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"Sad is How I Am!" Treating Dysthymia in Children and Adults
Dysthymia continuing education addiction counselor CEUs

Section 21
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The clinical spectrum of so-called "minor" depressions. (eng; includes abstract) By Akiskal HS, Weise RE, American Journal Of Psychotherapy [Am J Psychother], ISSN: 0002-9564, 1992 Jan; Vol. 46 (1), pp. 9-22; PMID: 1543256


The various terms used in describing these depressions embody concepts believed to be the key elements of these disorders.


This term suggests external causation by which is usually meant psychological causation. In Jasper's[ 11] conceptualization, the depression would not have occurred without the event (e.g., love loss) to which it is a reaction, it will continue for as long as the event were present, and it would terminate with the reversal of the event (e.g., the return of the lover). Depressions meeting all these features are not commonly encountered in clinical practice.[4] If they occur, they are more likely to be considered "adjustment disorders." With some support most individuals are able to face up to life reverses, which explains why adjustment disorders tend to be self-limiting conditions.
Conceptually, however, it is possible to envision chronically unsatisfactory life situations that might lead to chronic demoralization.[ 12] Such a "chronic adjustment disorder"--that one might also label a state of "chronic reactive depression"--is nonetheless a contradiction in terms. The question one would raise is why the individual elected to stay in that situation or felt unable to abandon it. This brings the concept of personality vulnerability that prevents an individual from taking adaptive action. Sometimes the concept of "masochism" is invoked to explain why certain individuals are unable to rid themselves of painful life situations, the implication being that they somehow contribute to their maintenance. This paper has a descriptive focus and discussion of a putative masochistic personality type[ 13-14]--based on metapsychological constructs--is beyond its purview. Suffice it to mention that at least some of the "self-defeating" traits believed to be indicative of masochism appear to be situation-specific, and tend to resolve with the elimination of the situation.[ 15]


Mixed anxiety-depressive states[ 16] acknowledge the simultaneous occurrence of anxious (e.g., the threat loss represents) and depressive (e.g., the despair of loss) cognitions when faced with a major aversive life situation. The admixture implies that the progress of psychopathology is from anxiety to depression, the patient's mental state is still in flux, and this ongoing dynamics in part explains the subacute or chronic nature of the disorder. This term is not an official diagnostic rubric, but it serves to point to the almost universal presence of anxiety in depressive states, and especially its greater visibility when the depression is less prominent, i.e., "milder."
Wolpe,[ 17] a pioneer in behavior therapy, argues that neurotic depression arises as a maladaptive response to anxiety and, on this etiologic ground, suggests retaining the neurotic depressive rubric.


"Neurasthenia," a century-old term developed by the American neuropsychiatrist Beard,[ 18] refers to a more chronic stage of anxious-depressive symptomatology. The anxiety generated by overstimulation is so excessive that it is replaced by a chronic disposition to fatigue, especially mental fatigue. It is, as it were, the sufferer's mind refused to take on new stresses.
Although this term today is more used in China than in the United States,[ 19] the recent popularity of the concept of chronic-fatigue states (152 articles indexed in Medline Search for 1990-91 alone at this writing) attests to the clinical acumen of classic physicians. Despite much energy invested on a viral etiology, current evidence[ 20-21] tends to support an affective origin for this syndrome. However, why in some individuals depression manifests primarily in fatigue is as elusive as it was 100 years ago.


This rubric[ 22-24] captures this sense of fatigue--superimposed on past history of somatic anxiety and phobias--together with reverse vegetative signs (mood worse in the evening, insomnia, tendency to oversleep and overeat). Because nighttime sleep is disturbed in the early part of the night, irritability, hypersomnolence, and daytime fatigue represent expected daytime stigmata of sleep deprivation.[ 25]


The term "hysteroid dysphoria," originally coined by Donald Klein who subsequently co-authored a classic paper on it,[ 26] emphasizes the foregoing features of atypical depressions plus the following characteristics that specifically represent contributions by his research team at Columbia: 1) giddy responses to romantic opportunities, and an avalanche of dysphoria (angry-depressive, even suicidal responses) upon romantic disappointment; 2) impaired anticipatory pleasure, yet perfectly capable of responding with pleasure when such is provided by others, i.e., preservation of consummatory reward; 3) craving for chocolate and sweets, which contain phenylethylamine compounds and/or sugars believed to facilitate cellular and neuronal intake of the amino-acid 1-tryptophan, leading hypothetically to the brain's synthesis of endogenous antidepressants. Interestingly, the use of the epithet "hysteroid" was meant to convey that what appeared to be character pathology was in reality secondary to a biologic disturbance in the substrates governing affect, drives, and reward.


This clinical colloquialism[6] is the final nosologic concept to be considered. It refers to patients with low-grade depression with intermittent fluctuating chronic course, thereby forming part of the sufferer's habitual self, such that it cannot be distinguished from his or her character structure. The characterologic pathology is variously believed to represent an admixture of dependent, avoidant, passive-aggressive, histrionic, narcissistic, and borderline features. For many authorities these features represent the core pathology of neurotic depressions; curiously there appears to be broad consensus on this point among authorities of both psychodynamic[ 27-29] and neo-Kraepelinian[ 30, 31] persuasion. Parker et al.[ 32] have expressed this position most eloquently in their inability to develop a clinical typology of neurotic depression that excludes personality variables. What remains unresolved is the origin of the personality pathology. Winokur would argue that it is related--possibly genetically--to antisocial and related personality disorders in their first-degree relatives, many of whom also suffer from alcoholism. However, the Copenhagen adoption study of alcoholism[ 33] suggests an environmental factor--i.e., being raised by an alcoholic parent--to be responsible for the pathologic depression-related character traits. The University of Tennessee study,[ 6] which demonstrated heterogeneity in characterologic depressions, tends to support the latter position for some, and an affective temperamental origin--to be elaborated later in this paper--for others.


DSM-III replaced the term "neurotic depression" with "dysthymic disorder" as a more accurate reflection of the long-standing pathology which predisposes to depression. At the same time, it classified the disorder under mood disorders based on emerging evidence that the character pathology itself reflected a more basic affective dysregulation.[ 9]
Shifting low-grade depressive pathology from the general category of neurosis to that of mood disorder represents a radical departure from traditional nosology. It was in part based on prospective outcome in 100 neurotic depressive[ 4] that demonstrated a recurrent unipolar or bipolar disorder in as many as 40 percent of neurotic depressives, 3 percent mortality from suicide, and overall unfavorable social outcome in 60 percent (Table I). This and related considerations necessitated reclassifying many neurotic depressions as major depressive or atypical bipolar disorders (atypical bipolar refers to the bipolar II sub-type characterized by major depressive episodes and non psychotic elations). There was a consequent need to create the rubric of "dysthymia," also subsumed under mood disorders, for the remaining cases of neurotic depression that pursued a low-grade intermittent or chronic course. These changes represent more than a revision; they counter a widespread clinical stereotype that equates protracted depressions with character pathology.
Dysthymic disorder in DSM-III subsumed all chronic depressions of two or more years. In DSM-III-R, low-grade depressive states following major depressive episodes are distinguished from dysthymia proper, a disorder of insidious onset, low-grade severity and chronic course. Although the dysthymic category in DSM-III-R can occur as a secondary complication of other psychiatric disorders, the core concept of dysthymia[10] refers to a primary mood disorder--with the following characteristics: low-grade chronicity--for at least two years--which is not sequel of a major depression; insidious onset with origin often in childhood or adolescence; persistent or interrmittent course; concurrent "character" pathology; and ambulatory disorder not incompatible with relatively "stable" functioning. This stability though is precarious at best; recent data from a series of studies summarized by Cassano et al.[34] have documented that many of these patients invest whatever "energy" they have in work, with none left for leisure and other family or social activities; hence the marital friction so characteristic of their colorless lives that appears to be one of overdedication to work. These empirical findings on the dysthymics' "work-orientation" echo earlier formulations on the melancholic personality by Tellenbach,[ 35] who was himself undoubtedly influenced by Kraepelin's[ 36] description of the depressive temperament:
Life with its activity is a burden which they habitually bear with dutiful self-denial without being compensated by the pleasures(s) of existence.
Chronicity does not imply presence of symptoms on a daily basis; intermittent symptoms are quite common. Furthermore, it is noteworthy that in DSM-III-R personality disorder is considered to be present concurrently with dysthymia. This is an important change from DSM-III which, despite its philosophy of considering personality disorders (Axis II) as orthogonal to the major psychiatric syndromes (Axis D, contained the ambiguous statement that "often the affective features of [dysthymia] are viewed as secondary to an underlying personality disorder." Clinicians who subscribe to the earlier DSM-III conceptualization would generally assume that the proper management of dysthymia requires major psychotherapeutic effort in altering the pathological character structure. The skeptics who prefer the newer DSM-III-R conceptualization, do not have the same degree of confidence in the necessity of a long-term investment in such effort; on the contrary, they point to evidence on the efficacy of thymoleptics[ 6, 37, 38] in attenuating not only the affective symptoms, but possibly, reversing much of the interpersonal disturbances.[ 39]


Unlike its precursors, DSM-III-R dysthymia is not defined as an etiologic construct; thus, neither anxiety and related neurotic conflicts, nor character pathology are necessary for its definition. Instead, dysthymia is operationally defined as a chronic subsyndromal depression. As formulated elsewhere,[ 10] insidious onset of depression dating back to late childhood or teens, preceding any superimposed major depressive episodes by years, or even decades, represents the most typical developmental background of dysthymia in DSM-III-R Return to the low-grade depressive pattern is the rule following recovery from superimposed episodes, if any; hence the designation "double depression."[ 40] Dysthymic patients often complain of being depressed "since conception" or of "feeling depressed all the time."[ 6] They also seem to view themselves as belonging to "an aristocracy of suffering."[ 41] These descriptions of chronic depression in the absence of observed signs of melancholia earn patients the label of "characterological depression." The fluctuating depressive picture often merges imperceptibly with that of major depression,[ 42] and the consequent difficulty of separating the fluctuating course of depression from the patient's personality gives rise to diagnostic uncertainties.
Such difficulty notwithstanding, it has been possible to delineate the symptom profile of dysthymic patients with sufficient precision[ 10] (Table II). The symptomatic picture obviously overlaps with that of major depression, but differs from it in that symptoms outnumber signs (more "subjective" than "objective" depression). Thus, marked disturbances in appetite and libido are uncharacteristic and severe psychomotor agitation or retardation are absent. All of this translates into a depression which is less intense in its symptomatic picture. A related feature that distinguishes it from major depression is lack of sharp demarcation from the sufferer's usual self. If the change from "dysthymia" to "major depression" occurs gradually, which is often the case, dysthymia should still be considered the basic disorder; in our opinion, only a precipitous fall into depression would qualify for a major depressive diagnosis. In other words, clinically, "double depressions" are more like dysthymia than episodic major depression, a conclusion supported by the recent findings of Klein et al.[43]
Although dysthymia manifesting the foregoing symptomatologic picture represents a more restricted concept than its parent neurotic depression,[ 4] it is still quite heterogeneous.[ 9] Anxiety is not a necessary part of its clinical picture, yet dysthymia is often diagnosed in patients with anxiety and neurotic disorders with sensitive-avoidant personality; such patients would typically meet the criteria of "atypical depression" as defined earlier, and might be classified under the DSM-III-R rubric of "secondary dysthymia." Another dysthymic variant is represented by patients with fluctuating lowgrade depressions associated with "histrionic-borderline" traits [44]; the occasional extraverted hypomanic-like behavior of these patients places them closer to bipolar II disorder. Strictly speaking, neither low-grade depressives with past or current indicators of anxiety, nor those with occasional extraverted or impulsive behavior fully meet the definition of classical primary dysthymia (i.e., dysthymia unexplained by another psychiatric disorder). This classic picture of dysthymia is that of an individual who is habitually gloomy, brooding, incapable of fun, and pre-occupied with inadequacy.[ 9] Dysthymia then is a chronic state of depressive anhedonia, so chronic that it can be considered a trait--in brief a "personality." Kurt Schneider[ 41] provided one of the most compelling descriptions of such a personality that has been put in operational terms at the University of Tennessee[ 9] (Table III).
To recapitulate, although dysthymia refers to a heterogeneity of lowgrade affective conditions, the core primary disorder[ 9, 10] is represented by intermittent or fluctuating subsyndromal depressive symptoms-with the obligatory presence of chronic anhedonia and related Schneiderian depressive personality traits.


Fifteen to 30 percent of patients with major mood disorders pursue a chronic course[ 45] (bipolar disorders usually at the lower range, and unipolar disorders at the upper range).[ 46] The chronicity rates obviously depend on the populations under study. Dysthymia and neurotic depression appear to have even more unfavorable outcome, with symptomatic chronicity and social disability occurring in up to 80 percent[ 40, 47]; reported completed suicide rates vary from 3 percent in the Memphis outpatient study[ 6] to 12 percent in the Munich inpatient study[ 47] of neurotic depressives. In community samples[ 2] 42 percent of low-grade depressives experience superimposed major depressive episodes; the corresponding figure in clinical populations[ 9, 40] is 85-90 percent. Furthermore, the onset of dysthymia occurs at a significantly younger age as compared with that of episodic major depression[ 6, 43] and pursues a chronic low-grade course punctuated by major episodes.
Family history in dysthymia has shown high loading for both unipolar and bipolar disorders in all studies that have examined it systematically.[ 6, 43, 48] These familial data support a strong kinship between dysthymia and major depressions, even hinting at greater familial-genetic loading in dysthymia. Not only the familial rates of mood disorders in dysthymia exceed those of major affective disorders without dysthymia, but significantly higher numbers of their first-degree relatives are hospitalized for mood disorders.[ 49] Higher concordance of neurotic depression in monozygotic twins[ 50] also suggests a hereditary component in the etiology of low-grade depressions. Sleep EEG data[ 6, 51, 52] further suggest that early-onset dysthymia and neurotic depression share with major (and endogenous) depressions the same neurophysiologic abnormalities such as short REM latency. This marker is present following recovery from depressive illness,[ 53] and may even be present before the overt onset of the illness as judged by examination of sleep records in the "well" relatives of affectively ill probands.[ 54] In brief, phase advance of circadian rhythms appears to characterize depressive illness throughout its course, including relatively asymptomatic subsyndromal phases.
Although psychodynamically oriented psychotherapy is probably the most common approach in treating the spectrum of characterologic depressives, [28] recent trends, beginning with the systematic Tennessee study published in 1980,[ 6] have supported the efficacy of a variety of thymoleptic medications in these patients often deemed "intractable." Indeed, the reader who has not followed these new trends may be surprised to learn of a large number of double-blind studies demonstrating efficacy of such medications in low-grade depressive conditions.[ 38] Sleep deprivation[ 55] too, appears useful in selected patients, though it must be avoided in those with concurrent panic and anxiety which is typically made worse by sleep loss.[ 4, 56] It is of both clinical and theoretical interest that hypomanic responses occur in about 10 percent of dysthymic patients treated with antidepressants.[ 6] Hypomania has also been reported during the prospective course of double-depressives compared with episodic major depressives,[ 43] as well as in dysthymic children prospectively followed through puberty.[ 57] Finally, dysthymia has been observed in the children of both unipolar[ 58] and bipolar probands.[ 59] These findings suggest that some dysthymics share the cyclic nature of cyclothymia.[79] This latter sub-bipolar form of dysthymia is best viewed as a series of brief minidepressions that either coalesce together, or cycle into major depression or hypomania (giving rise to the bipolar II picture discussed earlier).[ 44] It is in these patients often from a bipolar familial background--that a trial of lithium, given empirically in the Tennessee study[ 6] is most likely to be beneficial either as monotherapy or as "augmentation. "
Despite such progress in the treatment of dysthymic disorders, their response tends to be suboptimal.[ 60] Therefore, it should not come as a surprise that followup data[ 40, 47-49, 61-64] on dysthymic and related conditions have uniformly shown low rates of recovery and high rates of combined dysthymic-major depressive morbidity often extending over decades (Table IV). Likewise, long-term outcome in neurotic depression[ 65, 66] appears to be nearly as poor as in psychotic depression. Although ability to work per se might not be impaired, the chronic anhedonia of these patients robs their families of leisure activities, and their constant gloominess gives rise to longstanding marital conflicts.[ 34] Clinicians and researchers who consider dysthymic and related conditions as "minor" have either observed them over the short-term, or have selectively focused or treated those few with more favorable outcome. It is of course expected that treatment impacts positively on some of these patients, but naturalistic outcome is reported to be unfavorable in so many studies that one must conclude that the term "minor" represents a gross underestimation of the severity of the lifelong illness in many of its sufferers presenting for psychiatric treatment. Conceivably, the illness is milder in dysthymics in the community and those seeking advice from primary care physicians, but substantive data on their course and outcome in these settings are presently unavailable.
It would appear that dysthymia represents one of the substrates from which the more visible "major" episodes of affective illness erupt.[ 9, 10] Thus, trait and state seem to merge imperceptibly.[ 65, 66] Although conventional thinking would make a personality disorder out of the dysthymia underlying many major depressions, the considerations reviewed here suggest that the two are alternative manifestations of the same pathogenic process involved in the origin of mood disorders.[ 67-69]


Reviewing the recent literature on the overlapping spectrum of neurotic depressive and dysthymic conditions--unofficially referred to as "minor," "atypical" or "characterologic" depressives--the authors conclude that significant symptomatologic admixtures with anxiety disorders do not represent the prototypical features of these disorders as defined in DSM-III-R It is long-standing anhedonia on an intermittent or chronic basis which appears to characterize the trait illness of dysthymia. The emerging data on dysthymia suggest that it begins early in life, is often complicated by major depressions, and pursues a chronic--often pernicious--course. The development of hypomanic switches during the prospective course of some of these patients further suggests some kinship to bipolar disorder.
Although traditionally conceived as being largely "psychogenic," familial data and selected biologic indices--especially in the area of sleep--and thymoleptic responsiveness impart some credibility to the role of biologic factors in the origin of these disorders. Given the high prevalence of dysthymic conditions in clinical practice, new research strategies on their causes are needed as a precondition for more rational treatment approaches.



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