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|Classification and external resources|
|Classification and external resources|
Dysthymia (English pronunciation: /dɪs.ˈθaɪ.miː.ə/), also known as neurotic depression, dysthymic disorder, and chronic depression, is a mood disorder consisting of chronic depression, with less severe but longer lasting symptoms than major depressive disorder. The concept was coined by Dr. Robert Spitzer (an editor of the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders (DSM-III)) as a replacement for the term "depressive personality" in the late 1970s.
According to the DSM's definition of dysthymia, it is a serious state of chronic depression, which persists for at least 2 years; it is less acute and severe than major depressive disorder. As dysthymia is a chronic disorder, sufferers may experience symptoms for many years before it is diagnosed, if diagnosis occurs at all. As a result, they may believe that depression is a part of their character, so they may not even discuss their symptoms with doctors, family members, or friends.
Dysthymia has a number of typical characteristics: low drive, low self-esteem, and a low capacity for pleasure in everyday life. Mild degrees of dysthymia may result in people withdrawing from stress and avoiding opportunities for failure. In more severe cases of dysthymia people may even withdraw from daily activities. They will usually find little pleasure in usual activities and pastimes. Diagnosis of dysthymia can be difficult because of the subtle nature of the symptoms and patients can often hide them in social situations making it challenging for others to detect symptoms. Additionally, dysthymia often occurs at the same time as other psychological disorders, which adds a level of complexity in determining the presence of dysthymia, particularly because there is often an overlap in the symptoms of disorders.
There are no consistent or pervasive biological links to dysthymia. However, this may be a result of the diverse nature of the disorder. There are some links between dysthymia and possible causes however. "The rate of depression in the families of people with dysthymia is as high as fifty percent for the early-onset form of the disorder". This may indicate that there is some genetic predisposition to dysthymia. Other factors linked with the disorder include: stress, social isolation, or lack of social support.
"At least three-quarters of patients with dysthymia also have a chronic physical illness or another psychiatric disorder such as one of the anxiety disorders, cyclothymia, drug addiction, or alcoholism". Common co-occurring conditions include: major depression (up to 75%), anxiety disorders (up to 50%), personality disorders (up to 40%), somatoform disorders (up to 45%) and substance abuse (up to 50%). People with dysthymia have a higher-than-average chance of developing major depression. In a 10 year follow up study, it was found that 95% of dysthymia patients had an MDD episode.  When an intense episode of depression occurs on top of dysthymia the state is called "double depression."
Double-depression occurs when a person experiences a major depressive episode on top of the already-existing condition of dysthymia. It is difficult to treat as people accept these major depressive symptoms to be a natural part of their personality or as a part of their life that is outside of their control. Because people with dysthymia may accept these worsening symptoms as inevitable, it can delay treatment. If treatment is sought out, it is commonly treatment-resistant due to the fact that the major depressive symptoms are addressed, but often not the dysthymic symptoms. Hopelessness has been found to be a significant symptom of double-depression, with patients reporting higher levels of hopelessness. This can be a useful symptom for mental health services providers to focus on when working with the patient to treat the condition. Additionally, cognitive therapies can be effective for working with people with double-depression in order to help change negative thinking patterns and give individuals a new way of seeing themselves and their environment.
It has been suggested that the best way to prevent double-depression is by treating the dysthymia. A combination of antidepressants and cognitive therapies is thought to be helpful in preventing major depressive symptoms from occurring. Additionally, exercise and good sleep hygiene (e.g. improving sleep patterns) are thought to have somewhat of an additive effect on treating dysthymic symptoms and preventing them from worsening.
There is evidence indicating that there may be neurological indicators of early onset dysthymia. There are several brain structures (corpus callosum and frontal lobe) that are different between women with dysthymia and normal individuals. This may indicate that there is a developmental difference between these two groups.
Another study, which used fMRI techniques to assess the differences between individuals with dysthymia and other people found additional support for neurological indicators of the disorder. This study found several areas of the brain that function differently. The amygdala (associated with processing negative emotions such as fear) was more activated in dysthymia patients. The study also observed increased activity in the insula (which is associated with sad emotions). Finally, there was increased activity in the cingulate gyrus (which serves as the bridge between attention and emotion).
A study comparing healthy individuals to people with dysthymia indicates there are other biological indicators of the disorder. An anticipated result appeared as healthy individuals expected fewer negative adjectives to apply to them, whereas, people with dysthymia expected fewer positive adjectives to apply to them in the future. Biologically these groups are also differentiated in that healthy individuals showed greater neurological anticipation for all types of events (positive, neutral, or negative) than those with dysthymia. This provides neurological evidence toward the lack of emotion that individuals with dysthymia have compared to healthy people.
There is some evidence of a genetic basis for all types of depressions, including dysthymia. A study using identical and fraternal twins indicated that there is a stronger likelihood of identical twins both having depression than fraternal twins. This provides support for the idea that dysthymia is in part caused by heredity.
A new model has recently surfaced in the literature regarding the HPA Axis and its involvement with dysthymia (e.g. phenotypic variations of corticotropin releasing hormone (CRH) and arginine vasopressin (AVP), and down-regulation of adrenal functioning) as well as forebrain serotonergic mechanisms. Since this model is highly provisional, further research is still needed.
There is a common belief that low levels of the neurotransmitter serotonin play a central role in the development and course of affective disorders, dysthymia included. But, more recent research in the field of neuropsychology is trying to debunk this assumption based on the fact that there is no known scientific evidence to prove this as fact. The belief that low levels of serotonin contribute to the onset of depressive disorders is based on "backwards" reasoning, in that SSRIs have shown to improve depressed mood. Though this may be the case, it does not prove that serotonin, or any other sort of chemical imbalance is a cause of dysthymia. Further research is needed in this area, as no conclusive results have been found in the neurophysiological functioning of dysthymia.
The Diagnostic and Statistical Manual of Mental Disorders (DSM), published by the American Psychiatric Association, characterizes dysthymic disorder. The essential symptom involves the individual feeling depressed for the majority of days and parts of the day for at least two years. Low energy, disturbances in sleep or in appetite, and low self-esteem typically contribute to the clinical picture as well. Sufferers have often experienced dysthymia for many years before it is diagnosed. People around them often describe the sufferer in words similar to "just a moody person". Note the following diagnostic criteria:
In children and adolescents, mood can be irritable, and duration must be at least one year, in contrast to two years needed for diagnosis in adults.
Early onset (diagnosis before age 21) is associated with more frequent relapses, psychiatric hospitalizations, and more co-occurring conditions. For younger adults with dysthymia, there is a higher co-occurrence in personality abnormalities and the symptoms are likely chronic and may result from personality. However, in older adults suffering from dysthymia the psychological symptoms are associated with medical conditions and/or stressful life events and losses.
Dysthymia can be contrasted with major depressive disorder by assessing the acute nature of the symptoms. Dysthymia is far more chronic (long lasting) than major depressive disorder, in which symptoms may be present for as little as 2 weeks. Also Dysthymia often presents itself at an earlier age than Major Depressive Disorder.
Though there is no clear-cut way to prevent dysthymia from occurring, some suggestions have been made. Since dysthymia will often first occur in childhood, it is important to identify children who may be at risk. It may be beneficial to work with children in helping to control their stress, increase resilience, boost self-esteem, and provide strong networks of social support. These tactics may be helpful in warding off or delaying dysthymic symptoms.
Oftentimes, people with dysthymia will seek out treatment not necessarily because of depressed mood, but rather due to increasing levels of stress or because of personal difficulties that may be situation-related. This is hypothesized to be because of the chronic nature of the disorder, and how depressed mood is oftentimes thought to be a characterological pattern for the individual with the condition. Thus, it is only when the person experiences increasing stress that he or she thinks to go to some sort of trained professional for symptom relief. It is usually through the administration of the Structured Clinical Interview for DSM-IV that dysthymia is first diagnosed. At this point, with the help of a trained professional, a certain line of treatment is often discussed and then selected. It is important to consider all factors in the person's life that may be affected when deciding on a particular course of treatment. Additionally, if one method of treatment does not particularly work for a certain individual, it may be helpful to try something else.
Psychotherapy is often effective in treating dysthymia. Different modalities have been shown to be beneficial. Empirically-based treatments, such as cognitive-behavioral therapy, have been researched to show that through the proper course of treatment, symptoms can dissipate over time. Other forms of talk-therapy (e.g. psychodynamic psychotherapy, interpersonal psychotherapy) have also been said to be effective in treating the disorder. It may be helpful for people diagnosed with dysthymia to develop better coping skills, search for the root cause of symptoms, and work on changing faulty beliefs (e.g., I am worthless).
In addition to individual psychotherapy, both group psychotherapy and self-help, or support groups, can be an effective line of treatment for dysthymia as well. Through these treatment modalities, issues such as self-esteem, self-confidence, relationship issues/patterns, assertiveness skills, cognitive restructuring, etc., can be worked through and strengthened.
SSRIs are usually the first line of treatment via pharmacotherapy due to its more tolerable nature and reduced side effects versus the irreversible monoamine oxidase inhibitors or Tricyclic antidepressants. Studies have found that the mean response to antidepressant medications for people with dysthymia is 55% compared with a 31% response rate to a placebo. The most commonly prescribed antidepressants/SSRIs for dysthymia are fluoxetine, paroxetine, sertraline, and fluvoxamine. These medications will often take an average of 6–8 weeks before the patient will begin to feel its therapeutic effects. Additionally, STAR*D, a multi-clinic governmental study, found that people with overall depression will generally need to try different brands of medication before finding one that works specifically for them. Of those who switch medications, about 1 in 4 have been found to get better regardless of whether or not the second medication is an SSRI or some other type of antidepressant.
In a meta-analytic study from 2005, it was found that SSRIs and TCAs are equally effective in treating dysthymia. They also found that MAOIs have a slight advantage over the use of other medication in treating this disorder. Though, the author of this study cautions that MAOIs should not necessarily be the first line of defense in the treatment of dysthymia, as they are often less tolerable than their counterparts, such as SSRIs.
A combination of antidepressant medication and psychotherapy has consistently been shown to be the most effective line of treatment for people diagnosed with dysthymia. Working with a psychotherapist to address the causes and effects of the disorder, in addition to taking antidepressants to help eliminate the symptoms, can be extremely beneficial. This combination is often the preferred method of treatment for those who have dysthymia. Looking at various studies involving treatment for dysthymia, 75% of people responded positively to a combination of cognitive behavioral therapy (CBT) and pharmacotherapy, whereas only 48% of people responded positively to just CBT or medication alone.
In a meta-analytic study from 2008, researchers found an effect size of -.07 (Cohen's d) between pharmacologic treatments and psychological treatments for depressive disorders, suggesting pharmacologic treatments to be slightly more effective, though the results were not found to be statistically significant. This small effect is true only for SSRIs, with TCAs and other pharmacologic treatments showing no differences from psychological treatments. Additionally, there have been several studies yielding results that indicates that severe depression responds more favorably to psychotherapy than pharmacotherapy.
Because of dysthymia's chronic nature, treatment resistance can be somewhat common in dysthymic patients. In such a case, augmentation is often recommended. Such treatment augmentations can include lithium pharmacology, thyroid hormone augmentation, buspirone, bupropion, stimulants, and mirtazapine. Additionally, if the person also suffers from seasonal affective disorder, light therapy can be useful in helping augment therapeutic effects.
Globally dysthymia occurs in about 105 million people a year (1.5% of the population). It is slightly more common in women (1.8%) than in men (1.3%). The lifetime prevalence rate of dysthymia in community settings appears to range from 3 to 6% in the United States. However, in primary care settings the rate is higher ranging from 5 to 15 percent. United States prevalence rates tend to be somewhat higher than rates in other countries. Finally, the rate is higher among women than men.