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Abstract
Bipolar disorder is a recurring, often chronic, illness characterised by periods of mania and depression with variable inter-episode recovery. For the majority of patients it is the depressive component of this illness that contributes to most of the associated morbidity, social disability and mortality. Research and clinical experience suggest that acute treatment and prevention of depressive episodes is by far the most challenging aspect of the care of patients with the disorder. This review examines the contribution of depression to the course and outcome of bipolar disorder as well as diagnostic difficulties that often complicate treatment and may lead to inappropriate medication. Key studies that form the evidence base of treatment recommendation for bipolar depression are presented and areas of therapeutic uncertainty are highlighted.
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Jesulola E, Micalos P, Baguley IJ. Understanding the pathophysiology of depression: From monoamines to the neurogenesis hypothesis model - are we there yet? Behav Brain Res 2017; 341:79-90. [PMID: 29284108 DOI: 10.1016/j.bbr.2017.12.025] [Citation(s) in RCA: 223] [Impact Index Per Article: 27.9] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/16/2017] [Revised: 12/19/2017] [Accepted: 12/22/2017] [Indexed: 02/07/2023]
Abstract
A number of factors (biogenic amine deficiency, genetic, environmental, immunologic, endocrine factors and neurogenesis) have been identified as mechanisms which provide unitary explanations for the pathophysiology of depression. Rather than a unitary construct, the combination and linkage of these factors have been implicated in the pathogenesis of depression. That is, environmental stressors and heritable genetic factors acting through immunologic and endocrine responses initiate structural and functional changes in many brain regions, resulting in dysfunctional neurogenesis and neurotransmission which then manifest as a constellation of symptoms which present as depression.
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Affiliation(s)
- Emmanuel Jesulola
- Paramedicine Discipline, Charles Sturt University, Bathurst Campus, NSW Australia.
| | - Peter Micalos
- Paramedicine Discipline, Charles Sturt University, Bathurst Campus, NSW Australia
| | - Ian J Baguley
- Brain Injury Rehabilitation Service, Westmead Hospital, Hawkesbury Rd, Wentworthville, NSW Australia
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Abstract
Hyperactive intracellular calcium ion (Ca) signaling in peripheral cells has been a reliable finding in bipolar disorder. Some established mood stabilizing medications, such as lithium and carbamazepine, have been found to normalize elevated intracellular Ca concentrations ([Ca]i) in platelets and lymphocytes from bipolar disorder patients, and some medications the primary effect of which is to attenuate increased [Ca]i have been reported to have mood stabilizing properties.Hyperactive intracellular Ca signaling has also been implicated in epilepsy, and some anticonvulsants have calcium antagonist properties. This study demonstrated that levetiracetam, an anticonvulsant that has been shown to block N and P/Q-type calcium channels in animal studies does not alter elevated [Ca]i in blood platelets of patients with bipolar disorder. Review of published clinical trials revealed no controlled evidence of efficacy as a mood stabilizer.This study underscores the possibility that pharmacologic actions of a medication in animals and normal subjects may not necessarily predict its pharmacologic or clinical effects in actual patients. Effects of treatments on pathophysiology that is demonstrated in clinical subtypes may be more likely to predict effectiveness in those subtypes than choosing medications based on structural similarities to established treatments.
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Dubovsky SL, Daurignac E, Leonard KE. Increased platelet intracellular calcium ion concentration is specific to bipolar disorder. J Affect Disord 2014; 164:38-42. [PMID: 24856551 DOI: 10.1016/j.jad.2014.04.025] [Citation(s) in RCA: 18] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/18/2014] [Accepted: 04/11/2014] [Indexed: 01/02/2023]
Abstract
BACKGROUND Increased baseline ([Ca(2+)]B) and agonist-stimulated ([Ca(2+)]s) free intracellular calcium ion concentrations ([Ca(2+)]i) are well-replicated findings in bipolar disorder, but whether this finding is specific to that condition and if so, whether it is a marker of the mood disorder or a feature seen in other disorders such as psychosis has remained unclear. METHODS Platelet [Ca(2+)]i was assessed in 15 inpatients with psychotic and nonpsychotic mania, 17 schizophrenia inpatients, and 17 matched controls. RESULTS Platelet [Ca(2+)]B and [Ca(2+)]s were significantly higher than controls in bipolar disorder but not schizophrenia. Variability of [Ca(2+)]B was significantly increased in bipolar disorder regardless of the presence of psychosis, but not in schizophrenia. LIMITATIONS Use of antipsychotic drugs by the majority of both patient groups may have obscured elevated [Ca(2+)]i in schizophrenia, or may have masked a difference between psychotic and nonpsychotic bipolar disorder. Measurement of [Ca(2+)]i is too labor intensive to become a routine test for diagnosis or prediction of treatment response. CONCLUSIONS Elevated intracellular Ca(2+) signaling may be a marker of primary cellular hyperactivity that could contribute to comorbid conditions such as hypertension and neuronal apoptosis. Since lithium and carbamazepine attenuate increased [Ca(2+)]i, further research may demonstrate a correlation between normalization of [Ca(2+)]i and response to one of these medications, and further research may clarify whether a subgroup of patients may respond well to calcium channel antagonists.
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Affiliation(s)
- Steven L Dubovsky
- Department of Psychiatry, State University of New York at Buffalo, Buffalo, NY 14215, USA; Departments of Psychiatry and Medicine, University of Colorado, Denver, CO, USA.
| | - Elsa Daurignac
- Department of Psychiatry, State University of New York at Buffalo, Buffalo, NY 14215, USA
| | - Kenneth E Leonard
- Department of Psychiatry, State University of New York at Buffalo, Buffalo, NY 14215, USA; Research Institute on Addictions, University at Buffalo, Buffalo, NY, USA
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Different neural responses to a moral valence decision task in unipolar and bipolar depression. ISRN PSYCHIATRY 2013; 2013:568617. [PMID: 24455401 PMCID: PMC3877629 DOI: 10.1155/2013/568617] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 10/02/2013] [Accepted: 11/12/2013] [Indexed: 11/23/2022]
Abstract
Objectives. Patients affected by bipolar disorder (BP) and major depressive disorder (UP) share the susceptibility to experience depression and differ in their susceptibility to mania, but clinical studies suggest that the biological substrates of the two disorders could influence the apparently similar depressive phases. The few brain imaging studies available described different brain metabolic and neural correlates of UP and BP. Methods. We studied the BOLD neural response to a moral valence decision task targeting the depressive biases in information processing in 36 subjects (14 BP, 11 UP, and 11 controls). Results. Main differences between UP and controls and between UP and BP were detected in left ventrolateral prefrontal cortex (PFC, BA 47). Neural responses of BP patients differed from those of control subjects in multiple brain areas, including anterior cingulate cortex (ACC) and medial PFC, bilateral dorsolateral PFC, temporal cortex and insula, and parietal and occipital cortex. Conclusions. Our results are in agreement with hypotheses of dysfunctions in corticolimbic circuitries regulating affects and emotions in mood disorders and suggest that specific abnormalities, particularly in ventrolateral PFC, are not the same in UP and BP depression.
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Disorder-specific volumetric brain difference in adolescent major depressive disorder and bipolar depression. Brain Imaging Behav 2013; 8:119-27. [DOI: 10.1007/s11682-013-9264-x] [Citation(s) in RCA: 47] [Impact Index Per Article: 3.9] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/21/2023]
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Asor E, Ben-Shachar D. Platelets: A possible glance into brain biological processes in schizophrenia. World J Psychiatry 2012; 2:124-33. [PMID: 24175178 PMCID: PMC3782191 DOI: 10.5498/wjp.v2.i6.124] [Citation(s) in RCA: 35] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/11/2011] [Revised: 07/02/2012] [Accepted: 07/23/2012] [Indexed: 02/05/2023] Open
Abstract
Schizophrenia is a severe mental disorder, characterized by behavioral, emotional and cognitive disturbances, which commonly follows a chronic course. Diagnostic accuracy, management plans, treatment evaluation and prognosis are dependent on relatively subjective assessments. Despite extensive research and improvement in imaging technology, as well as modern genetic and molecular methodologies, the biological basis of this disease is still unclear. Therefore, there is a need for objective and valid biological markers. Platelets have often been used as a model in neurobiological research. The accessibility of platelets and their similarities with neurons turns them into an attractive candidate to search for biological markers for diagnosis and for unraveling pathophysiological processes relevant to the etiology of brain disorders, including schizophrenia. The present review addresses the main changes in platelet physiology observed in schizophrenia and its response to antipsychotic medication. We summarize numerous studies demonstrating impaired metabolism, uptake and receptor kinetics of schizophrenia-relevant neurotransmitters, abnormalities in membrane derived phospholipids and polyunsaturated fatty acids, as well as dysfunctions in the mitochondria. These changes fit with the various hypotheses raised for the etiology of schizophrenia, including the dopamine-glutamate hypothesis, the autoimmune hypothesis, the polyunsaturated fatty acid hypothesis and the impaired energy metabolism hypothesis. Despite extensive research in platelets, no conclusive reliable biomarker has been identified yet. This review suggests that the clinical heterogeneity and the biological complexity of schizophrenia lead to the inevitable conclusion that biomarkers will be identified only for subgroups characterized according to the different diagnostic criteria. Moreover, any biomarker would have to be an array of interrelated factors or even a set of several such arrays.
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Affiliation(s)
- Eyal Asor
- Eyal Asor, Dorit Ben-Shachar, Laboratory of Psychobiology, Department of Psychiatry, Rambam Medical Center and B. Rappaport Faculty of Medicine, Rappaport Family Institute for Research in the Medical Sciences, Technion, PO Box 9649, Haifa 31096, Israel
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8
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Abstract
Major depression is a serious disorder of enormous sociological and clinical relevance. The discovery of antidepressant drugs in the 1950s led to the first biochemical hypothesis of depression, which suggested that an impairment in central monoaminergic function was the major lesion underlying the disorder. Basic research in all fields of neuroscience (including genetics) and the discovery of new antidepressant drugs have revolutionized our understanding of the mechanisms underlying depression and drug action. There is no doubt that the monoaminergic system is one of the cornerstones of these mechanisms, but multiple interactions with other brain systems and the regulation of central nervous system function must also be taken into account In spite of all the progress achieved so far, we must be aware that many open questions remain to be resolved in the future.
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Affiliation(s)
- Bondy Brigitta
- Psychiatric Clinic of University Munich, Department of Neurochemistry, Munich, Germany
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Differential association of circadian genes with mood disorders: CRY1 and NPAS2 are associated with unipolar major depression and CLOCK and VIP with bipolar disorder. Neuropsychopharmacology 2010; 35:1279-89. [PMID: 20072116 PMCID: PMC3055337 DOI: 10.1038/npp.2009.230] [Citation(s) in RCA: 263] [Impact Index Per Article: 17.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/17/2023]
Abstract
Disruptions in circadian rhythms have been described in mood disorders (MD), but the involvement of genetic variation in genes pertaining to the molecular circadian machinery in the susceptibility to MD has not been conclusively determined. We examined 209 single-nucleotide polymorphisms (SNPs) covering 19 circadian genes (ADCYAP1, ARNTL, ARNTL2, BHLHB2, BHLHB3, CLOCK, CRY1, CRY2, CSNK1E, DBP, NPAS2, NR1D1, PER1, PER2, PER3, RORA, TIMELESS, VIP, and VIPR2) in a sample of 534 MD patients (335 with unipolar major mood depression (MDD) and 199 with bipolar disorder (BD)) and 440 community-based screened controls. Nominally, statistically significant associations were found in 15 circadian genes. The gene-wide test, corrected for the number of SNPs analyzed in each gene, identified significant associations in CRY1 (rs2287161), NPAS2 (rs11123857), and VIPR2 (rs885861) genes with the combined MD sample. In the MDD subsample, the same SNPs in CRY1 and NPAS2 of the combined sample remained associated, whereas in the BD subsample CLOCK (rs10462028) and VIP (rs17083008) were specifically associated. The association with an SNP located 3' near CRY1 gene in MDD remained statistically significant after permutation correction at experiment level (p=0.007). Significant additive effects were found between the SNPs that were statistically significant at the gene-wide level. We also found evidence of associations between two-marker haplotypes in CRY1 and NPAS2 genes and MD. Our data support the contribution of the circadian system to the genetic susceptibility to MD and suggest that different circadian genes may have specific effects on MD polarity.
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Grunze H, Vieta E, Goodwin GM, Bowden C, Licht RW, Möller HJ, Kasper S. The World Federation of Societies of Biological Psychiatry (WFSBP) Guidelines for the Biological Treatment of Bipolar Disorders: Update 2010 on the treatment of acute bipolar depression. World J Biol Psychiatry 2010; 11:81-109. [PMID: 20148751 DOI: 10.3109/15622970903555881] [Citation(s) in RCA: 242] [Impact Index Per Article: 16.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/05/2023]
Abstract
OBJECTIVES These guidelines are based on a first edition that was published in 2002, and have been edited and updated with the available scientific evidence until September 2009. Their purpose is to supply a systematic overview of all scientific evidence pertaining to the treatment of acute bipolar depression in adults. METHODS The data used for these guidelines have been extracted from a MEDLINE and EMBASE search, from the clinical trial database clinicaltrials.gov, from recent proceedings of key conferences, and from various national and international treatment guidelines. Their scientific rigor was categorised into six levels of evidence (A-F). As these guidelines are intended for clinical use, the scientific evidence was finally assigned different grades of recommendation to ensure practicability. RESULTS We identified 10 pharmacological monotherapies or combination treatments with at least limited positive evidence for efficacy in bipolar depression, several of them still experimental and backed up only by a single study. Only one medication was considered to be sufficiently studied to merit full positive evidence. CONCLUSIONS Although major advances have been made since the first edition of this guideline in 2002, there are many areas which still need more intense research to optimize treatment. The majority of treatment recommendations is still based on limited data and leaves considerable areas of uncertainty.
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Affiliation(s)
- Heinz Grunze
- Newcastle University, RVI, Division of Psychiatry, Institute of Neuroscience, Newcastle upon Tyne, UK.
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Konarski JZ, McIntyre RS, Kennedy SH, Rafi-Tari S, Soczynska JK, Ketter TA. Volumetric neuroimaging investigations in mood disorders: bipolar disorder versus major depressive disorder. Bipolar Disord 2008; 10:1-37. [PMID: 18199239 DOI: 10.1111/j.1399-5618.2008.00435.x] [Citation(s) in RCA: 213] [Impact Index Per Article: 12.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/19/2023]
Abstract
BACKGROUND As patients with mood disorders manifest heterogeneity in phenomenology, pathophysiology, etiology, and treatment response, a biological classification of mental disease is urgently needed to advance research. Patient and methodological variability complicates the comparison of neuroimaging study results and limits heuristic model development and a biologically-based diagnostic schema. OBJECTIVE We have critically reviewed and compared the magnetic resonance neuroimaging literature to determine the degree and directionality of volumetric changes in brain regions putatively implicated in the pathophysiology of major depressive disorder (MDD) versus bipolar disorder (BD). METHODS A total of 140 published magnetic resonance imaging investigations evaluating subjects with BD or MDD were selected to provide a summary and interpretation of volumetric neuroimaging results in MDD and BD. Further commentary on the pathophysiological implications, and putative cellular and pharmacological mechanisms, is also provided. RESULTS While whole brain volumes of patients with mood disorders do not differ from those of healthy controls, regional deficits in the frontal lobe, particularly in the anterior cingulate and the orbitofrontal cortex, appear to consistently differentiate subjects with mood disorders from the general population. Preliminary findings also suggest that subcortical structures, particularly the striatum, amygdala, and hippocampus, may be differentially affected in MDD and BD. CONCLUSIONS Structural neuroimaging studies have consistently identified regional abnormalities in subjects with mood disorders. Future studies should strive to definitively establish the influence of age and medication.
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Affiliation(s)
- Jakub Z Konarski
- Institute of Medical Science, University of Toronto, Toronto, Ontario, Canada
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Hensch T, Herold U, Brocke B. An electrophysiological endophenotype of hypomanic and hyperthymic personality. J Affect Disord 2007; 101:13-26. [PMID: 17207536 DOI: 10.1016/j.jad.2006.11.018] [Citation(s) in RCA: 34] [Impact Index Per Article: 1.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/06/2006] [Revised: 11/23/2006] [Accepted: 11/24/2006] [Indexed: 10/23/2022]
Abstract
BACKGROUND Hyperthymic Temperament (HYT) and a closely related trait, Hypomanic Personality (HYP), have both been related to bipolar affective disorder (BAD). Intensity dependence of auditory evoked potentials (IAEP) is a suggested inverse indicator of serotonergic neurotransmission and has been found to be elevated in BAD. Therefore the present study explored for the first time whether subclinical variance of HYT/HYP is also associated with IAEP in a healthy sample. As several traits from biological personality research are correlated with HYT/HYP and also with BAD, the specificity of results against these traits was further analyzed by calculating multiple regression analyses. METHODS Evoked potentials were recorded from a sample (N=87) homogenous for confounding variables influencing IAEP. For this reason, only 19 to 27-year-old non-smoker psychiatrically healthy male students were included. RESULTS Significant correlations were found between IAEP and both HYP and HYT. Including Sensation or Novelty Seeking and Extraversion in Regression Analyses did not weaken the associations of HYP with IAEP much, but did affect those of HYT. However, these competing biological personality traits were hardly able to predict IAEP themselves. Impulsivity, though, was able to reduce the predictive power of HYP and HYT and to explain unique IAEP-variance. This was even more the case for Behavioral-Activation-System-Sensitivity (BAS) subscale Fun Seeking clearly dominating all regression analyses. LIMITATIONS Homogeneity of sample. CONCLUSIONS The impact of BAS is in agreement with the assumption that heightened BAS-sensitivity is an underlying biological cause for HYP/HYT and for BAD. Future studies on BAD should include BAS and Impulsivity besides HYP/HYT to further explore uniqueness of the latter and to develop questionnaires based on those items of a hyperthymic-hypomanic-impulsive-funseeking item pool, which possess the most external validity.
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Affiliation(s)
- Tilman Hensch
- Department of Psychology II, Dresden University of Technology, Mommsenstr. 13, 01062 Dresden, Germany.
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Harvey M, Gagné B, Labbé M, Barden N. Polymorphisms in the neuronal isoform of tryptophan hydroxylase 2 are associated with bipolar disorder in French Canadian pedigrees. Psychiatr Genet 2007; 17:17-22. [PMID: 17167340 DOI: 10.1097/ypg.0b013e3280111877] [Citation(s) in RCA: 31] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/26/2022]
Abstract
OBJECTIVE Tryptophan hydroxylase is the rate-limiting enzyme in the serotonin biosynthetic pathway and plays an important role in the regulation of serotonin levels. Recently, a brain-specific isoform, tryptophan hydroxylase 2 or n-tryptophan hydroxylase, has been discovered. Some studies reported genetic and functional associations between this isoform and bipolar disorder and/or major depressive disorder. The aim of this study was to investigate further association of genetic variants in French Canadian samples with bipolar disorders. METHODS Genetic variants in the tryptophan hydroxylase 2 gene were genotyped in a case-control sample consisting of 225 affected individuals (191 bipolar I and 34 bipolar II) and 221 controls and in a collection of extended pedigrees and trios from the same population 357 nuclear families (201 bipolar I, 64 bipolar II, 79 recurrent major depressive disorder). RESULTS We determined linkage disequilibrium structure in our isolated population and analyzed six tagged single nucleotide polymorphisms in the case-control sample. Whereas no single, single nucleotide polymorphism gave any significant result, a three single nucleotide polymorphism haplotype gave a global P=0.01. Family-based association showed significant association (P=0.004) of one polymorphism (rs4290270) with the major allele overtransmitted to affected offspring. CONCLUSIONS Case-control and family-based association studies further support the presence of a susceptibility locus for bipolar disorder in tryptophan hydroxylase 2 by showing statistically significant associations with both, single nucleotide polymorphism alone and haplotype of single nucleotide polymorphism markers.
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Affiliation(s)
- Mario Harvey
- Department of Neuroscience, CHUL Research Centre and Laval University, Sainte-Foy, Quebec, Canada
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Roessner V, Weber A, Becker A, Beck G, Kornhuber J, Frieling H, Bleich S. Decreased serum semicarbazide sensitive aminooxidase (SSAO) activity in patients with major depression. Prog Neuropsychopharmacol Biol Psychiatry 2006; 30:906-9. [PMID: 16616983 DOI: 10.1016/j.pnpbp.2006.01.030] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Accepted: 01/30/2006] [Indexed: 11/22/2022]
Abstract
Semicarbazide sensitive aminooxidase (SSAO) is known to interplay with monoamine oxidases (MAO) and several antidepressants. Taking into account the monoamine hypothesis concerning the pathophysiology of depression, the aim of the present pilot study was to evaluate serum SSAO activity in depressed patients. A total of 21 inpatients with major depression and 41 healthy controls were studied. Serum SSAO activity was determined by HPLC on days 1, 5 and 10 of inpatient treatment. At baseline without medication including antidepressants, highly depressed patients (MADRS score>or=30) had significantly decreased serum SSAO activity (mean 385+/-161 mU/l) when compared to healthy controls (mean 526+/-141 mU/l; p=0.003). This SSAO decrease was less pronounced at day 5 and day 10 under an antidepressive drug regime. Decreased serum SSAO activity was observed in patients with major depression, especially in those with high MADRS scores. The present results support the hypothesis of dysfunctional monoaminergic metabolism in the pathogenesis of depressive disorders. The disputable association between depression and monoamine metabolism requires further investigation, particularly with regard to SSAO activity and medication status.
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Affiliation(s)
- Veit Roessner
- Department of Psychiatry and Psychotherapy, Friedrich-Alexander University of Erlangen-Nuremberg, Schwabachanlage 6, D-91054 Erlangen, Germany
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Schiavone P, Dorz S, Conforti D, Scarso C, Borgherini G. Comorbidity of DSM-IV Personality Disorders in unipolar and bipolar affective disorders: a comparative study. Psychol Rep 2004; 95:121-8. [PMID: 15460367 DOI: 10.2466/pr0.95.1.121-128] [Citation(s) in RCA: 14] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/15/2022]
Abstract
The aim of this study was to compare the prevalence of Personality Disorders assessed by Structured Clinical Interview for Axis-II in 155 inpatients diagnosed with Unipolar Disorder vs inpatients with Bipolar Disorder (39). The most frequent Axis II diagnoses among Unipolar inpatients were Borderline (31.6%), Dependent (25.2%), and Obsessive-Compulsive (14.2%) Personality Disorders. Among Bipolar inpatients, the most prevalent personality disorders were Borderline (41%), Narcissistic (20.5%), Dependent (12.8%), and Histrionic disorders (10.3%). Using chi squared analysis, few differences in distribution emerged between the two groups: Unipolar patients had more recurrent Obsessive-Compulsive Personality Disorder than Bipolar patients (chi(1)2=6.24, p<.005). Comorbid Narcissistic Personality Disorder was significantly more frequent in the Bipolar than in the Unipolar group (chi(1)2=6.34, P<.01). Considering the three clusters (DSM-IV classification), there was a significant difference between the groups, Cluster C (fearful, avoidant) diagnoses being more frequent in the Unipolar than in the Bipolar group (48.4% vs 20.5%, respectively). Cluster B (dramatic, emotionally erratic) diagnoses were found more frequently in patients with Bipolar Disorders (71.8% vs 45.2% in Unipolar patients, chi(2)2=10.1, p<.006). The differences in the distribution and prevalence of Personality Disorders between the two patient groups are discussed.
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Affiliation(s)
- Paolo Schiavone
- Affective Disorders Unit, Casa di Cura Parco dei Tigli, Padova, Italy
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SCHIAVONE PAOLO. COMORBIDITY OF DSM-IV PERSONALITY DISORDERS IN UNIPOLAR AND BIPOLAR AFFECTIVE DISORDERS: A COMPARATIVE STUDY. Psychol Rep 2004. [DOI: 10.2466/pr0.95.5.121-128] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/15/2022]
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Mück-Seler D, Pivac N, Sagud M, Jakovljević M, Mihaljević-Peles A. The effects of paroxetine and tianeptine on peripheral biochemical markers in major depression. Prog Neuropsychopharmacol Biol Psychiatry 2002; 26:1235-43. [PMID: 12502009 DOI: 10.1016/s0278-5846(02)00259-2] [Citation(s) in RCA: 55] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/23/2022]
Abstract
Depression is related to the alterations of the central serotonergic system and some antidepressants achieve their therapeutic effects through alteration of serotonin (5-HT) (re)uptake. Peripheral biochemical markers, platelet and serum 5-HT concentrations, platelet monoamine oxidase (MAO) activity, plasma levels of cortisol and prolactin (PRL), were investigated in patients with major depression before and after 4 weeks of treatment with paroxetine (an inhibitor of 5-HT uptake) or tianeptine (a stimulator of 5-HT uptake). Study was open, single center and included female depressed patients, 21 treated with tianeptine (37.5 mg/day) and 15 treated with paroxetine (20 mg/day), and 11 drug-free healthy women (controls). Before treatment, depressed patients as a group had significantly higher serum 5-HT and cortisol concentrations than healthy controls. There were no differences in the other biochemical markers. Response to antidepressant treatment was estimated according to the 50% fall in the initial scores of Hamilton Depression Rating Scale (HAMD) after 4 weeks of treatment. Good therapeutic response was observed in 47% and 45% patients treated with paroxetine and tianeptine, respectively. Paroxetine treatment induced significant decrease in platelet 5-HT concentrations in both responders and nonresponders, while no alterations in platelet 5-HT values were found in tianeptine-treated patients. There was a subgroup of depressed patients in paroxetine-treated group with high pretreatment platelet 5-HT concentration and later poor therapeutic response to paroxetine treatment. Serum 5-HT values, platelet MAO activity or plasma cortisol or PRL levels were unchanged after both treatments. The results suggest that pretreatment platelet 5-HT levels, but not other peripheral biochemical markers, might predict therapeutic outcome at least in paroxetine-treated patients.
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Affiliation(s)
- Dorotea Mück-Seler
- Ruder Bosković Institute, Division of Molecular Medicine, PO Box 180, HR-10002 Zagreb, Croatia.
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Abstract
OBJECTIVES The purpose of the present study has been to examine differences in the laterality of pain in patients with migraine and comorbid unipolar depressive (UP) and bipolar II (BP II) disorders. METHODS Semi-structured interviews of 102 patients with major affective disorders were conducted, using DSM-IV criteria for affective disorders combined with Akiskal's criteria for affective temperaments and International Headache Society criteria for migraine. The group of patients reported on in the present study encompass 47 subjects with UP (n = 24) or BP 11 (n = 23) disorders. Fifteen of the bipolar II patients fulfilled DSM-IV criteria while eight were diagnosed according to the broader criteria of Akiskal. RESULTS Sixteen of the 38 patients with migraine headaches had bilateral pain or pain equally often on the left or right side while 22 had pain predominantly located on one side. Among the UP patients the pain was most often on the right side (8/10) while among the BP II patients the pain was most often on the left (9/12, p = 0.01). Apart from the presence of hypomanic symptoms in the BP II group there were no clinical or demographic characteristics that distinguished these two sub-groups of affective disorders. CONCLUSIONS These results indicate that there may be a differential affection of the cerebral hemispheres in patients with migraine and comorbid unipolar depressive disorder versus patients with migraine and comorbid bipolar II disorder.
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Affiliation(s)
- Ole Bernt Fasmer
- Department of Psychiatry, University of Bergen, Haukeland Hospital, Bergen, Norway.
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Rossi A, Marinangeli MG, Butti G, Scinto A, Di Cicco L, Kalyvoka A, Petruzzi C. Personality disorders in bipolar and depressive disorders. J Affect Disord 2001; 65:3-8. [PMID: 11426507 DOI: 10.1016/s0165-0327(00)00230-5] [Citation(s) in RCA: 62] [Impact Index Per Article: 2.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/23/2022]
Abstract
The association of mood disorders with personality disorders (PDs) is relevant from a clinical, therapeutic and prognostic point of view. To examine this issue, we compared the prevalence of DSM-III-R personality disorders assessed with SCID-II in patients with depressive (n = 117) and bipolar (n = 71) disorders both recovered from a major depressive index episode that needed hospital admission. PDs prevalence and comorbidity with axis I were calculated. Avoidant PD (31.6%) (O.R. = 1.7, C.I. = 1.06-2.9. P < 0.01), borderline PD (30.8%) and obsessive-compulsive PD (30.8%) were the most prevalent axis II diagnoses among patients with depressive disorder. In bipolar disorder group, patients showed more frequently obsessive-compulsive PD (32.4%), followed by borderline PD (29.6%) and avoidant PD (19.7%). Avoidant PD showed a trend toward being significantly more prevalent among depressives (P < 0.07). A different pattern of PDs emerges between depressive and bipolar patients.
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Affiliation(s)
- A Rossi
- Department of Experimental Medicine, University of L'Aquila, Italy.
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Plein H, Berk M, Eppel S, Butkow N. Augmented platelet calcium uptake in response to serotonin stimulation in patients with major depression measured using Mn2+ influx and 45Ca2+ uptake. Life Sci 2000; 66:425-31. [PMID: 10670830 DOI: 10.1016/s0024-3205(99)00608-6] [Citation(s) in RCA: 14] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/29/2022]
Abstract
There is an augmented platelet intracellular calcium response to serotonin stimulation in major depression. The role that calcium influx has in this process is not known. The objective of this study was to determine platelet calcium influx in response to serotonin by two methods, Mn2+ influx and 45Ca2+ uptake, in order to observe if the uptake response to serotonin was augmented in major depression by comparing the response to normal controls. The use of the two methods of calcium influx showed that serotonin stimulates calcium uptake into platelets. Furthermore, patients with major depression have significantly augmented platelet calcium uptake in response to serotonin. The interesting finding was that calcium uptake into platelets is biphasic, occurring immediately and after five minutes. These results may support the two pool model for calcium oscillations within cells whereby extracellular calcium is needed for intracellular calcium release, and for replenishment of depleted stores once intracellular calcium is released.
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Affiliation(s)
- H Plein
- Department of Clinical and Experimental Pharmacology, University of the Witwatersrand, Faculty of Health Sciences, Parktown, Johannesburg
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Barbini B, Colombo C, Benedetti F, Campori E, Bellodi L, Smeraldi E. The unipolar-bipolar dichotomy and the response to sleep deprivation. Psychiatry Res 1998; 79:43-50. [PMID: 9676825 DOI: 10.1016/s0165-1781(98)00020-1] [Citation(s) in RCA: 67] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/30/2022]
Abstract
Fifty-one inpatients affected by a major depressive episode were divided into four groups according to mood disorder diagnosis and previous clinical history (bipolar disorder type I; bipolar disorder type II; major depressive disorder with at least three previous depressive episodes; and single depressive episode patients) and administered three consecutive total sleep deprivation (TSD) cycles. Mood changes were rated with a reduced version of the Hamilton Depression Rating Scale and with self-administered visual analogue scales. TSD caused better clinical effects in bipolar and single-episode patients; in particular, unipolar patients lacked effects in perceived mood after the first TSD and showed worse Hamilton ratings in respect to the other groups after the three TSD treatments. Discriminant function analysis could correctly classify 80% of bipolar patients, post hoc, based on TSD response. Further researches on the clinical efficacy of TSD must take into account the heterogeneity of depression and of its biological substrate.
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Affiliation(s)
- B Barbini
- IRCCS Istituto Scientifico Ospedale San Raffaele, Department of Neuropsychiatric Sciences, University of Milan, School of Medicine, Milano, Italy
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