Subtypes Of Affective Disorders Research Articles

Factors associated with tobacco consumption in patients with depression.

Smoking and depression are related in a bidirectional way: smoking is the primary avoidable cause of illness and death in patients with depression, and depression is one of the most consistent risk factors for smoking. The main objective of this study is to investigate the relationship between smoking and depression, analyzing sociodemographic and clinical variables such as severity of symptoms, subtype of affective disorder, and its impact on suicidal behavior in the clinical population.A sample of 201 patients, over 18 years of age [mean age (SD) = 53.76 (10.36) years; women = 132 (65.7%)], with a history of depressive episode (unipolar or bipolar) or dysthymia (ICD 10 criteria) was studied.Current smoking prevalence was 43.2% and life-time prevalence 61.2%. No statistically significant differences in smoking prevalence between men and women were found (X2 = 3.896, p = 0.143). The average age of onset was 17.81 (5.60) years. There was a tendency towards a linear association between number of cigarettes/day consumed and severity of depression according to the Hamilton Depression Scale (HDRS) in current smokers (Pearson's R = 0.298, p = 0.050). Multinomial logistic regression analysis showed that current tobacco consumption was associated with higher HDRS scores, with each additional point on the HDRS increasing the likelihood of smoking by 0.062 [p = 0.032; OR (95% CI) = 1.064 (1.005-1.125)].Our results showed that depressed patients present higher prevalence of current smoking than the general population, also suggesting a relationship between severity of consumption and severity of depressive symptoms.

A functional dopamine-β-hydroxylase gene promoter polymorphism is associated with impulsive personality styles, but not with affective disorders

Dopamine-beta-hydroxylase (DbetaH) catalyzes the conversion of dopamine to norepinephrine in central noradrenergic and adrenergic neurons and thus is critically involved in the biosynthesis of catecholamines. There are equivocal findings concerning the question whether or not DssH activity levels are altered in affective disorders or in subtypes of affective disorders. Moreover, information about the role of dopamine beta-hydroxylase (DBH) genotype, which explains a large part of the variance of enzymatic activity, in affective disorders and personality dimensions is limited. To resolve these inconsistencies, association tests were performed using four independent samples, healthy volunteers (N = 387), patients with affective disorders (N = 182), adult attention deficit hyperactivity disorder (ADHD) patients (N = 407), and patients with personality disorders (N = 637). In the latter two samples, the revised NEO personality inventory (NEO-PI-R) was administered. All participants were genotyped for a putatively functional single nucleotide polymorphism (C-1021T, rs1611115). No differences in DBH C-1021T genotype distribution were observed between patients with affective disorders and healthy control subjects. Also when the patient sample was divided into uni- and bipolar patients versus controls, no significant differences emerged. Furthermore, no clear-cut association was detected between the TT genotype and personality disorder clusters while there was a significant association with adult ADHD. However, personality disorder patients carrying the DBH TT genotype exhibited higher neuroticism and novelty seeking scores as compared to individuals with the CC or CT genotype. Analyses on the level of the neuroticism and novelty seeking subscales revealed that the DBH TT genotype was primarily associated with personality features related to impulsiveness and aggressive hostility. Also adult ADHD patients carrying the homozygous TT genotypes displayed by significantly increased neuroticism scores; when both personality disorder and adult ADHD patient were analyzed together, TT carriers also displayed by significantly lower conscientiousness levels. Our results thus do not implicate the DBH C-1021T polymorphism in the pathophysiology of depressive disorders or personality disorders, yet homozygosity at this locus appears to increase the risk towards personality traits related to impulsiveness, aggression and related disease states, namely adult ADHD. These data argue for a dimensional rather than categorical effect of genetic variance in DBH activity; accordingly, the inconsistency of previous findings concerning DbetaH levels in affective disorders might be caused by the underlying association of the TT genotype at DBH-1021 with impulsive personality traits.

Human Borna disease virus‐infection and its therapy in affective disorders

Patients with affective disorders show an enhanced prevalence of Borna disease virus (BDV)-infection. Furthermore, BDV causes latent infection preferably in limbic central nervous structures and is suggested to be causally related to subtypes of affective disorders, especially with melancholic clinical features or bipolarity. Such a possible link was highlighted by the first report of amantadine showing an antidepressive and an antiviral efficacy against BDV in a patient with a bipolar disorder. This article summarizes clinical studies which followed this first report on the use of amantadine in BDV-infected patients with an affective disorder. A special focus is given on an open clinical study in patients with depression (n = 25), a study in remitted patients with affective disorders (n = 16), and the effect of amantadine on severe hypomanic or moderately manic patients with a bipolar disorder in an on-off-on study. In these studies amantadine reduced clinical symptoms paralleled by a reduction of BDV-infection in depressive patients, it also reduced all three BDV-parameters (BDV-Ab, -AG, and -CICs) in remitted patients, and it even reduced severe hypomania and moderate mania in bipolar patients. These data suggest the existence of an etiopathogenetic link between BDV and subtypes of affective disorders.

Psychosocial disability and work role function compared across the long-term course of bipolar I, bipolar II and unipolar major depressive disorders

Objective The research literature on psychosocial disability and work in mood disorders has either focused on relatively short-term course, or did not consider direct comparisons of these domains across all three of the affective subtypes of bipolar I (BP-I), bipolar II (BP-II), and unipolar major depressive disorders (UP-MDD). Methods Mean composite measures of psychosocial impairment and months at specific levels of overall and work impairment were compared for 158 BP-I, 133 BP-II, and 358 UP-MDD patients based on semi-structured interviews conducted during 15 years of follow-up in the NIMH Collaborative Depression Study (CDS). These are contrasted with a single month of psychosocial impairment ratings for a sample of 1787 subjects with no current psychiatric disorder. Results Patients with mood disorders experienced some degree of disability during the majority of long-term follow-up (54 to 59% of months), including 19 to 23% of months with moderate and 7 to 9% of months with severe overall impairment. Severe disability occurred a substantial percentage of time only in the specific area of work role function. BP-I patients were completely unable to carry out work role functions during 30% of assessed months, which was significantly more than for UP-MDD and BP-II patients (21% and 20%, respectively). Conclusions These findings have public health, economic, and clinical importance, and underscore the need to reduce the chronicity and impairment associated with these three prevalent affective disorder subtypes. Interventional research is just beginning to address these challenges.

Abnormalities of the HPA axis in affective disorders: clinical subtypes and potential treatments.

New evidence is emerging regarding abnormalities of hypothalamic-pituitary-adrenal (HPA) axis function in subtypes of affective disorders. Adverse effects of HPA axis dysregulation may include dysfunction of monoaminergic transmitter systems, cognitive impairment and peripheral effects. Newer treatments specifically targeting the HPA axis are being developed. To review these developments focusing particularly on the glucocorticoid receptor (GR) antagonist mifepristone. A selective review of the literature. The function of GRs is increasingly being defined. The role of corticotrophin-releasing hormone (CRH) and dehydroepiandrosterone (DHEA) in the brain is also increasingly understood. HPA axis function is particularly likely to be abnormal in psychotic depression and bipolar disorder, and it is in these conditions that trials of the GR antagonist mifepristone are being focused. CRH antagonists and DHEA are also being investigated as potential treatments. Initial studies of mifepristone and other HPA-axis-targeting agents in psychotic depression and bipolar disorder are encouraging and confirmatory studies are awaited.

Subjective life satisfaction and objective functional outcome in bipolar and unipolar mood disorders: A longitudinal analysis

Background Quality of life (QOL) has gained increasing attention as an important yet underappreciated component of functional outcome in mood disorders. In particular, the relationship between subjective life satisfaction and objective measures of psychosocial adjustment has not been well-studied. The goal of the present study was to examine the longitudinal associations between subjective life satisfaction and objective functional outcome among individuals with bipolar and unipolar mood disorders. Method One hundred fifty-seven mood disordered subjects were assessed at index hospitalization for bipolar mania ( n = 35), unipolar psychotic depression ( n = 27), or unipolar nonpsychotic depression ( n = 95). All were prospectively followed up three times, at approximately 2, 4.5 and 7–8 years. Global outcome, work performance, social adjustment, recurrent depressive episodes, and dimensions of life satisfaction were assessed by semi-structured interviews using standardized ratings. Results Subjective life satisfaction strongly paralleled global functioning, work performance and social adjustment at each follow-up for patients with unipolar nonpsychotic depression, but not bipolar disorder or unipolar psychotic depression. Depressive symptoms and objective functional impairment contributed to poor QOL in most domains, independent of illness chronicity, medication use, or affective disorder subtype. Limitations Findings might have differed had a different QOL measure been used, although the present measure showed concurrent validity with a previously used instrument. Sample sizes for the bipolar and psychotic depression groups were sufficient to detect moderate, but not small, correlations between objective functioning and subjective QOL. Conclusions Recurrent depression remains a substantial contributor to poor life satisfaction across affective disorder subtypes. Subjective QOL in bipolar and unipolar psychotic depression patients may not accurately reflect objective functional outcome status, potentially due to diminished insight, demoralization, or altered life expectations over time.

New directions in the development of antidepressants: the interface of neurobiology and psychiatry.

There have been considerable advances in neurobiology in recent years that are providing new directions for the development of novel classes of antidepressants. For example, the finding that corticotropin-releasing factor (CRF) is hypersecreted in depressed patients and mediates certain symptoms of depression has led to the development of specific antagonists of the CRF(1) receptor. These are expected to prove highly effective for the treatment of mood and anxiety disorders. Another related avenue of research is based on evidence that cortisol is integral to the pathophysiology of major depression with psychotic features. One alternative for treating this subtype of affective disorder is, therefore, to block the action of glucocorticoids using a receptor antagonist such as mifepristone. These are just two of the many new directions that will likely lead to the development of antidepressants in the near future.

Mortality in affective disorders

Background: To investigate the mortality rates in affective disorders due to unnatural and natural causes with respect to illness subtype and social–demographic features. Methods: Mortality data were determined from a prospective study of 354 outpatients with affective disorders during a follow-up period of 5 years. Death from natural and unnatural causes was compared to sex- and age-specific expectations in the general population. Standardized mortality rates (SMR) in diagnostic subgroups and the influence of social–demographic features were investigated. Results: The observed 30 deaths represented nearly three times (SMR, 2.9) the number expected on the basis of age- and sex-standardized reference population rates. Death from natural causes occurred with the same rate as expected (SMR, 1.0), death from unnatural causes was 28.8 times higher than expected. Women with affective disorders had a considerable high risk to die from unnatural causes (SMR, 47.1). A significant excess of unnatural death was found in all subtypes of affective disorders, particularly in recurrent major depressive episodes (SMR, 46.7). Limitations: The sample was restricted in size. Therefore subgroup differences and multiple relationships of risk factors could not be analyzed with high statistical power. Conclusions: The results corroborate earlier findings of excess mortality in major affective disorders and strengthen the view that suffering from recurrent major depression confers per se an important biological risk for suicide. Natural causes of death in affective disorders are comparable to expectations from reference populations. Social–demographic characteristics may contribute to an additional risk of premature death by suicide, particularly in women.

Let There Be Dark: A Chrematogenic Presentation of Seasonal Affective Disorder

Seasonal affective disorder (SAD) is a well-accepted subtype of affective disorder. Its current criteria require that the patterns of mood changes correspond to seasons, not to ambient light, although the research makes it clear that it is the decreased light in the winter that results in the depressive symptoms. The authors present a case in which a patient with a demonstrated pattern of mild depression in the winter developed a severe depression when placed in a new job situation requiring her to work in virtually total darkness for 12-hour shifts. She was unable to work under these conditions and requested a change back to more normal lighting conditions. When this was refused, she was ultimately fired, despite an exemplary 25-year work record. The case is presented to illustrate that when diagnostic criteria are taken too literally, they may lead to unanticipated results in the legal arena.

CLINICAL PREDICTORS OF ANTIDEPRESSANT RESPONSE

We should not necessarily expect that all new antidepressants will be equally effective in all subtypes of affective disorder across all age groups. Data from a number of studies have suggested that the selective serotonin (5-HT) reuptake inhibitors (SSRIs) are significantly less effective than the tricyclics in the treatment of patients with melancholia. Two Danish studies that compared the effectiveness of chlorimipramine to either paroxetine or citalopram in depressed inpatients with melancholia found an approximately 60% response rate to the tricyclic compared to only a 30% response rate to the SSRI. Data from our own studies of nortriptyline or fluoxetine in treatment of depressed patients with heart disease show the same effect; 78% (25/32) melancholic patients responded to nortriptyline compared to 10% (1/10) treated with fluoxetine χ2=12.24, P<0.001. However, not all studies agree. Differences in patient populations with respect to severity, age, and gender, as well as methodological issues such as criteria for response (50% reduction in the Ham-D) vs. a final Ham-D ≤10), and adequacy of antidepressant trial explain most of the variance.

ANXIOUS–BIPOLAR COMORBIDITY: Diagnostic and Treatment Challenges

This article describes multiple anxiety comorbidity in the setting of unstable bipolar syndromes, associated with alcohol and substance abuse. Also described are panic attacks during mania, social phobia followed by hypomania as well as bipolar disorder manifesting as episodic obsessive-compulsive disorder. The use of psychotropic combinations is necessary because of the syndromic complexity and the contrasting effects of pharmacologic treatments. The identification of differential patterns of comorbidity may provide important information in distinguishing more homogeneous clinical subtypes of affective disorders from the genetic, temperamental, and therapeutic point of view. The pattern of complex relationships among these disorders requires better-designed prospective observations. This is also true for putative temperamental (e.g. cyclothymia, interpersonal sensitivity) and personality (e.g. histrionic and borderline) factors, which might play a predisposing role in several clinically comorbid syndromes.

Therapeutic strategies in refractory bipolar disorder

Lithium is still regarded as the first choice substance in the prophylactic treatment of bipolar disorder. However, approximately one third of patients with a "classic" course of bipolar affective disorder do not adequately respond to lithium prophylaxis. The introduction of carbamazepine and valproic acid allowed a more differential syndrome- and course-orientated approach to the prophylactic treatment of bipolar disorder for the first time. However, about 10 to 20 percent of patients still remain refractory to standard regimes. Therefore, criteria for resistance to prophylactic treatment have to be further established. It has been suggested that at least two adequate trials of more than 12 months duration with sufficient drug blood levels have to be performed before refractoriness should be assumed. A severe subtype of affective disorder with poor response to lithium and other treatment approaches is a rapid cycling course which is characterised by at least four affective episodes per year. Here we present an overview of the currently available alternatives for prophylactic treatment, i.e. anticonvulsants, combination treatment, adjunctive thyroxine, calcium channel blockers, and more experimental approaches for treating refractory bipolar disorder patients. Suggestions for optimizing the prophylactic treatment of bipolar disorder are summarized in an algorithm.

Apolipoprotein E-ε4 frequency in affective disorder

Background: The ε4 allele of apolipoprotein E (APOE) as well as affective disorder have been found to be associated with Alzheimer’s disease, but it is unclear whether cognitive impairment in affective disorder or subtypes of affective disorder is mediated by the ε4 allele of APOE. Methods: The genotype of APOE was analyzed in 106 unipolar patients, 21 bipolar patients, and 46 controls and correlated with cognitive function in the euthymic phase as measured by the Mini-Mental State Examination, the Cambridge Cognitive Examination, the Mattis Dementia Rating Scale, the Gottfries–Bråne–Steen Dementia Rating Scale, and the Global Deterioration Scale. Results: The frequency of APOE-ε4 allele was approximately the same in unipolar patients (.189) and in bipolar patients (.167). Although patients showed more cognitive impairment than controls, no significant overall difference was found between the frequency of APOE-ε4 allele in patients (.185) and controls (.131). In fact, the frequency of APOE-ε4 allele did not correlate with cognitive impairment. It was not possible to identify subgroups of patients with an increased frequency of APOE-ε4 allele, as no association was found with gender, age at onset, the number of affective episodes, the presence of psychotic features, or the prevalence of familial affective disorder. Conclusions: It seems that cognitive impairment in affective disorder can be attributed to pathways other than the APOE genotype.

Changes in CSF spaces differ in endogenous and neurotic depression: A planimetric CT scan study

Regional planimetric measurements of internal and external CSF spaces were performed in CT scans of 23 patients with endogenous depression (ICD 9, 296.1) and 28 patients with neurotic depression (ICD 9, 300.4) as compared to 56 control individuals without neuropsychiatric disorder. In female patients with endogenous depression, but not in men, the bilateral upper cortical sulci were widened, especially in the frontal regions, and the third ventricle was enlarged. In contrast, the female neurotic depressed group showed no enlargement of CSF spaces, but a narrowing of the Sylvian fissure and of the basal frontal lobe reaching level of significance in the right fronto-temporal region ( P=0.005). No narrowing of CSF spaces was observed in women with endogenous depression. A discriminant analysis of significantly changed CSF regions resulted in a correct classification in 82.4% of depressed women in either the endogenous or the neurotic group. Determination of divergent types of brain pathology might prove as a useful tool in validating the differential classification of these two main subtypes of affective disorders.

416. - Dawn simulation treatment of abstinent alcoholics with winter depression

Background: Recent data suggest that winter depression (seasonal affective disorder [SAD]) may be a subtype of affective disorder that is closely related to alcoholism. Dawn simulation has been shown in controlled trials to be effective in SAD. The present study examined the effectiveness of dawn simulation in abstinent alcoholics who met DSM-III-R criteria for major depression, or bipolar disorder, depressed with seasonal pattern. Method: All 12 subjects with winter depression had a history of either alcohol dependence or alcohol abuse according to DSM-III-R and had been abstinent from alcohol for at least 6 months. They also fulfilled criteria for SAD according to Rosenthal and were hypersomnic and drug free. After a 1-week baseline period, the subjects were randomly assigned to a 1-week treatment period at home with either a white 1.5-hour dawn from 4:30 a.m. to 6:00 a.m. peaking at 250 lux or a red 1.5-hour dawn from 4:30 a.m. to 6:00 a.m. peaking at 2 lux. The subjects were told that they would receive daily either a red or a white dawn reaching the same illuminance, an illuminance that would be much dimmer than standard bright light treatment. At the end of each week, the subjects were blindly assessed by a psychiatrist using the Structured Interview Guide for the Hamilton Depression Rating Scale-Seasonal Affective Disorder version (SIGH-SAD). Results: For the 6 subjects completing the white dawn treatment, the mean SIGH-SAD score decreased from 33.0 at baseline to 15.8 after treatment. For the 6 subjects completing the dim red dawn treatment, the mean SIGH-SAD score decreased from 34.3 to 32.7. The mean post-dawn SIGH-SAD score was significantly lower after the white dawn treatment than after the dim red dawn treatment (ANCOVA with baseline SIGH-SAD as the covariate, F = 12.95, p <.01). Superiority of the white dawn was also found by analogous analyses for the Hamilton Rating Scale for Depression (HAM-D) (p <.01) and the SAD Subscale (p <.05). Conclusion: The present study suggests that dawn simulation may be helpful in decreasing depression in abstinent alcoholics with SAD. Further study is necessary to confirm these preliminary findings and to determine whether dawn simulation might be helpful in preventing relapse in abstinent alcoholics who have SAD.

Functional Brain Imaging, Limbic Function, and Affective Disorders

For more than a century, mesial cerebral structures have been candidate substrates for the mediation of emotional experience. Although limbic structures were originally conceived as forming a midline ring, emerging evidence suggests that emotional processes may be related more closely to anterior paralimbic (anterior limbic and nearby cortical) regions than to posterior limbic regions. In addition, basal ganglia-thalamocortical circuits for various cerebral processes have been proposed, including one involving anterior paralimbic structures thought to mediate emotion. Recent brain imaging studies have advanced this thesis by demonstrating anterior paralimbic activation during affective arousal in healthy volunteers. The overwhelming majority of functional imaging studies of both primary and secondary depression has demonstrated decreased anterior paralimbic and prefrontal cortical activity, the latter of which often correlated with severity of depression and resolved with symptom remission. A few studies have noted increased activity in these same regions, which may reflect heterogeneity due to particular illness subtypes. Preliminary evidence has suggested that baseline functional abnormalities in these structures may relate to diagnostic subtypes and provide differential markers of therapeutic responses. New imaging methods with greater sensitivity, spatial and temporal resolution, and biochemical specificity promise to fuel further insights into the neurobiology of normal emotion in health, subtypes of affective disorders, and perhaps even improved targeting of therapeutic interventions.

Familial depression versus depression identified in a control group: are they the same?

Subjects who meet the criteria for an affective syndrome possibly are aetiologically heterogeneous. An approach to this possibility involves examining affectively ill subjects obtained by different methods of ascertainment. This study compares depressed and manic subjects who are related to affectively ill probands with affectively ill subjects who were obtained from a study of a control population, and, therefore, were less likely to be familial. The subjects were identified in a large collaborative study of depression where both family members as well as controls were personally interviewed and followed up for 6 years after admission to the study. Data were obtained on subtypes of affective disorder using the Research Diagnostic Criteria and information was gathered about psychiatric hospitalizations, suicide attempts, alcoholism and psychological functioning prior to admission. Similar assessments were made for the comparison groups for the 6 year period between intake and follow-up. Relatives of bipolar I/schizoaffective manic probands were more likely to show mania than affectively ill controls or relatives of unipolar/schizoaffective depressed probands. Affectively ill controls were less likely to be hospitalized and less likely to suffer from an incapacitating depression. They were also likely to have functioned in a more healthy fashion than the affectively ill relatives of the bipolars and unipolars, in the 5 years before admission to the study. In the 6 year follow-up, both the subjects themselves and raters assessed the depressed controls as functioning better than the affectively ill relatives of the probands. Further, assessment of global adjustment during the 6 year period was worse for the relatives of affectively ill probands than for the depressed controls. Length of major depression was longer in relatives of bipolar and unipolar probands than in controls. Though all of the subjects in this study met research criteria for an affective illness, there were marked differences in the qualitative aspects of these illnesses with the relatives of affectively ill probands, who functioned less well and had longer and more severe episodes and more hospitalizations.

Personality patterns in subjects at risk for affective disorders.

The main conclusions of this study on the familial links between personality patterns and affective disorders are: (1) The personality features with the greatest degree of symptomatic overlap with unipolar depression were more common among the first-degree relatives of probands with this diagnosis: thus dysthymic temperament and neuroticism are enhanced in this group of relatives compared to controls. Likewise personality features with a high degree of symptomatic overlap with bipolar affective disorder were more common among the first-degree relatives of probands with this diagnosis. Thus levels of dysthymic and cyclothymic temperament were elevated in this group of relatives compared to controls, whereas a familial link between neuroticism and bipolar disorder was not observed. (2) In addition, personality traits with only limited similarity with the syndromes of depression and mania were also found to be linked with affective disorders (obsessive-compulsive PD to bipolar disorders, rigidity to both subtypes of affective disorders). These associations have different implications regarding the association between personality/temperament conditions and disorders depending on the degree of overlap between symptoms and the personality trait. Those with substantial overlap may indicate the presence of a unitary disease process in which the enhancement of subthreshold affective traits may result in aggravation of behavior characteristics fulfilling the criteria of fullblown episodes of the disease. This relationship was particularly stressed by Kraepelin, Kretschmer, Clayton et al. and Akiskal. In this view personality and temperament patterns represent minor variants of the associate acute disorders. On the other hand, the relationship between dissimilar conditions may indicate the presence of a risk of underlying vulnerability factors which led to affective disorder only in the presence of additional risk factors. An example of the latter relationship in the present study is the aggregation of obsessive-compulsive and anancastic traits in families with affective disorders. Tellenbach focussed on this particular constellation. Epidemiological and family studies including these personality traits are too rare to fully appreciate the relevance of this particular relationship. Future prospective studies and family genetic studies which investigate the relationship between temperament, personality traits and disorders and affective syndromes are clearly indicated by the results presented herein.

Cerebral blood flow in major depression and dysthymia

Using single photon emission computerized tomography (SPECT) with a 99 m Tc-HMPAO perfusion technique, we studied the regional cerebral blood flow (rCBF) of 42 drug-free impatients suffering from Major Depression' ( n = 21) or dysthymia with the super-imposed diagnosis of a major depressive episode ( n = 21). The patients with Major Depression had a significantly lower frontal and posterior rCBF ratio than those with Double Depression. Left frontal region indices showed a slight overlap between the two groups. There was no correlation between the severity of the illness and the rCBF indices. Different qualitative cerebral dysfunctions may be implicated in these two affective disorder sub-types.

Biological and clinical features of recurrent brief depression: A comparison with major depressed and healthy subjects

Recurrent brief depression (RBD) has recently been proposed as a new subtype of affective disorder characterized by episodes of major depression which last less than two weeks. The aim of this study was to further evaluate the validity of this putative subtype by means of clinical and biological data. DST, TSH response to TRH and sleep EEG variables were compared in 25 RBD patients sex- and age-matched to 25 major depressed (MD) and 25 healthy subjects. Family history, age at onset, and psychiatric comorbidity did not discriminate RBD from MD. Recurrent unipolar depression was found to be more prevalent in MD. Although less severely depressed during the biological tests, patients with RBD did not significantly differ from those with MDD on basis of DST non-suppression, blunted TSH response and shortening of REM latency. Compared to controls, a greater sleep onset latency was observed both in RBD and MD and a lower total sleep time in MD patients only. These results suggest that RBD could be viewed as a subtype of affective disorder sharing many characteristics with MDD.