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516681 research-article2013 ANP0010.1177/0004867413516681ANZJP ArticlesWatson et al. Research Australian &

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New Zealand Journal of Psychiatry 2014, Vol. 48(6) 564­–570 DOI: 10.1177/0004867413516681 Childhood trauma in bipolar disorder © The Royal Australian and New Zealand College of Psychiatrists 2013 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav anp.sagepub.com Stuart Watson1, Peter Gallagher1, Dominic Dougall2, Richard Porter3, Joanna Moncrieff2, I Nicol Ferrier1 and Allan H Young4 Editor’s Choice Abstract Objective: There has been little investigation of early trauma in bipolar disorder despite evidence that stress impacts on the course of this illness. We aimed to compare the rates of childhood trauma in adults with bipolar disorder to a healthy control group, and to investigate the impact of childhood trauma on the clinical course of bipolar disorder. Methods: Retrospective assessment of childhood trauma was conducted using the Childhood Trauma Questionnaire (CTQ) in 60 outpatients with bipolar disorder being treated for a depressive episode and 55 control participants across two centres in north-east England and New Zealand. Results: Significantly higher rates of childhood trauma were observed in patients with bipolar I and bipolar II disorder compared to controls. Logistic regression, controlling for age and sex, identified emotional neglect to be the only significant CTQ subscale associated with a diagnosis of bipolar disorder. Childhood history of sexual abuse was not a significant predictor. Associations with clinical severity or course were less clear. Conclusions: Childhood emotional neglect appears to be significantly associated with bipolar disorder. Limitations include the relatively small sample size, which potentially increases the risk of type II errors. Replication of this study is required, with further investigation into the neurobiological consequences of childhood trauma, particularly emotional neglect. Keywords Bipolar disorder, childhood trauma, depression, emotional neglect Introduction The high prevalence and incidence (Merikangas et al., 2011), chronicity of symptoms (Judd et al., 2002, 2003), and psychosocial impairment (Judd et al., 2005) of bipolar disorder underlines the need to establish its aetiological and risk factors. Bipolar disorder is highly heritable (McGuffin et al., 2003); psychosocial stress also appears to increase the likelihood of first and possibly subsequent episodes (Etain et al., 2008; Post, 1992). Childhood trauma is a recognised indicator of poor prognosis in major depressive disorder (Douglas and Porter, 2012; Nanni et al., 2012) but, in bipolar disorder, whilst the impact of stressors in adulthood on the course of illness has been investigated (Cohen et al., 2004; Paykel, 2003), the impact of early trauma has been relatively neglected. One study has shown that early parental loss is more common (Agid et al., 1999), whilst others have shown that childhood stressful life events are less common (Horesh et al., 2011) or as common (Horesh Australian & New Zealand Journal of Psychiatry, 48(6) and Iancu, 2010) in bipolar disorder compared with healthy controls. Children and adolescents with bipolar disorder have been shown to be exposed to more negative life events and less positive events compared to controls (Romero et al., 2009), although interestingly, a recent paper suggested that the link between stressful events and bipolar disorder may be a consequence of the illness (Hosang et al., 1The Institute for Neuroscience, Newcastle University, Newcastle, UK of Brain Sciences, University College London, London, UK 3Department of Psychological Medicine, University of Otago, Christchurch, New Zealand 4Centre for Affective Disorders, Institute of Psychiatry, Kings College London, London, UK 2Faculty Corresponding author: Stuart Watson, The Wolfson Unit, Campus for Aging and Vitality, The Institute for Neuroscience, Newcastle University, Newcastle NE4 6BE, UK. Email: stuart.watson@newcastle.ac.uk 565 Watson et al. 2012). Studies using the Childhood Trauma Questionnaire (CTQ) (Bernstein et al., 2003) have reported a higher rate of childhood trauma (Fowke et al., 2012), particularly emotional abuse (Etain et al., 2010), in bipolar disorder. Retrospectively reported childhood abuse has been associated with an adverse illness course (Garno et al., 2005; Leverich et al., 2002), more depressive episodes (Garno et al., 2005), greater severity of mania (Garno et al., 2005; Leverich et al., 2002), with earlier onset (Carballo et al., 2008; Garno et al., 2005; Leverich et al., 2002), suicidal ideation (Carballo et al., 2008; Leverich et al., 2002), substance abuse (Brown et al., 2005; Carballo et al., 2008), and with impaired performance on tests of neuropsychological function (Savitz et al., 2008). However, interpretation of these findings is limited by the clinical and methodological heterogeneity of these studies (Daruy-Filho et al., 2011). In this study, childhood trauma, as measured by the CTQ, was compared in a sample of people with bipolar disorder recruited for a randomised trial (Watson et al., 2012) and in a healthy control group. It was predicted that higher CTQ scores would be associated with a diagnosis of bipolar disorder and secondly, that childhood trauma would be associated with measures of clinical severity. Methods Sample This analysis uses baseline assessment data from a randomised placebo-controlled trial of mifepristone treatment in bipolar depression (Watson et al., 2012). The study was carried out in two centres, Newcastle University in the north-east of England and Otago University in Christchurch, New Zealand. The main inclusion criterion was a diagnosis of bipolar disorder current episode depressed, confirmed with the Structured Clinical Interview for DSM-IV (SCID) (First et al., 1997). Additional inclusion criteria were: age between 18 and 65 years, stable medication for a minimum of 4 weeks, the ability to provide informed consent and the ability to adequately understand both written and verbal English. Both men and women were eligible. Potential participants were excluded if they fulfilled criteria for substance abuse or dependence (First et al., 1997), were pregnant, suffered significant medical illness which would render recruitment into the clinical trial unsafe (such as: suffered head trauma with persistent loss of consciousness, a neurological disorder or uncompensated endocrine disorder). A co-morbid axis II diagnosis was not an exclusion criterion. After a complete description of the study, written informed consent was obtained from all participants. The study received full approval from the local ethics committee. Participants were recruited from outpatient clinics allied to the respective centres. Sixty patients were randomized over a 5-year period from October 2004, of which 31 patients met SCID criteria for bipolar I and 25 the criteria for bipolar II. A cohort of 55 age- and sex-matched comparators, who were SCID confirmed as having no current or past history of an axis I disorder, was concurrently locally recruited. Assessment After an initial screening visit, baseline data was collected by trained psychiatrists with full history, case note and medication review. The data included demographic and clinical characteristics of sex, age, body mass index (BMI), pre-morbid IQ measured by the National Adult Reading Test (NART) (Nelson and Willison, 1991) and number of years of education. Measures which may indicate clinical severity included: the 17-item version of the Hamilton Depression Rating Scale (HDRS-17) (Hamilton, 1960); diagnosis of DSM-IV melancholia; length of the current depressive episode (weeks); number of previous hospitalisations; current alcohol intake (standard UK alcohol units per week); diagnosis of rapid cycling bipolar disorder; history of attempted suicide; any form of current suicidal ideation reported to the assessor. The childhood trauma questionnaire (CTQ) was also completed. The CTQ is a validated 28-item self-report questionnaire used to provide a retrospective measure of childhood trauma (Bernstein et al., 2003). It uses a fivepoint Likert-type scale. Twenty-five of the CTQ questions are split into five subscales of maltreatment: emotional abuse, physical abuse, sexual abuse, emotional neglect and physical neglect. The other three questions are used for detecting ‘false-negative’ answers involving a minimisation/denial scale. Statistical analyses Distributions of CTQ scores did not meet the assumption required for parametric analysis. Where appropriate, the bipolar group was divided into SCID (First et al., 1997) determined bipolar I and bipolar II subgroups. Chi-squared (χ2) test was used to compare sex distribution across bipolar and control groups. Age and BMI were normally distributed and were compared across bipolar and control groups using the independent samples t-test. The Mann–Whitney U-test and Spearman’s rank order correlations were used for all other comparisons of continuous variables. CTQ subscales for pooled bipolar and control data were examined using Spearman’s rho to identify significant correlations between subscales to determine suitability for inclusion in a regression analysis. Spearman’s rho was also used to examine relationships between CTQ subscale scores and the demographic variables, age, pre-morbid IQ (NART score) and years of education. CTQ subscale scores were compared between males and females. Step forward logistic regression of CTQ total scores and relevant demographic Australian & New Zealand Journal of Psychiatry, 48(6) 566 ANZJP Articles variables was performed to examine the overall relationship between trauma and bipolar disorder, with the binary outcome variable of bipolar or control group. A separate step forward logistic regression of the relevant CTQ subscales and demographic variables was performed to explore for relationships according to types of trauma. Results Patients and controls were matched for age, sex, pre-morbid IQ (NART score) and years of education, as reported in Table 1. A diagnosis of bipolar disorder was found to be significantly associated with a greater total CTQ score (Table 2). All subscale scores were significantly higher in the bipolar group, apart from sexual abuse. Similar results were found when the analysis was restricted to those with a diagnosis of bipolar I. In participants diagnosed with bipolar II, CTQ total, emotional abuse, emotional neglect and physical neglect scores were significantly greater than controls. Table 3 shows that in bipolar patients, CTQ scores did not differ between those with and those without suicidal ideation, although scores for the emotional neglect subscale showed a trend towards significance. Participants with a diagnosis of DSM-IV melancholia had significantly higher CTQ total scores, and significantly higher emotional neglect and emotional abuse scores than those without. Participants with a diagnosis of rapid cycling bipolar disorder had higher sexual abuse subscale scores than those who were not rapid cycling. In bipolar patients who reported one Table 1. Demographic and clinical characteristics of the bipolar group and control group. Bipolar patients % or mean (SD) Controls % or mean (SD) Comparison (p) Male (%) 53.3 54.5 χ2 = 0.02 (0.896) Age (mean years) 47.9 (9.4) 45.1 (13.1) t = 1.3 (0.193) BMI 29.8 (6.2) 26.0 (3.7) t = 3.0 (0.004) 110.6 (10.5) 113.3 (11.3) U = 1152.5 (0.089) 14.7 (3.3) 14.8 (4.3) U = 917.0 (0.554) NART IQ Years of education BMI: body mass index; NART IQ: National Adult Reading Test IQ. Table 2. CTQ scores in bipolar groups compared to controls.a All bipolar N = 60b Bipolar I N = 31b,c Comparison CTQ (SD) U p Bipolar II N = 25b,c Control N = 55% Comparison Comparison CTQ (SD) U p CTQ (SD) U p CTQ (SD) CTQ total 44.4 (19.1) 490.0 < 0.001 43.6 (20.6) 280.5 0.004 41.1 (13.1) 203.0 0.003 31.2 (8.0) Emotional abuse 10.4 (5.4) 780.0 < 0.001 10.2 (5.8) 470.0 0.012 9.7 (4.3) 294.0 0.005 6.8 (2.8) Physical abuse 7.5 (4.4) 903.0 0.005 7.9 (4.9) 461.0 0.005 6.0 (2.1) 439.5 0.387 5.4 (1.3) Sexual abuse 7.7 (5.4) 1092.5 0.131 7.9 (4.9) 584.5 0.182 7.1 (4.1) 428.5 0.224 6.2 (3.1) 12.4 (6.0) 767.0 < 0.001 12.7 (7.0) 459.5 0.011 11.1 (4.2) 299.0 0.008 8.2 (3.5) 7.9 (3.8) 787.5 < 0.001 8.1 (4.2) 446.0 0.002 7.2 (3.0) 306.5 0.003 5.7 (1.7) Emotional neglect Physical neglect aTable showing mean and SD of CTQ scores in different subject groups with a comparison using Mann–Whitney U-test of CTQ scores between the bipolar groups (all bipolar patients and those with a diagnosis of bipolar I or bipolar II) with controls. bNumbers vary due to the incomplete return of CTQs: all bipolar, N = 49–57; bipolar I, N = 25–31; bipolar II, N = 20–22; control, N = 39–45. cFour participants with bipolar disorder were not sub-classified as either bipolar I or II. CTQ: Childhood Trauma Questionnaire. Australian & New Zealand Journal of Psychiatry, 48(6) 567 vary due to the incomplete return of CTQs: history of attempted suicide, yes N = 23–29, no N = 21–23; current suicidal ideation, yes N = 11–13, no N = 34–40; rapid cycling, yes N = 6, no N = 38–46; DSM-IV melancholia, yes N = 21–24, no N = 23–27. CTQ: Childhood Trauma Questionnaire. aNumbers 0.046 222.0 (3.8) 6.9 (3.7) 8.9 137.0 0.976 (3.5) 7.8 9.3 9.2 Physical neglect (4.3) 6.6 (2.7) 218.5 0.029 6.8 (2.2) 8.2 (4.3) 235.0 0.597 (6.5) 0.031 210.0 (5.2) 10.9 (6.0) 129.5 0.807 14.3 (5.9) 12.6 12.5 13.7 Emotional neglect (6.4) 11.4 (5.4) 255.0 0.146 9.7 (5.9) 13.1 (6.0) 169.0 0.058 (6.7) 0.907 319.0 (5.3) 7.6 (6.0) 8.2 75.5 0.038 (5.0) 7.4 12.7 9.0 Sexual abuse (6.2) 6.7 (4.6) 265.0 0.198 8.4 (4.9) 7.7 (5.8) 190.0 0.184 (7.9) 0.227 264.5 (3.5) 7.0 (4.3) 7.8 116.0 0.503 (3.9) 7.2 10.2 8.3 Physical abuse (5.6) 6.9 (2.8) 322.5 0.831 6.8 (3.2) 7.9 (4.9) 234.0 0.569 (7.7) 0.216 259.0 (4.2) 8.9 (6.2) 113.5 0.479 11.6 (5.3) 10.1 12.3 11.5 Emotional abuse (5.9) 9.2 (5.0) 260.5 0.174 10.1 (5.6) 10.4 (5.6) 256.0 0.933 (6.4) 0.023 p U (14.9) 145.0 CTQ (SD) (20.8) 37.7 CTQ (SD) p U 92.0 0.451 49.8 (16.3) (SD) CTQ (32.6) 42.9 56.8 CTQ (SD) p U (20.3) 176.5 0.781 (SD) CTQ (19.4) 44.7 (SD) CTQ 42.8 0.051 p U Comparison (12.8) 158.5 CTQ (SD) (23.1) 38.3 CTQ (SD) No N = 42a Yes N = 14a No N = 24a Yes N = 31a 51.6 No N = 48a Yes N = 7a Comparison Rapid cycling Current suicidal ideation History of attempted suicide Table 3. Analyses of bipolar group clinical severity and clinical characteristics. CTQ total No N = 29a Yes N = 25a Comparison DSM-IV melancholia Comparison Watson et al. or more previous suicide attempts, CTQ total score was higher (p = 0.051), and scores significantly higher in the emotional abuse subscale. No significant correlations between CTQ total or CTQ subscale scores and length of current episode, number of previous hospitalizations, current severity of depression (HDRS-17 score), current alcohol intake were found (rs < 0.3, p > 0.1). Bivariate correlations between pooled bipolar and control scores of the five trauma subscales found significant correlations between all subscales (0.33 < rs < 0.64, p < 0.002), apart from between physical and sexual abuse (rs = 0.12, p = 0.17). All correlations were below 0.8 and therefore could be entered into a regression model without risk of multi-colinearity. Differences or associations with CTQ subscale scores and demographic characteristics were limited to age, which was significantly, but weakly, correlated with emotional neglect (rs = 0.14, p = 0.046) and sexual abuse scores which were significantly higher in females (U = 873.0, p < 0.001). NART scores or years of education were not significantly correlated with the CTQ subscales (rs < 0.2, p > 0.1). The factors considered to be plausible independent causal risk factors, i.e. CTQ total score, age and sex, were entered into step forward logistic regression, with the dependent variable of group (bipolar or control). This confirmed CTQ total score was the only significant predictor (β = 0.08, p = 0.001). The five subscale scores, age and sex, were then entered into a second step forward logistic regression, also with the dependent variable of group. Emotional neglect (β = 0.185, p < 0.001) remained the only significant predictor in the model (Table 4). Emotional abuse approached significance (p = 0.082). Discussion This paper demonstrates significant associations between childhood trauma and bipolar disorder. Higher CTQ scores were found in patients diagnosed with both bipolar I and bipolar II disorder compared to controls. Sexual abuse was the only subscale measure that was not higher in bipolar patients compared with controls. In bipolar patients with a diagnosis of DSM-IV melancholia, emotional neglect and physical neglect scores were higher. CTQ subscale scores were higher in those with a past history of attempted suicide or a diagnosis of rapid cycling bipolar disorder. Logistic regression showed CTQ total scores to differentiate bipolar patients from controls, and separately identified emotional neglect to be the only significant subscale of the CTQ to differentiate bipolar patients from controls. Emotional abuse approached significance and may therefore be considered as a potential contributor to the model. Our study is in line with the findings of two previous studies which also found that patients with a diagnosis of bipolar disorder reported higher rates of childhood trauma compared to healthy controls (Etain et al., 2010; Fowke et al., 2012). Exploring the subscales, we did not find Australian & New Zealand Journal of Psychiatry, 48(6) 568 ANZJP Articles Table 4. Logistic regression of CTQ subtypes predicting a diagnosis of bipolar disorder (I and II). Step 1 Age Gender Emotional abuse Physical abuse Sexual abuse Physical neglect Step 1a Emotional neglect Constant Score df 0.324 0.119 3.030 1.790 0.017 1.865 1 1 1 1 1 1 p 0.569 0.730 0.082 0.181 0.896 0.172 β Wald p 0.185 1.651 14.393 10.246 < 0.001 0.001 CTQ: Childhood Trauma Questionnaire. significant differences in the sexual abuse scale, which is in accord with one previous report (Etain et al., 2010) and is supported by a recent paper that found sexual abuse to be the least reported form of abuse by bipolar patients (Larsson et al., 2013), although other studies did find this association (Fowke et al., 2012; Hyun et al., 2000). Our findings differed in identifying emotional neglect, as opposed to an earlier finding of emotional abuse, to be the single significant subscale associated with bipolar disorder (Etain et al., 2010; Fowke et al., 2012). Methodological differences with the previous studies utilising the CTQ (Etain et al., 2010; Fowke et al., 2012) relate to the presence or absence of current episode and to the sample size. Our finding that a history of childhood trauma is related to a history of suicide attempts in bipolar patients is also in line with other studies (Alvarez et al., 2011; Carballo et al., 2008; Garno et al., 2005; Leverich et al., 2002), although two of these studies did not use a validated measure to retrospectively assess for childhood trauma (Carballo et al., 2008; Leverich et al., 2002). The allostatic impact of childhood trauma may be mediated through a range of biological systems with the hypothalamic–pituitary–adrenal (HPA) axis appearing to have a central role (Grande et al., 2012). It can also be argued that childhood trauma, at sensitive periods, may trigger an altered developmental pathway (Bateson et al., 2004), mediated in part by epigenetic processes (McGowan et al., 2009). For example, the regulation of hippocampal GR expression (McGowan et al., 2009) may induce ‘evolutionary appropriate’ responses such as increased vigilance, alertness to danger, responsivity to novel stressors and a willingness to explore new environments (Glover, 2011). The trade-off for such responses may be an increased risk of behavioural problems in childhood (Ramchandani et al., 2012) and of adult psychopathology including bipolar disorder (Watson et al., 2007) and suicidality (McGowan Australian & New Zealand Journal of Psychiatry, 48(6) et al., 2009). It is of interest that emotional neglect was the only subscale which significantly differentiated patients from controls. Emotional neglect suggests a pervasive deficiency in the parent–child relationship (Glaser, 2002), has been repeatedly linked with HPA axis dysregulation in adults (Gerra et al., 2008, 2010; Watson et al., 2007) and has been previously shown to be differentially related to depression (Spinhoven et al., 2010). It has been suggested that retrospective assessment of childhood trauma may be liable to recall bias in depressed patients (Lewinsohn and Rosenbaum, 1987). However, it should be noted that autobiographical recall of events (as measured using CTQ scores) in our study did not significantly correlate with severity of depression. CTQ scores have also been demonstrated to remain stable over time and to be independent of the current degree of abuse-related psychopathology (Paivio, 2001). Although there have been concerns that retrospective reporting overestimates associations between abuse and adult psychopathology compared to prospective assessment (Gilbert et al., 2009), a recent study found retrospective, compared to prospective, assessment of maltreatment predicted similar rates of mental disorder (Scott et al., 2012). A previous study has shown that recall bias accounted for less than 1% of reporting variance for measures of childhood abuse (Fergusson et al., 2011). However, emotional neglect is arguably the most subjective and difficult to define among forms of abuse, and hence further examination of the relationship between abuse and neglect and bipolar disorder in prospective studies which exclude recall bias would be useful. Investigations with euthymic bipolar patients would help to clarify the potential impact of current mood state. A weakness of this study is the relatively small sample size, which engenders the risk of type II errors. Further, the use of baseline data from a randomized controlled trial may have resulted in an under-sampling of more severe bipolar patients or those with comorbidities, which in turn may have resulted in an underestimation of the rates of childhood trauma in the bipolar group given the association between childhood trauma and poorer clinical outcomes (Garno et al., 2005; Leverich et al., 2002). Conclusions The association of perceived childhood trauma and depression is established (Nanni et al., 2012). This study adds to the literature suggesting a similar relationship in bipolar disorder, although confirmation in prospective studies is desirable. Emotional neglect may be particularly pernicious. Further consideration of its psychological and neurobiological mediation is warranted. Acknowledgements We are grateful to the participants who contributed to the research and to all those who helped in participant recruitment. Watson et al. Funding The study was funded by the Stanley Medical Research Institute (REF.: 03T-429) and the Medical Research Council (REF.: G0401207). Declaration of interest The authors declare that there is no conflict of interest. The funders did not influence the design or dissemination of the study. References Agid O, Shapira B, Zislin J, et al. (1999) Environment and vulnerability to major psychiatric illness: a case control study of early parental loss in major depression, bipolar disorder and schizophrenia. Molecular Psychiatry 4: 163–172. 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Question Name two different methods for evaluating evidence. Compare and contrast these two methods.

Statement 1

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Two methods for evaluating evidence:

Systemic review: a formal research study that “follows clear, predefined structure to find, assess, and analyze studies that have all tried to answer a similar question” (The PubMed Health, 2018). The steps for systemic review are: 1. Formulating Topic, 2. Developing the systematic review protocol, 3. Finding and assessing individual studies, 4. Synthesizing the body of evidence, 5. Providing a detailed comprehensive final report (The PubMed Health, 2018). Systemic review “objectively summarize large amounts of information, identifying gaps in medical research, and identifying beneficial or harmful interventions which will be useful for clinicians, researchers, and even for public and policymakers” (Gopalakrishnan & Ganeshkumar, 2013).
Meta-analysis: “Statistical analysis carried out to integrate and synthesize findings from completed studies to determine what is known and not known about a particular research area” (Grove, Gray, & Burns, 2015, p.507).
Both methods are “prepared with the aim of capacity building for general practitioners and other primary healthcare professionals in research methodology and day-to-day clinical practice” (Gopalakrishnan & Ganeshkumar, 2013). Some flaws identified by Gopalakrishnan and Ganeshkumar (2013) about both methods are loss of information on important outcomes, inappropriate subgroup analyses, and duplication of publication.

References:

Gopalakrishnan, S., & Ganeshkumar, P. (2013). Systematic Reviews and Meta-analysis: Understanding the Best Evidence in Primary Healthcare. Journal of Family Medicine and Primary Care, 2(1), 9–14. http://doi.org/10.4103/2249-4863.109934

Grove, S., Gray, J., Burns, N. (2015). Understanding Nursing Research, 6th Edition. [Pageburstl]. Retrieved from https://pageburstls.elsevier.com/#/books/978145577…

The PubMed Health. (2018). What is a Systematic Review? Retrieved from https://www.ncbi.nlm.nih.gov/pubmedhealth/what-is-a-systematic-review/

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Statement 2

Two methods for evidence evaluation is critical appraisal and meta-analysis. According to Grove, Gray, and Burns (2015), a critical appraisal is a literature review of qualitative or quantitative research that evaluates the weaknesses and strengths of a study to determine if the evidence is useful and whether the study results are reliable. Meta-analysis is the review of a combination of related studies to determine the validity of the evidence (Grove et al., 2015). Although both are determining the trustworthiness of the evidence provided in a study, the critical appraisal is looking at the study itself, assessing research methods, adequacy of sample size, and whether it was performed in an unbiased manner; whereas the meta-analysis looks at many different studies, with the same research question determining its validity based on the consistency of the findings (Grove et al., 2015). A personal preference would be to use the Meta–analysis for review because the congruency of the results would prove more reliable and the critical appraisal seems more time consuming.

References

Grove, S., Gray, J., Burns, N. (2015). Understanding Nursing Research, 6th Edition. [Pageburstl]. Retrieved from https://pageburstls.elsevier.com/#/books/978145577…

RESPOND TO THE STATEMENT WITH 175 WORDS APA FORMAT SOURCE EACH RESPONSE.

Statement 3

There are various methods that researchers use to evaluate evidence. When evaluating evidence it is imperative to ask questions such as: what forms of evidence are more reliable than others, how can one draw accurate conclusions from evidence, and how can the evidence be interpreted reliably.

Meta- analysis and systematic reviews have become increasingly important in healthcare settings. A systemic review is a critical assessment and evaluation of all research studies that address a particular issue. Researchers use an organized method of locating, assembling, and evaluating a body of literature on a particular topic using a set of specific criteria.

Systemic reviews have specific advantages in which they used methods to eliminate bias, and draw reliable and accurate conclusions. Systemic reviews are increasingly being used as a preferred research method and plays an important role in formulating evidence-based nursing practice. Meta-analysis is a method used for quantitatively integrating the results of multiple or similar studies addressing the same research question.

Both methods help to reduce bias, provide adequate power to demonstrate differences in outcomes and resolves the results of inconsistent studies (Gopalakrishnan & Ganeshkumar, 2013).

Gopalakrishnan, S., & Ganeshkumar, P. (2013). Systematic reviews and meta-analysis: understanding the best evidence in primary healthcare. Journal of Family Medicine and Primary Care, 2(1), 9–14. http://doi.org/10.4103/2249-4863.109934

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Statement 4

Systemic reviews and meta-analysis are two main ways to evaluate evidence in research articles. Often used in combination, these methods help to understand the broad view of research related to the topic. Systemic review focuses on getting specific criteria in order to evaluate the research application while reducing the amount of extraneous data material (Uman, 2011). Systemic review is considered to be the new standard for evaluating evidence since the goal is to accurately ascertain data that is replicable that will lead to the best clinical-making decisions.

Meta-Analysis is another important form of evidence evaluation which is used to assess collective data into one qualitative study. Systemic review often includes the meta-analysis in order to summarize the results to apply to clinical actions or changes (Uman, 2011). Meta-analysis is a more stastical analysis of the data which can be derived from the material gathered in a systemic review. This method may be problematic in the aspect that it lacks the specificity of data that a systemic review may identify. This may lead to skewed results from differences in the subject groups or variables in the study.

Combining these studies helps maximize the application of the data from the studies being assessed. Using both systematic and meta-analysis of the data helps to ensure the results are related to the topic as well as replicable in order to confirm validity.

Uman, L. (2011) Systemic Reviews and Meta-Analyses. Journal of the canadian academy of child and adolescant psychiatry 20(1) 57-59. Retreived from

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC30247…

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Statement 5

Systematic review is one of the common methods for evaluating evidence (PubMed Heath Team, 2018). This type of review clearly defines structure. It reviews and responds to a set of inquiries. The purpose of this method is to define

Literature Review

Literature Review

476458 8Violence Against WomenLevendosky et al. © The Author(s) 2011 VAWXXX10.1177/107780121347645

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Reprints and permission: http://www. sagepub.com/journalsPermissions.nav Article PTSD Symptoms in Young Children Exposed to Intimate Partner Violence Violence Against Women 19(2) 187­–201 © The Author(s) 2013 Reprints and permissions: sagepub.com/journalsPermissions.nav DOI: 10.1177/1077801213476458 vaw.sagepub.com Alytia A. Levendosky1, G. Anne Bogat1, and Cecilia Martinez-Torteya2 Abstract Intimate partner violence (IPV) places infants and young children at risk for development of trauma symptoms. However, this is an understudied consequence of IPV because young children pose particular difficulties for assessment of trauma symptoms. The authors collected maternal reports on mothers’ and children’s posttraumatic stress disorder (PTSD) symptoms and IPV yearly, from ages 1 to 7. Approximately half of the children exposed to IPV at each time period developed some trauma symptoms, and frequency of IPV witnessed was associated with PTSD symptoms. Maternal and child PTSD symptoms were correlated, suggesting that young children may be particularly vulnerable to relational PTSD due to their close physical and emotional relationship with their parents. Keywords childhood exposure, intimate partner violence, PTSD, trauma There is a dearth of research on posttraumatic stress disorder (PTSD) in young children that occurs as a result of exposure to intimate partner violence (IPV; defined here as male violence against a female romantic partner). This is unfortunate, as young children are at high risk for exposure to IPV. Families in which IPV occurs are more likely than the general population to have children under the age of 5 (Fantuzzo, Boruch, Beriama, Atkins, & Marcus, 1997). Also, young children are likely to witness the violence directly (i.e., see or hear it) because they are often in the presence of their mothers (DeJonghe, von Eye, Bogat, & Levendosky, 2006; Fantuzzo et al., 1997). Between 20% and 25% of school-age children 1 Michigan State University, East Lansing, MI, USA DePaul University, Chicago, USA 2 Corresponding Author: Alytia A. Levendosky, Department of Psychology, Michigan State University, East Lansing, MI 48824, USA. Email: levendo1@msu.edu 188 Violence Against Women 19(2) living in homes with IPV report that they directly witness it (McCloskey, Figueredo, & Koss, 1995; McCloskey & Walker, 2000; O’Brien, John, Margolin, & Erel, 1994). When IPV episodes involve law enforcement, the rate of child witnessing at all ages increases to 95% (Fusco & Fantuzzo, 2009). Exposure to IPV results in an increased risk of behavioral and emotional problems among children, as demonstrated by recent meta-analyses (e.g., Chan & Yeung, 2009; Evans, Davies, & DiLillo, 2008; Sternberg, Baradaran, Abbott, Lamb, & Guterman, 2006). The problems include externalizing (e.g., Davis & Carlson, 1987; Fantuzzo et al., 1991; Hughes, 1988; Graham-Bermann & Levendosky, 1998a) and internalizing symptoms (e.g., Grych, Jouriles, Swank, McDonald, & Norwood, 2000; Hughes, 1988), such as PTSD and dissociative symptoms (Bogat, DeJonghe, Levendosky, Davidson, & von Eye, 2006; Graham-Bermann & Levendosky, 1998b; Levendosky, Huth-Bocks, Semel, & Shapiro, 2002). The extant literature provides only a broad, generic understanding of the effects of IPV on children’s PTSD symptoms. The current research focused on children exposed to IPV during the time they were aged 1 to 7 years. The number of children exposed to IPV varied from 29 to 48 across these ages. Our unique, longitudinal data set allowed us to elucidate developmental differences in the symptom picture of these children. In addition, we examined why, because IPV is a unique interpersonal stressor, it is important to understand the child’s trauma symptoms in the context of the mother’s traumatic response as well as the severity of the IPV she experiences. Problems Diagnosing PTSD in Young Children A significant difficulty in accurately diagnosing very young children stems from their inability to report on their psychological symptoms (Scheeringa, Zeanah, Myers, & Putnam, 2003; Stover & Berkowitz, 2005); thus, children’s symptoms are generally assessed through parental report. However, because PTSD symptoms are more likely to be on the internalizing rather than the externalizing spectrum (e.g., feeling confused about the event) and, thus, not “visible” to the parent, there are inevitably problems with reliability. For example, all of the reexperiencing symptoms cannot be assessed by an external observer (parent or otherwise) in children below the age of 1 (e.g., bad dreams [with or without clear content] or flashbacks about the traumatic event) as, without significant language skills, the child cannot describe the content of his or her dreams. It is really only at age 3 that clinicians and researchers can begin to have more confidence in parental assessment of PTSD reexperiencing symptoms. There are two current sets of diagnostic criteria for PTSD in young children: the DSMIV-TR (Diagnostic and Statistical Manual of Mental Disorders, text rev., American Psychiatric Association, 2000) and DC: 0-3R (Diagnostic Classification of Mental Health and Developmental Disorders of Infancy and Early Childhood, rev. ed.; Zero to Three, 2005). The DSM-IV-TR criteria require A1 (exposure to trauma) and A2 (reaction of fear, helplessness, or horror) as well as one reexperiencing symptom, three avoidance symptoms, and two arousal symptoms (same as for adults). Some guidance is given for modifications of symptoms that are useful when diagnosing children. The major difference in the Levendosky et al. 189 two diagnostic systems is that the DC: 0-3R diagnosis of PTSD excludes the A2 criteria and reduces the number of criteria needed for the avoidance/numbing symptom cluster to one symptom. In addition, it eliminates some criteria that are clearly inappropriate for young children (“intense psychological distress at exposure to internal or external cues that symbolize or resemble the trauma” and “inability to recall an important aspect of the trauma”) and adds one new avoidance/numbing symptom (i.e., “social withdrawal”). The DC: 0-3R diagnosis shows predictive validity of children’s problems in functioning and is reliable over time (Meiser-Stedman, Smith, Glucksman, Yule, & Dalgleish, 2008; Scheeringa, Zeanah, Myers, & Putnam, 2005). However, some research indicates that very young children may experience additional/ different trauma symptoms that are not contained within either the DSM-IV-TR or the DC: 0-3R (Scheeringa & Zeanah, 1995, 2001). These include constriction of play, regression to earlier functioning (such as loss of toilet training), aggression, separation anxiety, and development of new fears (Scheeringa & Zeanah, 1995). This symptom cluster, called “New Symptoms,” was included in the diagnosis of Traumatic Stress Disorder (TSD) in the original DC: 0-3 (Diagnostic Classification of Mental Health and Developmental Disorders of Infancy and Early Childhood, Zero to Three, 1994). Thus, if using the DSMIV-TR or the DC: 0-3R, the more constricted range of symptoms that exclude those most applicable to young children may limit the clinician and researcher from diagnosing PTSD symptoms in young children. Assessment of PTSD symptoms needs to be developmentally sensitive. Recent studies suggest that the DC: 0-3R is the superior system for children aged 0 to 6 (Meiser-Stedman et al., 2008; Scheeringa, 2008); however, in our opinion, children under the age of 1 year cannot be reliably diagnosed. The data are unclear whether the criteria for the DC: 0-3R diagnosis of PTSD is the superior diagnostic system for childhood through adolescence (Scheeringa, Wright, Hunt, & Zeanah, 2006) or whether current DSM-IV-TR criteria are better (see Kearney, Wechsler, Kaur, & Lemos-Miller, 2010, for a review). It is difficult to ascertain the most accurate diagnostic system for specific age groups because most research is cross-sectional and thus it aggregates data from children of a wide variety of ages. A recent meta-analysis that examined 96 studies of children aged 3 to 18 found that exposure to traumatic events was significantly associated with both posttraumatic symptoms and PTSD and that there were no age effects in this association (Furr, Comer, Edmunds, & Kendall, 2010). However, the data were analyzed by comparing those children aged 3 to 12 with children older than age 12. This procedure did not allow for examination of the potential developmental differences between infants, preschoolers, and school-age children. Our longitudinal data provided a unique opportunity to examine these differences. There are few studies solely focused on trauma symptoms of very young children. Research finds that young children exposed to single event or chronic traumatic events (e.g., IPV) exhibit symptoms that fit the three DSM-IV-TR clusters (see Coates & Gaensbauer, 2009, for a review). However, the rates of PTSD diagnosis in traumaexposed young children are only consistent with rates of older children when developmentally sensitive versus DSM-IV-TR criteria are used (25%-69% vs. 0%-20%, 190 Violence Against Women 19(2) respectively; Ghosh-Ippen, Briscoe-Smith, & Lieberman, 2004; Levendosky et al., 2002; Meiser-Stedman et al., 2008; Ohmi et al., 2002; Scheeringa, Peebles, Cook, & Zeanah, 2001; Scheeringa, Zeanah, Drell, & Larrieu, 1995; Scheeringa & Zeanah, 2008; Scheeringa et al., 2003). A similar pattern of results is found in the few studies that have specifically examined PTSD symptoms and diagnoses in children exposed to IPV. Research on PTSD in Young Children Exposed to IPV Extant studies find that, among young children, witnessing IPV is associated with PTSD symptoms (e.g., Jarvis, Gordon, & Novaco, 2005; Kilpatrick & Williams, 1997). However, while these studies generally find that mothers and/or children report high rates of symptoms, low rates of PTSD diagnosis are reported for children, particularly when DSM-IV (American Psychiatric Association, 1994) criteria are used. Across studies of young children (including studies that assessed PTSD symptoms in both younger and older children exposed to IPV), the rates of children who endorsed symptoms in each of the criteria sets were as follows: 52% to 85% for reexperiencing, 3% to 98% for avoidance, and 31% to 73% for arousal, while the rates of DSM-IV-TR PTSD reported were between 3% and 25% (Graham-Bermann, DeVoe, Mattis, Lynch, & Thomas, 2006; Graham-Bermann & Levendosky, 1998; Levendosky et al., 2002; Mertin & Mohr, 2002; Rossman, Bingham, & Emde, 1997). The large discrepancies in percentages of symptoms in each of the PTSD clusters that different researchers find are probably due to the cross-sectional nature of the research methods that assessed children from a wide age range (e.g., young childhood to middle childhood or adolescence; Graham-Bermann et al., 2006; Mertin & Mohr, 2002; Rossman et al., 1997). Across ages, reexperiencing symptoms seem to be most prevalent, with avoidant symptoms least prevalent. In addition, the discrepancy between the large percentages of children who have symptoms of PTSD and the much lower percentages of children who meet diagnostic criteria for PTSD suggests that PTSD criteria as defined by the DSM-IV-TR are not as valid for young children as they are for adolescents and adults. Finally, when examining PTSD diagnoses or symptoms in young children, it is important to also examine the mother’s symptoms in order to understand fully the child’s symptom picture. For example, prior research with infants in the current study revealed that while mothers reported that more than one third of the infants who witnessed IPV had at least one symptom of PTSD, these symptoms of PTSD were associated with maternal PTSD symptoms, especially when mothers had been exposed to severe IPV (Bogat et al., 2006). IPV and PTSD in Mothers In very young children there is some evidence that the mother’s trauma symptoms are associated with those of her child (e.g., Bogat et al., 2006; Scheeringa & Zeanah, 2001). This is significant because rates of PTSD across studies of women experiencing IPV typically range from 31% to 84% (Golding, 1999). Scheeringa and Zeenah propose that in situations where mothers experience trauma, relational PTSD can result—a situation in Levendosky et al. 191 which the emotional relationship between the mother and child causes an enhancement of the trauma symptoms of each of them. Young children, compared to older children, are considered to be particularly vulnerable to the effects of the mother’s trauma response due to their increased physical proximity to and more significant emotional dependence on the mother. Thus, for young children, trauma symptoms may be more highly related to the severity of the mother’s trauma symptoms, rather than the frequency of witnessing IPV (or other traumas), compared with older children and adults. Current research has not examined developmental changes in relational PTSD, nor has it examined whether specific symptom clusters of mothers and children are more likely than others to be related. Again, longitudinal data allowed us to examine changes in relational PTSD over time. The Current Study The data from the current longitudinal study allowed for a fine-grained description of the PTSD symptom clusters at six different ages. At each age, we measured PTSD symptoms using developmentally appropriate criteria. In contrast to most studies, we chose to examine symptoms for each of the six age groups separately because of the significant developmental changes that occur over the course of 1 year during early childhood. This allowed us to examine variation in symptom picture across age groups. We addressed the following research questions. First, does age influence the types of symptoms and symptom clusters that children exhibit? Second, do the three different diagnostic schemes (DSM-IV-TR, DC: 0-3R, and DC: 0-3) show age differences in rates of diagnosis? Third, is the frequency of witnessed IPV related to children’s PTSD symptoms? Fourth, controlling for frequency of witnessed IPV, is there a significant relationship between maternal and child PTSD symptoms, and does this change as a function of the child’s age? Method Participants The participants were drawn from the Mother-Infant Study (Bogat, Levendosky, & Davidson, 1999; Levendosky, Bogat, Davidson, & von Eye, 2000). Two hundred and six women were interviewed during the last trimester of their pregnancy. After the child was born, they were assessed yearly at the child’s birthday through age 7. In the current study, we are presenting data from ages 1, 2, 3, 4, 5 and 7. We did not collect data on the children’s PTSD symptoms at age 6. The demographics for the full sample are shown in Table 1. The children in the current research are those whose mothers reported that they witnessed IPV at any age. For each data collection, if the mother reported that her child had witnessed IPV (note, the mother may have experienced IPV but the child did not witness it), then she was asked to report on her child’s symptoms of PTSD. Because in any given year the women may not have experienced IPV or the child may not have witnessed what occurred, the data at each time point are not necessarily for the same children (see Table 1 for the children witnessing IPV each year and the percentage with any PTSD symptoms and full diagnosis). 192 Violence Against Women 19(2) Table 1. Children Who Witnessed IPV With PTSD Symptoms at Ages 1 to 7. Age of Child IPV, n Witness, n PTSD symptoms, n Percentage of witnessing with any symptoms Percentage of witnessing with DSMIV-TR diagnosis Percentage of witnessing with DC: 0-3R diagnosis Percentage of witnessing with DC: 0-3 diagnosis 1 2 3 4 5 7 77 48 18 38 83 43 26 60 55 29 23 79 65 38 29 76 51 33 16 48 47 29 17 86 N/A 0 0 2 2 4 N/A 1 9 14 6 21 N/A 4% 12% 17 N/A N/A Note: DSM-IV-TR = Diagnostic and Statistical Manual of Mental Disorders (text rev.); DC: 0-3R = Diagnostic Classification of Mental Health and Developmental Disorders of Infancy and Early Childhood (rev. ed.). Measures IPV. IPV was assessed with the Severity of Violence Against Women Scales (SVAWS: Marshall, 1992), a 46-item questionnaire that measures the frequency of threats of violence, actual physical violence, and sexual violence during the past year. A total frequency score at each time point was used. Mothers also indicated whether their children witnessed the violence. Marshall reported coefficient alphas among a community sample ranging from .86 to .96 for the subscales. Maternal PTSD. This was assessed using the Posttraumatic Stress Disorder Scale for Battered Women (Saunders, 1994). This self-report questionnaire asks women to endorse how often they experience 17 symptoms that are consistent with the DSM-IV-TR symptom list (Criteria B-D) for PTSD. A total score as well as scores for the individual cluster symptoms were used in these analyses. Saunders reported a .94 reliability coefficient, and a high correlation (r = .58) with other PTSD scales. Child PTSD. This was assessed with maternal report on three different measures, based on the appropriateness of the measure for the developmental level of the child. The infants were assessed with a measure developed for this study based on the DC: 0-3 criteria (Zero to Three, 1994)—the Infant Traumatic Stress Questionnaire (ITSQ: Bogat, 1999). The preschool children (ages 2-4) were assessed with a measure based on the DSM-IV-TR and DC: 0-3 (Zero to Three, 1994) criteria—the Child Traumatic Stress Questionnaire (CTSQ: Bogat & Levendosky, 2002). The 5- and 7-year-old children were assessed with the Child Domestic Violence PTSD scale (Pynoos, Rodriguez, Steinberg, Stuber, & Frederick, 1998), a measure based on the DSM-IV (American Psychiatric Association, 1994) criteria. All of these measures yielded symptoms for the three clusters Levendosky et al. 193 of reexperiencing, avoidance, and arousal, with the exception of the ITSQ, which did not assess reexperiencing. The ITSQ and the CTSQ also assessed symptoms in the new fears category from the DC: 0-3R. Procedures Women were recruited into this study during their pregnancy. We oversampled for women who had experienced IPV so that more than half of them had experienced IPV during the pregnancy (see Huth-Bocks, Levendosky, Bogat, & von Eye, 2004) for a detailed description of recruitment and screening. The current study analyzes data collected when the children were ages 1, 2, 3, 4, 5 and 7. At each wave, data include only those children whose mothers indicated that they witnessed IPV during the past year. Interviews were scheduled near the child’s birthday. Women were paid for their time, and children were given a small gift. Results The children who witnessed IPV at each of the six ages were assessed for their PTSD symptoms and whether they met criteria for PTSD. There was no linear developmental pattern to the number of children who lived in homes where IPV occurred or to the number of children who witnessed the IPV (see Table 1). At ages 1 and 2, children were more likely to have IPV in their homes and to witness it compared to children at other ages. Across the different ages, there was a general rise in the percentage of children witnessing IPV who experienced symptoms, with the exception of age 5 when there was a decline. The percentage of children diagnosed with PTSD based on the DC: 0-3 or DC: 0-3R criteria was higher at all ages compared to when the DSM-IV-TR diagnostic criteria were used (see Table 1). There were developmental patterns in the three PTSD clusters of symptoms: reexperiencing, avoidance, and arousal (see Figure 1). Arousal was the most frequently endorsed at all ages, except age 4. At age 4 reexperiencing was the most highly endorsed symptom. The percentage of children with reexperiencing symptoms peaked at age 4 and then declined. The percentage of children who experienced avoidance rose from ages 1 to 3 and then stayed fairly stable, with mild fluctuation between ages 4 and 7. The percentage of children who experienced arousal symptoms increased from ages 1 to 3, dropped at ages 4 and 5, and was then fairly stable until age 7, when it increased dramatically. In addition, the percentage of new symptoms (a category of symptoms unique to DC: 0-3 diagnostic criteria) also showed a nonlinear pattern (see Figure 1). The percentage of children with these symptoms was similar at ages 1 and 2, more than doubled at age 3, and then declined at age 4, but to levels higher than ages 1 and 2. These symptoms were not measured at ages 5 and 7. Frequency of IPV witnessed by the children influenced the relationship between symptoms and the age at which they were expressed (see Table 2). Again, though, the results were not consistent. Frequency of IPV was significantly related to total PTSD symptoms at 194 Violence Against Women 19(2) 80 % with Symptoms 70 60 Avoidance 50 Re-experiencing 40 Arousal 30 New Fears 20 10 0 1 2 3 4 Age 5 7 Figure 1. Percentage of Children Experiencing the Four Types of Symptoms at Each Age. Note: Figure is available in full color in the online version at vaw.sagepub.com Table 2. Relationship Between Frequency of IPV Witnessed and Child PTSD Symptoms. Age of Child Total PTSD Reexperiencing Avoidance Arousal New symptoms 1 2 3 4 5 7 .46* N/A .28* .30* .09 .24* –.15 –.02 .17 .17 .70* .04 .08 .36* .44* .48* .16 .21 .29* .35* .72* .34* .36 .52* N/A .48* .41* .36* .23 N/A Note: IPV = intimate partner violence; PTSD = posttraumatic stress disorder. *p < .05. all ages. None of the symptom clusters follows this pattern. Reexperiencing was only associated with severity of IPV at age 7. Avoidance was only associated with frequency of IPV at ages 1, 5, and 7. Arousal was associated with frequency of IPV at ages 1, 3, 4, and 5. The new symptoms cluster from the DC: 0-3 (Zero to Three, 1994) was associated with frequency of witnessing IPV at ages 3 and 4. Finally, we examined the relationship between mothers’ and children’s PTSD symptoms, controlling for frequency of witnessed IPV (see Table 3). These revealed inconsistent significant relationships across ages without a clear developmental pattern. In fact, the patterns that existed seemed to be related to symptom clusters rather than to age. The most consistent relationships were found for arousal symptoms across ages, showing significance for ages 1, 2, 4, and 7. In contrast, there were no significant relationships between reexperiencing symptoms for mothers and children. 195 Levendosky et al. Table 3. Relationship Between Child and Maternal PTSD Symptoms Controlling for Frequency of IPV Witnessed. Age of Child Total PTSD Reexperiencing Avoidance Arousal 1 2 3 4 5 7 .47* N/A .44* .39* .19 .15 .18 .32* .25 .01 .04 .21 .43* .17 .45* .44* .44* –.02 .44* .19 .13 .28 .07 .31* Note: IPV = intimate partner violence; PTSD = posttraumatic stress disorder. *p < .05. Discussion Overall, our findings indicate that children are affected by the IPV they witness and often show a traumatic response. The likelihood of traumatic symptoms increases as children age; this is consistent with the trajectory of other anxiety disorders and internalizing disorders generally (Kovacs, Feinberg, Crouse-Novak, Paulauskas, & Finkelstein, 1984; Leve, Kim, & Pears, 2005). In addition, maternal report of child PTSD symptoms changes across development such that some symptoms are more likely to be endorsed in infancy and others during preschool. The “new symptoms” category in the original DC: 0-3 (Zero to Three, 1994) was relatively highly endorsed by the mothers in our sample, and the correlations with frequency of witnessing IPV were in the same direction and generally of the same strength as the other three groups of symptoms. In addition, these symptoms contributed to several additional cases of diagnosed TSD in ages 2 to 4. One possible interpretation is that these symptoms are in fact other ways of responding to trauma and a comprehensive assessment of early childhood traumatic responses should include these symptoms. Rates of diagnosed PTSD were low in this study, compared with studies of older children exposed to trauma (Graham-Bermann et al., 2006; Lehmann, 1997). Only the PTSD diagnosis rate of 21% in the 7-year-olds (using the DC: 0-3R criteria) approaches rates typical of older children reported in the literature (i.e., 25%-69%; Ghosh-Ippen et al., 2004; Levendosky et al., 2002; Meiser-Stedman et al., 2008; Ohmi et al., 2002; Scheeringa et al., 2001, 1995; Scheeringa & Zeanah, 2008; Scheeringa et al., 2003). It may be that young children rarely meet all criteria for a PTSD diagnosis, similar to the low rates for other anxiety and internalizing disorders. The low rates of PTSD diagnosis, even using the DC: 0-3R or DC: 0-3 criteria suggest that young children witnessing IPV do not fit the same profile of responses to IPV as older children and adults. Their high rates of symptoms suggest that they do experience affective and behavioral dysregulation but that it is not adequately captured with the various instruments that assess PTSD diagnoses. Our findings suggest that alternative conceptions of posttraumatic consequences for young children are important to consider, such as the Developmental Trauma Disorder (DTD), currently under 196 Violence Against Women 19(2) development by van der Kolk and colleagues (see van der Kolk, Roth, Oelcovitz, Sunday, & Spinazzola, 2005). Another explanation for the low rates of PTSD diagnosis among the young children in our sample may relate to the difficulty mothers have reliably reporting internalizing symptoms. At this stage of development, mothers may have underestimated the symptoms, thus depressing the rates of PTSD. Consistent with this hypothesis is the finding that arousal symptoms were generally the most frequently endorsed by mothers. Arousal symptoms are more amenable to external observation than are reexperiencing and avoidance symptoms. The total number of children’s symptoms was related to the frequency of IPV that they witnessed. This is consistent with previous findings (e.g., Graham-Bermann et al., 2006; Levendosky et al., 2002; Rossman et al., 1997) and suggests that young children are directly affected by witnessing violence, even if most of them do not meet criteria for PTSD. Arousal was significantly associated with witnessing IPV for ages 1 to 5 (with the exception of age 2). In contrast, avoidance was only associated with witnessing IPV at ages 5 and 7, and reexperiencing was only associated at age 7. This may indicate a developmental shift such that in the youngest children, affective dysregulation is the most dominant response to witnessing IPV, but as children get older, more cognitive and behavioral dysregulation as a response to witnessing IPV become prominent, as seen in reexperiencing and avoidance. This may reflect the increasing differentiation of symptoms of emotional distress that occur with development and are associated with particular psychopathologies (Carter, Briggs-Gowan, Jones, & Little, 2003; Eisenberg et al., 2001). Age 2 was an exception to the trend, with no specific symptom clusters related to witnessing IPV. The inconsistency of the age 2 data may be a valid finding. This is the age when children first attempt to separate and develop independence; this may be a particularly trying and conflictual experience in families where IPV takes place. A mother may be unable to distinguish her toddler’s traumatic response from other difficult behaviors. Our findings also indicated a high co-occurrence of maternal and child PTSD symptoms, controlling for frequency of IPV witnessed, across all the ages. One interpretation of these findings is support for relational PTSD. Young children who are likely to be in close physical and emotional proximity to their mothers are likely to influence and be influenced by her traumatic response to the IPV. In particular, maternal symptoms of arousal were associated with children’s arousal symptoms. This suggests young children are responding directly to their mothers’ affective dysregulation in reaction to IPV as well as demonstrating similar affective dysregulation. In contrast, maternal reexperiencing symptoms were not related to those of the children. This may be due to children’s lack of awareness of maternal reexperiencing symptoms or that these symptoms in their mothers may be less distressing to children than their mother’s arousal symptoms. Finally, the lack of a significant relationship also may be due to the difficulty mothers have in ascertaining children’s reexperiencing symptoms, as noted above. There are several limitations to this study. The first is the reliance on the mother as the sole reporter of her experiences of IPV as well as her and her child’s trauma symptoms. Mothers may underreport witnessing of IPV because, at the time it is occurring, their involvement in the episode may have distracted them from attending to whether or not their Levendosky et al. 197 child heard or saw the IPV. In addition, they may defensively imagine that they protect their children from exposure to IPV. The second limitation is related to the size of the sample. Our sample was sufficient to allow for examination of symptoms at each age, rather than aggregating different age children as prior studies have done. However, our study method was to assess PTSD symptoms at each age only for those children whose mothers reported that they witnessed IPV. Thus, we could not examine whether and how PTSD symptoms change throughout an individual child’s development. Unfortunately, because women’s experiences of IPV are rarely consistent (e.g., overall rates of IPV decrease as women and men age, women often leave and return to abusive partners multiple times) an enormous epidemiological sample would be necessary to track children’s trauma symptoms over time. In summary, similar to other studies, the ratio between children who had symptoms of PTSD in response to witnessing IPV, compared with those who met criteria for PTSD under any of the diagnostic schemes, was low. This adds evidence to the growing movement to include DTD in the DSM-5 (van der Kolk et al., 2005). This disorder is designed to address the very significant problem that most children exposed to traumatic events, including witnessing IPV, do not meet criteria for PTSD, even the modified criteria by Scheeringa et al. (2003) for younger children. Van der Kolk et al. argue that many children who have a posttraumatic disorder are not currently diagnosed, with the implication that children often do not get services they need. Many of these children, instead, may be receiving treatment for other disorders, such as ADHD (attention-deficit hyperactive disorder) or depression, rather than the treatment they need. Among children who witness IPV, DTD may better capture the posttraumatic problems than current diagnostic schemas. Future studies should continue to examine the trajectories of symptoms of PTSD in response to trauma across children’s ages. Our study suggests that children may exhibit different PTSD symptom clusters across development in response to witnessing IPV. Finally, there are some clinical implications from the current study. It is critical that assessment instruments used by clinicians and researchers with young children exposed to IPV include developmentally sensitive symptom items. Physicians and mental health professionals should assess young children exposed to IPV for trauma symptoms and consider the consequences for children’s functioning and development, even when children do not fit criteria for the DSM-IV PTSD diagnosis. Finally, this study highlights the importance of clinicians being aware of the differences in the types of posttraumatic symptoms across early childhood. Declaration of Conflicting Interests The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article. 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Reconsideration of harm’s way: Onsets and comorbidity patterns of disorders in preschool children and their caregivers following Hurricane Katrina. Journal of Clinical Child and Adolescent Psychology, 37, 508-518. Scheeringa, M. S., Zeanah, C. H., Drell, M. J., & Larrieu, J. A. (1995). Two approaches to the diagnosis of posttraumatic stress disorder in infancy and early childhood. Journal of the American Academy of Child & Adolescent Psychiatry, 34, 191-200. Levendosky et al. 201 Scheeringa, M. S., Zeanah, C. H., Myers, L., & Putnam, F. W. (2003). New findings on alternative criteria for PTSD in preschool children. Journal of the American Academy of Child & Adolescent Psychiatry, 42, 561-570 Scheeringa, M. S., Zeanah, C. H., Myers, L., & Putnam, F. W. (2005). Predictive validity in a prospective follow-up of PTSD in preschool children. Journal of the American Academy of Child & Adolescent Psychiatry, 44, 899-906. Sternberg, K. J., Baradaran, L. P., Abbott, C. B., Lamb, M. E., & Guterman, E. (2006). Type of violence, age, and gender differences in the effects of family violence on children’s behavior problems: A mega-analysis. Developmental Review, 26, 89-112. Stover, C. S., & Berkowitz, S. (2005). Assessing violence exposure and trauma symptoms in young children: A critical review of measures. Journal of Traumatic Stress, 18, 707-717. van der Kolk, B., Roth, S., Pelcovitz, D., Sunday, S., & Spinazzola, J. (2005). Disorders of extreme stress: The empirical foundation of a complex adaptation to trauma. Journal of Traumatic Stress, 18, 389-399. Zero to Three. (1994). The diagnostic classification of mental health and developmental disorders of infancy and early childhood. Washington, DC: Author. Zero to Three. (2005). Diagnostic classification of mental health and developmental disorders of infancy and early childhood (rev. ed.). Washington, DC: Author. Author Biographies Alytia A. Levendosky is a professor of clinical psychology and director of clinical training at Michigan State University. Her research focuses on the intergenerational transmission of intimate partner violence. She is particularly interested in the perinatal period and the psychological and biological mechanisms through which intimate partner violence influences the mother–child relationship and child behavior. G. Anne Bogat is a professor of clinical psychology at Michigan State University. Her research focuses on risk and resilience factors related to women and children living with intimate partner violence, including social, psychological, and biological correlates related to psychological outcomes. She is particularly interested in understanding the longitudinal trajectory of the effects of intimate partner violence. Cecilia Martinez-Torteya is a postdoctoral fellow at the Department of Psychiatry of the University of Michigan. She studies the effects of prenatal and early traumatic stress on children’s development. Using a developmental psychopathology framework, her research addresses the biological, psychological, and environmental mechanisms that promote resilience or increase risk for psychopathology in the context of early adversity.
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Literature Review

Literature Review

435289 2012 ANP46410.1177/0004867411435289BassettANZJP Articles Review Borderline personality disorder and

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bipolar affective disorder. Spectra or spectre? A review Australian & New Zealand Journal of Psychiatry 46(4) 327­–339 DOI: 10.1177/0004867411435289 © The Royal Australian and New Zealand College of Psychiatrists 2012 Reprints and permission: sagepub.co.uk/journalsPermissions.nav anp.sagepub.com Darryl Bassett1,2 Abstract Objective: Bipolar affective disorder and borderline personality disorder have long been considered to have significant similarities and comorbidity. This review endeavours to clarify the similarities and differences between these disorders, with an effort to determine whether they reflect different forms of the same illness or separate illness clusters. Method: The published literature relating to bipolar affective disorders, borderline personality disorders, and related areas of knowledge was reviewed using searches of several electronic databases (AMED, CINHAL, Embase, Ovid, ProQuest, MEDLINE, Web of Science, ScienceDirect) and published texts. These findings were combined with the personal clinical experience of the author, and information gathered from colleagues, to create a review of this topic. Results: Bipolar affective disorders and borderline personality disorders differ with respect to sense of self, disruption of relationships, family history of bipolar disorders, the benefits of medications, the extent of cognitive deficits, the form of affective dysregulation and mood cycling, the incidence of suicide and suicide attempts, the form of psychotic episodes, the incidence of early sexual abuse but not early trauma in general, the loss of brain substance, alterations in cortical activity, glucocorticoid receptor sensitivity, and mitochondrial dysfunction. They are similar with respect to non-specific features of affective dysregulation, the incidence of atypical depressive features, the incidence of self-mutilation, the incidence of transporter polymorphisms, possible genetic linkages, overall reduction in limbic modulation, reduction in the size of hippocampi and amygdala, and the incidence of sleep disruption. Conclusions: This review concludes that bipolar affective disorders and borderline personality disorder are separate disorders, but have significant elements in common. Keywords Atypical depressive disorder, bipolar disorder, bipolar spectrum, borderline personality disorder, cyclothymia Fundamentals The relationship between borderline personality disorder and bipolar affective disorder has been a topic of debate since at least 1979 (Boyce and Wilson, 2011; Siever and Gunderson, 1979; Stone, 1979). The presumed associations have been multiplied by increasing interest in patients who suffer less severe forms of mania but still suffer significant affective instability (the bipolar spectrum disorders) (Benazzi, 2009; Howland and Thase, 1993; Kwapil et al., 2011; Perugi et al., 2011; Thomas, 2004; Tiller and Schweitzer, 2010; Van Meter et al., 2011; Youngstrom et al., 2010). While such interest has captured recent attention, the concept of bipolar disorder with relatively mild forms of mania is not a recent development (Baethge et al., 2003; Brieger and Marneros, 1997; Slater and Roth, 1969). Our current major diagnostic systems have added to the confusion with long lists of criteria for each of these diagnostic groups, which permit the inclusion of a wide range of clinical presentations (Meares et al., 2011a). While bipolar disorder has been recognised as a diagnostic entity for a very long time (at least since Aretaeus of Cappadocia, circa AD 150–200) (Adams, 1972; Hornblower and Spawforth, 1School of Medicine, University of Notre Dame, Fremantle Australia of Psychiatry and Clinical Neurosciences, University of Western Australia, Nedlands, Australia 2School Corresponding author: Darryl Bassett, Suite 25, Hollywood Specialist Centre, 95 Monash Avenue, Nedlands, WA 6009, Australia. Email: dbassett@iinet.net.au Australian & New Zealand Journal of Psychiatry, 46(4) 328 1996), borderline personality disorder as currently defined is a relatively more recent construct (Stern, 1938). The problem of misdiagnosis of bipolar disorder has been well recognised and is the subject of considerable comment (Benazzi, 2000, 2006, 2008; Boyce and Wilson, 2011; Chilakamarri et al., 2011; George et al., 2003; Little and Richardson, 2010; Paris, 2010; Paris et al., 2007; Patfield, 2011; Ruggero et al., 2010a, 2010b; Smith et al., 2004; Tiller and Schweitzer, 2010; Yatham et al., 2009). One can readily appreciate that, among patients, a diagnosis of bipolar disorder gives a sense of optimism that treatment for their distressing illness is available. Conversely, in the context of our current service structure, a diagnosis of borderline personality disorder carries greater stigma and the implication that treatment may be unavailable (Aviram et al., 2006). A more biological diagnosis also externalises the locus of control, which is of appeal to some patients and therapists. Nevertheless, bipolar disorder is both frequently overdiagnosed and frequently missed (Hadjipavlou and Yatham, 2009; Leboyer and Kupfer, 2010). Evidence is steadily accumulating that bipolar disorder is associated with significant risks to brain structure and function, making early and effective treatment particularly important (Berk et al., 2009, 2010a, 2010b, 2011; Macneil et al., 2011). On the other hand, the positive misdiagnosis of bipolar disorder brings significant potential adverse consequences, including inappropriate medication exposure, insurance complications, employment implications, stigma and a distorted perception of health status. The failure to diagnose borderline personality disorder also has significant potential adverse consequences, as targeted psychotherapy and psychosocial management have proven efficacy. In the context of several shared elements, the complex phenomenological differences between the two disorders will emerge with greater clarity as they are examined in this paper (Berk et al., 2004). It would seem helpful to begin by reflecting upon what might be considered the ‘core’ elements of each group of disorders. Meares et al. (2011a) used factor analysis to define four core elements for borderline personality disorder: ‘painful incoherence’ (highly intense emotional pain reflecting a fragmented sense of self; the most significant factor); ‘role absorption’ (loss of identity); ‘inconsistency’; and ‘lack of commitment’ (the least significant factor) (Meares et al., 2011a). Although other significant features of borderline personality disorder such as a fear of abandonment, impulsivity, recurrent self-injurious behaviour, affective instability (rapidly fluctuating moods provoked by life events), episodic explosive rage and episodic psychotic phenomena were clearly significant, they were not regarded as ‘core’ features. Previous factor analyses identified disturbed relatedness (identity disturbance, chronic perceptions of internal emptiness, unstable relationships), behavioural dysregulation (self-injurious behaviour, impulsivity) and Australian & New Zealand Journal of Psychiatry, 46(4) ANZJP Articles affective dysregulation (inappropriate anger, efforts to avoid abandonment, affective instability) as the three prime features of borderline personality disorder (Clifton and Pilkonis, 2007). Significantly, Clifton and Pilkonis (2007) established that these latter factors correlated so highly together that they statistically reflected one comprehensive construct. It would be helpful to identify that construct in a clinically meaningful way. Like Meares et al. (2011a), I suggest that an ‘emotionally noxious sense of self” (an emotionally painful disruption of self-identity, a recurring fear of abandonment and chronic emptiness) is that core entity. Zanarini et al. (2007) argue for a similar concept, and also suggest that the interaction of this core element with a ‘kindling’ life event converts this predisposition into a clinical syndrome. However, Trull et al. (2011), in their discussion of the proposed diagnostic criteria for DSM-V, maintain that there is no single ‘latent’ group identity for borderline personality disorder and therefore a categorical diagnostic structure is unsatisfactory. Instead, they argue for a combination of the dimensions of clinical signs and symptoms derived from factor analyses, combined with the core features of affective dysregulation, impulsivity, and interpersonal hypersensitivity. This seems consistent with the notion of a fundamental core element of a noxious sense of self. Young et al. (2003), and Kellogg and Young (2006), have formulated the core elements of borderline personality disorder using a schema-based model. They describe these core schema elements as five modes which reflect the impact of childhood traumatic experiences: (1) ‘the abandoned and abused child’: fear of isolation and abandonment; (2) ‘the angry and impulsive child’: rage over perceived abuse, deprivation, rejection, subjugation and punishment; (3) ‘the detached protector’: emotional withdrawal, disconnection, isolation and behavioural avoidance; (4) ‘the punitive parent’: identification with a devaluing and rejecting parent; and (5) ‘the healthy adult mode’: the least common mode which allows the patient to meet essential needs and to seek containment of the recurring emotional pain. Their formulation is largely consistent with those described above, although they do not place emphasis upon self-observation and evaluation. However, their model has the added value of constructing a framework for a cognitive approach to psychotherapy. Bipolar disorder would seem to have a very different nature when the fundamental features of this disorder are considered. These consist of elements of depressive disorder (dysphoric mood, anhedonia, psychomotor disorder) and elements of mania (unusually and significantly increased energy evident in several forms, impaired judgement with disinhibition, unusually elevated or irritable mood), with subjective experiences linked to these elements (emotional emptiness, irrational guilt, suicidal thoughts, grandiose thoughts, elevated or depressed mood, increased creativity or impaired cognitive function, and a 329 Bassett number of other features) (Hosokawa et al., 2009; Parker, 2000, 2009; Parker et al., 2006). Importantly, disruption of a sense of self and an incapacity to maintain mutually satisfying relationships with others are not core features of bipolar disorder. As a consequence, the approach to effective psychotherapy for bipolar disorder is different to that for borderline personality disorder (Basco and Rush, 2005; Goodwin and Jamison, 2007d; Kellogg and Young, 2006; Linehan, 1993). Matters of difference Mania and hypomania in various ways define bipolarity, but some uncertainty arises when the milder forms of mania, such as those seen in cyclothymia, are considered (Akiskal and Benazzi, 2006; Alloy et al., 2011; Diagnostic and Statistical Manual of Mental Disorders, 2000; Goodwin and Jamison, 2007e; International Classification of Mental and Behaviour Disorders, 1994; Phelps, 2009; Smith et al., 2005). Perugi et al. (2011) report evidence of cyclothymic temperament in patients diagnosed with bipolar disorder, borderline personality disorder and atypical major depressive disorder, although their criteria for cyclothymia were not clearly defined (Perugi et al., 2011). Further, they did not separate cyclothymia as a syndrome from cyclothymic temperament as an element of personality. Ghaemi et al. (2004) maintain that cyclical patterns of mood shifts are a common element of bipolar disorder, recurrent major depressive disorder and atypical major depressive disorder, but that atypical depressive features and early onset are more common in bipolar disorder. The absence of mania in major depressive disorder and atypical major depressive disorder would seem critically important, despite the cyclical nature of their symptom profiles. As noted previously, a family history of major mood disorders helps to reinforce the diagnosis of a bipolar disorder (Galione and Zimmerman, 2010; Ghaemi et al., 2004; Mitchell et al., 2008; Souery et al., 2012), and the life trajectories of disabling symptoms of bipolar disorder tend to be more prolonged than with borderline personality disorder (Paris, 2004; Paris et al., 2007). However, both disorders are associated with a significant incidence of childhood trauma (approximately 50% in bipolar disorder and 60–80% in borderline personality disorder) (Alvarez et al., 2011; Ball and Links, 2009; Conus et al., 2010; Etain et al., 2008; Fowke et al., 2011; Garno et al., 2005; Herman et al., 1989; Hyun et al., 2000), and early life trauma may play an aetiological role in both (Holmes, 2003; Joyce et al., 2003; Watson et al., 2006). Patients with bipolar disorders and borderline personality disorders may differ in the form of childhood trauma, or their vulnerability to such trauma, but the possible details of such differences remain uncertain. Mackinnon and Pies (2006) offer support for the notion that rapid cycling of mood states is a common element of both bipolar and borderline states. The suggestion has some clinical support but appears inconsistent with the nonaffective components, as well as the details of affective disruptions discussed later, observed in both disorders. Self-mutilation has been observed with similar frequency in both bipolar disorder, particularly mixed states (Joyce et al., 2010), and borderline personality disorder. Therefore, such self-injury does not distinguish these disorders diagnostically. The separation of bipolar disorder and borderline personality disorder must then be achieved with criteria other than the presence of affective dysregulation and cyclicity of symptoms and signs alone. Importantly, however, the time course of the cyclicity is helpful: the presence of discrete, prolonged periods of affective symptoms, as opposed to rapidly shifting states, does suggest a bipolar diagnosis. Differences have also been identified in thinking styles between bipolar and borderline patients, with implications for their emotional health and relationship quality. Wupperman et al. (2009) identified significant deficiencies in mindfulness (attention, awareness and acceptance of the moment) in patients with borderline personality disorder. These included reduced interpersonal effectiveness, as well as passive and impulsive emotion regulation, even when they controlled for neuroticism. Nilsson et al. (2010), using the Temperament Evaluation of Memphis, Pisa, Paris and San Diego Autoquestionnaire, and the Young Schema Questionnaire, found that bipolar patients exhibited a higher level of maladaptive schemas and affective temperaments compared with controls. In contrast, borderline patients exhibited a higher level of cyclothymic temperament and reduced self-control. Quantitative clinical studies There have been numerous attempts to quantify the similarities and differences between bipolar disorder and borderline personality disorder, as well as their comorbidity (Paris et al., 2007). Perugi et al. (2011) studied a population of patients diagnosed with atypical major depressive disorder, 32% of whom they subsequently found could be diagnosed with bipolar disorder (24% without antidepressant-induced bipolarity and increased to 78% if hyperthymia or cyclothymic temperaments were considered indicative of bipolarity). When these atypically depressed patients were divided into those who also suffered from borderline personality disorder (42%), the only significant differences in demographic and a range of clinical features were shorter durations of the current illness and a higher rate of suicide attempts. The presence of bipolar features, however, defined in their study, did not identify comorbid borderline personality disorder in these atypical major depressive disorder patients. Galione and Zimmerman (2010) examined the clinical features of patients suffering depressive disorders (unipolar and bipolar), both with and without comorbid borderline Australian & New Zealand Journal of Psychiatry, 46(4) 330 ANZJP Articles Table 1. Significant differences between borderline personality disorder and bipolar disorder. Borderline personality disorder Bipolar disorder Altered sense of self No altered sense of self Relationships severely disrupted Relationships not as severely disrupted No family history of bipolar disorder Family history of bipolar disorder Increased glucocorticoid receptor sensitivity Reduced glucocorticoid receptor sensitivity Mood stabilizers modestly effective Mood stabilizers very effective Atypical antipsychotics modestly effective Atypical antipsychotics very effective Cognitive deficits less severe Cognitive deficits more severe Affective dysregulation between anger and depression prominent Affective dysregulation between euphoria and depression prominent Higher incidence of suicide attempts Higher incidence of completed suicide Very rapid mood cycling Less rapid mood cycling Early sexual abuse prominent Early sexual abuse not prominent Limited loss of gray matter More loss of gray matter Limited loss of white matter More loss of white matter Alterations of insula activity Uncertain changes in insula activity No changes in dorsolateral or dorsomedial prefrontal cortices Reduced activity of dorsolateral and dorsomedial prefrontal cortices No changes in cuneus and lingual Reduced activity of cuneus and lingual gyri No mitochondrial dysfunction Mitochondrial dysfunction Psychosis – non-specific features and sometimes persistent long-term Psychosis – most often linked to affective state and not persistent long-term personality disorder. They found the following differences when depressive disorders were comorbid with borderline personality disorder: earlier age of onset of depressive symptoms, greater frequency of depressive episodes, greater frequency of ‘atypical’ depressive symptoms, higher prevalence of comorbid anxiety disorders and substance abuse, and a greater number of suicide attempts. They also found that a history of bipolar disorder in first-degree relatives was not significantly associated with the presence of borderline personality disorder. They concluded that overall their data did not support the inclusion of borderline personality disorder as a component of the bipolar spectrum. On the other hand, it is interesting that Mitchell et al. (2008) found that the probability of a depressive disorder being part of a bipolar disorder was increased by the presence of features of atypical major depressive disorder, an earlier age of onset of first depressive episode, a history of multiple and shorter depressive episodes, and/or a family history of bipolar disorder. While there is overlap in their findings with the probability of borderline personality Australian & New Zealand Journal of Psychiatry, 46(4) disorder being present, the family history of bipolar disorder is again a prominent distinguishing feature. Paris et al. (2007), in their review of the bipolar disorder/borderline personality disorder interface, also concluded that bipolar disorder and borderline personality disorder were most likely separate disorders. Specifically, they found that while episodes of mania in bipolar disorder contrasted with more affective instability in borderline personality disorder, there was a significantly higher frequency of bipolar disorder in first-degree relatives of bipolar disorder patients, the benefits of mood stabilizers were more predictable in bipolar disorder than borderline personality disorder, and the prognosis for borderline personality disorder was generally better than for bipolar disorder. They also reviewed the relative incidence of borderline personality disorder and bipolar disorder comorbidity in several studies (Paris et al., 2007). They record that after combining the data, the median incidence of bipolar disorder-I in patients with borderline personality disorder was 9%. Similarly, the median incidence of bipolar disorder-II in patients with 331 Bassett Table 2. Similarities between borderline personality disorder and bipolar disorder. Affective dysregulation – non-specific Atypical depressive features more common than in major depressive disorder Self-mutilation common High heritability Transporter polymorphisms relevant Possible genetic linkage Fronto-limbic dysregulation: reduced modulation of limbic activity Reduced hippocampal size Increased activity of the amygdale Reduced size of the corpus callosum Low comorbidity between bipolar disorder and borderline personality disorder Early life trauma significant Some common sleep disruption Psychotic symptoms may arise borderline personality disorder was 11%. Cyclothymia was identified in 22% of patients with borderline personality disorder, but only one study was cited (Levitt et al., 1990). Conversely, borderline personality disorder was identified in 11% of patients with bipolar disorder-I and 16% of those with bipolar disorder-II. Perugi et al. (2003) found borderline personality disorder in 62% of patients with atypical major depressive disorder and cyclothymic temperament. These low rates of overlap argue in favour of the disorders being discrete entities. Henry et al. (2001) found that while affective instability was evident in both bipolar disorder and borderline personality disorder, there were important differences. Significantly, the instability seen in bipolar disorder was more often between euthymia and depression, euthymia and elation, or depression and elation. In contrast, the lability seen in borderline personality disorder was more often between euthymia and anger. Indeed, there is an increasing consensus that the high ranking of irritability in the DSM-IV criteria for bipolar disorder is a problem, and this is likely to be amended in the DSM-V system (Ghaemi et al., 2008). Benazzi (2006), using a measure of personality factors, found borderline personality traits were significantly more common in bipolar disorder-II than in major depressive disorder. However, while the ‘affective instability’ factor did not separate bipolar disorder and borderline personality disorder, the ‘impulsivity’ factor was significantly more common in borderline personality disorder compared with bipolar disorder. Other personality disorders were also identified in patients with bipolar disorder, with histrionic personality disorder being the most common co-morbid subtype. Yen et al. (2002) found that in women with borderline personality disorder, the level of affect intensity and affect control were significantly associated with the number of borderline traits. Both affect intensity (raised) and affect control (reduced) remained significant in association, even when controlled for depression. Affect control remained significant, even when controlled for affect intensity. Reich et al. (2011) found several significant differences in affective lability between bipolar and borderline disorders. Bipolar patients exhibited higher scores on the EuthymiaElation subscale of the Affective Lability Scale (ALS), as well as higher total scores using the Affect Intensity Measure. The latter scale also revealed higher Positive Emotion subscale scores in this group. In contrast, borderline personality disorder patients scored more highly on the AnxietyDepression subscale of the ALS. They also found that, using the Affective Lability Interview for Borderline Personality Disorder Scale, borderline patients exhibited more frequent shifts between euthymia and anxiety, anger and depression, as well as depression and anxiety. Becerra is currently conducting the first known study measuring emotional dysregulation using the Difficulties with Emotion Regulation Scale in patients with bipolar disorder. His preliminary data reveal a current mean score of 90 (maximum possible = 180) (Becerra R, 2011, unpublished data). This can be compared to a mean score of 126 in patients with borderline personality disorder (Gratz et al., 2006) and a mean of 80 in college students (Gratz and Roemer, 2004). While sufficient data is not yet available to permit a statistical analysis, the trend is toward a difference in scores between bipolar and borderline patients. Altamura et al. (2011) reported lower rates of comorbidity of bipolar disorder and borderline personality disorder than, for example, of panic disorder, substance abuse and attention deficit hyperactivity disorder. Similarly, comorbidity of both disorders has been identified with atypical major depressive disorder and major depressive disorder. A family history of bipolar disorder tends to be more prominent in patients with bipolar disorder than borderline personality disorder. While affective dysregulation can be identified in both disorders, there appear to be qualitative as well as quantitative differences. Finally, similar forms of cognitive deficits can be identified in both disorders, but the severity tends to be greater in bipolar disorder. Subtypes of bipolar disorder The current DSM-IV and ICD-10 descriptions of criteria for bipolar disorder-I, bipolar disorder-II, and cyclothymia (with the added variants of mixed affective episodes, rapid Australian & New Zealand Journal of Psychiatry, 46(4) 332 cycling, psychotic affective symptoms and schizoaffective disorder), contain essentially the same criteria for manic and depressed episodes, separated only by severity and duration of episodes. This is a clumsy and largely meaningless exercise, in which arbitrary criteria of duration are cited and severity remains a subjective evaluation by the observer. Only the variants of mixed affective episodes, rapid cycling and affective psychosis can be said to have further objectivity, and even then the frequency of episodes to identify ‘rapid cycling’ is itself arbitrary. Indeed, the decision to admit to a hospital, with all its significant non-clinical variables, is regarded by many as an inappropriate criterion for separating bipolar disorder-I from bipolar disorder-II (Akiskal and Benazzi, 2006). The presence of affective psychosis is not even given its own separate subtype in current classifications, although clinically these bipolar disorder-I patients suffer from a particularly destructive illness and there may be significant differences in the nature of this form of bipolar disorder. Cyclothymia is a useful, valid, but heterogeneous clinical entity (Akiskal and Benazzi, 2006; Akiskal et al., 2000; Howland and Thase, 1993). While cyclothymia can be considered a personality trait or temperament, it can also be defined as a form of bipolar disorder (DSM-IV and ICD10). It is usefully considered as a disorder which includes a range of bipolar signs and symptoms (Phelps, 2009), but the manic features are of a severity which is only spontaneously evident to ‘significant others’ (such as family or friends), and often evident to the patient only through reflection. While many observers may notice various emotional, cognitive and behavioural features consistent with bipolar disorders, they will frequently consider these to be personality traits, and not recognise their significantly disabling quality. This may rely on a less than precise definition of ‘significant others’, but it carries at least some objectivity. Patients rarely present with well-manicured illness syndromes and the interplay of significant bipolar features and numerous other disorders is considerable. In clinical practice, cyclothymia is diagnosed largely by historical review, collateral information from family and friends, current observation and self-report. Many patients suffering from cyclothymia are not spontaneously aware that their experience of pressured thoughts, fluctuating moods, bursts of expansive thinking, periods of heightened libido and significant fluctuations in sleeping habits, for example, are components of an illness. Yet these patients are usually well aware of the adverse consequences of their disorder, and are often perplexed by their own behaviour and internal experiences. The intrusion of personality disorders (defined by the persistence of major disruption of the experience of self and interpersonal relationships), and a variety of other psychological disorders (such as anxiety disorders, eating disorders, attention deficit disorders and substance abuse), only obfuscate our understanding of bipolarity if included Australian & New Zealand Journal of Psychiatry, 46(4) ANZJP Articles under the umbrella of bipolar spectrum disorders. It is more parsimonious to consider these as comorbid disorders, rather than forme frustes of bipolar disorders. Neuropsychological studies Neuropsychological studies have revealed deficits in cognitive function in both borderline personality disorder and euthymic bipolar disorder. The most prominent common features are defects in verbal learning and memory, and subtle impairment of executive functions have also been identified in both borderline personality disorder and bipolar disorder (Kurtz and Gerraty, 2009; Ruocco, 2005). However, Mann-Wrobel et al. (2011) report that the cognitive changes in bipolar disorder tend to be ‘generalized’ (evident in more brain regions) and potentially involve any cognitive functions. The precise deficits are modified by numerous illness and age-related factors. Only ‘crystallized’ verbal functions appeared relatively spared in their analysis. The severity of deficits from all of these studies tends to be greater in bipolar disorders and less generalized in borderline personality disorder (Kurtz and Gerraty, 2009; Ruocco, 2005). Genetics In 2000, Torgersen et al. (2000) reported a twin study of personality disorders, in which borderline personality disorder was revealed to be associated with a level of heritability of 0.7 (or 70%), consistent with measures of heritability in other personality disorders in that study. However, in 2008, he and his colleagues (Torgersen et al., 2008) reported a study of cluster B personality disorders, revealing a measure of heritability for borderline personality disorder traits of 0.35 (35%). Heritability in borderline personality disorder has been variously found in a number of studies to be between 0.35 and 0.8 (Torgersen et al., 2000, 2008). Kendler et al. (2011) also found significantly heritable personality traits in a large genetic study of personality disorders in general. Heritability in bipolar disorder has been estimated to be between 0.68 and 0.80 (Goodwin and Jamison, 2007a). Familial coaggregation of borderline personality disorder and bipolar disorder has been identified, but similar coaggregation has been identified with other mood disorders (major depressive disorder and atypical major depressive disorder) as well as anxiety disorders, somatoform disorders and substance abuse (Zanarini et al., 2009). More rigorous measures of genetic linkage between bipolar disorders and borderline personality disorder have not yet been employed. The serotonin transporter gene ‘short’ polymorphism has been found to be significantly associated with both borderline personality disorder (Maurex et al., 2010; Wagner et al., 2009) and bipolar disorder (Daray Bassett et al., 2010; Levinson, 2006), but the associations are not strong. Joyce et al. (2006) found a significant association between the 9-repeat allele of the DAT1 dopamine transporter gene and borderline personality disorder. This association persisted when relevant developmental factors (childhood abuse or neglect, borderline temperament) were controlled. The association was larger in older patients, suggesting a possibly greater significance in ‘poorer prognosis’ patients. Nemoda et al. (2010) present similar evidence of an association between dopamine transporter polymorphisms and borderline personality disorder. However, dopamine transporter polymorphisms appear significant in bipolar disorders as well (Pinsonneault et al., 2011). The similarities and differences remain uncertain. Neurobiology While reduced suppression of corticotrophic releasing hormone production by dexamethasone (using the Dexamethasone Suppression Test) has been well observed in depressive disorders (unipolar and bipolar), increased suppression has been observed in borderline personality disorder (Carrasco et al., 2007; Goodman et al., 2010; Zimmerman and Choi-Kain, 2009). Post-traumatic stress disorder has also been associated with increased suppression, but the presence or absence of this disorder did not alter the findings in these studies. There may be a similar reduction in blunting of the suppression of thyrotropinreleasing hormone (thyroliberin) production by thyroxine in borderline personality disorder (Carrasco et al., 2007). Decreased serotonergic responsivity and increased cholinergic responsivity have been observed in borderline personality disorder and major depressive disorder, with suggestions that a similar pattern may be the case in bipolar disorder (Goodman et al., 2010). Sleep architecture in borderline personality disorder is associated with a longer duration of rapid eye movement sleep, less slow-wave sleep and more stage 2 sleep than in major depressive disorder or healthy controls (De La Fuente et al., 2001, 2004). Similar disruptions of sleep architecture have been observed in bipolar disorder (Goodwin and Jamison, 2007e; Srinivasan et al., 2009), but more detailed research is required to clarify the similarities and differences which may be present in these two groups of disorders. Hallahan et al. (2011) performed a very thorough megaanalysis of morphometric MRI studies in bipolar disorder and found evidence of increases in the volumes of the right lateral ventricle, left temporal lobe and right putamen, while a reduced size of right and left amygdalae and hippocampi have been observed in borderline personality disorder (Nunes et al., 2009). Previous studies in bipolar disorders found inconsistent evidence of changes in the volumes of the third ventricle, subgenual prefrontal cortex, hippocampal/amygdala complex, thalamus and caudate 333 (Mcdonald et al., 2004). There is some evidence that adolescent females with borderline personality disorder may have reductions in dorsolateral prefrontal cortex and orbitofrontal gray matter, but the separation from healthy adolescent subjects is uncertain (Brunner et al., 2010). Disruption of white matter integrity has been the subject of attention, with abnormalities detected in the internal capsules and adjacent areas of the striatum, thalamus and frontal white matter in bipolar spectrum disorders (Haznedar et al., 2005). Benedetti et al. (2011) found structural white matter injury in the pathways between the amygdala and a variety of regions, including the cingulate gyri (subgenual, anterior and posterior), the parahippocampal gyri, the orbitofrontal cortex and the dorsolateral prefrontal cortex, in patients with bipolar disorder. Of further interest, disruption of white matter integrity has been detected in the internal capsules and left temporal regions of unaffected first-degree relatives of patients with bipolar disorder (Sprooten et al., 2011). Altered white matter integrity in the inferior frontal lobes has also been described in females with borderline personality disorder and a history of self-injury (Grant et al., 2007). The significance and consistency of white matter changes are uncertain and await further clarification in both bipolar and borderline personality disorders. Bandelow et al. (2010) suggest that many features of borderline personality disorder could potentially be explained as consequences of endogenous opioid dysfunction. These features include attention-seeking behaviours, over-activation of reward pathways with fear of abandonment, anhedonia and subjective emptiness as consequences of endogenous opioid deprivation and self-injury as an attempt to activate endogenous opioid function. They argue that the benefits of opioid receptor antagonists for self-injurious behaviour is supportive of their hypothesis. Unfortunately, the supportive evidence appears scant and confirmation of their hypothesis is lacking at this time. Vollm et al. (2004) found that, using a Go/No Go task in borderline personality disorder and antisocial personality disorder patients, metabolic activation measured by Functional Magnetic Resonance Imaging (fMRI) was distributed across the medial, superior and inferior frontal gyri extending to the anterior cingulate. This contrasted with healthy controls whose activation was mainly limited to the prefrontal cortex. Schulze et al. (2011) used fMRI to examine differences in metabolic activity associated with emotional reactivity in female patients with borderline personality disorder and healthy controls during a delayed reappraisal paradigm using aversive pictures and cognitive reappraisal strategies. They found that borderline personality disorder patients exhibited enhanced emotional reactivity as well as deficits in voluntarily reducing aversive emotions by cognitive reappraisal. Reviews by Mauchnik and Schmahl (2010) for borderline personality disorder, and Kupferschmidt and Zakzanis (2011), as well as Chen et al. (2011) for bipolar disorders, Australian & New Zealand Journal of Psychiatry, 46(4) 334 examined the neuroimaging research for both of these disorders. They note reports of reduced hippocampal and corpus callosum size in both borderline and bipolar patients, increased size of the amygdala in borderline patients, but inconsistent reports of alteration in the size of the amygdala in bipolar patients. In addition, they report reduced size of gray matter in the rostral and ventral regions of the anterior cingulate gyri in borderline patients, but no consistent reports of change in the anterior cingulate size of bipolar patients. Amygdala activity (measured by fMRI or Positron Emission Tomography scans) was reported to be increased in both borderline and bipolar patients, while hippocampal activity has been variously altered in bipolar patients. Activity of the anterior cingulate gyri and insular cortices were reportedly increased in borderline patients, but the reports of altered activity in these regions in bipolar patients have not been consistent. The reported failure of the activity of the insular cortices to increase when under emotional stress in borderline patients is of interest given their difficulty regulating emotional responses to such challenges. Bipolar patients have been reported to show reduced activity in the dorsolateral prefrontal cortices, the dorsomedial prefrontal cortices, the orbitofrontal cortices, the inferior frontal cortices and in the cuneus as well as lingual gyri. These changes in activity are of interest, given the evidence of fronto-limbic dysregulation and dorsoventral dysregulation in bipolar patients. The precise nature of morphological and metabolic changes in the brains of patients with bipolar and borderline personality disorders remains clouded by clinical heterogeneity, variations in technical assessment and the complexity of the neurobiology in these disorders. The physiological response to facially expressed emotion, as measured by cerebral blood flow, has been studied in both bipolar disorder and borderline personality disorder. The findings reveal complex variations related to the nature of the expressed emotion, but possible differences between bipolar disorder and borderline personality disorder were difficult to define (Minzenberg et al., 2007; Wessa and Linke, 2009). Meares et al. (2011b) report neurophysiological evidence of reduced inhibitory activity in the right hemisphere from fronto-medial structures in borderline personality disorder. However, similar defects in evoked potentials have been observed in bipolar disorder and schizophrenia, and may represent a marker of a broad neurophysiological dysfunction (Bestelmeyer et al., 2009). Indeed, one of the difficulties of biological markers in general is their broad failure to respect our current diagnostic systems. This is not really a surprise, since in no other branch of medicine does phenomenology accurately reflect pathophysiology. Importantly, however, all of these studies have provided further evidence of fronto-limbic dysregulation in both bipolar disorder and borderline personality disorder, compared with healthy controls. Australian & New Zealand Journal of Psychiatry, 46(4) ANZJP Articles The finding that the sensitivity of glucocorticoid receptors is reduced in bipolar disorder and increased in borderline personality disorder is of considerable interest, as it suggests a major separation in the neuroendocrine response to stress (Goodwin and Jamison, 2007c; Zimmerman and Choi-Kain, 2009). There is also some evidence that there may be reduced responsivity in serotonergic and acetylcholinergic circuits in both disorders. Altered function of endogenous opioid systems is a tempting hypothesis for some features of borderline personality disorder but is poorly supported. Dysregulation of neural circuits in the prefrontal regions, with disruption of some executive cognitive functions and reduced modulation by fronto-limbic pathways, appears supported in borderline personality disorder and in bipolar disorder (Berdahl, 2010). The differences in both structural and functional activity of neural circuits in both disorders remain uncertain, but exhibit similarities to changes in mental state and interpersonal functions. Andreazza et al. (2010) and Berk et al. (2011) note the significance of mitochondrial dysfunction in bipolar disorders, with likely relevance to the disruption of energy evident in the clinical states of these disorders. There are no reports of mitochondrial dysfunction in borderline personality disorders. Pharmacology It is evident that antidepressants, anticonvulsant-mood stabilizers and atypical antipsychotic medications have value in the management of both bipolar disorder and borderline personality disorder. However, the benefits in bipolar disorder appear significantly more prominent than in borderline personality disorder, and their use in the latter remains limited (Ripoll et al., 2011). Given the broad utility of antidepressants, antipsychotics and anticonvulsants across a wide range of disorders, treatment response does not appear to have diagnostic implications. The only exception appears to be lithium, which does not show efficacy in non-affective psychoses nor display clear utility in personality disorders (Bellino et al., 2008). Clinical observations Clinical observation and documentation by many clinicians suggest that borderline personality disorder is associated with an emotionally painful disruption of the sense of self, as well as rapidly changing affective instability, high impulsivity and a pattern of severely unsatisfactory interpersonal relationships (Meares et al., 2011a, 2011b; Paris et al., 2007). Bipolar disorder is much less commonly associated with such disruption of self-experience, and is less often associated with high impulsivity and repeatedly unsatisfactory relationships. Patients with bipolar disorder are more often observed to have a positive family history of bipolar 335 Bassett disorder, and their experience of affective instability is characterised by less rapid changes and less reactivity to environmental events than patients with borderline personality disorder. Psychosis can arise in both bipolar disorder and borderline personality disorder. The form of psychosis in bipolar disorder is most frequently mood congruent, but mood incongruent psychotic phenomena can arise. The psychotic episodes are almost always limited in duration and rarely extend beyond several months (Goodwin and Jamison, 2007b). The content of the psychotic episodes is usually dominated by delusional thinking, but a variety of perceptual disorders are common and severe disorganisation (delirious mania and catatonia) may develop (Goodwin and Jamison, 2007b). Psychotic phenomena in borderline personality disorder are less consistent in content, may be linked to early life trauma, and may persist for many years. However, severe psychotic disorganization is rare and usually very brief (mainly hours) (Adams and Sanders, 2011; Barnow et al., 2010). Acute psychiatric illness of many forms can test underlying personality structures, and the temporary emergence of behaviours suggestive of underlying personality disorder is common. During episodes of acute illness, patients with bipolar disorder (particularly mixed states) sometimes exhibit prominent affective instability, high impulsivity, self-injury, manipulative interpersonal behaviour and explosive rage. This may lead to an incorrect diagnosis of borderline personality disorder. Tiller has named this phenomenon ‘state borderline’ (Tiller J, 2002, personal communication). Longitudinal observation of the patient through historical assessment and personal observation by therapists is vitally important for accurate diagnosis. These observations chime with experience. Conclusions While bipolar disorder and borderline personality disorder have many clinical and biological features in common, the evidence suggests that they remain essentially distinct entities which may occur together or separately (see Tables 1 and 2). They share some elements of psychopathology and pathophysiology, but their differences are more significant. Acknowledgements I am indebted to several colleagues, who have given very generously of their time and expertise to critically comment upon the preparation of this paper. Professors Michael Berk and Sean Hood have been of considerable assistance. My good friends Drs Robert Segal and Nick de Felice have also provided invaluable comment. Dr Sherylee Bassett has given expert advice, assisted generously with literature searches, provided professional editing and tireless devotion to the quality of presentation. Their contributions are gratefully acknowledged. Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors. Declaration of interest The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper. References Adams B and Sanders T (2011) Experiences of psychosis in borderline personality disorder: A qualitative analysis. Journal of Mental Health 20: 381–391. Adams F (1972) Digital Hippocrates: the extant works of Aretaeus the Cappadocian: On the causes and symptoms of chronic disease. Chapter vi. On madness. Boston, MA: Milford House Inc., 1972 (republication of the 1856 edition). Available at: www.chlt.org/sandbox/dh/aretaeusEnglish/page.55.a.php (accessed 19 April 2011). 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Healthy People Initiative

Healthy People Initiative

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This week’s graded discussion topic relates to the following Course Outcomes (COs).

CO1 Utilize prior knowledge of theories and principles of nursing and related disciplines to explain expected client behaviors, while differentiating between normal findings, variations, and abnormalities. (PO 1)
CO3 Utilize effective communication when performing a health assessment. (PO 3)
The topic this week asks you to apply what you have learned to the following case study.

As the school nurse working in a college health clinic, you see many opportunities to promote health. Maria is a 40-year-old Hispanic who is in her second year of nursing school. She complains of a 14-pound weight gain since starting school and is afraid of what this will do to both her appearance and health if the trend continues. After conducting her history, you learn that she is an excellent cook and she and her family love to eat foods that reflect their Hispanic heritage. She is married with two school-age children. She attends class a total of 15 hours per week, plus she must be present for 12 hours of labs and clinical. She maintains the household essentially by herself and does all the shopping, cooking, cleaning, and chauffeuring of the children. She states that she is lucky to get 6 hours of sleep per night, but that is okay with her. She lives 1 hour from campus and commutes each day. Using Healthy People 2020 (Links to an external site.)Links to an external site. and your text as a guide, answer the following questions.

What additional information would you like to gather from Maria?
What are Maria’s real and potential health risks?
Why is Maria’s culture important when obtaining the health assessment?
Pick one of Maria’s health risks. What would be one reasonable short-term goal for this risk?
What nursing interventions would you incorporate into Maria’s plan of care to assist her with meeting your chosen goal? Please provide rationale for your selections.
Class,

As we begin this week starting to talk about Healthy People 2020, I am looking forward to your input and answers to the questions with the scenario and Maria. As you are reviewing the Healthy People 2020 new topic areas, in this week’s lesson, what are your thoughts on them? Do any of these topics apply to your current workplace setting? Can you share an example of the scenario or a workplace example, and would these new areas benefit you in your practice?

Healthy People Initiative (1)

Healthy People Initiative (1)

Professor,

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Additional information I would gather would be: height and weight to calculate BMI, daily log of what food she is eating and how often, and family history, history of present illness.

Marias health risks include: hypertension, anxiety, depression, diabetes, obesity.

Marias culture is important in doing a health assessment because Hispanic /Latinos have a higher risk for obesity and diabetes. “Latinos have disproportionately higher rates of obesity and diabetes mellitus. Other health problems include stress, neurocysticercosis, and tuberculosis” (Juckett, 2013). Many Latinos believe in herbal healing.

“Approximately 43 percent of Mexican Americans older than 20 years are obese, compared with 33 percent of the non-Latino white population.12 (Links to an external site.)Links to an external site. Diabetes and hypertension are closely linked with obesity; 11.8 percent of Latinos older than 20 years have type 2 diabetes (13.3 percent of Mexican Americans), making it the foremost health issue in this population.14 (Links to an external site.)Links to an external site. A higher-calorie diet, a more sedentary lifestyle, and genetic factors contribute to this problem” (Juckett, 2013).

The health risk I would choose would be risk for obesity or Imbalanced nutrition: more than body requirements. A goal for this would be to improve healthy food choices and reduce caloric intake.

Nursing interventions would include: Daily food diary- to record calorie intake and establish healthy eating patterns, discuss emotions and situations related to times of eating to identify what times and what emotions may be causing the cravings and learn ways to cope, formulate an eating plan to set a specific meal plan to assist with healthy eating patterns , weigh periodically(weekly)and record measurements to track progress, implement restrictions of salt and carb intake if needed, consult with a dietitian when able.

Juckett, G. (2013, January 01). Caring for Latino Patients. Retrieved April 30, 2018, from https://www.aafp.org/afp/2013/0101/p48.html

Healthy People Initiative (2)

Healthy People Initiative (2)

Dear Professor Yesenosky and class,

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Some additional information that I would need to gather would be Maria’s eating habits and activity levels. I would need to know how often she eats, her servings and what types of food she consumes. Is she eating a variety of fruits, vegetables, lean meats and whole grains? How often does she exercise? What medications she is currently prescribed, including all over the counter medications? I would also like to know her past and current medical history, along with her family history. Is there a history of diabetes, obesity, or cardiac issues?

Maria’s real health risk would be obesity, of course we would need to obtain an accurate weight first. Her potential risks would include diabetes, hypertension and heart disease.

Maria’s culture is important when obtaining a health assessment because her Hispanic culture could influence her dietary habits and medications. Her culture could also increase her risk of developing other health concerns such as heart disease, stroke, type 2 diabetes and certain types of cancer (Tung, 2015).

The health risk of obesity can be managed by providing nutrition education and initiating a physical activity schedule. Maria could start by watching her calorie intake, eating healthy foods and consuming food in moderation. She can do this by documenting in a food diary and recording her weight. Maria could also begin exercising daily or at least every other day until she can free up some of her time. She could set a short-term goal of losing 5 pounds in a 3-month time frame.

A nursing intervention that I would incorporate into Maria’s plan of care to assist her with meeting a 5-pound weight loss would be exercising daily or every other day for 20-30 minutes, she could do this at the college gym, in between classes. She could also begin documenting in a food diary, and limit sweets and foods high in sugar. The food diary will assist her in determining foods that are high in calories and fat, and how she can eliminate them.

Thank you, Kelly

References

Tung, W., & McDonough, J. (2015). Overweight and obesity among Hispanic/Latino American women. Health Care Diversity, 27(3) 162-165. Doi 10.11771084822314563075

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Poor Patient Outcome

Poor Patient Outcome

Relying solely on the classic features of a disease may be misleading. That’s because the clinical presentation of a

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disease often varies: the symptoms and signs of many conditions are non-specific initially and may require hours, days, or even months to develop.

Generating a differential diagnosis; that is, developing a list of the possible conditions that might produce a patient’s symptoms and signs — is an important part of clinical reasoning. It enables appropriate testing to rule out possibilities and confirm a final diagnosis.

This case portrays a poor patient outcome after a misdiagnosis.

Case scenario

A previously healthy 35-year-old lawyer presents to a primary care office with a chief complaint of chest pain and a non-productive cough. The pain started suddenly 2 hours prior to coming to the office while the patient was sitting at his desk. The patient describes the pain as sharp in nature, constantly present but made worse with inspiration and movement, and with radiation to the base of the neck. His blood pressure in the right arm and other vital signs are normal.

On physical examination the only findings of note are chest wall tenderness and a faint cardiac murmur. The ECG in the office is normal. The patient is observed for an hour in the office and assessed. He is diagnosed with viral pleurisy and sent home on non-steroidal analgesics.

The following day the patient collapses at home and cannot be resuscitated by the paramedic service. An autopsy reveals a Type 1 aortic dissection with pericardial tamponade.

Developing a list of possible conditions that might produce a patient’s symptoms and signs is an important part of clinical reasoning.

As an NP in primary care what would you have done differently?
Discuss the importance of creating a list of differentials for this patient. How could it have changed this outcome?
If a serious diagnosis comes to mind based on a patient’s symptoms:

Ask yourself; Have you considered the likelihood of it and whether it needs to be ruled out by testing or referral?

Because many serious disorders are challenging to diagnose, have you considered ruling out the worst case scenario?
Ask yourself: Do you have sufficient understanding of the clinical presentation to offer an opinion on the diagnosis?
What other diagnosis could it be? How might the treatment to date have altered the patient outcome?
What other diagnostic and laboratory or imaging was needed in order to make a complete differential list? What support tools would you consider using in helping to create a differential diagnosis list?
Are you familiar with the current clinical practice guidelines for the investigation of a suspected condition such as chest pain?

Nursing Discussion Question

Nursing Discussion Question

After discussion with your mentor, name one financial aspect, one quality aspect, and one clinical aspect that need

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to be taken into account for developing the evidence-based practice project. Explain how your proposal will directly and indirectly impact each of the aspects.

MY EBP PROJECT TOPIC IS NURSING SHORTAGE/UNDER STAFFING AND YOUR ANSWER SHOULD BE CO-RELATED TO THAT (FIXING THIS ISSUE) TRY TO WRITE FROM FIRST PERSON PERSPECTIVE, AS IN USING ‘I’ ‘ME’ etc.

APA REFERENCES REQUIRED.

Nursing Discussion 2

Nursing Discussion 2

Now that you have completed a series of assignments that have led you into the active project planning and

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development stage for your project, briefly describe your proposed solution to address the problem, issue, suggestion, initiative, or educational need and how it has changed since you first envisioned it. What led to your current perspective and direction?

MY EBP PROJECT TOPIC IS NURSING SHORTAGE/UNDER STAFFING AND YOUR ANSWER SHOULD BE CO-RELATED TO THAT (FIXING THIS ISSUE) TRY TO WRITE FROM FIRST PERSON PERSPECTIVE, AS IN USING ‘I’ ‘ME’ etc.

APA REFERENCES REQUIRED.