Borderline personality disorder and depressive disorder.
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Biomarkers↗
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Results for “Depressive Disorder”
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Sertraline versus imipramine treatment of comorbid panic disorder and major depressive disorder.
OBJECTIVE: To evaluate the efficacy and tolerability of sertraline and imipramine in patients with comorbid panic disorder and major depressive disorder. METHOD: Outpatients meeting a DSM-IV diagnosis of panic disorder and concurrent major depressive disorder were randomized in a 2:1 ratio to 26 weeks of double-blind treatment with either sertraline, in daily doses of 50 to 100 mg, or imipramine, in daily doses of 100 to 200 mg. Primary outcome measures were panic attack frequency (derived from patient diaries) and the Montgomery-Asberg Depression Rating Scale (MADRS). RESULTS: 138 patients were treated with sertraline (76% female; mean age = 40 years) and 69 with imipramine (70% female; mean age = 40 years). The symptoms of both major depressive disorder and panic disorder responded significantly and equivalently to both drugs. Endpoint improvement with sertraline versus imipramine, respectively, on the MADRS was 11.1 +/- 10.8 versus 11.2 +/- 10.4, and on the Clinical Global Impressions-Improvement scale (CGI-I) was 2.1 +/- 1.3 versus 2.4 +/- 1.6. Among study completers, CGI-I responder rates were 88% with sertraline and 91% with imipramine. Treatment outcome was concordant for both diagnoses in approximately 70% of patients and discordant in approximately 30%. Overall, sertraline was significantly better tolerated with significantly fewer discontinuations due to adverse events (11% vs. 22%; chi(2) = 4.39, df = 1, p =.04). CONCLUSION: Both sertraline and imipramine were found to be highly effective treatments for both major depressive disorder and panic disorder, with sertraline showing significantly greater tolerability and compliance during long-term treatment than imipramine.
Adult↗
The risk for early-adulthood anxiety and depressive disorders in adolescents with anxiety and depressive disorders.
BACKGROUND: Various studies find relationships among anxiety and depressive disorders of adolescence and adulthood. This study prospectively examines the magnitude of longitudinal associations between adolescent and adult anxiety or depressive disorders. METHODS: An epidemiologically selected sample of 776 young people living in upstate New York received DSM-based psychiatric assessments in 1983, 1985, and 1992 using structured interviews. The magnitude of the association between adolescent and adult anxiety or depressive disorders was quantified using odds ratios generated from logistic regression analyses and from a set of latent Markov analyses. We focus on longitudinal associations among narrowly defined DSM anxiety or depressive disorders. RESULTS: In simple logistic models, adolescent anxiety or depressive disorders predicted an approximate 2- to 3-fold increased risk for adulthood anxiety or depressive disorders. There was evidence of specificity in the course of simple and social phobia but less specificity in the course of other disorders. Results from the analyses using latent variables suggested that while most adolescent disorders were no longer present in young adulthood, most adult disorders were preceded by adolescent disorders. CONCLUSIONS: An anxiety or depressive disorder during adolescence confers a strong risk for recurrent anxiety or depressive disorders during early adulthood. Most anxiety and depressive disorders in young adults may be preceded by anxiety or depression in adolescence.
Adolescent↗
Expression of ZNF804A in human brain and alterations in schizophrenia, bipolar disorder, and major depressive disorder: a novel transcript fetally regulated by the psychosis risk variant rs1344706.
IMPORTANCE: The single-nucleotide polymorphism rs1344706 in the zinc finger protein 804A gene (ZNF804A) shows genome-wide association with schizophrenia and bipolar disorder. Little is known regarding the expression of ZNF804A and the functionality of rs1344706. OBJECTIVES: To characterize ZNF804A expression in human brain and to investigate how it changes across the life span and how it is affected by rs1344706, schizophrenia, bipolar disorder, and major depressive disorder. DESIGN, SETTING, AND PARTICIPANTS: Molecular and immunochemical methods were used to study ZNF804A messenger RNA (mRNA) and ZNF804A protein, respectively. ZNF804A transcripts were investigated using next-generation sequencing and polymerase chain reaction-based methods, and ZNF804A protein was investigated using Western blots and immunohistochemistry. Samples of dorsolateral prefrontal cortex and inferior parietal lobe tissue were interrogated from 697 participants between 14 weeks' gestational age and age 85 years, including patients with schizophrenia, bipolar disorder, or major depressive disorder. MAIN OUTCOMES AND MEASURES: Quantitative measurements of ZNF804A mRNA and immunoreactivity, and the effect of diagnosis and rs1344706 genotype. RESULTS: ZNF804A was expressed across the life span, with highest expression prenatally. An abundant and developmentally regulated truncated ZNF804A transcript was identified, missing exons 1 and 2 (ZNF804AE3E4) and predicted to encode a protein lacking the zinc finger domain. rs1344706 influenced expression of ZNF804AE3E4 mRNA in fetal brain (P = .02). In contrast, full-length ZNF804A showed no association with genotype (P > .05). ZNF804AE3E4 mRNA expression was decreased in patients with schizophrenia (P = .006) and increased in those with major depressive disorder (P < .001), and there was a genotype-by-diagnosis interaction in bipolar disorder (P = .002). ZNF804A immunoreactivity was detected in fetal and adult human cerebral cortex. It was localized primarily to pyramidal neurons, with cytoplasmic as well as dendritic and nuclear staining. No differences in ZNF804A-immunoreactive neurons were seen in schizophrenia or related to rs1344706 (P > .05). CONCLUSIONS AND RELEVANCE: rs1344706 influences the expression of ZNF804AE3E4, a novel splice variant. The effect is limited to fetal brain and to this isoform. It may be part of the mechanism by which allelic variation in ZNF804A affects risk of psychosis. ZNF804A is translated in human brain, where its functions may extend beyond its predicted role as a transcription factor.
Adolescent↗
Reward-related decision-making in pediatric major depressive disorder: an fMRI study.
BACKGROUND: Although reward processing is considered an important part of affective functioning, few studies have investigated reward-related decisions or responses in young people with affective disorders. Depression is postulated to involve decreased activity in reward-related affective systems. METHODS: Using functional magnetic resonance imaging (fMRI), we examined behavioral and neural responses to reward in young people with depressive disorders using a reward decision-making task. The task involved choices about possible rewards involving varying magnitude and probability of reward. The study design allowed the separation of decision/anticipation and outcome phases of reward processing. Participants were 9-17 years old and had diagnoses of major depressive disorder (MDD), anxiety disorders, or no history of psychiatric disorder. RESULTS: Participants with MDD exhibited less neural response than control participants in reward-related brain areas during both phases of the task. Group differences did not appear to be a function of anxiety. Depressive and anxiety symptoms were associated with activation in reward-related brain areas. CONCLUSIONS: Results suggest that depression involves altered reward processing and underscore the need for further investigation of relations among development, affective disorders, and reward processing.
Adolescent↗
Does temperamental instability support a continuity between bipolar II disorder and major depressive disorder?
BACKGROUND: The current categorical split of mood disorders in bipolar disorders and depressive disorders has recently been questioned. Two highly unstable personality features, i.e. the cyclothymic temperament (CT) and borderline personality disorder (BPD), have been found to be more common in bipolar II (BP-II) disorder than in major depressive disorder (MDD). According to Kraepelin, temperamental instability was the "foundation" of his unitary view of mood disorders. STUDY AIM: The aim was to assess the distributions of the number of CT and borderline personality items between BP-II and MDD. Finding no bi-modal distribution (a "zone of rarity") of these items would support a continuity between the two disorders. METHODS STUDY SETTING: an outpatient psychiatry private practice. Interviewer: A senior clinical and mood disorder research psychiatrist. PATIENT POPULATION: A consecutive sample of 138 BP-II and 71 MDD remitted outpatients. Assessment instruments: The structured clinical interview for DSM-IV Axis I Disorders-Clinician Version (SCID-CV), the SCID-II Personality Questionnaire for self-assessing borderline personality traits (BPT) by patients, the TEMPS-A for self-assessing CT by patients. Interview methods: Patients were interviewed with the SCID-CV to diagnose BP-II and MDD, and then patients self-assessed the questions of the Personality Questionnaire relative to borderline personality, and the questions of the TEMPS-A relative to CT. As clinically significant distress or impairment of functioning is not assessed by the SCID-II Personality Questionnaire, a diagnosis of BPD could not be made, but BPT could be assessed (i.e. all BPD items but not the impairment criterion). The distribution of the number of CT and BPT items was studied by Kernel density estimate. RESULTS: CT and BPT items were significantly more common in BP-II versus MDD. The Kernel density estimate distributions of the number of CT and BPT items in the entire sample had a normal-like shape (i.e. no bi-modality). CONCLUSIONS: The expected finding, on the basis of previous studies and of the present sample features, was a clustering of CT and BPT items on the BP-II side of the curves. Instead, no bi-modality was present in the distributions of the number of CT and BPT items in the entire sample, showing a normal-like shape. By using the bi-modality approach, a continuity between BP-II and MDD seems supported, questioning the current categorical splitting of BP-II and MDD based on classic diagnostic validators.
Adult↗
Disease-specific alterations in frontal cortex brain proteins in schizophrenia, bipolar disorder, and major depressive disorder. The Stanley Neuropathology Consortium.
Severe psychiatric disorders such as schizophrenia, bipolar disorder and major depressive disorder are brain diseases of unknown origin. No biological marker has been documented at the pathological, cellular, or molecular level, suggesting that a number of complex but subtle changes underlie these illnesses. We have used proteomic technology to survey postmortem tissue to identify changes linked to the various diseases. Proteomics uses two-dimensional gel electrophoresis and mass spectrometric sequencing of proteins to allow the comparison of subsets of expressed proteins among a large number of samples. This form of analysis was combined with a multivariate statistical model to study changes in protein levels in 89 frontal cortices obtained postmortem from individuals with schizophrenia, bipolar disorder, major depressive disorder, and non-psychiatric controls. We identified eight protein species that display disease-specific alterations in level in the frontal cortex. Six show decreases compared with the non-psychiatric controls for one or more diseases. Four of these are forms of glial fibrillary acidic protein (GFAP), one is dihydropyrimidinase-related protein 2, and the sixth is ubiquinone cytochrome c reductase core protein 1. Two spots, carbonic anhydrase 1 and fructose biphosphate aldolase C, show increase in one or more diseases compared to controls. Proteomic analysis may identify novel pathogenic mechanisms of human neuropsychiatric diseases.
Amino Acid Sequence↗
Hypochondriacal concerns in panic disorder and major depressive disorder: a comparison.
OBJECTIVE: To gain perspective on the relationship between hypochondriasis and panic disorder, we compared the occurrence of hypochondriasis in patients with panic disorder (N= 59) and major depressive disorder (N= 27). METHODS: Patients who participated in separate drug treatment trials were assessed at baseline and eight weeks using the Whiteley Index of Hypochondriasis. RESULTS: At baseline, the Whiteley Index score was greater for patients with panic disorder than for those with major depressive disorder. At eight weeks, a statistically significant reduction in the mean hypochondriasis score was observed in panic patients who had improved but not in major depressive patients who had improved. Modest correlations were observed between hypochondriasis and symptoms of panic and major depressive disorder, but in depressed patients, hypochondriasis was positively correlated with anxiety symptoms as well. CONCLUSION: A unique relationship appears to exist between hypochondriasis and panic disorder. The nature of this relationship and its implications for classification are discussed.
Adult↗
[Treatment of major depressive disorder. Comorbidity, depression and anxiety: dangerous liaisons].
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Anti-Anxiety Agents↗
The functioning and well-being of patients with unrecognized anxiety disorders and major depressive disorder.
This study examines the degree to which untreated anxiety disorders and major depressive disorder, occurring either singly or in combination, reduce functioning and well-being among primary care patients. Adult patients were screened using the SCL-52 to identify those with clinically significant anxiety symptoms. They also completed the Rand Short-Form (SF-36) to measure self-reported patient functioning and well-being. Patients with untreated disorders were identified using the Q-DIS-III-R to diagnose six DIS-anxiety disorders (generalized anxiety disorder, post-traumatic stress disorder (PTSD), simple phobia, social phobia, panic/agoraphobia, obsessive/compulsive disorder) and major depression. Of 319 patients identified, 137 (43%) had a single disorder and 182 (57%) had multiple disorders. Regression models estimated the relative effects of these disorders on health status (SF-36) by comparing patients with the disorders to patients screened as being not-anxious. Estimates of these effects were consistent with available national norms. The estimated effect of each single disorder on all subscales for physical, social and emotional functioning was negative, often as much as a 20-30 point reduction on this 100-point scale. Major depression had the greatest negative impact, followed by PTSD and panic/ agoraphobia. For patients with multiple disorders, the presence of major depression was associated with the greatest reduction in functioning status. The impact of untreated anxiety disorders and major depressive disorder on functioning was comparable to, or greater than, the effects of medical conditions such as low back pain, arthritis, diabetes and heart disease.
Adult↗
Transcriptional profiling reveals evidence for signaling and oligodendroglial abnormalities in the temporal cortex from patients with major depressive disorder.
Major depressive disorder is one of the most common and devastating psychiatric disorders. To identify candidate mechanisms for major depressive disorder, we compared gene expression in the temporal cortex from 12 patients with major depressive disorder and 14 matched controls using Affymetrix HgU95A microarrays. Significant expression changes were revealed in families of genes involved in neurodevelopment, signal transduction and cell communication. Among these, the expression of 17 genes related to oligodendrocyte function was significantly (P < 0.05, fold change > 1.4) decreased in patients with major depressive disorder. Eight of these 17 genes encode structural components of myelin (CNP, MAG, MAL, MOG, MOBP, PMP22, PLLP, PLP1). Five other genes encode enzymes involved in the synthesis of myelin constituents (ASPA, UGT8), or are essential in regulation of myelin formation (ENPP2, EDG2, TF, KLK6). One gene, that is, SOX10, encodes a transcription factor regulating other myelination-related genes. OLIG2 is a transcription factor present exclusively in oligodendrocytes and oligodendrocyte precursors. Another gene, ERBB3, is involved in oligodendrocyte differentiation. In addition to myelination-related genes, there were significant changes in multiple genes involved in axonal growth/synaptic function. These findings suggest that major depressive disorder may be associated with changes in cell communication and signal transduction mechanisms that contribute to abnormalities in oligodendroglia and synaptic function. Taken together with other studies, these findings indicate that major depressive disorder may share common oligodendroglial abnormalities with schizophrenia and bipolar disorder.
Adult↗
Density and distribution of white matter neurons in schizophrenia, bipolar disorder and major depressive disorder: no evidence for abnormalities of neuronal migration.
The neurodevelopmental hypothesis of schizophrenia suggests that this disorder may result from a disruption of normal brain development. While widely cited, neuropathological evidence for this is far from conclusive. Alterations in the density and position of white matter neurons have been previously described in the frontal and temporal lobes and have led to suggestions that abnormal neuronal migration may play a role in the aetiology of schizophrenia. However, these findings have not been replicated. Furthermore, developmental abnormalities may not be specific to schizophrenia. The aim of this study was to examine the density and spatial pattern distribution of white matter neurons in psychiatric and control subjects using sophisticated computerised image analysis techniques. White matter neurons immunoreactive for microtubule associated protein-2 were quantified in the frontal lobe in schizophrenia, bipolar disorder, major depressive disorder and matched controls (each group n = 15). Analysis showed that the density and spatial distribution of white matter neurons did not differ significantly between the control and psychiatric groups. This study cannot replicate the earlier findings of white matter abnormalities in schizophrenia and finds no evidence for abnormal brain development in any of the disorders studied.
Adult↗
Generalized Anxiety Disorder and major depressive disorder comorbidity in the National Survey of Mental Health and Well-Being.
We report population data on DSM-IV Generalized Anxiety Disorder (GAD) from the Australian National Survey of Mental Health and Well-Being, obtained from a nationwide household survey of adults using a stratified multistage sampling process. A response rate of 78.1% resulted in 10,641 persons being interviewed. Diagnoses were made using the Composite International Diagnostic Interview. The interview was computerised and conducted by trained lay interviewers. We investigated comorbidity between GAD and major depressive disorder (MDD). The results indicate that sociodemographic correlates of GAD, and associated disablement and service use, are influenced by the presence of a comorbid depressive disorder but cannot be fully explained by the presence of that disorder. In addition, GAD was confirmed as significantly disabling, even as a single disorder. We conclude that the results are consistent with the view that GAD has a significant and independent impact on the burden of mental disorders.
Adolescent↗
An investigation of the Wnt-signalling pathway in the prefrontal cortex in schizophrenia, bipolar disorder and major depressive disorder.
The Wnt-signalling pathway has been implicated in a variety of processes including cortical development and plasticity. We have previously demonstrated a reduction in glycogen synthase kinase-3beta (GSK-3beta) levels in the prefrontal cortex in schizophrenia and aimed to further elucidate the abnormalities of the Wnt-signalling pathway in this and other psychiatric disorders. Immunoblotting was performed to quantify the levels of three members of the Wnt-signalling pathway, GSK-3beta, beta-catenin and dishevelled-2 (Dvl-2), in the prefrontal cortex in schizophrenia, bipolar disorder and major depressive disorder and in matched controls. We found no significant differences between the disease and control groups for any of the proteins studied, and therefore, cannot confirm our earlier findings of abnormalities of GSK-3beta in schizophrenia.
Adaptor Proteins, Signal Transducing↗
Differences in Axis I and II comorbidity between bipolar I and II disorders and major depressive disorder.
OBJECTIVE: To obtain a comprehensive view of differences in current comorbidity between bipolar I and II disorders (BD) and (unipolar) major depressive disorder (MDD), and Axis I and II comorbidity in BD in secondary-care psychiatric settings. METHOD: The psychiatric comorbidity of 90 bipolar I and 101 bipolar II patients from the Jorvi Bipolar Study and 269 MDD patients from the Vantaa Depression Study were compared. We used DSM-IV criteria assessed by semistructured interviews. Patients were inpatients and outpatients from secondary-care psychiatric units. Comparable information was collected on clinical history, index episode, symptom status, and patient characteristics. RESULTS: Bipolar disorder and MDD differed in prevalences of current comorbid disorders, MDD patients having significantly more Axis I comorbidity (69.1% vs. 57.1%), specifically anxiety disorders (56.5% vs. 44.5%) and cluster A (19.0% vs. 9.9%) and C (31.6% vs. 23.0%) personality disorders. In contrast, BD had more single cluster B personality disorders (30.9% vs. 24.6%). Bipolar I and bipolar II were similar in current overall comorbidity, but the prevalence of comorbidity was strongly associated with the current illness phase. CONCLUSIONS: Major depressive disorder and BD have somewhat different patterns in the prevalences of comorbid disorders at the time of an illness episode, with differences particularly in the prevalences of anxiety and personality disorders. Current illness phase explains differences in psychiatric comorbidity of BD patients better than type of disorder.
Adolescent↗
Obesity in bipolar disorder and major depressive disorder: results from a national community health survey on mental health and well-being.
OBJECTIVE: We aimed to ascertain the prevalence of obesity in individuals with a mood disorder (MD) (that is, bipolar disorder or major depressive disorder), compared with the general population. We further aimed to examine the likelihood of an association between obesity and MD, while controlling for the influence of sociodemographic variables. METHOD: The analysis was based on data from Statistics Canada's Canadian Community Health Survey: Mental Health and Well-Being (CCHS 1.2), conducted in 2002. The sample (n = 36 984; > or = aged 15 years) was drawn from the Canadian household-dwelling population. The CCHS used diagnostic criteria outlined in the DSM-IV to screen respondents. RESULTS: Individuals with a lifetime history of MD were more likely to be obese (body mass index [BMI] > 30) than were individuals without lifetime MD (19%, compared with 15%, respectively; P < 0.001). In sex-specific multivariate analysis, lifetime MD was associated with elevated odds of obesity in female respondents (95%CI, 1.03 to 1.46, odds ratio 1.22), but not in male respondents. Antipsychotic pharmacotherapy was also associated with obesity. CONCLUSIONS: This is the first Canadian epidemiologic investigation to specifically evaluate anthropometric indices and associated factors in people with MDs. The results herein supplement substantial clinical evidence documenting the association between MDs and stress-sensitive somatic disorders (for example, obesity). These data also underscore the metabolic consequences of some psychotropic agents.
Adolescent↗
Fluoxetine vs. tricyclic antidepressants in women with major depressive disorder.
Major depressive disorder and dysthymia are twice as prevalent in women as in men, and the lifetime risk of a woman's developing a major depressive disorder is about 20%. Yet depression is often unrecognized or misdiagnosed in women, and only about one quarter of women who meet criteria for major depressive disorder receive appropriate therapy. Until recently, women were generally excluded from clinical drug trials because of concerns of inadvertent pregnancy and risk of teratogenicity. Thus, information on safety and efficacy in those most likely to require antidepressant therapy is lacking. Studies have shown that the antidepressant fluoxetine, a selective serotonin reuptake inhibitor (SSRI) has a more tolerable side effect profile than do tricyclic amine (TCA) antidepressants, but few data have been reported on the efficacy and tolerability of fluoxetine or other SSRIs in female patients. In this study, a retrospective analysis of 11 randomized, double-blind, well-controlled trials was done to compare data from 427 female patients on fluoxetine and 423 female patients on TCAs. Both fluoxetine and TCAs significantly reduced the HAMD17 total mean score from baseline to end point, week 5 (fluoxetine, 24.35 to 14.37; TCAs, 24.57 to 14.43; p < 0.001). Both treatment groups were associated with significant reductions in the HAMD17 anxiety/somatization and insomnia subfactor scores. Abnormal vision, constipation, dizziness, dry mouth, and somnolence occurred more frequently (p < 0.05) in the TCA group. Insomnia and nausea were the only adverse events more common (p < 0.05) in the fluoxetine group. This study demonstrates that fluoxetine is an effective and tolerable agent for the treatment of major depressive disorder in women.
Adult↗
Dissociation of inflammatory markers and natural killer cell activity in major depressive disorder.
Major depressive disorder is associated with increases in infectious disease risk as well as the incidence of inflammatory disorders. Declines of natural killer (NK) cell activity are reliably found in depression, whereas other studies report evidence of inflammation in depressed patients. The potential association between NK activity and circulating markers of immune activation has not been previously examined in the context of major depression. In this study, we measured levels of NK activity, circulating levels of interleukin-6 (IL-6), soluble interleukin-2 receptor, and acute phase proteins in 25 male patients with current major depressive disorder and 25 age, gender, and body weight comparable controls. As compared to controls, patients with major depressive disorder showed lower NK activity (p = .05) and higher circulating levels of IL-6 (p < .05). Levels of NK activity were not correlated with IL-6 or with other markers of immune activation. The independent effect of depression on inflammatory markers and natural killer immune responses has implications for understanding individual differences in the adverse health effects of major depressive disorder.
Acute-Phase Proteins↗