The term ‘dysthymia’ (meaning ‘bad mood’) originated in classical Greek and is still in current use in that country with the same connotation.
In the Hippocratic School, it was considered as part of the broader concept of melancholia (meaning ‘black bile’). A temperament predisposed to melancholia was also delineated, and referred to individuals who were lethargic, brooding, and insecure. It was not until the early nineteenth century that dysthymia was reintroduced into medicine by the German physicians, Stark and Fleming to describe depressions in inpatients that pursued a chronic course.⁽¹⁴⁾ Eventually, dysthymia came to subsume all mood disorders. The major residue of dysthymia in the latter sense in Europe today is the French rubric of les dysthymies, as a synonym for troubles de l’humeur; the DSM-IV or ICD-10 ‘dysthymic disorder’ in that country is translated as le trouble dysthymique.

The more direct lineage of our current usage of the term dysthymia is to be found in the latter part of the nineteenth century in the work of Kraepelin, who delineated the depressive disposition as one of the constitutional foundations of affective episodes. The condition often began early in life, such that by adolescence many showed an increased sensitivity to life’s sorrows and disappointments: they were tormented by guilt, had little confidence in their abilities, and suffered from low energy. As they grew into adulthood, they experienced ‘life with its activity [as] a burden which they habitually [bore] with dutiful self-denial without being compensated by the pleasures of existence’. In some, these temperamental peculiarities were so marked that they could be considered ‘morbid without the appearance of more severe, delimited attacks …’ (clearly foreshadowing the modern concept of trait dysthymia). In other cases, recurrent melancholia arose from this substrate without definite boundaries (again anticipating the concept of ‘double-depression’).

Subsequently, Kurt Schneider in his opus Psychopathic Personalities devoted considerable space to a depressive type whose entire existence was entrenched in suffering. Building on this rich phenomenological tradition, our research in Memphis⁽¹⁵⁾ helped in operationalizing the core characteristics of such patients encountered in contemporary practice: gloomy, sombre, and incapable of having fun; brooding, self-critical, and guilt-prone; lack of confidence, low self-esteem, preoccupation with failure; pessimistic, easily discouraged; easy to tire, sluggish, and bound to routine; non-assertive, self-denying, and devoted; shy and sensitive. These traits have excellent internal consistency and discriminatory ability.⁽¹⁶⁾ Similar concepts have also appeared in the Japanese literature,⁽¹⁷⁾ with particular emphasis on self-critical attitudes, persistence in work habits, and devotion to others. Finally, the French construct of la depression constitutionelle⁽¹⁸⁾ has emphasized the lethargic aspects with a sense of inadequacy. A self-rated scale in all of these languages⁽⁸⁾ now can assist in reliable and valid assessment of depressive temperament traits.

The classical tenet in psychiatry has been that affectively ill patients recover from their acute episodes with relatively little symptomatic residua and dysfunction. Community psychiatry, which has given renewed visibility to the temperamentally expressed low-grade fluctuating depressive disorders, has challenged this classic view. With the advent of DSM-III, such patients are now officially designated as ‘dysthymic.’ In the ICD-10 classification, the low-grade depressive baseline is considered the main pathology; only an occasional superimposed depressive episode is permitted, provided that it is mild. In DSM-IV, at least two patterns have been described: pure dysthymia uncomplicated by major depression and a more prevalent pattern of dysthymia complicated by major depressive episodes that could be even moderate or severe in intensity (and which has been dubbed ‘double depression’).

The mystery of this incapacitating depressive subtype—long recognized, but only recently sanctioned in official diagnostic manuals—is that, in their habitual condition, sufferers lack the classical ‘objective’ or ‘major’ signs of acute clinical depression, such as profound changes in psychomotor and vegetative functions. Instead, patients consult their doctors for more fluctuating complaints consisting of gloominess, lethargy, self-doubt, and lack of joie de vivre; they typically work hard, but do not enjoy their work; if married, they are deadlocked in bitter and unhappy marriages which lead neither to reconciliation nor separation; for them, their entire existence is a burden: they are satisfied with nothing, complain of everything, and brood about the uselessness of existence. As a result, in the past those who could afford it were condemned to the couch for what often proved to be interminable analysis. The legitimization of dysthymia as a clinically significant variant of affective disorder in both the United States and WHO classifications has helped the cause of more cost-effective treatments.

To sum up, for nearly 2500 years physicians have described individuals with a low-grade chronic depressive profile marked by gloominess, pessimism, low enjoyment of life, relatively low drive, yet endowed with self-critical attitudes and suffering for others.⁽¹⁹⁾This constellation is as much a virtue as it is a disposition to melancholy, and many dysthymic patients presenting clinically have various admixtures of major depression. This is compatible with a spectrum-concept of depressive illness, which defines various degrees of severity.

Diagnostic criteria for dysthymia in both DSM-IV and ICD-10 stipulate a two-year duration of low-grade depressive symptoms, exclusive of such indicators of severity as suicidality and psychomotor disturbances. Dysthymia is distinguished from chronic major depressive disorder by the fact that it is not a sequel to wellde fined major depressive episodes. Instead, patients often complain that they have always been depressed. Most are of early onset (less than 20 years). A late-onset subtype first manifesting after the age of 50 is much less prevalent and has not been well characterized clinically, but it has been identified largely through studies in the community.

At their best, dysthymic individuals invest whatever energy they have in work, leaving none for leisure or social activities. According to Tellenbach, such dedication to work represents overcompensation against depressive disorganization. Kretschmer had earlier suggested that such persons were the ‘backbone of society,’ devoting their lives to jobs that require dependability and great attention to detail. These features represent the obsessoid facet of dysthymia. Such individuals may seek outpatient counseling and psychotherapy for what some clinicians might consider ‘existential depression’: individuals who complain that their life lacks lustre, joy, and meaning. Others present clinically because of an intensification of their gloom to the level of clinical depression; history of lifelong lowgrade
depressive symptoms would distinguish them from episodic major depressive patients.

The proverbial dysthymic patient will often complain of having been ‘depressed since birth’. In the eloquent words of Kurt Schneider, “they view themselves as belonging to an ‘aristocracy of suffering”. These hyperbolic descriptions of suffering in the absence of more objective signs of depression earn such patients the label of ‘characterological depression’. The description is further reinforced by the fluctuating depressive picture that merges imperceptibly with the patient’s habitual self, leading to the customary clinical uncertainty as to whether dysthymic disorder belongs to the affective or personality disorder domains.

At their worst, patients with low-grade depression having an intermittent course can present such instability in their life, including suicidal crises, that some clinicians would entertain the diagnosis of borderline personality disorder. This is not consistent with the classic picture of dysthymia arising from a temperamental type with more mature ego structure described above. Depressives with unstable (that is to say, ‘borderline’) personality structure more often belong to the irritable cyclothymic–bipolar II spectrum.

The greatest overlap of dysthymia is with major depressive disorder, but differs from it in that symptoms tend to outnumber signs (more subjective than objective depression). Thus, marked disturbances in appetite and libido are uncharacteristic, and psychomotor agitation or retardation is not observed. Nonetheless, subtle ‘endogenous’ features are not uncommonly reported: inertia, lethargy, and anhedonia that are characteristically worse in the morning. Because many patients with dysthymia presenting clinically fluctuate in and out of a major depression, the core DSM-IV criteria for dysthymia tend to emphasize vegetative dysfunction, whereas the alternative criterion B for dysthymia in a DSM-IV appendix lists cognitive symptoms; although the latter appear more characteristic of trait dysthymia, the DSM-IV field trial could not demonstrate their specificity for dysthymia.

A Milan-San Diego collaboration of a large sample from community and primary-care medical settings revealed that negative mood (by definition), along with low energy, poor concentration, low self-esteem, sleep and appetite disturbance, and hopelessness (in descending order) were the most common symptoms of dysthymia. These data suggest that the cognitive and somatic symptoms are not easily separable in practice. None the less, this study did raise the possibility that factors could be discerned along two different axes: ‘negative affectivity’ and ‘lassitude with poor concentration’. In our experience, patients loading on the latter factor often complain of hypersomnia and may exhibit subtle bipolar signs; alternatively, they might have some link to the poorly defined constructs of neurasthenia, chronic fatigue syndrome, and fibromyalgia. In terms of differential diagnosis, patients with chronic fatigue syndrome present with disabling fatigue and, typically, deny depressive symptoms; patients with fibromyalgia complain of pain; by contrast, the typical patient with dysthymia cannot stop relating to the physician his or her litany of depressive symptoms. Polysomnography, though not yet definitive, may shed some light on differentiating fibromyalgia from dysthymia proper.

Although dysthymic disorder represents a more restricted concept than does its parent, neurotic depression, it is still quite heterogeneous. Anxiety is not a necessary part of its clinical picture, yet dysthymia is sometimes diagnosed in patients with anxiety and neurotic disorders. That clinical situation is perhaps to be regarded as a secondary or ‘anxious dysthymia’ or, as some British authors seem to prefer, as part of a ‘general neurotic syndrome’ (an implicit partial return to the now defunct concept of neurotic depression).

The clinical picture of dysthymic disorder that emerges from the foregoing descriptions is quite varied, with many who fluctuate in and out of major depression, whereas in others the pathology is woven into the habitual self. Prospective follow-up supports a continuum between temperament, dysthymia and major depression. These considerations suggest that a clinically satisfactory operationalization of dysthymia must include both symptoms and trait characteristics (Table 4.5.9.1). The following vignette illustrates this more prototypical form of dysthymic suffering.

Case Study: This 37-year-old never-married male teacher presented with the complaint that he was ‘tired of living’ and was considering ‘ending it all’. He said that much of his life had been ‘wasted’, he had never known any joy, and that all human existence for him was a ‘tragic mistake of God’. He was known to be a dedicated and talented teacher, but he felt all his efforts had been ‘useless and in vain’. He said he probably was ‘born depressed’, because he had not known any happiness and that the only utility he could have for mankind was ‘to serve as a specimen to be researched—to shed light on human misery’. Although he conceded that some women found him interesting, even intellectually stimulating, he said he could not enjoy physical intimacy, that even orgasm lacked passion; nonetheless, he masturbated frequently, fantasizing about married female teachers—only to feel guilty. We could not document any major affective episodes. He stated that he had always functioned at a ‘mediocre level’ (which was at variance with the good feedback students had given him year after year); but did admit he ‘appreciated work, because there was nothing else to do’. He denied alcohol and drug habits. There had never been any periods of hypomania, but one of his maternal aunts had been treated for a ‘cyclical depression’ and was apparently doing well on lithium. The patient’s mother was a sombre serious work-oriented woman who had raised three children and had done voluntary work for the church, but had no depressive complaints. His father had died from a coronary attack, but his side of the family was otherwise unremarkable.

Although both DSM-IV and ICD-10 omit suicidal preoccupations in their diagnostic criteria for dysthymia, as testified by the above case, this is what often brings patients to clinical attention.

An insidious onset of depression dating back to late childhood or the teens, preceding any superimposed major depressive episodes by years, even decades, is the most typical developmental
background of dysthymic disorder. A return to the low-grade depressive pattern is the rule following recovery from superimposed major depressive episodes, if any, hence the designation ‘double depression’.

Few studies have studied the phenomenology of dysthymia in childhood. DSM-IV does not seem to distinguish between childhood and adult dysthymia, yet current clinical experience indicates that the main symptoms in childhood dysthymia include irritability, low self esteem, fatigue, low mood, guilt, poor concentration, anhedonia, and hopelessness; as in adults, comorbid anxiety disorders were prevalent; suicidality was more common in adolescents. These findings should be useful in dysthymic children in future studies. A long-term prospective Pittsburgh study of prepubertal children has revealed an episodic course of dysthymia with remissions and exacerbations, and eventual complication by major depressive episodes, as well as hypomanic, manic, or mixed episodes postpubertally. Persons with dysthymic disorder presenting clinically as adults tend to pursue a chronic ‘unipolar’ course, which may or may not be complicated by major depression: they rarely develop spontaneous hypomania or mania. However, when treated with antidepressants, some adult patients with dysthymia may experience brief hypomanic switches that typically disappear when the antidepressant dose is decreased. Although ICD-10 and DSM-IV would not ‘allow’ the occurrence of such switches in dysthymia, systematic clinical observation have verified their occurrence in between 10 and 30 per cent of dysthymic patients. In that special dysthymic subgroup, the family histories are typically positive for bipolar disorder. Such patients, often conforming to the double depressive pattern, represent a clinical bridge between major depressive disorder and bipolar II.

A 12-year NIMH prospective study has shown that patients with major depressive disorder spent 44 per cent of their course in low-grade depression (versus 15 per cent of time in major depressive episodes). This suggests that major depression, dysthymia, or otherwise subsyndromal depression constitute somewhat artificial conventions on the threshold and duration of depressive illness, representing alternative manifestations of the same diathesis. In this context, residual intermorbid depressive symptoms have been confirmed as being strongly predictive of a rapid relapse into a new major depressive episode. Various ‘major’ and ‘minor’ depressive conditions described in DSM-IV and its appendix must not be viewed as distinct depressive subtypes, but part of a symptomatic continuum. Fig. 4.5.9.1 shows a diagram of these putative relationships within a broad depressive spectrum.

From 1966 to 1980, Index Medicus listed no more than 10 articles on chronic depressions. Since 1980, when dysthymia was first introduced in DSM-III, at least 500 articles have appeared on chronic depression, mostly on dysthymia. This phenomenal growth in research interest parallels the increasing public health significance of this disorder. It is estimated that 3–5 per cent of the world population is suffering from dysthymia. Like major depressive disorders, dysthymia is twice as common in women as in men. Because of its chronicity, dysthymia is among the most prevalent psychiatric conditions in clinical practice. Dysthymia is more disabling, as far as quality of life in social and personal areas, work, and leisure, than depression in the setting of a severe anxiety disorder like agoraphobia. Celibacy is also common in early-onset dysthymia, but not for long; modern successful treatments often lead to a change in marital status!

UCLA research in primary care has focused on depressive symptoms falling short of the major depressive threshold, as far as symptom intensity is concerned, as well as falling short of the two year duration criterion for dysthymia. Despite its chronicity, 50 per cent of people remain unrecognized by general practitioners. Despite the low-grade nature of their depressive complaints, these patients report high degrees of morbidity and impairment in a variety of health domains and quality of life, including ‘bed days’ (namely, the number of days per year they stayed ill in bed). Actually, these impairments are generally more pronounced than those of patients with a variety of medical conditions, such as hypertension, diabetes, arthritis, and chronic lung disease; only coronary artery disease exceeded the disability of low-grade depression in several domains. Stroke has recently been added on this list.

In light of the foregoing developments, both the World Psychiatric Association⁽²¹⁾ and the World Health Organization⁽²²⁾ have developed programmes to address the challenges of educating general practitioners in the proper recognition and treatment of dysthymia.

Some sensitivity to suffering, a cardinal feature of the depressive temperament, represents an important attribute in a species like ours, where caring for young and sick individuals is necessary for survival. This temperament, historically the Anlage of dysthymia, in the extreme often leads to clinical depression. The constitutional viewpoint, while dominant in the early part of the twentieth century, gradually disappeared from psychiatric thinking. One reason was that Kurt Schneider preferred to conceptualize such conditions as ‘psychopathy’, by which he meant abnormal personality development. Independently, Freud’s disciples took this one step further and, eventually in outpatients, all milder depressions with a tendency to chronicity came to be considered as the expressions of a character neurosis. In support for this position, these authors could point to the long-standing nature of the interpersonal difficulties in the lives of these individuals. When, and if, antidepressants were prescribed, they were given in homeopathic doses; worse, many patients received stimulants or benzodiazepines rather than genuine antidepressants. Failure to respond to these incorrectly chosen pharmaceutical agents seemed to further reinforce the notion of a ‘character’ defect.

Several lines of observation during the latter part of the 20th century have challenged the concept of ‘character neurosis’ as an explanation for low-grade depression, and thereby forced a return to the more classical European concept of temperament with its biological underpinnings. First, in a 1980 Memphis study of rapid eye movement (REM) latency (normally 90 min, measured from sleep onset to the first REM period) conducted in ‘depressive characters’ who were not in a state of major depression, we reported that REM latency was less than 60 min, and REM was redistributed to the early part of the night (which was the reverse of what we observed in chronic anxious patients). Moreover, a family history for major affective illness (including bipolar) was significantly high in short-REM latency patients. (The reverse was true for those with familial alcoholism and sociopathy.) The sleep findings were so reminiscent of those seen in major affective illness that we were compelled to give our patients systematic open trials with desipramine and nortriptyline (the best-tolerated secondary amine tricyclics in those days) or lithium carbonate if antidepressants failed (based on the observation of familial bipolar disorder in some). Nearly 40 per cent remitted, of whom one out of three developed brief hypomania. The sleep findings have been replicated in other laboratories. Furthermore, a Hungarian study has shown that patients with dysthymia experience transient lifting of their mood with sleep deprivation. Other studies have shown high rates of affective illness in a systematic familial investigation of dysthymic probands. There also exist dysthymic patients whose lifelong suffering and discontent appear, in retrospect, a legacy of an unsatisfactory childhood marked by deprivation or abuse at the hands of alcoholic and/or sociopathic parents or step-parents. Although it is clinically attractive to invoke the notion of ‘learned helplessness’ secondary to such inescapable childhood traumata, an alternative hypothesis is that the helplessness of these individuals might develop secondary to an inherited diathesis which biases these children’s early experiences in a dysphoric direction.

As for neuroendocrine markers, thyroid-releasing hormonethyroid-stimulating hormone challenge and electrodermal activity similar to those with major depressive disorders are the main findings; by contrast, dexamethasone suppression and catecholamine metabolism are essentially unaltered in dysthymia. These observations, along with the REM latency findings, suggest that dysthymia represents trait depression. Coupled with the family history data, this traitness can be postulated to be of constitutional origin. Certainly, the occurrence of major affective episodes in the longterm course of dysthymia, in both community and clinical samples, is in line with this position. It is, therefore, of great theoretical and practical significance that shortened REM latency has been reported in the offspring of the affectively ill. More recently a variety of other biological findings have been reported in dysthymia, further strengthening the link with major depression: low testosterone and adrenal-gonadal steroid levels,⁽²⁴⁾ neuro-immune abnormalities,⁽²⁵⁾ effects of prenatal maternal dysthymia on foetal growth,⁽²⁶⁾ as well as small genual corpus callosum volume⁽²⁷⁾ and enlarged amygdalar volume.⁽²⁸⁾ Coupled with s-allele polymorphism of the serotonin transmitter,^(29,30) that subthreshold depression, however defined, is not a ‘neurotic’ phenomenon in the traditional psychodynamic sense of the term, but part of the spectrum of depressive illness! Table 4.5.9.2 summarizes the foregoing links between dysthymia and major depressive disorder, and which support its inclusion within the family of mood disorders.

There are also exist medical and neurological factors that may contribute to dysthymic symptom formation. Actually, joint medicalneurological and non-affective psychiatric disease is often contributory to extreme refractoriness among the chronic depressive states of these patients. Such patients are at risk for suicide, especially those with epilepsy or progressive degenerative neurological disease. Interestingly, living with a medically disabled spouse or family member, too, can be associated with some chronicity of depression.

The emergence of pathogenetic understanding, as outlined above, is all the more impressive, given the controversies on the very nature of dysthymia and its legitimacy as a nosological entity.⁽³¹⁾