DSM-III Criteria For Major Depression Research Articles

The Loss of Sadness: How Psychiatry Transformed Normal Sorrow Into Depressive Disorder

The Loss of Sadness: How Psychiatry Transformed Normal Sorrow Into Depressive Disorder . Allan V. Horwitz and Jerome C. Wakefield. New York: Oxford University Press, 2007, 312 pp., $31.95 (hardcover). Beginning with the 1980 publication of the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders ( DSM-III, 3rd ed.), mental health professionals and, consequently, various other disciplines including sociology and journalism used a much more inclusive diagnostic definition of depression. Eschewing both psychodynamic understanding and the contexts of depression, the DSM-III criteria for major depression were satisfied by a mere listing of symptoms, an assumption allowing normal responses to stressors to be mischaracterized as disorder. Sadness, with the exception of some bereavement reactions, was officially transformed from normality to pathology by psychiatric declaration. Perhaps it is not coincidental that the number of prescriptions for antidepressants and the people on these drugs have increased exponentially from 1980 to the present. Illustrating this trend, ". . . spending for antidepressants increased by 600% in the United States, exceeding $7 billion annually by the year 2000" (p. 5). As the title of their richly illuminating book suggests, Horwitz, a PhD sociologist, and Wakefield, who has both a PhD and a DSW in social work, show that sadness, that is normal sorrow-a human emotion that has vital adaptive utility grounded in our biological nature-has been lost in the relentless process of diagnosing even normal human sensibility to loss as depression. Thus, the new psychiatry, ostensibly based on scientific knowledge of our biological natures, has violated its own premise. In his foreword to their book, psychiatrist Robert Spitzer, who headed the task force that created the DSM-III, remarks "Because their analysis is anchored in psychiatry's own assumptions, it will be hard for those now constructing the DSM-V (expected publication in 2011) to ignore" (p. ix). Meanwhile, the DSM-III and its successor DSM-IV have persuaded more and more professionals and the lay public to regard sadness as a kind of pathology that should be quelled, particularly by prescribed drugs. Looking at the massive personal and societal effects thus generated since 1980, one is reminded of Aldous Huxley's 1932 book Brave New World and the 1956 and 1978 versions of the movie Invasion of the Body Snatchers. In Brave New World, unrelenting social pressure is used to persuade people to ingest soma, a drug that causes imbibers to lose their normal human nature and become like those who have already submitted to the ersatz normalization-by-soma. In Body Snatchers, humans who resist giving up their bodies to aliens are exploited by their normality, their biological need to sleep, a vulnerability used to steal their humanity. Seeing now what has happened via the new biological psychiatry bears out some of the ominous portents of the fictional soma and snatching societies. Horwitz and Wakefield present the findings of their thorough study soberly, patiently, and methodically as they proceed to their inexorable conclusions. Attesting to its thoroughness, the book's 11 chapters comprise: the concept of depression, the anatomy of normal sadness, sadness with and without cause, depression in the twentieth century, depression in the DSM-IV, importing pathology into the community, the surveillance of sadness, the DSM and biological research about depression, the rise of antidepressant drug treatments, the failure of the social sciences to distinguish sadness from depressive disorder, and the conclusion. Every chapter is well worth reading. The authors immediately present their central tenet: "We argue that the recent explosion of putative depressive disorder . . . does not stem primarily from a real rise in this condition. Instead, it is largely a product of conflating the two conceptually distinct categories of normal sadness and depressive disorder and thus classifying many instances of normal sadness as mental disorders" (p. …

Issues for DSM-V: The Medical Diagnostic Model

Back to table of contents Previous article Next article EditorialFull AccessIssues for DSM-V: The Medical Diagnostic ModelMax Fink M.D.Michael A. Taylor M.D.Max Fink M.D.Search for more papers by this authorMichael A. Taylor M.D.Search for more papers by this authorPublished Online:1 Jul 2008https://doi.org/10.1176/appi.ajp.2008.08020245AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail Early in the modern psychopharmacologic era, treatment response was considered verification for a diagnosis. A well-developed response to lithium in excited patients was consistent with a diagnosis of manic depression. A response to anticonvulsants supported a diagnosis of a seizure disorder. As syndrome categories broadened in scope and became less specific (e.g., the easily met criteria for major depression), the usefulness of such responses fell and interest waned. In the 1970s, hypercortisolemia was reported among severely depressed patients but not in patients with other mental disorders. Initial observations were made in patients with melancholic depression who were so ill they were referred for electroconvulsive therapy. The abnormality disappeared with remission and reappeared with relapse. The development of a simplified dexamethasone suppression test encouraged studies. However, when the test was applied as diagnostic criterion to populations classified according to DSM-III criteria for major depression, specificity was lost and the test was precipitously discarded. Recent interest in rigorously diagnosed examples of melancholia and psychotic depression based on narrowly defined mood, motor, and vegetative symptoms suggests that hypercortisolemia may be a verifying criterion and the response to specific treatments a validating criterion (1) . Psychiatric classification has swollen into a kaleidoscope of putative disorders. It is not likely that any one rule of taxonomy will define the many entities that may be included in DSM-V. But a medical diagnostic model will define those conditions for which we already have a biological interest in their identification and, more importantly, methods of resolution.Address correspondence and reprint requests to Dr. Fink, PO Box 457, St. James, NY 11780; [email protected] attglobal.net (e-mail). Editorial accepted for publication March 2008 (doi: 10.1176/appi.ajp.2008.08020245).The authors report no competing interests.Editorials discussing other DSM-V issues can be submitted to the Journal at http: //mc.manuscriptcentral.com/appi-ajp. Submissions should not exceed 500 words.Reference1. Taylor MA, Fink M. Melancholia: The Diagnosis, Pathophysiology, and Treatment of Depressive Illness. Cambridge, UK, Cambridge University Press, 2006Google Scholar FiguresReferencesCited byDetailsCited BySchizophrenia Research, Vol. 150, No. 1Diagnostic and statistical manual of mental disorders 5: A quick glanceIndian Journal of Psychiatry, Vol. 55, No. 3 Volume 165Issue 7 July, 2008Pages 799-799THE AMERICAN JOURNAL OF PSYCHIATRY July 2008 Volume 165 Number 7 Metrics PDF download History Published online 1 July 2008 Published in print 1 July 2008

Standardised nortriptyline and psychotherapy were more effective and more expensive than usual care in major depression

Lave JR, Frank RG, Schulberg HC , et al. Cost-effectiveness of treatments for major depression in primary care practice. Arch Gen Psychiatry1998 Jul; 55 : 645 –51 [OpenUrl][1][CrossRef][2][PubMed][3][Web of Science][4]...

Treating panic and depression in primary care

A meta-analysis of an earlier multicenter, double-blind efficacy study comparing placebo, oxaprotiline and amitriptyline was performed in order to test the survival-analytical approach in modelling the onset of improvement and response to treatment with antidepressants.The sample consisted of moderately depressed male (n=154) and female (n=275) patients (aged 17–73), diagnosed according to DSM-III criteria for major depression. Of these, 120 were treated with oxaprotiline, 120 with amitriptyline and 189 with placebo. Efficacy criteria were Hamilton Depression (HAMD) and Anxiety (HAMA) and Zung Self-Rating scales. Up to eight ratings over a period of 40 days were available for analysis.The results showed that the sensitivity in discriminating between groups was substantially enhanced through the inclusion of drop-outs and consideration of the effect of time to widthrawal from the study due to lack of improvement. Withdrawal from the trial due to inefficacy occurred earliest under placebo (50% within the first 8 days), whereas less than 40% dropped out within the first 12 days under active treatments. The most interesting and unexpected finding of the analysis was that the time course of improvement among responders was independent of the treatment modality, and thus identical in all three groups. Specifically, the efficacy of any of the given treatments was reflected only by the total number of responders or nonresponders. Once triggered, the time course of recovery from illness becomes identical to that of spontaneous remissions as observed, for example, under placebo. This finding strongly suggests that antidepressants may not change the pattern (‘Gestalt’) of the natural course of recovery from depression, but rather, they seem only to trigger recovery in a group of patients. Consequently, the efficacy of antidepressants appears to consist in their ability to change the boundary between the two populations of ‘responders’ and ‘nonresponders’.

Priorities of treatment in panic disorder

A meta-analysis of an earlier multicenter, double-blind efficacy study comparing placebo, oxaprotiline and amitriptyline was performed in order to test the survival-analytical approach in modelling the onset of improvement and response to treatment with antidepressants.The sample consisted of moderately depressed male (n=154) and female (n=275) patients (aged 17–73), diagnosed according to DSM-III criteria for major depression. Of these, 120 were treated with oxaprotiline, 120 with amitriptyline and 189 with placebo. Efficacy criteria were Hamilton Depression (HAMD) and Anxiety (HAMA) and Zung Self-Rating scales. Up to eight ratings over a period of 40 days were available for analysis.The results showed that the sensitivity in discriminating between groups was substantially enhanced through the inclusion of drop-outs and consideration of the effect of time to widthrawal from the study due to lack of improvement. Withdrawal from the trial due to inefficacy occurred earliest under placebo (50% within the first 8 days), whereas less than 40% dropped out within the first 12 days under active treatments. The most interesting and unexpected finding of the analysis was that the time course of improvement among responders was independent of the treatment modality, and thus identical in all three groups. Specifically, the efficacy of any of the given treatments was reflected only by the total number of responders or nonresponders. Once triggered, the time course of recovery from illness becomes identical to that of spontaneous remissions as observed, for example, under placebo. This finding strongly suggests that antidepressants may not change the pattern (‘Gestalt’) of the natural course of recovery from depression, but rather, they seem only to trigger recovery in a group of patients. Consequently, the efficacy of antidepressants appears to consist in their ability to change the boundary between the two populations of ‘responders’ and ‘nonresponders’.

The Effect of Nortriptyline on Cognition

Despite widespread belief that antidepressants cause cognitive dysfunction, there has been surprisingly little systematic research that supports this view. With this in mind, our group sought to evaluate the effects of the tricyclic antidepressant nortriptyline on a variety of cognitive and psychomotor tasks. For the purposes of this report, we will focus on Buschke Total Recall. Seventy-eight patients (age range 21-81, mean age 49.95) who met RDC and DSM-III criteria for major depression (mean Hamilton score 20.82) voluntarily agreed to participate in a 6 week double-blind trial whereby they received either notriptyline (NT) or placebo (PBO) following a 1 week single-blind placebo. At each weekly visit the patient received a comprehensive neuropsychological battery which included the Buschke Selective Reminding Task. In addition at baseline, the patient was acutely challenged with the medication to which he was randomized (either PBO or 50 mg NT) and the neuropsychological battery including Buschke selective reminding test was repeated at 1.5 and 4 hrs. All patients received another acute challenge (either placebo or 50 mg nortriptyline) after 6 weeks of chronic treatment. Doses of NT were adjusted weekly to maintain therapeutic plasma levels. Data were analyzed by an analysis of variance with age group (young vs old-55 was the cutoff) and drug status (drug vs PBO) the between subject factors and time of assessment (weekly for the chronic effect and 1.5 & 4 hrs for the acute effect) as the within subject factor. In view of the effect of depression on memory, we used weekly Hamilton depression score as a covariate. The results indicated that there was no statistically significant difference between the NT (mean plasma level 87.94 ng/ml at wk6) vs PBO group with respect to the chronic effects on Buschke Total Recall. There was also no difference between NT vs PBO with respect to Buschke Total Recall after acute challenge at baseline and after acute rechallenge following 6 weeks chronic treatment with either NT or PBO.

Depression following myocardial infarction: a one year longitudinal study.

The purpose of this study was to examine the course and clinical correlates of depression during the first year after myocardial infarction. A group of seventy patients hospitalized for the treatment of myocardial infarction (MI) were assessed for the presence of mood disorders during their hospital admission and at three, six, nine, and twelve months follow-up. Patients were evaluated and diagnosed using the Present State Examination and DSM-III criteria. Impairment in activities of daily living was measured by the Johns Hopkins Functioning Inventory and impairment in social functioning was measured by the Social Functioning Examination. A total of twenty-four patients met DSM-III criteria for major depression at some time during the study (18 in the acute stage, 6 during follow-up). There were two patients with minor depression (dysthymia) at intake and six developed minor depression during the follow-up period. The median duration of major depression was 4.5 months. Patients with depression at intake had greater impairment in activities of daily living than non-depressed patients. Depressions lasting more than six months were more likely to be anxious depressions than those lasting less than six months. After the acute MI period, there was a consistent relationship between the existence of depression and impaired social functioning. This is a pilot study and needs further replication due to the low rate of follow-up participation. However, these data suggest that there may be two types of depression following MI: an acute depression associated with greater functional impairment, and a prolonged depression that may be associated with inadequate social support.

The P300 ERP component: an index of cognitive dysfunction xin depression?

A number of measures of brain function have suggested that depression is associated with cerebral hypoactivity. This study examines the late components of the event-related potential (ERP), in particular the P300 component, in depression. The P300 component is thought to index the updating of neurocognitive models which are concerned with the prediction of future events. Cognitive theories of depression include the proposition that depression may be characterized by abnormalities in the prediction of future events. The P300 component may therefore provide one neurophysiological index of cognitive dysfunction in depression. Twenty-seven subjects (14 medicated, 13 drug-free) fulfilling DSM-III criteria for Major Depression were compared to 27 age- and sex-matched normal controls. The amplitudes and latencies of N100, P200, N200 and P300 ERP components, reaction time and task accuracy were recorded during a standard auditory discrimination task. No significant differences were found in any ERP component measure or in reaction-time between the groups. Depressed subjects performed the experimental task significantly less accurately than normal controls, but this was not reflected in the ERPs.

Screening for major depressive disorder in the community: A comparison of measures.

Self-administered questionnaires are frequently used as case-finding instruments in community studies of depression. The Center for Epidemiological Studies Depression Scale (CESD) is one of the most commonly used questionnaires, though several studies have found poor concordance between CESD- and interview-based diagnoses. The authors made the CESD more closely correspond to the DSM-III criteria for major depression by adding 11 items to the original 20, and this enabled them to apply DSM-III's diagnostic algorithm to the CESD items to identify cases of depression. As part of a family study, they interviewed relatives of psychiatric patients and normal controls with the Diagnostic Interview Schedule (DIS) and gave them the CESD and Inventory to Diagnose Depression (IDD) to complete on their own

Time course of improvement under antidepressant treatment: A survival-analytical approach

A meta-analysis of an earlier multicenter, double-blind efficacy study comparing placebo, oxaprotiline and amitriptyline was performed in order to test the survival-analytical approach in modelling the onset of improvement and response to treatment with antidepressants. The sample consisted of moderately depressed male (n=154) and female (n=275) patients (aged 17–73), diagnosed according to DSM-III criteria for major depression. Of these, 120 were treated with oxaprotiline, 120 with amitriptyline and 189 with placebo. Efficacy criteria were Hamilton Depression (HAMD) and Anxiety (HAMA) and Zung Self-Rating scales. Up to eight ratings over a period of 40 days were available for analysis. The results showed that the sensitivity in discriminating between groups was substantially enhanced through the inclusion of drop-outs and consideration of the effect of time to widthrawal from the study due to lack of improvement. Withdrawal from the trial due to inefficacy occurred earliest under placebo (50% within the first 8 days), whereas less than 40% dropped out within the first 12 days under active treatments. The most interesting and unexpected finding of the analysis was that the time course of improvement among responders was independent of the treatment modality, and thus identical in all three groups. Specifically, the efficacy of any of the given treatments was reflected only by the total number of responders or nonresponders. Once triggered, the time course of recovery from illness becomes identical to that of spontaneous remissions as observed, for example, under placebo. This finding strongly suggests that antidepressants may not change the pattern (‘Gestalt’) of the natural course of recovery from depression, but rather, they seem only to trigger recovery in a group of patients. Consequently, the efficacy of antidepressants appears to consist in their ability to change the boundary between the two populations of ‘responders’ and ‘nonresponders’.

Magnetic resonance imaging of the caudate nuclei in depression. Preliminary observations.

A role of the caudate nucleus in depression has been suggested from relevant clinical conditions, such as patients with Huntington's disease or caudate infarcts, as well as animal studies. Correlations of caudate nucleus disease with depressive symptoms have been limited to autopsy studies and cases of gross pathological disorder, such as large infarcts. We used serial axial high-field magnetic resonance images and an unbiased stereological technique to estimate the volumes of the caudate nuclei in 50 patients who met DSM-III criteria for major depression (23 men, 48.3 +/- 17 years old) in comparison with 50 age- and gender-matched normal controls free of major neurological and psychiatric disorders. Depressed patients had smaller caudate nucleus volumes (5.2 +/- 1.6 cm3) compared with controls (6.2 +/- 1.7 cm3). Right and left caudate nucleus volumes were smaller in depressed patients compared with controls. Age was negatively correlated with caudate nucleus volumes in depressed patients as well as in controls. Caudate nucleus volumes in depressed patients were inversely correlated with the bicaudate and bifrontal indices. These results may be the first demonstration of diminished caudate nucleus volumes in depression and suggest a role for the caudate nucleus in the pathogenesis of major depression.

Natural history of symptoms of depression and anxiety during inpatient treatment on general medicine wards

To establish the frequency of criteria-based depression and anxiety in newly admitted medical inpatients and to determine the natural history of depressive and anxiety symptoms during hospitalization. Prospective structured assessment of criteria-based depression and anxiety diagnoses within 24 hours of hospitalization with routine follow-up depression and anxiety questionnaires until discharge. A tertiary care university hospital and an affiliated Veterans Administration hospital. One hundred twenty-eight adult patients admitted to internal medicine inpatient units between May 1990 and August 1990. On admission, 43 of the 128 patients inducted met the DSM-III criteria for major depression, while an additional six met the criteria for adjustment disorder with depressed mood. Only six patients met the criteria for panic disorder, generalized anxiety disorder, or adjustment disorder with anxious mood at the time of admission to the study. Patients with high symptom scores on the anxiety and depression scales showed significant decreases in these scores without specific psychiatric intervention. Those who remained in the hospital 20 days or longer showed initial improvement and subsequently returned to baseline symptom levels of depression and anxiety. In approximately 9% of patients, symptoms of depression persisted or worsened. Major depression occurs more commonly than anxiety disorder in newly admitted medical inpatients but both resolve spontaneously in the majority during the course of hospitalization without specific psychiatric intervention unless the hospitalization is prolonged. One in ten will continue to show symptoms of depression.

Affective symptoms associated with the onset of major depression in the community: findings from the US National Institute of Mental Health Epidemiologic Catchment Area Program

This study examined the strength of relationships between forms of depressive symptoms over a one-year period and the onset of major depression. The data analyzed were collected in 4 sites of the US National Institute of Mental Health Epidemiologic Catchment Area Program (NIMH-ECA, 1981-1985). The Diagnostic Interview Schedule's specifications of DSM-III criteria for major depression were employed. Overall, the results indicated a strong positive association between an onset episode and the following depressive symptoms over 1 year: diminished sexual drive, feelings of worthlessness or excessive guilt and trouble concentrating or thinking. Sleep disturbance among women and fatigue among males were also significantly associated with experiencing an onset of major depression. The implications of the findings for secondary prevention efforts are explored.

Platelet [ 3H]-imipramine binding and leukoencephalopathy in geriatric depression

We examined the relationship between platelet [ 3H]-imipramine binding and leukoencephalopathy as assessed by 1.5 Tesla Magnetic Resonance Imaging (MRI) in 21 elderly depressed patients who satisfied DSM-III criteria for major depression. Both drug-free platelet [ 3H]-imipramine binding and brain MRI studies were obtained during the same episode of depression. Our findings show a significant inverse relationship between frequency of subcortical hyperintensity (SCH) and the number ( B max of platelet [ 3H]-imipramine binding sites. Patients with B max less than 850 fmol/mg protein had significantly larger SCH compared with patients with a higher B max. These data provide further support to the potential use of platelet [ 3H]-imipramine binding studies and brain MR imaging as diagnostic adjuncts in geriatric depression and suggest, moreover, that these two biological markers may be linked in geriatric patients with depression.

In-patient major depression: is rolipram as effective as amitriptyline?

The antidepressant efficacy and adverse-effects of rolipram (a dialkoxyphenyl-2-pyrrolidone) were compared to those of amitriptyline in the treatment of depressive illness requiring hospital admission in a double-blind study. Fifty patients meeting DSM-III criteria for Major Depression whose scores on the Hamilton Rating Scale for Depression (HRSD) remained above 17 after 5 to 7 days on placebo were randomly allocated to either treatment. The rate of recovery in those patients treated by amitriptyline was substantially greater than in those patients treated by rolipram. Twice as many patients dropped out of treatment by rolipram because of lack of efficacy or adverse-effects compared with patients treated by amitriptyline. Rolipram produced fewer adverse-effects attributable to cholinergic blockade, but more nausea. We conclude that amitriptyline is more effective than rolipram in the treatment of depressed hospital in-patients.

Phenylthiocarbamide (PTC) tasting, genetics, and depression

Twenty-three (23) females who satisfied the Diagnostic Interview Schedule (DIS) DSM-III criteria for Major Depression were assessed with the Beck Depression Inventory (BDI), the Hamilton Rating Scale for Depression (HRS), the genetically based phenylthiocarbamide (PTC) taste test, and each subject provided a family history of depression. Results show that, compared with PTC nontasters, the tasters suffered deeper depressions, longer periods of sadness, symptoms that resembled "endogenous depression," and the tasters reported more family members afflicted with depression. The PTC taste test accounted for 20% of the variance on the BDI and on the HRS.

Neuroendocrine challenge tests in depression: a study of growth hormone, TRH and cortisol release

Thirty drug-free patients fulfilling the DSM-III criteria for major depression serially underwent the dexamethasone suppression test (DST), thyroid stimulating hormone (TSH) test and a growth hormone (GH) challenge test with oral desipramine. Fifty-three per cent of the sample showed a blunted GH response, 47% were DST non-suppressors while 26% had a blunted TSH response. Eighty per cent of patients showed some biological abnormality. There was no clear association between any of these abnormalities. Neither was there any association between the neuroendocrine parameters studied and the severity of depression or patient gender. There was a trend for increasing GH blunting and DST non-suppression with increasing age.

Elevated Plasma Concentrations of α1-Acid Glycoprotein, a Putative Endogenous Inhibitor of the Tritiated Imipramine Binding Site, in Depressed Patients

The plasma concentration of alpha 1-acid glycoprotein, a putative endogenous inhibitor of the site labeled by tritiated imipramine, was measured by a radial immunodiffusion assay in 36 normal human volunteers and 51 drug-free patients who fulfilled DSM-III criteria for major depression. The depressed patients exhibited a significant elevation in the plasma concentration (+/- SEM) of alpha 1-acid glycoprotein (79.6 +/- 4 mg/dL) when compared with the age- and sex-matched controls (61.7 +/- 3 mg/dL). Fourteen of the 51 patients with major depression had plasma alpha 1-acid glycoprotein concentrations that were higher than the highest values of the normal controls. There was no relationship between plasma alpha 1-acid glycoprotein concentrations and sex or affinity of platelet tritiated imipramine binding of either the normal volunteers or the depressed patients. In the depressed patients, there was a significant positive correlation between plasma concentrations of alpha 1-acid glycoprotein and postdexamethasone plasma cortisol concentrations, and two measures of depression severity, the Montgomery-Asberg Rating Scale for Depression and the Center for Epidemiologic Studies-Depression Scale, and a significant negative correlation with age. These data provide the first evidence of alterations of an endogenous inhibitor of the tritiated imipramine binding site/serotonin transporter in depressed patients.

Transient post-partum thyroid dysfunction and postnatal depression

In the course of a population study of thyroid dysfunction in pregnancy and the post-partum period, 65 women, considered to be antibody-positive (microsomal and thyroglobulin), and 82 antibody-negative women were assessed for postnatal depression at 6–8 weeks post partum. The women were also assessed for the development of post-partum thyroid dysfunction. Of the 147 women, 22 met DSM-III criteria for major depression. The presence of autoantibodies showed little association with depressed mood but there was a minor association of postnatal depression with actual thyroid dysfunction in that the incidence of the latter condition was higher in depressed women (Raskin scale P < 0.01; Edinburgh scale P < 0.05; Montgomery–åsberg scale P < 0.1). Three of eight mothers with thyroid dysfunction had major depression and were depressed on all three scales.

Differences between patient and family assessments of depression in Alzheimer's disease.

A structured interview covering the DSM-III criteria for major depression was adapted for separate use with Alzheimer's disease patients and with their families. Data from 36 patients yielded a depression rate of 13.9%, whereas information from their families indicated that the rate was 50.0%. This disagreement reflected greater family endorsement of patients' loss of interest or pleasure, irritability, fatigue, and feelings of worthlessness. Use of DSM-III-R criteria narrowed but did not eliminate the discrepancy between patients' and families' assessments of the patients' depression. Uniform procedures for gathering and integrating data from the family that are relevant to diagnosis in this group are indicated.