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OBJECTIVE: To evaluate the CORE measure of melancholia, against the DSM-IV construct of melancholia. To evaluate the validity of both the CORE and DSM-IV constructs of melancholia against psychosocial risk factors, anxiety and personality disorder comorbidity, neuroendocrine markers and differential anti depressant response to fluoxetine and nortriptyline. METHOD: One hundred and ninety-five outpatients with major depression were evaluated for melancholia with both the DSM-IV criteria and the CORE evaluation. Both constructs were evaluated for validity against psychosocial risk factors, comorbidity, biological markers and differential antidepressant response. RESULTS: The CORE measure has satisfactory interrater reliability when used dimensionally, but has unacceptably low agreement for making a categorical diagnosis of melancholia. There is remarkably poor agreement (kappa = 0.11) between the CORE and DSM-IV criteria for melancholia. Neither the DSM-IV nor CORE criteria for melancholia identified subgroups of patients with better childhood environments or less anxiety or personality disorder comorbidity. The CORE criteria for melancholia, but not DSM-IV, identified patients with neuroendocrine disturbance. CORE scores also were associated with differential responses to fluoxetine and nortriptyline, but not in anticipated directions. Thus, high CORE scores were associated with a higher recovery rate with fluoxetine than nortriptyline. CONCLUSION: While the episode specifier of melancholia should be retained in diagnostic systems, the DSM-IV criteria were not validated against any of the variables examined in this study. The CORE construct of melancholia, was validated against neuroendocrine measures, and was associated with a differential antidepressant response. However, the limits imposed by interrater reliability,suggest the CORE measure should be used dimensionally and not to make a categorical diagnosis of melancholia.
BACKGROUND: Assuming that psychomotor disturbances represent the core and are specific of melancholia, Parker et al. have developed the CORE, an 18-item scale assessing retardation, agitation and non-interactivity by behavioural observation which is able to distinguish melancholia from other depressive disorders. We report an inter-rater reliability study of the French version of the CORE. METHODS: 35 French-speaking in-patients, with ICD-10 criteria for major depression underwent a video-recorded interview aimed to rate the CORE. Each patient's recording was rated by 5 psychiatrists. We tested the inter-rater reliability of the total CORE score and of each of its three subscales' scores using the intra-class correlation coefficient (ICC). A cut-off score for melancholia was established against the opinion of the psychiatrist in charge of the patient using a ROC curve. We used Cohen's kappa to assess the agreement between raters as to rate patients above the cut-off, namely the allocation of melancholia. RESULTS: The global ICC for the total score was 0.88 and ranged from 0.97 to 0.75 for the varying rater dyads. A ROC curve yielded an optimal cut-off of 5 for melancholia. The global kappa for the agreement on melancholia allocation was good (0.65). LIMITATIONS: The five raters had not exactly the same condition of quotation. The agreement for the "agitation" subscale was poor. CONCLUSION: The French version of the CORE, has a good to excellent inter-rater reliability for the total score as for the allocation of melancholia according to a cut-off. Further validation studies are required to allow research application.
AIM: To examine if melancholic depression is over-represented in those with 'bipolar depression' and, if confirmed, to use that phenomenon to assist the clinical definition of melancholia. METHODS: We contrast 83 bipolar and 904 unipolar depressed patients on three melancholic sub-typing systems (DSM, Clinical and CORE system) and compare representation of their clinical depressive features. RESULTS: By all three melancholic sub-typing systems, the bipolar patients were more likely to receive diagnoses of 'melancholia' and of psychotic depression. To the extent that this differential prevalence of depressive sub-types was reflected in varying patterns of clinical features, we so indirectly identified a set of items defining 'melancholia'. By such a strategy, melancholia was most clearly distinguished by behaviourally-rated psychomotor disturbance. While a number of 'endogeneity symptoms' were significantly over-represented, logistic regression analyses refined the set to psychomotor disturbance (both as a symptom and as a sign) and pathological guilt. We also established a distinctly higher prevalence of bipolar depression in those where a refined diagnosis of melancholia was made. CONCLUSIONS: Bipolar depression appears to be more likely to be 'melancholic' in type, thus providing an indirect strategy for the clinical definition of melancholia.
The plasma norepinephrine (NE) level was measured in 45 depressed patients and in 41 normal control subjects. Patients who met DSM-III criteria for a major depressive episode with melancholia (MDE-MEL; N = 16), and those with MDE but with melancholia in a previous episode (MDE-PMEL; N = 8), had significantly higher levels of plasma NE than normal control subjects while lying and standing and a greater change in the levels; whereas, patients with MDE alone (N = 10) and patients with dysthymic disorder (N = 11) had levels of NE comparable with control levels. Bipolar patients (N = 7), all with current melancholia or a history of it, had significantly lower levels of NE while lying down or standing than depressed unipolar patients with similar histories of melancholia. Among unipolar patients with melancholia, nonsuppressors on the dexamethasone suppression test had significantly higher lying-down NE values than did suppressors, suggesting that dysregulation of both the hypothalamic-pituitary-adrenal axis and the peripheral sympathetic nervous system occur together in this subgroup of depressed patients.
Melancholia is most commonly distinguished from non-melancholic depression by the presence of psychomotor disturbance (PMD) and a set of 'endogeneity' symptoms. We examine the capacity of an operationalized clinician-rated measure of PMD (the CORE system) to predict diagnostic assignment to 'melancholic/endogenous' classes by the DSM-III-R and Newcastle systems. Examining a pre-established CORE cut-off score (> or = 8) against independent diagnostic assignment, PMD was present in 51% of those assigned as melancholic by DSM-III-R, and 85% of those assigned as endogenous by the Newcastle system, quantifying the extent to which it is 'necessary' to the two definitions of 'melancholia'. Additionally, multivariate analyses established that the addition of a refined set of historically suggested endogeneity symptoms added only slightly to overall discrimination of melancholic and non-melancholic depressives. While only few endogeneity symptoms independent of psychomotor disturbance were suggested, their specific relevance varied against system definition of melancholia (appetite/weight loss and terminal insomnia being identified for DSM-III-R; anhedonia for Newcastle; and diurnal variation in mood and energy for both systems). Results allow consideration of the relative importance of two domains (psychomotor disturbance and 'endogeneity' symptoms) to clinical definition of melancholia, and have the potential to assist both classification and pursuit of neurobiological determinants. We interpret findings as suggesting a 'core and mantle' model for conceptualizing the clinical features of melancholia, with psychomotor disturbance as the core and with independent endogeneity symptoms as only a thin mantle.
This psychopathological study about the experience of anxiety in 160 melancholic and 93 neurotic depressive patients (diagnostic criteria acc. to ICD-9) aims at reconsidering earlier findings about the anthropological essence of melancholia. Anxiety seems to be especially appropriate to examine changes in time experience emphasized by phenomenological authors. Only 5% of the melancholic patients spontaneously report on alterations of the experience of time. Self reports point to a "basic disturbance of temporal development" (von Gebsattel) in melancholia. The temporal structure of the experience of anxiety however, more depends on the respective content of anxiety than on the patient group examined. On the contrary the natural matter of course in dealing with hitherto familiar affairs gets lost more often in melancholia than in non-melancholic states: Anxiety about all and everything and anxiety related to depersonalization prove to be characteristic of melancholia, even with regard to the severity of depression. The data confirm that beyond changes of time experience a "separateness from the essential conditions of natural experience" (Binswanger) comes to light in melancholia.
We describe the syndrome of 'organic melancholia', i.e. the form of melancholia which in addition to the endogenous symptoms also shows organic psychopathological symptoms and is connected with brain damage. We found considerable differences between organic and cryptogenic melancholia: the development of organic melancholia has a regular course which can be distinguished into four stages: (1) the asthenic-hypochondriac, (2) the purely depressive, (3) the organically depressive and (4) the purely organic stage. The outcome of organic melancholia - a severe organic psychodeficiency, often combined with neurological symptoms, and the irreversible destruction of the professional life of the patient - is one of the more important differences distinguishing the organic and the cryptogenous type. Our findings are based on long-term observations of 30 patients.
The DSM-III criteria for melancholia are intended to define an endogenomorphic subcategory of major depressive episode for which somatic treatment is usually required. One hundred twenty-three inpatients having a major depressive episode were examined retrospectively to determine the ability of the melancholia criteria to identify patients observed to have an autonomous syndrome during the first week of hospitalization and to distinguish them from patients observed to be responsive to psychosocial intervention without drug treatment. The melancholia criteria correctly classified 77% of the sample. In comparison with the primary affective disorder criteria, the melancholia criteria appeared to be selective; fewer responsive patients were falsely identified. The predictive values of individual symptom criteria were examined. Of the current symptom criteria, two observed signs, lack of reactivity and psychomotor change, were most useful for making the autonomous-responsive distinction.
In the medical literature of the eighteenth century melancholia came to be defined as partial insanity. Seventeenth-century English law introduced the term and influenced later forensic concerns about the concept. But the history of melancholia reveals a gradual development of such a concept of limited derangement associated with the delusions usually cited in accounts of this disease. In the early nineteenth century the relationship of melancholia and this concept weakened and was gradually abandoned, the content of the syndrome of melancholia was reduced, and out of this complex process emerged the notion of monomania.
The nineteenth century was the site of radical changes in understanding mental illness. The professionalization of psychiatry consisted primarily of the discipline's aspiration to the status of an expert medical subspecialty. While all forms of insanity were eventually reframed in medical terms, melancholia--for moral and nosological reasons--assumed a special role that made it an ideal diagnosis for conceptual reframing. Our analysis of the journal literature of the nineteenth and early twentieth centuries in North America and Germany traces several ways in which melancholia was medicalized. As the care for the insane shifted into the professional realm of physicians and medical terminology came to replace prior descriptors of mental illness, melancholia was replaced by depression. In addition, the process of delineating affective pathology assumed a distinctly medical flavor. Finally, melancholia was firmly medicalized when its boundaries blurred with neurasthenia. Differences in how ordinary affective terms became medicalized in German and North American psychiatry illustrate the importance of local historical approaches.
A taxometric analysis was conducted to test the hypothesis that the latent structure of melancholia in adolescents is categorical. Two taxometric procedures were used: Mean Above Minus Below a Cut (MAMBAC) and Maximum Covariance (MAXCOV) analyses. Participants were 378 adolescents presenting for a depression evaluation. Indicators of melancholia were constructed using items from the Schedule for Affective Disorders and Schizophrenia for School Aged Children (K-SADS) and the Beck Depression Inventory (BDI). The indicators of melancholia were consistent with a categorical latent variable. The findings suggest that the latent structure of melancholia in adolescents is similar to its previously identified categorical structure in adults. Implications for clinical research are discussed.
BACKGROUND: We pursue an observation that age may influence the clinical features of melancholia and, in particular, psychomotor disturbance. METHODS: Two large clinical databases were amalgamated allowing the clinical features of 124 depressed subjects meeting DSM-III-R and clinical criteria for melancholia to be contrasted with 218 subjects diagnosed as having a non-melancholic depression by both criteria sets. Psychomotor disturbance was assessed by the CORE measure and by seven classical endogeneity symptoms of melancholia which, when summed, created a ENDOG score. RESULTS: There was no impact of age on ENDOG scores in either the melancholics or non-melancholics. In the melancholics, increasing age was associated with increasing CORE scores and with agitation scale scores in particular. In a set of discriminant function analyses seeking to identify the comparative utility of a set of predictors of melancholic (versus non-melancholic) groups, age was significant, and while CORE and ENDOG scores were individual predictors, their combined entry established that the CORE score alone made the ENDOG score redundant, and that the addition of age then made little impact. CONCLUSIONS: Melancholia appears to have a later age of onset than non-melancholic depression, while its phenotypic expression appears to change with age, with psychomotor disturbance being more distinct in older subjects. Such an effect may have a number of clinical implications, including possible differential effects of varying antidepressant treatments.
Major depression is a heterogeneous condition, and the search for neural correlates specific to clinically defined subtypes has been inconclusive. Theoretical considerations implicate frontostriatal, particularly subgenual prefrontal cortex (PFC), dysfunction in the pathophysiology of melancholia--a subtype of depression characterized by anhedonia--but no empirical evidence has been found yet for such a link. To test the hypothesis that melancholic, but not nonmelancholic depression, is associated with the subgenual PFC impairment, concurrent measurement of brain electrical (electroencephalogram, EEG) and metabolic (positron emission tomography, PET) activity were obtained in 38 unmedicated subjects with DSM-IV major depressive disorder (20 melancholic, 18 nonmelancholic subjects), and 18 comparison subjects. EEG data were analyzed with a tomographic source localization method that computed the cortical three-dimensional distribution of current density for standard frequency bands, allowing voxelwise correlations between the EEG and PET data. Voxel-based morphometry analyses of structural magnetic resonance imaging (MRI) data were performed to assess potential structural abnormalities in melancholia. Melancholia was associated with reduced activity in the subgenual PFC (Brodmann area 25), manifested by increased inhibitory delta activity (1.5-6.0 Hz) and decreased glucose metabolism, which themselves were inversely correlated. Following antidepressant treatment, depressed subjects with the largest reductions in depression severity showed the lowest post-treatment subgenual PFC delta activity. Analyses of structural MRI revealed no group differences in the subgenual PFC, but in melancholic subjects, a negative correlation between gray matter density and age emerged. Based on preclinical evidence, we suggest that subgenual PFC dysfunction in melancholia may be associated with blunted hedonic response and exaggerated stress responsiveness.
This multicenter study compared the efficacy and safety of citalopram and placebo in a population of moderately to severely depressed patients with melancholia. This randomized, double-blind, parallel-group study compared citalopram (flexible dose; 20-80 mg/day) with placebo in 180 psychiatric outpatients with a DSM-III diagnosis of major depression or bipolar disorder, depressed, who also met DSM-III criteria for melancholia. Following a 1-week placebo washout period, patients meeting study entry criteria were randomized to 4 weeks of double-blind treatment with either citalopram or placebo. Efficacy measures included the Hamilton Rating Scale for Depression (HAM-D), the Clinical Global Impressions (CGI) Scale, and the Zung Self-Rating Depression Scale. Patients treated with citalopram showed significantly greater improvement at endpoint than placebo patients on the HAM-D, CGI, and Zung scales. On the HAM-D, citalopram patients exhibited significantly greater improvement than placebo patients after 1 week of double-blind treatment and at all subsequent study visits. Endpoint analyses of the HAM-D subscales demonstrated that citalopram produced significant improvement of the psychomotor retardation, cognitive disturbance, sleep disturbance, and melancholia symptom clusters. Nausea, dry mouth, somnolence, dizziness, and increased sweating were reported at higher rates by citalopram-treated patients than by placebo-treated patients, but there were no significant citalopram-placebo differences in the incidence of activation (e.g., anxiety, nervousness, insomnia) or sexual dysfunction. Analysis of electrocardiograms, vital signs, and laboratory tests did not reveal any clinically significant effects of citalopram treatment. The results of this study indicate that citalopram is safe and effective in the treatment of depressed patients with melancholia, and is associated with a favorable side effect profile and a potentially rapid onset of action.
Four hundred thirty-eight subjects underwent an overnight dexamethasone suppression test (DST) to standardize the test for the diagnosis of melancholia (endogenous depression). Abnormal plasma cortisol concentrations within 24 hours after dexamethasone administration occurred almost exclusively in melancholic patients. The best plasma cortisol criterion concentration, above which a DST result may be considered abnormal, was 5 microgram/dL. The optimal dose of dexamethasone was 1 rather than 2 mg. Two blood samples obtained at 4 and 11 PM after dexamethasone administration detected 98% of the abnormal test results. This version of the DST identified melancholic patients with a sensitivity of 67% and a specificity of 96%. Baseline nocturnal plasma cortisol concentrations were not useful. Abnormal DST results were found with similar frequency among outpatients and inpatients with melancholia; but they were not related to age, sex, recent use of psychotropic drugs, or severity of depressive symptoms. Extensive evidence validates this practical test for the diagnosis of melancholia.
Five scales were evaluated for the diagnosis of melancholia or endogenous depression. Of 21 total items, none appeared in all five scales, but four items occurred in four of the scales: autonomy of mood, prevasive anhedonia, psychomotor change, and guilt. Vegetative changes were represented inconsistently, with anorexia and weight loss in three scales, as was distinct quality of mood. Thereafter, item agreement between the scales fell off. Scale performance was tested in 50 depressive patients. Major differences were found in frequency of melancholia and scale orientation toward inpatients and outpatients. A number of old controversies remain dormant in these scales. Unresolved are the relationship between melancholia and severity of depression; the relevance of precipitating events, previous depressive episodes, type of onset, and adequacy of personality; and whether to classify by category or continuum. The merits of statistically and consensually derived scales also need to be evaluated.
A previous study reported that unipolar depressives excrete significantly lower amounts of urinary tyramine-O-sulfate following oral administration of a tyramine hydrochloride load than do normal control subjects. This study replicates and extends those findings by showing that within the heterogeneous group of unipolar depressives, patients with melancholia and bipolar patients with a history of melancholia manifest a tyramine excretion deficit. A small subgroup of medication-free patients in remission from episodes of melancholia had abnormally low tyramine sulfate excretion levels while they were euthymic, supporting the suggestion that reduced tyramine sulfate excretion following oral tyramine loading is a trait marker for depression. Further study of the role of trace amines in affective illness is warranted. Clinical application is not warranted until further evaluation of the sensitivity, specificity, and reproducibility of this oral tyramine challenge test.