Cloninger's temperament and character dimensions of personality in patients with major depressive disorder

In this present study, we examined the relationship between the Cloninger's dimensional psychobiologic model of personality and depression in an outpatient population with major depressive disorder. Eighty-one depressed outpatients (67 women, 14 men) and 51 healthy controls (35 women, 16 men) filled out the Turkish version of the Temperament and Character Inventory (TCI). Depression severity was evaluated by using the 17-item Hamilton Depression Rating Scale and the 21-item Beck Depression Inventory. Depressed patients exhibited statistically significant higher scores for harm avoidance and lower scores for self-directedness compared to healthy controls. Sentimentality (RD1) and dependence (RD4) subscale scores of reward dependence and spiritual acceptance (ST3) subscale of self-transcendence were significantly higher; attachment (RD3) subscale of reward dependence, responsibility (SD1), purposefulness (SD2), resourcefulness (SD3), and congruent second nature (SD5) subscales of self-directedness were significantly lower in the depressed group. In the depressed patient group, main effects of sex were significant for reward dependence and cooperativeness; the scores of both dimensions were higher for women. The Beck Inventory was positively correlated with harm avoidance and negatively correlated with novelty seeking and self-directedness dimensions (P < .05). The duration of depression (16.33 ± 20.18 months) or the mean onset age of depression (28.68 ± 8.11 years) did not show significant correlations with TCI scales. This study confirms the relationship between harm avoidance and depression and suggests a relationship between self-directedness and depression.     

Alexithymia and temperament and character model of personality in patients with major depressive disorder

Alexithymia is thought to be a stable personality trait and a predisposing risk factor for depression. In this study, we aimed to identify the prevalence of alexithymia in a depressed and nondepressed sample and examined the relationship between Cloninger's psychobiological model of personality with alexithymia. The Turkish version of the 20-item Toronto Alexithymia Scale (TAS-20), the Turkish version of the Temperament and Character Inventory, and the 21-item Beck Depression Inventory (BDI) were administered to 81 depressed patients and 51 controls. The mean age of the groups was 30.5 ± 7.7 and 32.75 ± 8.73, respectively. Depression severity was evaluated with the BDI. In the depressed group, 33.3% were alexithymic, and alexithymic subjects had significantly higher BDI scores. Depressed individuals were significantly more alexithymic than the controls on the total and all the 3 subscales of TAS-20. The TAS-20 total score was negatively correlated with the temperament dimension of Reward Dependence (RD) and the character dimension of Self-Directedness (SD). In the TAS-20 subscale, difficulties in identifying feelings was positively correlated with Self-Transcendence and negatively correlated with SD. The difficulties in expressing feelings subscale was negatively correlated with RD and SD. In the depressed patient group, the temperament dimension of RD was significantly lower in the alexithymic group. The rate of alexithymia is found high among this sample of Turkish depressed patients, and the results suggested a strong connection between alexithymia and depression. Alexithymia is explained by specific dimensions and subscale within Cloninger's psychobiological model of personality in this sample of depressed Turkish patients.     

Partial validation of the atypical features subtype of major depressive disorder.

BACKGROUND: Symptoms of the atypical features subtype of major depressive disorder include mood reactivity, hypersomnia, hyperphagia, leaden paralysis, and rejection sensitivity. This subtype was introduced into the mood disorders section of the DSM-IV following a series of antidepressant trials showing that such patients responded preferentially to monoamine oxidase inhibitors. Studies aimed at validating the atypical features subtype have yielded inconsistent results. Our study sought to reevaluate the validity of atypical depression by examining the demographic and clinical features of a large cohort of depressed patients who met DSM-IV criteria for atypical features. METHODS: We evaluated 579 psychiatric outpatients with a current diagnosis of major depressive disorder for the presence of atypical features. Detailed demographic and clinical information was obtained for each patient through semistructured interviews. Using the available literature, we made a series of a priori hypotheses regarding how depressed patients with atypical features (n = 130) would differ from those without atypical features (n = 449). In addition, we tested the strength of the associations between each of the 5 atypical symptoms. RESULTS: Although many of the predicted hypotheses were substantiated, an equal number were not. Correlation analyses revealed modest associations between several of the atypical symptoms, but mood reactivity was not associated with any of the other symptom criteria. CONCLUSION: Our results provide partial support for the validity of the atypical features subtype of major depressive disorder.     

Subcortical shape alterations in major depressive disorder: Findings from the ENIGMA major depressive disorder working group

Alterations in regional subcortical brain volumes have been investigated as part of the efforts of an international consortium, ENIGMA, to identify reliable neural correlates of major depressive disorder (MDD). Given that subcortical structures are comprised of distinct subfields, we sought to build significantly from prior work by precisely mapping localized MDD-related differences in subcortical regions using shape analysis. In this meta-analysis of subcortical shape from the ENIGMA-MDD working group, we compared 1,781 patients with MDD and 2,953 healthy controls (CTL) on individual measures of shape metrics (thickness and surface area) on the surface of seven bilateral subcortical structures: nucleus accumbens, amygdala, caudate, hippocampus, pallidum, putamen, and thalamus. Harmonized data processing and statistical analyses were conducted locally at each site, and findings were aggregated by meta-analysis. Relative to CTL, patients with adolescent-onset MDD (≤ 21 years) had lower thickness and surface area of the subiculum, cornu ammonis (CA) 1 of the hippocampus and basolateral amygdala (Cohen's d = ?0.164 to ?0.180). Relative to first-episode MDD, recurrent MDD patients had lower thickness and surface area in the CA1 of the hippocampus and the basolateral amygdala (Cohen's d = ?0.173 to ?0.184). Our results suggest that previously reported MDD-associated volumetric differences may be localized to specific subfields of these structures that have been shown to be sensitive to the effects of stress, with important implications for mapping treatments to patients based on specific neural targets and key clinical features.     

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.     

The relationship between depressive personality disorder and major depressive disorder: a population-based twin study

OBJECTIVE: One of the most important controversies regarding depressive personality disorder is the overlap with mood disorders. The aim of this study was to estimate the genetic and environmental sources of covariance between depressive personality disorder and major depressive disorder and to what extent genetic, shared, and unique environmental factors are specific to each disorder. METHOD: A total of 2,801 young adult twins from the Norwegian Institute of Public Health Twin Panel were assessed at personal interview for depressive personality disorder and major depressive disorder with the Structured Interview for DSM-IV Personality and the Composite International Diagnostic Interview. Bivariate Cholesky models were fitted to the data by using the Mx statistical program. RESULTS: In the best-fitting model, the covariation between depressive personality disorder and major depressive disorder were accounted for by genetic and unique environmental factors only. A model that did not include genetic factors specific to major depressive disorder was rejected. The authors found no clear evidence for gender differences in sources of comorbidity of depressive personality disorder and major depressive disorder. CONCLUSIONS: Although depressive personality disorder and major depressive disorder share a substantial proportion of genetic and environmental risk factors, the results from this study support the hypothesis that the two disorders are distinct entities with overlapping, but not identical, etiologies.     

Tachyphylaxis in unipolar major depressive disorder

BACKGROUND: Major depressive disorder is usually a recurring illness, and maintenance treatment is used to forestall or prevent recurrent episodes of depression. This study describes recurrence of major depression despite maintenance pharmacotherapy, termed tachyphylaxis. METHOD: The study sample consisted of 103 subjects who participated in the NIMH Collaborative Depression Study, a multicenter longitudinal observational study of the mood disorders. Subjects diagnosed with unipolar major depressive disorder according to Research Diagnostic Criteria were enrolled from 1978-1981 and prospectively followed for up to 20 years. As an observational study, treatment was recorded but not controlled by anyone connected with the study. Subjects were selected for the present study if at some point during follow-up they received antidepressant medication for treatment of an episode of major depressive disorder, recovered from this episode, and subsequently received maintenance pharmacotherapy. Some subjects were successfully treated for multiple episodes of major depressive disorder and then received maintenance medication after each of these episodes, resulting in multiple maintenance treatment intervals. Data were collected using the Longitudinal Interval Follow-Up Evaluation, and mixed-effects logistic regression was used to test the association of sociodemographic and clinical variables with tachyphylaxis. RESULTS: For the 103 subjects, there were 171 maintenance treatment intervals in which a subject received maintenance pharmacotherapy after having recovered from an episode of major depressive disorder. The median duration of maintenance treatment was 20 weeks. Tachyphylaxis occurred during 43 (25%) of these 171 maintenance treatment intervals. The subtype of melancholic (endogenous) major depressive disorder significantly elevated the risk of tachyphylaxis during the subsequent maintenance treatment interval. CONCLUSIONS: Despite the use of maintenance pharmacotherapy, major depression recurs in a considerable number of patients. Improved prophylaxis for these patients requires other treatment strategies based upon a greater understanding of recurrence.     

Lymphocyte function in major depressive disorder

Lymphocyte stimulation by phytohemagglutinin, concanavalin A, and pokeweed mitogen was significantly lower in a group of hospitalized depressed patients than in matched controls. The absolute number of T and B cells was lower in the depressed group, but the percentage of these cell types did not differ between the groups. These findings may be related to the altered neuroendocrine function found in patients with depressive disorders.     

Ego-rotation and object-rotation in major depressive disorder

Mental rotation (MR) performance provides a direct insight into a prototypical higher-level visuo-spatial cognitive operation. Previous studies suggest that progressive slowing with an increasing angle of orientation indicates a specific wing of object-based mental transformations in the psychomotor retardation that occurs in major depressive disorder (MDD). It is still not known, however, whether the ability of object-rotation is associated with the ability of ego-rotation in MDD. The present study was designed to investigate the level of impairment of mental transformation abilities in MDD. For this purpose we tested 33 MDD (aged 18–52 years, 16 women) and 30 healthy control subjects (15 women, age and education matched) by evaluating the performance of MDD subjects with regard to ego-rotation and object-rotation tasks. First, MDD subjects were significantly slower and made more errors than controls in mentally rotating hands and letters. Second, MDD and control subjects displayed the same pattern of response times to stimuli at various orientations in the letter task but not the hand task. Third, in particular, MDD subjects were significantly slower and made more errors during the mental transformation of hands than letters relative to control subjects and were significantly slower and made more errors in physiologically impossible angles than physiologically possible angles in the mental rotation hand task. In conclusion, MDD subjects present with more serious mental rotation deficits specific to the hand than the letter task. Importantly, deficits were more present during the mental transformation in outward rotation angles, thus suggesting that the mental imagery for hands and letters relies on different processing mechanisms which suggest a module that is more complex for the processing of human hands than for letters during mental rotation tasks. Our study emphasises the necessity of distinguishing different levels of impairment of action in MDD subjects.     

Social functioning in major depressive disorder

Depression is associated with social risk factors, social impairments and poor social functioning. This paper gives an overview of these social aspects using the NIMH Research and Domain Criteria ‘Systems for Social Processes’ as a framework. In particular, it describes the bio-psycho-social interplay regarding impaired affiliation and attachment (social anhedonia, hyper-sensitivity to social rejection, competition avoidance, increased altruistic punishment), impaired social communication (impaired emotion recognition, diminished cooperativeness), impaired social perception (reduced empathy, theory-of-mind deficits) and their impact on social networks and the use of social media. It describes these dysfunctional social processes at the behavioural, neuroanatomical, neurochemical and genetic levels, and with respect to animal models of social stress. We discuss the diagnostic specificity of these social deficit constructs for depression and in relation to depression severity. Since social factors are importantly involved in the pathogenesis and the consequences of depression, such research will likely contribute to better diagnostic assessments and concepts, treatments and preventative strategies both at the diagnostic and transdiagnostic level.     

Circadian genes in major depressive disorder

Abstract

Background: Sleep disturbances are a common symptom of major depressive disorder (MDD). Sleep is highly regulated by circadian rhythms, controlled by circadian genes, that act through a series of feedback loops to regulate the sleep-wake cycle.

Objectives: To the best of our knowledge, a systematic review regarding the core circadian genes and their role in MDD has not been published recently. Also, a review of these genes and their role in sleep disturbances in depressed individuals appears to have never been done. We decided to integrate both concepts into one comprehensive review.

Method: The review was done using the appropriate search terms in the following search engines: OVID Medline, Embase, PsycINFO and Pubmed.

Results: Based on the data reviewed, none of the circadian genes appear to be associated with MDD, but some are more promising than others. These genes are: CRY1, CRY2, PER2 and NPAS2. When investigating the role of circadian genes in sleep disturbances among individuals with MDD, the most promising candidate gene is TIMELESS. Although the results in this area are limited.

Conclusion: Given the promising leads from this review, future studies should investigate circadian genes in sleep disturbances among the depressed population.     

Neuroendocrine interrelationships in major depressive disorder

The authors administered the thyrotropin-releasing hormone (TRH) stimulation test and the dexamethasone suppression test (DST) to 54 patients who met DSM-III criteria for major depressive disorder and to 19 nondepressed patients. A blunted thyrotropin (TSH) response to TRH injection was noted in 18 depressed patients (33%) but in no nondepressed patients. An escape from dexamethasone suppression was noted in 23 depressed patients (43%) but in only 2 nondepressed patients (11%). The combined sensitivity of the DST and the TRH test in identifying major depressive disorder was 67% with 92% specificity. Only 6 depressed patients (11%) had abnormal responses to both the DST and the TRH test, suggesting that the hypothalamic-pituitary-adrenal axis dysregulation and hypothalamic-pituitary-thyroid axis dysregulation are independent phenomena. These findings support the combined use of these neuroendocrine tests in clinical practice.     

Executive dysfunction in major depressive disorder

Executive dysfunction is commonly seen in major depression. The types of executive deficits seen in depression include problems with planning, initiating and completing goal-directed activities. Executive dysfunction may vary as a function of the severity of depression. In addition, a subset of geriatric depression is also characterized by prominent deficits in executive functioning. The presence of executive dysfunction in depression is associated with vocational disability and possibly poorer treatment response. While few studies have examined the treatment of executive dysfunction in depression, preliminary work suggests that both pharmacologic interventions and psychosocial interventions such as problem solving therapy may be efficacious.     

Recovery and relapse from major depressive disorder in the elderly.

OBJECTIVE: Results from the National Institute of Mental Health (NIMH) Collaborative Study of the Psychobiology of Depression raised serious concerns about the longer-term prognosis for major depressive disorder in younger persons. However, little research has examined the prognosis for major depressive disorder in the elderly despite suggestions that they have poorer clinical outcomes than younger adults. The objective of this study was to 1) document rates of recovery and relapse from major depressive disorder in a large group of inpatient elderly and 2) compare recovery and relapse rates from major depressive disorder in the elderly with those in a mixed-age patient group from the NIMH collaborative study. METHOD: The psychiatric status of 127 elderly inpatients diagnosed with major depressive disorder by Research Diagnostic Criteria was evaluated for 1 year. The same diagnostic and follow-up method to assess psychiatric symptoms employed in the NIMH study were used. RESULTS: One year after study admission, 72% of elderly patients had recovered. Nineteen percent of recovered patients, however, had a subsequent episode of major depressive disorder. Recovery and relapse rates in the elderly did not significantly differ from those reported for the mixed-age group in the NIMH study. CONCLUSIONS: It is erroneous to single out the elderly as being more likely to have poorer longitudinal treatment outcomes than others. Study findings indicate the need for continued refinement of somatic and nonsomatic treatments for the elderly to improve rates of sustained recovery from depression.     

Challenges and algorithm-guided treatment in major depressive disorder

Major depressive disorder is complicated and difficult to treat, primarily because of its chronic and recurrent nature and the poor efficacy of most pharmacologic treatment options. Until more effective treatments become available, clinicians must focus on optimizing patient outcomes through patient care. Implementing measurement-based care and using treatment algorithms can reduce symptoms of depression and help patients achieve and maintain remission.