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		<title>BMC Psychiatry - Most viewed articles</title>
		<link>http://www.biomedcentral.com/bmcpsychiatry/mostviewed/</link>
		<description>Most viewed articles in last 30 days from BMC Psychiatry (ISSN 1471-244X) published by 
				
				BioMed Central
		</description>
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				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-244X/8/70"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-244X/8/71"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-244X/8/81"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-244X/8/78"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-244X/8/84"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-244X/8/77"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-244X/3/17"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-244X/8/80"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-244X/8/83"/>			    
            
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		<item rdf:about="http://www.biomedcentral.com/1471-244X/8/70">
            
            <title>A systematic review of mental disorder, suicide, and deliberate self harm in lesbian, gay and bisexual people</title>
			<description>Background:
Lesbian, gay and bisexual (LGB) people may be at higher risk of mental disorders than heterosexual people.MethodWe conducted a systematic review and meta-analysis of the prevalence of mental disorder, substance misuse, suicide, suicidal ideation and deliberate self harm in LGB people. We searched Medline, Embase, PsycInfo, Cinahl, the Cochrane Library Database, the Web of Knowledge, the Applied Social Sciences Index and Abstracts, the International Bibliography of the Social Sciences, Sociological Abstracts, the Campbell Collaboration and grey literature databases for articles published January 1966 to April 2005. We also used Google and Google Scholar and contacted authors where necessary. We searched all terms related to homosexual, lesbian and bisexual people and all terms related to mental disorders, suicide, and deliberate self harm. We included papers on population based studies which contained concurrent heterosexual comparison groups and valid definition of sexual orientation and mental health outcomes.
Results:
Of 13706 papers identified, 476 were initially selected and 28 (25 studies) met inclusion criteria. Only one study met all our four quality criteria and seven met three of these criteria. Data was extracted on 214,344 heterosexual and 11,971 non heterosexual people. Meta-analyses revealed a two fold excess in suicide attempts in lesbian, gay and bisexual people [pooled risk ratio for lifetime risk 2.47 (CI 1.87, 3.28)]. The risk for depression and anxiety disorders (over a period of 12 months or a lifetime) on meta-analyses were at least 1.5 times higher in lesbian, gay and bisexual people (RR range 1.54&#8211;2.58) and alcohol and other substance dependence over 12 months was also 1.5 times higher (RR range 1.51&#8211;4.00). Results were similar in both sexes but meta analyses revealed that lesbian and bisexual women were particularly at risk of substance dependence (alcohol 12 months: RR 4.00, CI 2.85, 5.61; drug dependence: RR 3.50, CI 1.87, 6.53; any substance use disorder RR 3.42, CI 1.97&#8211;5.92), while lifetime prevalence of suicide attempt was especially high in gay and bisexual men (RR 4.28, CI 2.32, 7.88).
Conclusion:
LGB people are at higher risk of mental disorder, suicidal ideation, substance misuse, and deliberate self harm than heterosexual people.</description>
			<link>http://www.biomedcentral.com/1471-244X/8/70</link>		
			<dc:creator>Michael King, Joanna Semlyen, Sharon See Tai, Helen Killaspy, David Osborn, Dmitri Popelyuk and Irwin Nazareth</dc:creator>
			<dc:source>BMC Psychiatry 2008, 8:70</dc:source>
			<dc:subject>Number of accesses: 1081</dc:subject>
			<dc:date>2008-08-18</dc:date>
			<dc:identifier>doi:10.1186/1471-244X-8-70</dc:identifier>
			
			
							
					<prism:publicationName>BMC Psychiatry</prism:publicationName>
					
			
							
					<prism:issn>1471-244X</prism:issn>
					
			
							
					<prism:volume>8</prism:volume>
					
			
							
					<prism:startingPage>70</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-08-18</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-244X/8/71">
            
            <title>Acute maternal stress in pregnancy and schizophrenia in offspring: A cohort prospective study</title>
			<description>Schizophrenia has been linked with intrauterine exposure to maternal stress due to bereavement, famine and major disasters. Recent evidence suggests that human vulnerability may be greatest in the first trimester of gestation and rodent experiments suggest sex specificity. We aimed to describe the consequence of an acute maternal stress, through a follow-up of offspring whose mothers were pregnant during the Arab-Israeli war of 1967. A priori, we focused on gestational month and offspring's sex.MethodIn a pilot study linking birth records to Israel's Psychiatric Registry, we analyzed data from a cohort of 88,829 born in Jerusalem in 1964&#8211;76. Proportional hazards models were used to estimate the relative risk (RR) of schizophrenia, according to month of birth, gender and other variables, while controlling for father's age and other potential confounders. Other causes of hospitalized psychiatric morbidity (grouped together) were analyzed for comparison.
Results:
There was a raised incidence of schizophrenia for those who were in the second month of fetal life in June 1967 (RR = 2.3, 1.1&#8211;4.7), seen more in females (4.3, 1.7&#8211;10.7) than in males (1.2, 0.4&#8211;3.8). Results were not explained by secular or seasonal variations, altered birth weight or gestational age. For other conditions, RRs were increased in offspring who had been in the third month of fetal life in June 1967 (2.5, 1.2&#8211;5.2), also seen more in females (3.6, 1.3&#8211;9.7) than males (1.8, 0.6&#8211;5.2).
Conclusion:
These findings add to a growing literature, in experimental animals and humans, attributing long term consequences for offspring of maternal gestational stress. They suggest both a sex-specificity and a relatively short gestational time-window for gestational effects on vulnerability to schizophrenia.</description>
			<link>http://www.biomedcentral.com/1471-244X/8/71</link>		
			<dc:creator>D Malaspina, C Corcoran, KR Kleinhaus, MC Perrin, S Fennig, D Nahon, Y Friedlander and S Harlap</dc:creator>
			<dc:source>BMC Psychiatry 2008, 8:71</dc:source>
			<dc:subject>Number of accesses: 932</dc:subject>
			<dc:date>2008-08-21</dc:date>
			<dc:identifier>doi:10.1186/1471-244X-8-71</dc:identifier>
			
			
							
					<prism:publicationName>BMC Psychiatry</prism:publicationName>
					
			
							
					<prism:issn>1471-244X</prism:issn>
					
			
							
					<prism:volume>8</prism:volume>
					
			
							
					<prism:startingPage>71</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-08-21</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-244X/8/81">
            
            <title>Early trauma-focused cognitive-behavioural therapy to prevent chronic post-traumatic stress disorder and related symptoms: A systematic review and meta-analysis</title>
			<description>Background:
Early trauma-focused cognitive-behavioural therapy (TFCBT) holds promise as a preventive intervention for people at risk of developing chronic post-traumatic stress disorder (PTSD). The aim of this review was to provide an updated evaluation of the effectiveness of early TFCBT on the prevention of PTSD in high risk populations.
Methods:
We performed a systematic literature search in international electronic databases (MEDLINE, EMBASE, PsycINFO, CENTRAL, CINAHL, ISI and PILOTS) and included randomised controlled trials comparing TFCBT delivered within 3 months of trauma, to alternative interventions. All included studies were critically appraised using a standardised checklist. Two independent reviewers selected studies for inclusion and assessed study quality. Data extraction was performed by one reviewer and controlled by another. Where appropriate, we entered study results into meta-analyses.
Results:
Seven articles reporting the results of five RCTs were included. All compared TFCBT to supportive counselling (SC). The study population was patients with acute stress disorder (ASD) in four trials, and with a PTSD diagnosis disregarding the duration criterion in the fifth trial. The overall relative risk (RR) for a PTSD diagnosis was 0.56 (95% CI 0.42 to 0.76), 1.09 (95% CI 0.46 to 2.61) and 0.73 (95% CI 0.51 to 1.04) at 3&#8211;6 months, 9 months and 3&#8211;4 years post treatment, respectively. A subgroup analysis of the four ASD studies only resulted in RR = 0.36 (95% CI 0.17 to 0.78) for PTSD at 3&#8211;6 months. Anxiety and depression scores were generally lower in the TFCBT groups than in the SC groups.
Conclusion:
There is evidence for the effectiveness of TFCBT compared to SC in preventing chronic PTSD in patients with an initial ASD diagnosis. As this evidence originates from one research team replications are necessary to assess generalisability. The evidence about the effectiveness of TFCBT in traumatised populations without an ASD diagnosis is insufficient.</description>
			<link>http://www.biomedcentral.com/1471-244X/8/81</link>		
			<dc:creator>Hege Korn&#248;r, Dagfinn Winje, &#216;ivind Ekeberg, Lars Weis&#230;th, Ingvild Kirkehei, Kjell Johansen and Asbj&#248;rn Steiro</dc:creator>
			<dc:source>BMC Psychiatry 2008, 8:81</dc:source>
			<dc:subject>Number of accesses: 663</dc:subject>
			<dc:date>2008-09-19</dc:date>
			<dc:identifier>doi:10.1186/1471-244X-8-81</dc:identifier>
			
			
							
					<prism:publicationName>BMC Psychiatry</prism:publicationName>
					
			
							
					<prism:issn>1471-244X</prism:issn>
					
			
							
					<prism:volume>8</prism:volume>
					
			
							
					<prism:startingPage>81</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-09-19</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-244X/8/78">
            
            <title>Early evaluation of patient risk for substantial weight gain during Olanzapine treatment for schizophrenia, schizophreniform, or schizoaffective disorder</title>
			<description>Background:
To make well-informed treatment decisions for their patients, clinicians need credible information about potential risk for substantial weight gain.  We, therefore, conducted a post-hoc analysis of clinical trial data, examining early weight gain as a predictor of later substantial weight gain. 
Methods:
Data from 669 (Study 1) and 102 (Study 2) olanzapine-treated patients diagnosed with schizophrenia, schizophreniform, or schizoaffective disorder were analyzed to identify and validate weight gain cut-offs at Weeks 1-4 of treatment that were predictive of substantial weight gain (>=5, 7, 10 kg or 7% of baseline weight) after approximately 30 weeks of treatment. Baseline characteristics alone, baseline characteristics plus weight change from baseline to Weeks 1, 2, 3 or 4, and weight change from baseline to Weeks 1, 2, 3, or 4 alone were evaluated as predictors of substantial weight gain.  
Results:
At Weeks 1 and 2, predictions based on early weight gain plus baseline characteristics were more robust than those based on early weight gain alone. However, by Weeks 3 and 4, there was little difference between the operating characteristics associated with these two sets of predictors. 
Conclusions:
Negative predictive values based on data from these studies suggest approximately 88% of patients who gain less than 2 kg by Week 3 will gain less than 10 kg after 26-34 weeks of olanzapine treatment. Further research in larger patient populations for longer periods is necessary to confirm these results.</description>
			<link>http://www.biomedcentral.com/1471-244X/8/78</link>		
			<dc:creator>Ilya Lipkovich, Jennie G Jacobson, Thomas A Hardy and Vicki POOLE Hoffmann</dc:creator>
			<dc:source>BMC Psychiatry 2008, 8:78</dc:source>
			<dc:subject>Number of accesses: 645</dc:subject>
			<dc:date>2008-09-15</dc:date>
			<dc:identifier>doi:10.1186/1471-244X-8-78</dc:identifier>
			
			
							
					<prism:publicationName>BMC Psychiatry</prism:publicationName>
					
			
							
					<prism:issn>1471-244X</prism:issn>
					
			
							
					<prism:volume>8</prism:volume>
					
			
							
					<prism:startingPage>78</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-09-15</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-244X/8/84">
            
            <title>Relative risk of diabetes, dyslipidaemia, hypertension and the metabolic syndrome in people with severe mental illnesses. 
Systematic review and metaanalysis 
</title>
			<description>Background:
Severe mental illnesses  (SMI) may be independently associated with cardiovascular risk factors and the metabolic syndrome. We aimed to systematically assess studies that compared diabetes, dyslipidaemia, hypertension and metabolic syndrome in people with and without SMI.MethodWe systematically searched MEDLINE, EMBASE, CINAHL &amp; PsycINFO. We hand searched reference lists of key articles. We employed three search main themes: SMI, cardiovascular disease, and each cardiovascular risk factor. We selected cross-sectional, case control, cohort or intervention studies comparing one or more risk factor in both SMI and a reference group. We excluded studies without any reference group. We extracted data on: study design, cardiovascular risk factor(s) and their measurement, diagnosis of SMI, study setting, sampling method, nature of comparison group and data on key risk factors.
Results:
Of 14592 citations, 134 papers met criteria and 36 were finally included.  26 reported on diabetes, 12 hypertension, 11 dyslipidaemia, and 4 metabolic syndrome. Most studies were cross sectional, small and several lacked  comparison data suitable for extraction. Meta-analysis was possible for diabetes, cholesterol and hypertension; revealing a pooled risk ratio of 1.70 (1.21 to 2.37) of diabetes and 1.11 (0.91 to 1.35) of hypertension. Restricting SMI to schizophreniform illnesses yielded a pooled risk ratio of 1.87 (1.68 to 2.09). Total cholesterol was not higher in people with SMI (Standardized Mean Difference -0.10 (-0.55 to 0.36)) and  there were inconsistent data on HDL, LDL and triglycerides with some, but not all, reporting low levels of HDL cholesterol and raised triglyceride levels. Metabolic syndrome appeared more common in SMI.
Conclusions:
Diabetes (but not hypertension) is more common in SMI.  Data on other risk factors were limited by poor quality or inconsistent research findings, but a small number of studies show greater prevalence of the metabolic syndrome in SMI. </description>
			<link>http://www.biomedcentral.com/1471-244X/8/84</link>		
			<dc:creator>David PJ Osborn, Christine A Wright, Gus Levy, Michael B King, Raman Deo and Irwin Nazareth</dc:creator>
			<dc:source>BMC Psychiatry 2008, 8:84</dc:source>
			<dc:subject>Number of accesses: 560</dc:subject>
			<dc:date>2008-09-25</dc:date>
			<dc:identifier>doi:10.1186/1471-244X-8-84</dc:identifier>
			
			
							
					<prism:publicationName>BMC Psychiatry</prism:publicationName>
					
			
							
					<prism:issn>1471-244X</prism:issn>
					
			
							
					<prism:volume>8</prism:volume>
					
			
							
					<prism:startingPage>84</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-09-25</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-244X/8/77">
            
            <title>Design and methods for a randomized clinical trial treating comorbid obesity and major depressive disorder</title>
			<description>Background:
Obesity is often comorbid with depression and individuals with this comorbidity fare worse in behavioral weight loss treatment. Treating depression directly prior to behavioral weight loss treatment might bolster weight loss outcomes in this population, but this has not yet been tested in a randomized clinical trial.Methods and designThis randomized clinical trial will examine whether behavior therapy for depression administered prior to standard weight loss treatment produces greater weight loss than standard weight loss treatment alone. Obese women with major depressive disorder (N = 174) will be recruited from primary care clinics and the community and randomly assigned to one of the two treatment conditions. Treatment will last 2 years, and will include a 6-month intensive treatment phase followed by an 18-month maintenance phase. Follow-up assessment will occur at 6-months and 1- and 2 years following randomization. The primary outcome is weight loss. The study was designed to provide 90% power for detecting a weight change difference between conditions of 3.1 kg (standard deviation of 5.5 kg) at 1-year assuming a 25% rate of loss to follow-up. Secondary outcomes include depression, physical activity, dietary intake, psychosocial variables and cardiovascular risk factors. Potential mediators (e.g., adherence, depression, physical activity and caloric intake) of the intervention effect on weight change will also be examined.DiscussionTreating depression before administering intensive health behavior interventions could potentially boost the impact on both mental and physical health outcomes.Trial registrationNCT00572520</description>
			<link>http://www.biomedcentral.com/1471-244X/8/77</link>		
			<dc:creator>Kristin L Schneider, Jamie S Bodenlos, Yunsheng Ma, Barbara Olendzki, Jessica Oleski, Philip Merriam, Sybil Crawford, Ira S Ockene and Sherry L Pagoto</dc:creator>
			<dc:source>BMC Psychiatry 2008, 8:77</dc:source>
			<dc:subject>Number of accesses: 535</dc:subject>
			<dc:date>2008-09-15</dc:date>
			<dc:identifier>doi:10.1186/1471-244X-8-77</dc:identifier>
			
			
							
					<prism:publicationName>BMC Psychiatry</prism:publicationName>
					
			
							
					<prism:issn>1471-244X</prism:issn>
					
			
							
					<prism:volume>8</prism:volume>
					
			
							
					<prism:startingPage>77</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-09-15</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-244X/3/17">
            
            <title>High vitamin B12 level and good treatment outcome may be associated in major depressive disorder</title>
			<description>Background:
Despite of an increasing body of research the associations between vitamin B12 and folate levels and the treatment outcome in depressive disorders are still unsolved. We therefore conducted this naturalistic prospective follow-up study. Our aim was to determine whether there were any associations between the vitamin B12 and folate level and the six-month treatment outcome in patients with major depressive disorder. Because vitamin B12 and folate deficiency may result in changes in haematological indices, including mean corpuscular volume, red blood cell count and hematocrit, we also examined whether these indices were associated with the treatment outcome.
Methods:
Haematological indices, erythrocyte folate and serum vitamin B12 levels were determined in 115 outpatients with DSM-III-R major depressive disorder at baseline and serum vitamin B12 level again on six-month follow-up. The 17-item Hamilton Depression Rating Scale was also compiled, respectively. In the statistical analysis we used chi-squared test, Pearson's correlation coefficient, the Student's t-test, analysis of variance (ANOVA), and univariate and multivariate linear regression analysis.
Results:
Higher vitamin B12 levels significantly associated with a better outcome. The association between the folate level and treatment outcome was weak and probably not independent. No relationship was found between haematological indices and the six-month outcome.
Conclusion:
The vitamin B12 level and the probability of recovery from major depression may be positively associated. Nevertheless, further studies are suggested to confirm this finding.</description>
			<link>http://www.biomedcentral.com/1471-244X/3/17</link>		
			<dc:creator>Jukka Hintikka, Tommi Tolmunen, Antti Tanskanen and Heimo Viinam&#228;ki</dc:creator>
			<dc:source>BMC Psychiatry 2003, 3:17</dc:source>
			<dc:subject>Number of accesses: 478</dc:subject>
			<dc:date>2003-12-02</dc:date>
			<dc:identifier>doi:10.1186/1471-244X-3-17</dc:identifier>
			
			
							
					<prism:publicationName>BMC Psychiatry</prism:publicationName>
					
			
							
					<prism:issn>1471-244X</prism:issn>
					
			
							
					<prism:volume>3</prism:volume>
					
			
							
					<prism:startingPage>17</prism:startingPage>
					
			
							
					<prism:publicationDate>2003-12-02</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-244X/8/80">
            
            <title>Discontinuation of hypnotics during cognitive behavioural therapy for insomnia</title>
			<description>Background:
In practical sleep medicine, therapists face the question of whether or not to discontinue the ongoing use of hypnotics in patients, as well as the possible effects of discontinuation. The aim of this study was to evaluate the effects of discontinuing third-generation hypnotics on the results of cognitive-behavioural therapy (CBT) for primary insomnia in patients after long-term abuse.
Methods:
Twenty-eight outpatients were treated by CBT for 8 weeks. The treatment outcome was estimated by means of differences among subjective clinical scales and polysomnography variables assessed before and after the treatment period. The therapeutic effect in a subgroup of 15 patients who had previously received hypnotics and were successively withdrawn during weeks 2&#8211;6 was compared to the effect achieved in patients who had not used hypnotics before CBT.
Results:
There were no significant differences in baseline subjective and objective sleep characteristics between the hypnotic abusers and non-abusers. According to clinical scales and most polysomnographic measures, CBT was highly effective in both groups of subjects; it produced the greatest changes in total sleep time, REM sleep and sleep efficiency. Unexpectedly, discontinuation of hypnotics, as a factor in the analysis, was followed by an additional improvement of sleep efficiency and wake after sleep onset parameters.
Conclusion:
Our study confirmed the efficacy of CBT in both hypnotic-abusing and non-abusing patients with chronic insomnia. The results of this study suggest that tapered withdrawal of third-generation hypnotics during CBT therapy for chronic insomnia could be associated with improvement rather than worsening of sleep continuity.</description>
			<link>http://www.biomedcentral.com/1471-244X/8/80</link>		
			<dc:creator>Lucie Zavesicka, Martin Brunovsky, Milos Matousek and Peter Sos</dc:creator>
			<dc:source>BMC Psychiatry 2008, 8:80</dc:source>
			<dc:subject>Number of accesses: 466</dc:subject>
			<dc:date>2008-09-18</dc:date>
			<dc:identifier>doi:10.1186/1471-244X-8-80</dc:identifier>
			
			
							
					<prism:publicationName>BMC Psychiatry</prism:publicationName>
					
			
							
					<prism:issn>1471-244X</prism:issn>
					
			
							
					<prism:volume>8</prism:volume>
					
			
							
					<prism:startingPage>80</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-09-18</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-244X/8/83">
            
            <title>Longitudinal population-based studies of affective disorders: Where to from here?</title>
			<description>Background:
Longitudinal, population-based, research is important if we are to better characterize the lifetime patterns and determinants of affective disorders. While studies of this type are becoming increasingly prevalent, there has been little discussion about the limitations of the methods commonly used.
Methods:
Discussion paper including a brief review of key prospective population-based studies as the basis for a critical appraisal of current approaches.
Results:
We identified a number of common methodological weaknesses that restrict the potential of longitudinal research to characterize the diversity, prognosis, and determinants of affective disorders over time. Most studies using comprehensive diagnostic instruments have either been of relatively brief duration, or have suffered from long periods between waves. Most etiologic research has focused on first onset diagnoses, although these may be relatively uncommon after early adulthood and the burden of mental disorders falls more heavily on individuals with recurring disorders. Analysis has tended to be based on changes in diagnostic status rather than anges in symptom levels, limiting study power. Diagnoses have generally been treated as homogeneous entities and few studies have explored whether diagnostic subtypes such as atypical depression vary in their etiology or prognosis. Little research has considered whether there are distinct trajectories of symptoms over time and most has focused on individual disorders such as depression, rather than considering the relationship over time between symptoms of different affective disorders. There has also been limited longitudinal research on factors in the physical or social environment that may influence the onset, recurrence or chronicity of symptoms.
Conclusion:
Many important, and in some respects quite basic, questions remain about the trajectory of depression and anxiety disorders over the life course and the factors that influence their incidence, recurrence and prognosis. Innovative approaches that consider symptoms of all affective disorders, and how these change over time, has the potential to greatly increase our understanding of the heterogeneity of these important conditions and of the individual and environmental characteristics that influence their life course.Using longitudinal research to define sub classes of affective disorders may also be of great benefit for studies seeking to define the genetic determinants of susceptibility to these conditions.</description>
			<link>http://www.biomedcentral.com/1471-244X/8/83</link>		
			<dc:creator>John R Beard, Sandro Galea and David Vlahov</dc:creator>
			<dc:source>BMC Psychiatry 2008, 8:83</dc:source>
			<dc:subject>Number of accesses: 415</dc:subject>
			<dc:date>2008-09-23</dc:date>
			<dc:identifier>doi:10.1186/1471-244X-8-83</dc:identifier>
			
			
							
					<prism:publicationName>BMC Psychiatry</prism:publicationName>
					
			
							
					<prism:issn>1471-244X</prism:issn>
					
			
							
					<prism:volume>8</prism:volume>
					
			
							
					<prism:startingPage>83</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-09-23</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-244X/7/7">
            
            <title>The improved Clinical Global Impression Scale (iCGI): development and validation in depression</title>
			<description>Background:
The Clinical Global Impression scale (CGI) is frequently used in medical care and clinical research because of its face validity and practicability. This study proposes to improve the reliability of the Clinical Global Impression (CGI) scale in depressive disorders by the use of a semi-standardized interview, a new response format, and a Delphi procedure.
Methods:
Thirty patients hospitalised for a major depressive episode were filmed at T1 (first week in hospital) and at T2 (2 weeks later) during a 5' specific interview. The Hamilton Depressive Rating Scale and the Symptom Check List were also rated. Eleven psychiatrists rated these videos using either the usual CGI response format or an improved response format, with or without a Delphi procedure.
Results:
The new response format slightly improved (but not significantly) the interrater agreement, the Delphi procedure did not. The best results were obtained when ratings by 4 independent raters were averaged. In this situation, intraclass correlation coefficients were about 0.9.
Conclusion:
The Clinical Global Impression is a useful approach in psychiatry since it apprehends patients in their entirety. This study shows that it is possible to quantify such impressions with a high level of interrater agreement.</description>
			<link>http://www.biomedcentral.com/1471-244X/7/7</link>		
			<dc:creator>Alane Kadouri, Emmanuelle Corruble and Bruno Falissard</dc:creator>
			<dc:source>BMC Psychiatry 2007, 7:7</dc:source>
			<dc:subject>Number of accesses: 410</dc:subject>
			<dc:date>2007-02-06</dc:date>
			<dc:identifier>doi:10.1186/1471-244X-7-7</dc:identifier>
			
			
							
					<prism:publicationName>BMC Psychiatry</prism:publicationName>
					
			
							
					<prism:issn>1471-244X</prism:issn>
					
			
							
					<prism:volume>7</prism:volume>
					
			
							
					<prism:startingPage>7</prism:startingPage>
					
			
							
					<prism:publicationDate>2007-02-06</prism:publicationDate>
					

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