of HD patients. 3HANA levels continued to be decreased for the HD patients after loading. This may suggest degradation of 3HKYN and 3HANA by autoxidation producing reactive oxygen species which could contribute to the high levels of oxidative stress found in these patients. Tryptophan loading in healthy control subjects showed significant increases in the inflammatory marker, neopterin, and in the lipid peroxidation products. These results should be considered when tryptophan loading is used in psychiatric practice and in diets high in tryptophan, such as the Atkins diet. Patients with severe chronic brain injury showed similar alterations in kynurenine pathway metabolism as HD patients, at baseline and throughout the loading and depletion protocols. Although the brain injury had occurred at least one year previously, these patients showed persistent inflammation and oxidative stress, demonstrated by their increased levels of neopterin and lipid peroxidation products compared with healthy controls. In baseline blood samples, there were increased K:T ratios indicating greater IDO activity in the patients. Patients with chronic brain injury showed decreased concentrations of the neuroprotectant, KYNA, as well as low KAT activity, indicated by the decreased KYNA: kynurenine ratios. After tryptophan loading, K:T ratios decreased and the KYNA: kynurenine ratios increased in patients in comparison with controls, suggesting a reversal in the activities of the enzymes IDO and KAT. Similar levels of the inflammatory marker, neopterin, were observed in patients and controls after tryptophan loading. This suggests that these changes in IDO and KAT activities may be related to inflammation. As for the HD patients, patients with chronic brain injury showed lower levels of 3HKYN and 3HANA in their blood, with no change in QUIN levels. These metabolites may be undergoing autoxidation, producing reactive oxygen species which contribute to the ongoing oxidative stress in these patients.The kynurenine pathway was activated following an acute stroke, as indicated by the increased K:T ratios, suggesting greater IDO activity. Stroke patients also had raised levels of neopterin and lipid peroxidation products, indicating inflammation and oxidative stress. There were no changes in the blood concentrations of kynurenines, neopterin or lipid peroxidation products during the fourteen days after a stroke. Stroke patients had reduced levels of 3HANA in their blood, as observed for the HD and chronic brain injury patients. There were negative correlations between the concentration of 3HANA and the volume of the brain lesion, measured by computed tomography (CT) scan, demonstrating the importance of the decreased concentrations of 3HANA. In addition, there were increased levels of ANA in the blood of the stroke patients and the ratios of 3HANA: ANA also correlated with brain lesion volume. Another measurement which correlated with lesion volume was lipid peroxidation, suggesting that oxidative stress contributes to the extent of the brain damage after a stroke. This may suggest that the role of 3HANA in stroke is related to its autoxidation and the generation of reactive oxygen species. Increased concentrations of KYNA were observed in patients who died within three weeks of having a stroke. These high levels of KYNA may have been produced following excitotoxicity and the generation of free radicals, and may cause excessive NMDA receptor blockade or reduced mitochondrial adenosine triphosphate (ATP) synthesis, thus contributing to cell death. The kynurenine pathway was activated and showed abnormal metabolism in all the patient groups, suggesting a potential role for these metabolites in neuronal dysfunction in HD, chronic brain injury and acute stroke. Further work is required to elucidate the role of tryptophan metabolites and whether they may have a direct contribution to neuronal damage in neurological disorders.
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Wilshere, Veronica. "Mentalization and eating disorders." Thesis, University of Surrey, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.543931.
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Nicholson, Josie. "Relationships and Eating Disorders." Thesis, City University London, 2010. http://openaccess.city.ac.uk/1150/.
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Sarberg, Maria. "Sleep disorders during pregnancy." Doctoral thesis, Linköpings universitet, Avdelningen för kliniska vetenskaper, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-117869.
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Background Sleep disorders are known to increase in prevalence during pregnancy, and associations between disturbed sleep during pregnancy and adverse outcomes for mother and child have been reported in a number of studies. However, most of these studies were retrospective and too small to satisfactorily demonstrate the association. Aims To prospectively investigate the development of snoring during pregnancy and assess if there is an association between snoring and sleepiness or adverse pregnancy outcomes. To study the development of restless legs syndrome during and after pregnancy, and whether it is associated with snoring or other pregnancy-related symptoms. To investigate the possible association between depressive symptoms in the postpartum period and sleep related problems during pregnancy, using screening instruments. To objectively evaluate sleep disordered breathing in pregnant women compared to non-pregnant controls and to evaluate differences in Epworth Sleepiness Scale scores between the two groups. Methods Questionnaires containing subjective rating of snoring, Epworth Sleepiness Scale and symptoms of restless legs were used in all studies. Information from the medical records of the pregnant women was also utilized. For objective evaluation of sleep disordered breathing, nocturnal respiratory recordings were used. In the research for the first three papers the same cohort of 500 pregnant women was followed on three occasions during pregnancy and also after delivery, and for the last paper, 100 other pregnant women were compared to 80 nonpregnant controls. Results and conclusions Both snoring and restless legs syndrome increase during pregnancy, but this had no convincing impact on obstetric outcome. Sleep recordings could not verify an increased prevalence of obstructive sleep apnea among pregnant women. Restless legs syndrome was associated with snoring and could persist after delivery. Women who had high scores on the Epworth Sleepiness Scale in the last trimester of pregnancy showed more depressive symptoms in the postpartum period. No difference in item scoring of the Epworth Sleepiness Scale was found between pregnant women and controls.
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Kalinowski, Katherine. "Eating disorders : between people." Thesis, City University London, 2015. http://openaccess.city.ac.uk/14512/.
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The National Institute of Health and Clinical Excellence (NICE) has suggested that 1.6 million people in the UK are affected by eating disorders (NICE, 2004). Generally speaking, eating disorders have major physical, psychological and social consequences (Hjern et al., 2006), often characterized by a poor quality of life (De la Rie et al., 2007) and a high health burden (Mond et al., 2009). Furthermore, anorexia nervosa has the highest rate of mortality of any psychiatric disorder, due to both medical complications associated with the disorder and suicide (BEAT, 2014). This statistic alone is indicative of the vitality of eating disorder research particularly that focused on treatment and prevention. Though the ‘poor quality of life’ and ‘high health burden’ are attributed to the individual sufferer, these adverse complications often seep into the immediate family, including children (Stitt & Rupert, 2014). The majority of studies in this field have explored the impact of parental eating disorders on their children; with a focus on the quantitative relationship between the maternal eating disorder and child development, birth weight and feeding logistics (Stitt & Rupert, 2014). The mother’s subjective experience has been widely neglected. Linville et al. have explored the sociocultural influences on the development of eating disorders. Their evidence suggested that the parents, as the primary socialization agents to their children, significantly influence the development of body image disturbances and disordered eating (Linville et al., 2011). Familial eating disorder pathology has long been a source of ongoing investigation, as studies have consistently indicated that the immediate relatives of individuals with anorexia nervosa show an increased risk of developing an eating disorder themselves (Watkins, Cooper & Lask, 2012). Though the degree of correlation pertaining to genetic and environmental influence is unclear, the link itself is consistent and compelling (Lilenfeld & Kaye, 1998). This chapter will consider the literature surrounding mothers’ experiences of feeding her children while having a disordered relationship with food. First I will consider the impact that parental psychiatric disorders have on their children, specifically, the relationship between maternal eating disorders and child development. I will then review the evidence that characterizes the children of mothers with eating disorders as a ‘at risk’ population. Previous research has identified a number of difficulties that mothers with eating disorders encounter within their parenting role; these will be explored, with a particular focus on the mothers’ subjective experience of feeding their children. And finally, the literature on the transgenerational transmission of eating disorders from mother to child will be reviewed. Treatment options will be contemplated, with a view to creating interventions specifically tailored to mothers with eating disorders and their families. A look forward in the direction of future research will be explored, specifically the effectiveness of family therapy for adults with eating disorders. There is an uneven distribution in the literature of research focused on the quantitative impact of maternal eating disorders on children and the risk of transmission. This bias manifests in an unsaturated body of evidence exploring the mothers’ experience. The current chapter will reflect this disproportionate emphasis and attend to both the majority and minority perspectives. This literature review will illuminate the need for more qualitative research, exploring the mothers’ experience of being a parent while having an eating disorder, specifically, her subjective account of engaging in the function of feeding her children.
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Симоненко, Наталія Олександрівна, Наталия Александровна Симоненко, Nataliia Oleksandrivna Symonenko, and N. Vasko. "Endocrine system and disorders." Thesis, Вид-во СумДУ, 2009. http://essuir.sumdu.edu.ua/handle/123456789/16782.
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Rice, Judy A. "Pediatric Behavioral Health Disorders." Digital Commons @ East Tennessee State University, 2002. https://dc.etsu.edu/etsu-works/7610.
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Fagelson, Marc A. "Disorders of Sound Tolerance." Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/etsu-works/7810.
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Wexler, Isaiah David. "Disorders of pyruvate metabolism." Case Western Reserve University School of Graduate Studies / OhioLINK, 1995. http://rave.ohiolink.edu/etdc/view?acc_num=case1057937741.
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