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Chapter 4

Classifying Mood Disorders

The Official Nomenclature

Classification of the mood disorders has evolved in the more than 50 years since the American Psychiatric Association’s first diagnostic and statistical manual was published. As research and theory have advanced, they have been reflected in the four editions and two revisions of the manual.

The current criteria for classifying Major Depressive Episodes and Manic Episodes are listed in Tables 4-1 and 4-2 from DSM-IV-TR.¹ It might be noted that the DSM-IV criteria for major depressive episode (as in Table 4-1) include “biological” or physiological symptoms along with cognitive ones. For example, these four symptoms are largely physiological in nature: (3) weight loss (or, in children, failure to make expected weight gains); (4) insomnia or hypersomnia; (5) psychomotor agitation or retardation; and (6) fatigue or loss of energy nearly every day. These five are cognitive or motivational symptoms: (1) depressed mood (or, in children and adolescents, irritability); (2) markedly diminished interest or pleasure in activities; (7) feelings of worthlessness or excessive or inappropriate guilt; (8) diminished ability to think or concentrate, or indecisiveness; (9) recurrent thoughts of death or suicidal ideation. The various types of mood disorder are listed in Table 4-3.¹

To find the various types of depression in the earlier nomenclature of the American Psychiatric Association,^2,3 compared to subsequent versions,^1,4,5,6 it was necessary to hunt through many sections. This scattering of the affective disorders contrasted with the consolidation found in other classification systems (e.g., the British Classification).⁷ This prior scattering of the mood disorders was a reflection of several historical trends, including the dissolution of Kraepelin’s grand union of all affective disorders into the manic-depressive category, the isolation of new entities such as neurotic-depressive reaction, and the attempt to separate the disorders on the basis of presumed etiological differences.

Schizoaffective disorder, which has salient affective features, was at one time listed as a subtype of the schizophrenic reaction. In terms of its historical conceptualization, its course, and its prognosis, this disorder may be more closely allied to bipolar disorder (see Chapter 8).

TABLE 4-1. Criteria for Major Depressive Episode

A.	Five (or more) of the following symptoms have been present during the same 2-week period and represent a change from previous functioning; at least one of the symptoms is either (1) depressed mood or (2) loss of interest or pleasure. Note: Do not include symptoms that are clearly due to a general medical condition, or mood-incongruent delusions or hallucinations.
	(1) depressed mood most of the day, nearly every day, as indicated by either subjective report (e.g., feels sad or empty) or observation made by others (e.g., appears tearful). Note: In children and adolescents, can be irritable mood. (2) markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day (as indicated by either subjective account or observation made by others). (3) significant weight loss when not dieting or weight gain (e.g., a change of more than 5% of body weight in a month), or decrease or increase in appetite nearly every day. Note: In children, consider failure to make expected weight gains. (4) insomnia or hypersomnia nearly every day. (5) psychomotor agitation or retardation nearly every day (observable by others, not merely subjective feelings of restlessness or being slowed down). (6) fatigue or loss of energy nearly every day. (7) feelings of worthlessness or excessive or inappropriate guilt (which may be delusional) nearly every day (not merely self-reproach or guilt about being sick). (8) diminished ability to think or concentrate, or indecisiveness, nearly every day (either by subjective account or as observed by others). (9) recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a specific plan, or a suicide attempt or a specific plan for committing suicide.
B.	The symptoms do not meet criteria for Mixed Episode.
C.	The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.
D.	The symptoms are not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a general medical condition (e.g., hypothyroidism).
E.	The symptoms are not better accounted for by bereavement, i.e., after the loss of a loved one, the symptoms persist for longer than 2 months or are characterized by marked functional impairment, morbid preoccupation with worthlessness, suicidal ideation, psychotic symptoms, or psychomotor retardation.

Adapted from DSM-IV-TR.

Derivation of System of Classification

In its original development, the DSM system of classification represented a composite of the ideas of three schools of thought: those of Emil Kraepelin, Adolph Meyer, and Sigmund Freud. The division of the various nosological categories, particularly of the psychoses, reflected the original boundaries drawn by Kraepelin. The major modification in the terminology reflected the Meyerian influence. Meyer rejected the Kraepelinian concept of disease entities and formulated in its place a theory of “reaction types.” The reaction types were conceived by him to be the result of the interaction between the specific hereditary endowment and the matrix of psychological and social forces impinging on the organism. The term reaction in the nomenclature reflected the Meyerian view.

TABLE 4-2. Criteria for Manic Episode

A.	A distinct period of abnormally and persistently elevated, expansive, or irritable mood, lasting at least 1 week (or any duration if hospitalization is necessary).
B.	During the period of mood disturbance, three (or more) of the following symptoms have persisted (four if the mood is only irritable) and have been present to a significant degree:
	(1) inflated self-esteem or grandiosity; (2) decreased need for sleep (e.g., feels rested after only 3 hours of sleep); (3) more talkative than usual or pressure to keep talking; (4) flight of ideas or subjective experience that thoughts are racing; (5) distractibility (i.e., attention too easily drawn to unimportant or irrelevant external stimuli); (6) increase in goal-directed activity (either socially, at work or school, or sexual or psychomotor agitation; (7) excessive involvement in pleasurable activities that have a high potential for painful consequences (e.g., unrestrained buying sprees, sexual indiscretions, or foolish business investments).
C.	The symptoms do not meet criteria for Mixed Episode.
D.	The mood disturbance is sufficiently severe to cause marked impairment in occupational functioning or in usual social activities or relationships with others, or to necessitate hospitalization to prevent harm to self or others, or there are psychotic features.
E.	The symptoms are not due to the direct physiological effects of a substance (e.g., drug of abuse, a medication, or other treatment) or a general medical condition (e.g., hyperthyroidism). Note: Maniclike episodes that are clearly caused by somatic antidepressant treatment (e.g., medication, electroconvulsive therapy, light therapy) should not be counted toward a diagnosis of Bipolar I Disorder.

Adapted from DSM-IV-TR.

Freud’s influence was seen in the descriptions of the specific categories in the glossary section of the original APA manual.² Here the syndromes were outlined according to the psychoanalytic theories; the various affective disorders were presented in terms of the concepts of guilt, retroflected hostility, and defense against anxiety. More recently, Jerome Wakefield has contributed some important ideas on the concept of mental disorder as harmful dysfunction.^8,9,10

TABLE 4-3. Types of Mood Disorder

Disorder	Characterizations
Depressive Disorders
Major Depressive Disorder	One or more Major Depressive Episodes (i.e., at least 2 weeks of depressed mood or loss of interest accompanied by at least four additional symptoms of depression)
Dysthymic Disorder	At least 2 years of depressed mood for more days than not, accompanied by additional depressive symptoms that do not meet criteria for a Major Depressive Episode
Depressive Disorder Not Otherwise Specified	Included for coding disorders with depressive features that do not meet criteria for Major Depressive Disorder, Dysthymic Disorder, Adjustment Disorder with Depressed Mood, or Adjustment Disorder with Mixed Anxiety and Depressed Mood (or depressive symptoms about which there is inadequate or contradictory information)
Bipolar Disorders
Bipolar I Disorder	One or more Manic or Mixed Episodes, usually accompanied by Major Depressive Episodes
Bipolar II Disorder	One or more Major Depressive Episodes accompanied by at least one Hypomanic Episode
Cyclothymic Disorder	At least 2 years of numerous periods of Hypomanic symptoms that do not meet criteria for a Manic Episode and numerous periods of depressive symptoms that do not meet criteria for a Major Depressive Episode
Bipolar Disorder Not Otherwise Specified	Included for coding disorders with bipolar features that do not meet criteria for any of the specific Bipolar Disorders defined in this section (or bipolar symptoms about which there is inadequate or contradictory information)
Other Mood Disorders
Mood disorder due to a general medical condition	A prominent and persistent disturbance in mood that is judged to be a direct physiological consequence of a general medical condition
Substance-induced mood disorder	A prominent and persistent disturbance in mood that is judged to be a direct physiological consequence of a drug of abuse, a medication, another somatic treatment for depression, or toxin exposure
Mood Disorder Not Otherwise Specified	Included for coding disorders with mood symptoms that do not meet the criteria for any specific Mood Disorder and in which it is difficult to choose between Depressive Disorder Not Otherwise Specified and Bipolar Disorder Not Otherwise Specified (e.g., acute agitation)

Adapted from DSM-IV-TR.

Reliability and Validity of Classification

Early studies in the United States and the United Kingdom cast doubt on the reliability of the official nomenclatures. Some investigators, however, suggested at the time that the essential problem may be in the application of the nomenclature, rather than in its construction.^11,12,13 Substantial discrepancies were found among diagnosticians concurrently interviewing the same patients. Diagnostic agreement improved considerably by formulating operational definitions of the categories in the official nomenclature.

The validity of a nomenclature refers to the accuracy with which the diagnostic terms designate veridical entities. Unfortunately, in the case of the so-called functional psychiatric disorders, there has been no known pathology or physiological abnormality to provide guidelines in the construction of the nomenclature. The basic definition of the nosological categories has rested largely on clinical criteria.

In assessing the validity of a medical or psychiatric classification, it is appropriate to ask whether the specific groups or syndromes isolated from each other are different in ways that are of medical or psychiatric significance, that is, in terms of symptoms, duration, outcome, tendency to recur, and response to treatment. In general, the studies seem to justify the isolation of the group of depressive disorders from other psychiatric disorders; in addition, there is some support for the separation within the affective (now mood disorders) group of the endogenous depressions from the reactive (now adjustment disorder¹) depressions.

In the early 1960s, Clark and Mallet¹⁴ conducted a follow-up study of cases of depression and schizophrenia in young adults, in which 74 cases diagnosed as manic-depressive psychosis or reactive depression and 76 initially diagnosed with schizophrenia were followed for three years. During the follow-up period, 70 percent of those with schizophrenia were readmitted, as were 20 percent of the depressives. Thirteen (17 percent) of those with schizophrenia became chronic, compared with only one (1.3 percent) of the depressives. Of the 15 depressed patients requiring readmission to the hospital, four were considered to have schizophrenia at that time. Of the 76 patients initially diagnosed with schizophrenia, none were considered to have a depressive disorder on readmission.

Several inferences may be drawn from the clinical studies. Two major categories are distinguishable (as Kraepelin suggested) when rate of recovery and chronicity are examined as parts of the clinical picture. These are (1) depressive disorders having a relatively high rate of recovery, a moderate rate of relapse within three years of the initial diagnosis, and a moderate rate of chronicity; and (2) schizophrenia having a high rate of relapse and a high rate of chronicity. Some cases that initially evince the clinical picture of depression ultimately develop symptoms of schizophrenia. But it is rare for a patient who has symptoms of schizophrenia to develop bipolar disorder symptoms later. Lewis and Piotrowski¹⁵ suggested that many cases are diagnosed incorrectly as bipolar disorder because of insufficient recognition of certain signs of schizophrenia.

Dichotomies and Dualisms: Past and Present

Aubrey Lewis¹⁶ and Paul Hoch¹⁷ regarded depression as essentially a single entity, while others sliced the syndrome along various planes to produce several dichotomies. This controversy reflected fundamental differences between the unitary and the separatist schools.¹⁸ The unitary school (gradualists) maintained that depression is a single clinical disorder that can express itself in a variety of forms; the separatists stated that there are several distinguishable types.

Endogenous Versus Exogenous

This division attempted to establish the basic etiology of depression. Cases of depression were divided into those caused essentially by internal factors (endogenous) and those caused by external factors (exogenous). Although originally the exogenous group included such environmental agents as toxins and bacteria, writers have equated exogenous with psychogenic factors. This dichotomy will be discussed at greater length below.

Autonomous Versus Reactive

Some writers have distinguished between types of depression on the basis of degree of reactivity to external events. Gillespie¹⁹ described several groups of depressed patients that differed in their responsiveness to external influences. He labeled those cases that followed a relentless course irrespective of any favorable environmental influences as “autonomous.” Those that responded favorably to encouragement and understanding were labeled “reactive.”

Agitated Versus Retarded

Depression has often been characterized in terms of the predominant activity level. Many authors considered agitation as characteristic of depressions of the so-called involutional period and retardation of activity as characteristic of earlier depressions. Several studies (see Chapter 7) have discounted this hypothesis.

Psychotic Versus Neurotic

Most authors have drawn a sharp line between psychotic and non-psychotic depressions. The gradualists, however,^16,17 believed that this distinction is artificial and that the differences are primarily quantitative. They asserted that the reported distinctions are based entirely on differences in the severity of the illness.

Endogenous and Exogenous Depressions

The focus of the controversy between the separatists and the gradualists was primarily on the etiological concepts of depression. The separatists favored two distinct entities. One category consisted of cases that were thought to be endogenous, that is, caused primarily by some biological derangement in the human organism. The second category, reactive depressions, consisted of cases caused primarily by some external stress (bereavement, financial reverses, loss of employment). The unitary school considered these distinctions artificial and did not recognize the validity of labeling some cases endogenous and others reactive.

The concept of two etiologically different types of depression was not new. In 1586 Timothy Bright, a physician, wrote a monograph, Melancholy and the Conscience of Sinne, in which he distinguished two different types of depression. He described one type “where the peril is not of the body” and requires “cure of the minde” (psychotherapy). In the second type, “the melancholy humour, deluding the organical actions, abuseth the minde”; this type requires physical treatment.

Origin of Endogenous-Exogenous Model

The words “endogen” and “exogen” were coined by the Swiss botanist Augustin de Candolle.²⁰ The concept was introduced into psychiatry toward the end of the nineteenth century by the German neuropsychiatrist P. J. Moebius (for a more complete discussion of the evolution of the concept, see Heron²²). Moebius attached the label of “endogenous” to the group of mental disorders considered at that time to be due to degeneration or hereditary factors (internal causes). He further distinguished another group of mental disorders that he considered to be produced by bacterial, chemical, and other toxins (external causes); this group was given the label of “exogenous.” The endogenous-exogenous view of psychiatric disorders was a completely organic dichotomy that left no room for a different order of causative agents, namely the social or psychogenic. The exclusiveness of this doctrine caused semantic difficulties when the concept later had to be adapted to include social determinants of abnormal behavior.

The dualism inherent in the endogenous-exogenous concept is apparent in Kraepelin.²¹ He accepted Moebius’s classification and stated that the principal demarcation of the etiology of mental disorders is between internal and external causes. He proposed that there was a natural division between the two major groups of diseases, exogenous and endogenous. In manic-depressive illness, “the real causes of the malady must be sought in permanent internal changes which very often, perhaps always, are innate.” Environment could at most be a precipitant of manic-depressive disease, because by definition an endogenous illness could not at the same time be an exogenous illness.

“The Great Debates”

The controversy regarding the endogenous-exogenous concept was most prominent in Great Britain, and a number of outstanding authorities took part on both sides of the argument.¹⁸ Earlier, Kraepelin had endeavored to include almost all forms of depression under one label, manic-depressive disorder. Later, German writers almost uniformly split depressions into endogenous and exogenous. The British, however, were sharply divided on this point, and as a result of the clash of opinions in a series of great debates, the concepts of depression were considerably refined (although unanimity has not as yet been attained).

The first of the debates was touched off by Mapother in 1926, when he attacked the notion of a clinical distinction between neurotic depressions and psychotic depressions. (This argument later shaded into the controversy of endogenous versus reactive depression.) He held that the only reason for making a distinction was the practical difficulties connected with commitment procedures. He claimed that he could “find no other basis for the distinction; neither insight, nor cooperation in treatment, nor susceptibility to psychotherapy.” He attacked the notion that there are neurotic conditions that are purely psychogenic and psychotic conditions that are dependent on structural change. His view was that all depressions, whether ostensibly psychogenic or seemingly endogenous, are mediated by essentially the same means.

Mapother’s concept is an interesting statement of the phenomenon of depression: “The essence of an attack is the clinical fact that the emotions for the time have lost enduring relation to current experience and whatever their origin and intensity they have achieved a sort of autonomy.” There were a number of rebuttals in the discussion of Mapother’s paper, and then another debate in 1930, which touched off another series of discussions and papers (see Partridge).

Klein and Wender²³ note that the labels “neurotic,” “reactive,” and “endogenous” depression are beginning to disappear. They speculate that one of the major reasons for their fading is the increasing evidence that diverse types of mood disorders are often triggered by life events, but nonetheless are treatable by “physical methods” (p. 93). However, as reviewed in Chapters 14, 15, and 16, the somatic and psychological therapies overall appear equally capable of providing treatment and prevention of the mood disorders.

Distinction Between Endogenous and Reactive Depressions

From the various conflicting as well as complementary opinions regarding the validity of differentiating endogenous from reactive or neurotic depressions, it is possible to make a composite picture of endogenous depression as it emerged from the debates. This may be helpful in understanding the referents of the term endogenous, which appeared widely in the earlier literature, although it was not included in any official nomenclature.

In general, there are two major defining characteristics of the category endogenous depression. First, it was generally equated with psychosis and consequently distinguished from neurotic depressions. Second, it was regarded as arising primarily from internal (physiological) factors and could thus be contrasted with reactive depressions produced by external stress. To complicate the distinctions, however, reactive depressions, although often equated with neurotic depressions, were sometimes distinguished from them.

The etiology of endogenous depression was ascribed to a toxic chemical agent, a hormonal factor, or a metabolic disturbance.^24,25 Autonomy from external environmental stimuli was considered an essential feature. Crichton-Miller likened the mood variation to the swinging of a pendulum, completely independent of the environment. Neurotic variations in mood, in contrast, were compared to the motion of a boat with insufficient keel, subject to the oscillations in its milieu.

The specific symptomatology was characterized as a diffuse coloring of the whole outlook, phasic morning-evening variation, continuity, detachment from reality, loss of affection, and loss of power to grieve.²⁶ To this should be added Gillespie’s observation that the symptoms seemed alien to the individual and not congruent with her or his premorbid personality.

The role of heredity in endogenous depressions was stressed by a number of writers. Gillespie¹⁹ reported that a family history of psychosis was common in this group, and Buzzard²⁶ suggested that suicide and alcoholism were frequent in the family background. Constitutional factors as reflected in body build were emphasized by Strauss.

Reactive depressions were distinguished from endogenous depressions because they were said to fluctuate according to ascertainable psychological factors.¹⁹ In terms of symptomatology, the distinguishing features were seen to be a tendency to blame the environment and insight into the abnormal nature of the condition.

Systematic Studies

Several investigators tried to determine whether depressive illnesses are simply drawn from different points along a single continuum, or whether a number of qualitatively distinct entities exist. Kiloh and Garside²⁷ reported a study designed to differentiate between endogenous and neurotic (exogenous) depression. Their article reviewed the historical development of the controversy and the experimental literature and presented data collected by the authors.

They studied the records of 143 depressed outpatients and abstracted data relevant to their investigation; 31 of the patients had been diagnosed as having endogenous depression, 61 as having neurotic depression, and 51 as doubtful. Thirty-five clinical features of the illness were selected for additional study. A factor analysis was carried out, and two factors were extracted. The first was a general factor; the bipolar second factor was considered by the authors to differentiate between neurotic and endogenous depression. The second factor accounted for a greater part of the total variance than the general factor and was therefore more important in producing the correlations among the 35 clinical features analyzed.

Kiloh and Garside found significant correlation between certain clinical features and each of the diagnostic categories. The clinical features that correlated significantly (p < .05) with the diagnosis of neurotic depression were, in decreasing order of the magnitude of their correlations, reactivity of depression; precipitation; self-pity; variability of illness; hysterical features; inadequacy; initial insomnia; reactive depression; depression worse in evening; sudden onset; irritability; hypochondriasis; obsessionality. The features that correlated significantly with endogenous depression were early awakening; depression worse in morning; quality of depression; retardation; duration one year or less; age 40 or older; depth of depression; failure of concentration; weight loss of seven or more pounds; previous attacks.

Another study by Carney et al.²⁸ extended to inpatients the overall approach used by Kiloh and Garside in their study of outpatients. Carney and his coworkers studied 129 inpatient depressives treated with ECT. All patients were followed up for three months, and 108 patients were followed for six months. Initially, all were scored for the presence or absence of 35 features considered to discriminate between endogenous and neurotic depressions. Diagnoses were made before or shortly after treatment was started. Improvement was rated on a four-point scale at the termination of ECT, at three months, and at six months. At three months, only 12 of 63 neurotic depressives (19 percent) were found to have responded well to ECT, whereas 44 of 53 endogenous depressives (83 percent) had responded well.

A factor analysis of the clinical features produced three significant factors: a bipolar factor “corresponding to the distinction between endogenous and neurotic depression”; a general factor with high loadings for many features common to all the depressive cases studied; and a “paranoid psychotic factor.” The bipolar factor closely resembled that which was extracted in the study by Kiloh and Garside. Among features with high positive loadings on the first factor, and thus corresponding to a diagnosis of endogenous depression, were adequate premorbid personality; absence of adequate psychogenic factors in relation to illness; a distinct quality to the depression; weight loss; pyknic body build; occurrence of previous depressive episode; early morning awakening; depressive psychomotor activity; nihilistic, somatic, and paranoid delusions; and ideas of guilt. Among features with a negative loading, corresponding to a diagnosis of neurotic depression, were anxiety; aggravation of symptoms in the evening; self-pity; a tendency to blame others; and hysterical features.

By means of multiple regression analysis, three series of 18 weighted coefficients for the differential diagnosis between the two varieties of depression and for the prediction of ECT response at three and six months were calculated. The multiple correlations between the summed features, on the one hand, and diagnosis and outcome at three and six months, on the other, were 0.91, 0.72, and 0.74 respectively. It was found that ECT response could be better predicted by the direct use of the weights for ECT response than from the diagnostic weights alone. The weights based on the 18 clinical features were complex, and therefore a table was constructed giving simplified weights based on ten features of diagnosis. When the weighted scores for each patient were computed, it was found that, of the patients with a score of six or higher, 52 had been diagnosed clinically as endogenous and three as neurotic. Those patients scoring below six included one endogenous and 60 neurotic depressives. The amount of overlap, consequently, was small, and the findings supported the two-type hypothesis.

Methodological Problems

Several methodological questions may be raised in connection with these studies. First, the reliability of the ratings of the clinical material was not reported. As has been pointed out in many papers, interjudge agreement tends to be relatively low when applied to clinical material; low reliability automatically imposes a limit on the validity of any findings based on these ratings. In addition, since the psychiatrists making the ratings were cognizant of the underlying hypotheses, the possibility of bias in making their judgments cannot be excluded.

The second methodological problem concerned the differences between the two groups studied with respect to uncontrolled variables of importance, such as age and sex. For example, relative sleeplessness and loss of appetite are characteristic of older patients. (We found a relatively high correlation between age and loss of appetite among our psychiatric patients.) There was also evidence that females and males reacted differently to stress. Since these studies did not control adequately for either age or sex (or for other demographic variables), we cannot be certain that the salient differences between the two groups are explained by the dualistic hypothesis.

There is also a problem in the interpretation of the factor analysis. The authors extracted a bipolar factor that seemed to indicate a division of the patient sample into two independent groupings. In order to prove that these groupings apply to different kinds of patients rather than simply to different clusters of signs and symptoms, it is necessary to show that there is a clear-cut splitting of the patient sample into two independent groups. Kiloh and Garside²⁷ did not present any information regarding the distribution of the cases. In the study by Carney, Roth and Garside,²⁸ however, a separation of the endogenous and neurotic groups was achieved by weighting items based on the statistical analysis.

Studies of Symptomatology

Hamilton and White²⁹ performed a factor analysis on data obtained from 64 severely depressed patients who had been evaluated with the use of Hamilton’s rating scale.³⁰ The first of the four factors obtained included such clinical features as depressed mood, guilt, retardation, loss of insight, suicidal attempt, and loss of interest. It proved, according to the authors, to be correlated with a clinical diagnosis of retarded depression. Significantly different mean scores between the endogenous and reactive groups were obtained for this first factor. It should be emphasized, however, that this finding does not specify whether the difference is qualitative or merely quantitative.

Unfortunately, the so-called precipitating factors given to justify the diagnosis of reactive depression seemed unconvincing. In the three cases of reactive depression presented, the authors refer to the following as the psychological precipitating factors: one patient was left alone for prolonged periods while his wife went to look after their sick daughter; another was put in charge of a program that was beyond his capabilities; the third learned that the pulmonary tuberculosis he had had for nine years was bilateral.

Findings contradictory to those reported by Hamilton and White were contained in a study by Rose.³¹ This investigator used the same clinical rating scale in studying 50 depressed patients. The patients were divided into endogenous, reactive, and doubtful groups. In contrast to Hamilton and White, Rose found no significant differences in symptoms among the three groups.

Physiological Responses and Tests

Kiloh and Garside referred to the work on sedation threshold by Shagass and Jones,³² which indicated that cases of endogenous depression had lower sedation thresholds than those of neurotic depression. They also cited the work of Ackner and Pampiglione³³ and Roberts,³⁴ which failed to confirm Shagass’s results. The work of Shagass and Schwartz³⁵ on cortical excitability following electrical stimulation of the ulnar nerve was also cited. They found that in 21 patients with psychotic depression, the mean recovery time was significantly increased. However, controls for age were not included in these early studies, thus confounding the variables of interest.

The Funkenstein test was cited by Sloan et al. as additional evidence supporting the distinction between these two types of depression.³⁶ Better designed studies failed to substantiate these findings (see Chapter 9). More recent research supports an interactive perspective on the development of depression, including cognitive vulnerability, stress, early experiences, and genetic components (see Chapter 13).

Body Build

Kiloh and Garside quoted a study by Rees³⁷ that demonstrated an association between neurotic depression and leptomorphic physique, and between eurymorphic physique and manic-depressive disorder. Here again, the mean age of the manic-depressive group was significantly higher than that of the neurotic-depressive group. As will be indicated in Chapter 9, body build becomes more eurymorphic with increasing age.

Response to Treatment

Kiloh and Garside cited several studies suggesting that exogenous depression reacts poorly to electroconvulsive therapy but endogenous depression reacts favorably. Some evidence to support this claim is contained in a study by Rose,³¹ who found that better response was obtained only for the women who had endogenous depression. There was no difference in treatment response among the men in this study. (The study by Carney et al.²⁸ described in detail above helped substantiate the claim of a differential response.)

Depressive Equivalents

Many writers attempted to spread the umbrella of depression to cover cases showing clinical symptoms or behaviors different from those generally indicative of depression. The term depressive equivalents was introduced by Kennedy and Wiesel³⁸ to describe patients who had various somatic complaints but did not show any apparent mood depression. They reported three cases characterized by somatic pain, sleep disturbance, and weight loss, all of whom recovered completely after a course of ECT.

A number of other terms have been applied at various times to designate such cases of concealed depression. These include incomplete depression, latent depression, atypical depression, and masked depression. Various psychosomatic disorders, hypochondriacal reactions, anxiety reactions, phobic reactions, and obsessive-compulsive reactions have also been implicated as masking the typical picture of depressive reactions.³⁹

TABLE 4-4. Diagnostic Criteria for Mood Disorder Due to General Medical Condition

A.	A prominent and persistent disturbance in mood predominates in the clinical picture and is characterized by either (or both) of the following:
	(1) depressed mood or markedly diminished interest or pleasure in all, or almost all, activities; (2) elevated, expansive, or irritable mood.
B.	There is evidence from the history, physical examination, or laboratory findings that the disturbance is the direct physiological consequence of a general medical condition.
C.	The disturbance is not better accounted for by another mental disorder (e.g., adjustment disorder with depressed mood in response to the stress of having a general medical condition).
D.	The disturbance does not occur exclusively during the course of a delirium.
E.	The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.

Adapted from DSM-IV-TR.

The use of such a term as depressive equivalents raised several difficult conceptual, semantic, and diagnostic problems. (1) How could a syndrome substitute for a depressive reaction? (2) Since the usual indices of depression are lacking, how can the diagnosis of masked depression, etc. be made? (3) Since the concept of depressive equivalent is so loose, it could be stretched to encompass practically any psychiatric or somatic syndrome.

One of the main criteria for diagnosing a depressive equivalent has been the response of patients with formerly intractable symptoms to ECT.³⁸ Denison and Yaskin,⁴⁰ in a report titled “Medical and Surgical Masquerades of the Depressed State,” listed several criteria for the diagnosis of an underlying depression. These include previous attacks of somatic complaints similar to the present attack, with complete recovery after several months; disturbance of sleep cycle; loss of appetite; loss of energy disproportionate to the somatic complaints; diurnal variation in intensity of somatic symptoms; and feeling of unreality. In the consideration of disguised depressions, it is worth emphasizing the truism that depression may mask organic disease as well as vice versa.

Depressions Secondary to Somatic Disorders

It has long been understood that depressions are associated with a wide variety of nonpsychiatric disorders. In some instances, the depression appears to be a manifestation of the physiological disturbance caused by structural disease or toxic agents. The current American Psychiatric Association criteria for diagnosing depressions secondary to somatic disorders are in Table 4-4. In other instances, the depression seems to be a psychological reaction to being acutely or chronically ill—that is, the illness is a nonspecific precipitating factor. In either event, the depressive symptomatology per se, is not distinguishable from that observed in primary depressions.^1,41

Conditions that specifically impair the normal functioning of the nervous system have long been known to produce depression.⁴² These conditions may be acute (the acute brain syndromes) such as those associated with alcohol, drugs, head trauma, or post-ictal states. Or the conditions may be chronic (chronic brain syndromes) such as those associated with cerebral arteriosclerosis, dementia, neurosyphilis, multiple sclerosis, malnutrition, and various vitamin deficiency syndromes.

Depression as a complication of the use of the tranquilizing drugs has frequently been reported. Early reports of the use of reserpine in the treatment of hypertension implicated this drug as a causative agent in many depressions. Also, the phenothiazines have been suspected. Simonson,⁴³ for instance, interviewed 480 patients who were having their first acknowledged depression. He found that 146 (30 percent) had been taking a phenothiazine prior to the depression. Ayd,⁴⁴ however, was skeptical of the role of tranquilizers in producing a depression. He studied 47 cases of so-called drug-induced depression, and concluded that each case presented a history of predisposition to psychic disturbance and of physical and psychological stresses that helped precipitate the depression. This is not surprising, since the people in this study were presumably prescribed the tranquilizers due to some identified “psychic disturbance” in the first place.

Depressive symptomatology was found in a substantial proportion of patients hospitalized for medical disorders.⁴⁵ Yaskin⁴⁶ and Yaskin et al.⁴⁷ reported a high frequency in patients with organic disease of the abdominal organs, particularly carcinoma of the pancreas. Dovenmuehle and Verwoerdt⁴⁸ reported that 64 percent of 62 patients hospitalized for definitely diagnosed cardiac disease had depressive symptoms of moderate or severe degree.

Other types of generalized somatic disorders that, according to Castelnuovo-Tedesco, are likely to be complicated by depression are (1) certain infectious diseases—especially infectious hepatitis, influenza, infectious mononucleosis, atypical pneumonia, rheumatic fever, and tuberculosis; (2) so-called psychosomatic disorders such as ulcerative colitis, asthma, neurodermatitis, and rheumatoid arthritis; (3) anemias; (4) malignancies; and (5) endocrine disturbances.

In view of the longstanding theory that primary depression is caused by an endocrine disturbance, it is interesting that certain diseases of the endocrine glands are associated with a high frequency of depression. Michael and Gibbons⁴⁹ pointed out that the adrenocortical hyperfunction of Cushing’s syndrome is almost always accompanied by mood change. The alteration in mood is generally depressive, but it may also be characterized by emotional lability and overreactiveness. In their review of the reports of psychiatric disturbance related to Cushing’s syndrome, Michael and Gibbons stated that the incidence of psychiatric disturbance generally exceeded 50 percent. Severe mental disturbance, extreme enough to warrant the label psychotic, was found in 15–20 percent of the cases. In one series, 12 of 13 patients with Cushing’s syndrome were reported to be consistently or intermittently depressed. There was, however, no close correlation between the symptoms of depression and the steroid output.

Michael and Gibbons also reviewed the incidence of depression in Addison’s disease. They noted that depression occurred in 25 percent of the cases, and, somewhat surprisingly, euphoria occurred in 50 percent. Psychiatric disturbances have also been reported in cases of hypopituitarism. In longstanding untreated cases, the symptoms may appear in an extreme form. The most prominent symptom tends to be apathy and inactivity. Mild depression, occasionally interrupted by brief episodes of irritability and quarrelsomeness, is also prominent. Additional studies on the biological aspects are reviewed in Chapter 9.