Adult Dysthymia

Adult Dysthymia Melancholia, a word once used to describe a multitude of symptoms, has since been shoved aside by more clinical-sounding terminology (Taylor and Fink, 2006, p. 1-9). Melancholia is now referred to as depression, major depression, dysthymia, seasonal affective disorder, hypomanic episodes, brief recurrent depression, postpartum depression and several others. Some may even conjure a terrifying image for laypersons, such as double depression.

This multitude of terms is intended to help clinicians determine both the possible causes of the condition and the best ways to intervene and for researchers to establish common diagnostic criteria so that empirical data from different studies can be compared, but there can also be considerable functional overlap between these classifications. These diagnostic distinctions may therefore have more to do with the descriptive needs of clinicians and researchers, rather than distinct neurochemical and cognitive mechanisms.

A small library could be filled with information about melancholia, so it is impractical to write a detailed review of this topic in a relatively short essay. However, since there is considerable overlap between the many forms depression takes, choosing one classification should provide a good view of melancholia as a whole. Towards this goal, adult dysthymia will be reviewed here in detail, both to provide insight into melancholia generally and to dissect a specific form of depression.

Defining Adult Dysthymia Dysthymia and major depression represent the two most common forms of melancholia, with dysthymia representing a milder and longer lasting form (Harvard Health Publications, 2012). The current clinical definition is an almost daily experience of sadness lasting for at least two years (Taylor and Fink, 2006, p. 100). If dysthymia should emerge during childhood, the main symptom could be irritability, rather than sadness (American Psychiatric Association, 2000, p. 376).

People suffering from dysthymia often experience bouts of major depression as well, which gave rise to the term 'double depression.' The clinical diagnostic criteria for dysthymia includes a period of duration lasting for 2 years in adults or 1 year in children, and sadness together with two of the following: poor appetite or overeating, insomnia or hypersomnia, fatigue, low self-esteem, poor concentration or decision-making, and feelings of hopelessness (American Psychiatric Association, 2000, p. 376).

Other symptoms that could emerge include feelings of inadequacy, apathy, inability to experience pleasure, social isolation, feeling guilty, brooding about the past, irritable, angry, and decreased activity or productivity. In addition, the patient cannot be symptom free for more than two months and the initial 2-year period must not co-occur with a major depressive episode, although approximately 75% of patients with dysthymia will eventually experience a major depressive episode within 5 years.

Another distinguishing feature of patients with dysthymia is that in comparison to patients with major depression, they often present with personality disorders (Axis II). Another term used interchangeably with dysthymia is neurotic depression. Neurosis is defined as feelings of distress and anxiety sufficient to impair everyday functioning, but not due to psychosis (Encyclopedia of Mental Disorders, 2012). In other words, people who suffer from neurotic depression live within the real world, but experience persistent sadness and anxiety due to an internal conflict.

Regardless of whether this condition is called dysthymia or neurotic depression, it is important to remember that the symptoms are invariably severe enough to interfere with the sufferer's ability to negotiate their life and take care of their own needs. The Historical Origins of Dysthymia and the First Cases The Greek derivation of the word dysthymia means, "bad state of mind" or "ill humor" (Harvard Health Publications, 2012).

Hippocrates (460-377 BC) defined melancholia as phobia combined with dysthymia (bad mood), so this word and the associated mood disorder has a long historical record (Brieger and Marneros, 1997, p. 118). The modern use of the word can be traced to Carl Friedrich Flemming (1799-1880), who founded the first successful psychiatric journal in Germany in which he distinguished between disorders of the intellect, mood (dysthymia), and mood plus intellect.

At the turn of the 20th century, the term dysthymia fell out of popular use, as the classification system developed by Kraepelin became popular (Brieger and Marneros, 1997, p. 120). Even though use of the term may have faded, there is little doubt that Kraepelin and his contemporaries were well aware that dysthymia represented a distinct form of melancholia that is easily recognizable using current diagnostic criteria.

It was not until 1979, with publication of the third version of the American Psychiatric Association's Diagnostic and Statistical Manual that the term dysthymia was again popularized (Taylor and Fink, 2006, p. 8). The proposed 5th edition of the Diagnostic and Statistical Manual will replace dysthymia with "Chronic Depressive Disorder (Dysthymia)" (American Psychiatric Association, 2012). The primary subcategories will be early and late onset, which will be used to indicate whether the first episode began before or after the age of 21, respectively.

The rationale behind this change is the overwhelming evidence that laboratory measures, disease course, outcome, and family history are not significantly different between major depression and dysthymia. Dysthymia is therefore increasingly viewed as a chronic version of major depression, requiring the same or similar treatment approaches. Consistent with this change, the 'chronic' modifier for major depression will be eliminated and these patients will be diagnosed as having chronic depressive disorder (dysthymia). Etiology The vast majority of patients develop dysthymia during adolescence or early adulthood (Kocsis, 1998, p. 13-14).

Early onset tends to be associated with personality disorders, but onset during late adulthood is associated with significant adverse life events. Older dysthymic patients also have fewer comorbid mental conditions (10% versus 50%) and fewer episodes of major depression (20% versus 80%). Dysthymia in older adults (> 50 years of age) appears to be unrelated to early onset dysthymia, since the mean duration of this condition in geriatric patients was just 12.5 years.

The close association of early onset dysthymia with personality disorders was confirmed in a recent study, which found a significant association between schizotypal signs and dysthymia (p < 0.0001) (Rossler et al., 2011, p. 20-21). Some of the criteria for schizotypal signs included blaming others for personal problems, generally untrusting of others, feeling watched, having thoughts others do not share, feeling marginalized and exploited, and unable to feel comforted by the company of others.

In adolescents or young adults, the primary causative factor may be internal (neurotic) conflicts that lead to feeling uncomfortable in their own skin (Akiskal and Cassano, 1997, p. 5). This anxious type of depression can often be traced to the emergence of self-defeating traits and is consistent with the theory that this type of dysthymia may represent a neurotic or anxious for of depression.

In contrast, researchers have found that dysthymia in older adults (> 50 years of age) may have arisen due to the onset of major medical illnesses, such as cardiovascular disease, and therefore represents primarily a reactive form of depression (Kocsis, 1998, p. 14). There does appear to be a significant genetic component to melancholia as well, although it is uncertain to what degree disease severity or its prevalence is determined by a shared environment or genetic predispositions.

A recent study examined how often monozygotic or dizygotic twins developed the same unipolar depressive conditions (Edvardsen et al., 2009). The concordance ratio between monozygotic and dizygotic twins, when dysthymia was included in the analysis, was found to be 1.87, which suggests that monozygotic twins are 25.7% (p = 0.002) more likely to develop depressive symptoms than dizygotic twins. Genetic susceptibility would therefore explain 26% of dysthymia prevalence and environmental factors would account for the other 74%.

Epidemiology Dysthymia is a common form of depression and an estimated 6% of the population will develop this condition within their lifetime (American Psychiatric Association, 2000, p. 376). At any one time, approximately 3% of the population is suffering from dysthymia. Women are three times more likely to have dysthymia during their adult years, but this gender difference is absent in children with dysthymia. A Case Study Since the vast majority of dysthymia patients develop symptoms during childhood, case studies of adult dysthymia patients are rare, but not impossible to find.

A 28-year-old unmarried, bicultural (Mexican mother/Palestinian father) native-born American male, enrolled in law school for 3 years, presented with complaints of depression lasting for more than 2 years and frequent negative self-directed verbalizations (Elligan, 1997). A family history showed that his mother was unemployed and his father worked part-time as a garbage man. His two younger siblings have also been successful in college and the patient claims he is proud of their accomplishments.

There is a possibility the father suffers from schizophrenia, yet the patient began to experience symptoms only after beginning law school. The stress of graduate school and interactions with faculty and staff from a much higher socioeconomic standing seems to be the precipitating events, which is consistent with a theory of reactive depression. What motivated the patient to seek mental health services was the feeling that the self-directed negative comments were self-destructive and interfering with his ability to function socially and at school (Elligan, 1997).

The self-directed verbalization generally consisted of statements like "I hate myself" and the patient would inevitably feel more depressed afterwards and withdraw socially. The self-directed verbalizations also increased the level of anxiety being experienced, to such a degree that the threat of encroaching insanity was constantly on his mind. The treating clinician diagnosed dysthymia and a psychotherapeutic intervention was prescribed.

Having grown up in a working class, minority neighborhood in Baltimore, Maryland the patient found it difficult to interact with the predominantly white, and relatively wealthy, law students and faculty at the Washington DC law school he was attending (Elligan, 1997). This cultural 'shock' was understood to be the primary contributing factors to the patient's condition. Previous unfruitful interactions with a White psychotherapist suggested the patient might benefit from working with a therapist of color having a similar socioeconomic background as the patient.

Session topics included establishing a relationship with a professor of color at the law school and professional Hispanic mentors in the Washington DC area, seeking out and fostering relationships with other students he felt comfortable with, and developing a supportive social network apart from school. The therapist was able to share personal experiences of racist attitudes at academic institutions, which helped the patient feel free to discuss the anti-Palestinian sentiments expressed by several of the law faculty he had interacted with.

The patient reported feeling 'empowered' after making considerable progress towards these goals. After three weeks of supportive therapy, a cognitive-behavioral assessment was performed to identify the precise factors that triggered the self-loathing episodes (Elligan, 1997). A diary was maintained by the patient for four weeks, which revealed morning interactions with White students and professors were the primary triggers. A treatment approach was devised that relied heavily on mindfulness techniques to reduce overall stress and to restructure negative though processes.

The diary was again used to track progress and after 11 weeks, the 3-times daily negative self-directed statements were eliminated and remained absent from the patient's life for at least two months. The intervention for this dysthymic patient was based on the assumption that it represented a reactive depression. Understanding the historical events that led to developing dysthymia was an important part of the treatment regimen, yet the use of mindfulness techniques, improved coping skills, and adverse cognitive habit restructuring could have still been used without this history.

Pharmocological intervention was unnecessary, probably because the depressive symptoms were so responsive to psychotherapy. Treatment Chronic depression is currently classified as dysthymia, double depression, chronic major depression, or recurrent major depression with incomplete remission between episodes (Kriston, von Wolff, and Holzel, 2010, p. 1). These patients tend to suffer from worse treatment outcomes, tend to be resistant to pharmacological interventions, are frequently hospitalized, and commit suicide more often than patients with major depression.

The most common form of dysthymia encountered in the clinical setting is double depression, rather than pure dysthymia (Akiskal and Cassano, 1997, p. 13-14). The clinical bias against pure dysthymia exists because the symptoms of pure dysthymia tend to be subtle enough to remain undetected by both the sufferer and their primary care physician, and therefore remains untreated unless major depressive symptoms develop. Current treatment guidelines recommend first ruling out an underlying medical or substance abuse problem (National Institute of Mental Health, n.d.).

If dysthymia is eventually diagnosed, patients may be prescribed any of a number of antidepressant medications, such as Prozac, Zoloft, Paxil, Luvox, Celexa, Lexapro, Wellbutrin, tricyclic antidepressants, and monoamine oxidase inhibitors (PubMed Health, 2012). Psychotherapy may also be prescribed and consist of cognitive behavioral therapy, psychodynamic therapy, and/or a dysthymia support group. The most effective intervention has been shown to be a combination of both psychotherapeutic and pharmacological (Kriston, von Wolff, and Holzel, 2010, p. 2; PubMed Health, 2012).

Prevention If dysthymia for a particular person was triggered by a significant adverse life event (reactive depression) there is not much that can be done to prevent this from occurring; however, those impacted should be closely monitored for the development of subclinical.