|Dysthymic disorder/persistent depressive disorder|
|Classification and external resources|
Dysthymia (// dis-THY-mee-ə, from Ancient Greek δυσθυμία, "bad state of mind"), sometimes also called neurotic depression, dysthymic disorder, or chronic depression, is a mood disorder consisting of the same cognitive and physical problems as in depression, with less severe but longer-lasting symptoms. The concept was coined by Robert Spitzer as a replacement for the term "depressive personality" in the late 1970s.
According to the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders, published in 1994 (DSM-IV), dysthymia is a serious state of chronic depression, which persists for at least two years (one year for children and adolescents). Dysthymia 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 often co-occurs with other mental disorders. A "double depression" is the occurrence of episodes of major depression in addition to dysthymia. Switching between periods of dysthymic moods and periods of hypomanic moods is indicative of cyclothymia, which is a mild variant of bipolar disorder.
In the DSM-5, dysthymia is replaced by persistent depressive disorder (PDD). This new condition includes both chronic major depressive disorder and the previous dysthymic disorder. The reason for this change is that there was no evidence for meaningful differences between these two conditions.
Signs and symptoms
Dysthymia has a number of typical characteristics: low energy and 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 is a high incidence of comorbid illness in those with dysthymia. Suicidal behavior is also a particular problem with persons with dysthymia. It is vital to look for signs of major depression, panic disorder, generalised anxiety disorder, alcohol and substance misuse and personality disorder.
There are no known biological causes that apply consistently to all cases of dysthymia, which suggests diverse origin of the disorder. However, there are some indications that there is a genetic predisposition to dysthymia: "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". Other factors linked with dysthymia include stress, social isolation, and lack of social support.
In a study using identical and fraternal twins, results 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.
"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. A 10-year follow-up study was found that 95% of dysthymia patients had an episode of major depression. 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 sufferers accept these major depressive symptoms as a natural part of their personality or as a part of their life that is outside of their control. The fact that people with dysthymia may accept these worsening symptoms as inevitable can delay treatment. When and if such people seek out treatment, the treatment may not be very effective if only the symptoms of the major depression are addressed, but not the dysthymic symptoms. Patients with double depression tend to report significantly higher levels of hopelessness than is normal. This can be a useful symptom for mental health services providers to focus on when working with patients 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 can be helpful in preventing major depressive symptoms from occurring. Additionally, exercise and good sleep hygiene (e.g., improving sleep patterns) are thought to have an additive effect on treating dysthymic symptoms and preventing them from worsening.
There is evidence 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 those without dysthymia. 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 of the dulling of emotion that individuals with dysthymia have learned to use to protect themselves from overly strong negative feelings, compared to healthy people.
There is some evidence of a genetic basis for all types of depression, 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 caused in part by heredity.
A new model has recently surfaced in the literature regarding the HPA axis (structures in the brain that get activated in response to stress) 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.
The Diagnostic and Statistical Manual of Mental Disorders IV (DSM-IV), 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:
- During a majority of days for two years or more, the adult patient reports depressed mood, or appears depressed to others for most of the day.
- When depressed, the patient has two or more of:
- During this two-year period, the above symptoms are never absent longer than two consecutive months.
- During the duration of the two-year period, the patient may have had a perpetual major depressive episode.
- The patient has not had any manic, hypomanic, or mixed episodes.
- The patient has never fulfilled criteria for cyclothymic disorder.
- The depression does not exist only as part of a chronic psychosis (such as schizophrenia or delusional disorder).
- The symptoms are often not directly caused by a medical illness or by substances, including drug abuse or other medications.
- The symptoms may cause significant problems or distress in social, work, academic, or other major areas of life functioning.
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. 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.
Often, 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 often 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 (such as when patients believe themselves to be 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.
The first line of pharmacotherapy is usually SSRIs due to their more tolerable nature and reduced side effects compared to 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 escitalopram, citalopram, sertraline, fluoxetine, paroxetine, and fluvoxamine. It often takes an average of 6–8 weeks before the patient begins to feel these medications' 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. Research shows that 1 in 4 of those who switch medications get better results regardless of whether 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. However, 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 indicate that severe depression responds more favorably to psychotherapy than pharmacotherapy.
Because of dysthymia's chronic nature, treatment resistance is somewhat common. In such a case, augmentation is often recommended. Such treatment augmentations can include lithium pharmacology, thyroid hormone augmentation, amisulpride, 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.
- Anhedonia, a symptom of dysthymia characterized by a decreased or absent ability to enjoy a sense of pleasure
- Blunted affect, a symptom of PTSD, schizophrenia, and ASPD involving decreased or absent emotional response
- Atypical depression
- List of medications used to treat major depressive disorder or dysthymia
- "Neurotic Depression". Dr-Elze.com. Retrieved 2015-06-18.
- Gilbert, Daniel T.; Schacter, Daniel L.; Wegner, Daniel M., eds. (2011). Psychology (2nd ed.). New York: Worth Publishers. p. 564. ISBN 978-1-4292-3719-2.
- "Dysthymic Disorder". BehaveNet. Retrieved 2013-06-23.
- Brody, Jane (30 January 1995). "Help awaits those who live with sadness". The News-Journal. Daytona Beach, Florida. p. 54.
- "Dysthymia". Harvard Health Publications. Harvard University. February 2005. Archived from the original (February 2005 issue of the Harvard Mental Health Letter) on 6 January 2010. Retrieved 12 December 2009.
- American Psychiatric Association (2013). Diagnostic and Statistical Manual of Mental Disorder, Fifth Edition. Washington, DC: American Psychiatric Publishing. ISBN 978-0-89042-554-1.
- John M. Grohol, Psy.D. (18 May 2013). "DSM-5 Changes: Depression & Depressive Disorders". Psych Central. Retrieved 2 December 2013.
- Niculescu, A.B.; Akiskal, H.S. (2001). "Proposed Endophenotypes of Dysthymia: Evolutionary, Clinical, and Pharmacogenomic Considerations". Molecular Psychiatry. 6 (4): 363–366. doi:10.1038/sj.mp.4000906.
- Sansone, R. A. MD; Sansone, L. A. MD (2009). "Dysthymic Disorder: Forlorn and Overlooked?". Psychiatry. 6 (5): 46–50. PMC . PMID 19724735.
- Baldwin, Rudge S.; Thomas S. (1995). "Dysthymia: Options in Pharmacotherapy". Practical Therpeutics. 4 (6): 422 to 430. doi:10.2165/00023210-199504060-00005.
- "Double Depression: Hopelessness Key Component Of Mood Disorder". Science Daily. 26 July 2007. Archived from the original on 7 September 2008. Retrieved 17 July 2008.
- Klein, DN; Shankman, SA; Rose, S (2006). "Ten-year prospective follow-up study of the naturalistic course of dysthymic disorder and double depression". The American Journal of Psychiatry. 163 (5): 872–80. doi:10.1176/appi.ajp.163.5.872. PMID 16648329.
- Double Depression: Definition, Symptoms, Treatment, and More. Webmd.com (2012-01-07). Retrieved on 2012-07-01.
- Lyoo, I.K., Kwon, J.S., Lee, S.J., Hann, M.H., Chang, C., Seo, Lee, S.I., and Renshaw, P.F. (2002). "Decrease in Genu of the Corpus Callosum in Medication-Naïve, Early-Onset Dysthymia and Depressive Personality Disorder". Biological Psychiatry. 52 (12): 1134–1143. doi:10.1016/S0006-3223(02)01436-1.
- Ravindran, A. V., Smith, A. Cameron, C., Bhatal, R., Cameron, I., Georgescu, T. M., Hogan, M. J. (2009). "Toward a Functional Neuroanatomy of Dysthymia: A Functional Magnetic Resonance Imaging Study". Journal of Affective Disorders. 119: 9–15. doi:10.1016/j.jad.2009.03.009.
- Casement, M. D.; Shestyuk, A. Y.; Best, J. L.; Casas, B. R.; Glezer, A.; Segundo, M. A.; Deldin, P. J. (2008). "Anticipation of Affect in Dysthymia: Behavioral and Neurophysiological Indicators". Biological Psychiatry. 77 (2): 197–204. doi:10.1016/j.biopsycho.2007.10.007.
- Edvardsen, J.; Torgersen, S.; Roysamb, E.; Lygren, S.; Skre, I.; Onstad, S.; and Oien, A. (2009). "Unipolar Depressive Disorders have a Common Genotype". Journal of Affective Disorders. 117: 30–41. doi:10.1016/j.jad.2008.12.004.
- Schacter, Gilbert, Wegner (2011). Psychology (2nd ed.). Worth. p. 631.
- J Griffiths; A V Ravindran; Z Merali; H Anisman (2000). "Dysthymia: a review of pharmacological and behavioral factors". Molecular Psychiatry. 5 (3): 242–261. doi:10.1038/sj.mp.4000697.
- American Psychiatric Association, ed. (June 2000). Diagnostic and Statistical Manual of Mental Disorders DSM-IV-TR (4th ed.). American Psychiatric Publishing. ISBN 978-0-89042-024-9.
- Turner, Samuel M.; Hersen, Michel; Beidel, Deborah C., eds. (2007). Adult Psychopathology and Diagnosis (5th ed.). Hoboken, New Jersey: John Wiley. ISBN 978-0-471-74584-6. OCLC 427516745.
- 300.4, ICD9, Accessed 2009 May 2
- Bellino, S.; Patria, L.; Ziero, S.; Rocca, G.; Bogetto, F. (2001). "Clinical Features of Dysthymia and Age: a Clinical Investigation". Psychiatry Review. 103 (2–3): 219–228. doi:10.1016/S0165-1781(01)00274-8.
- Goodman, S. H., Schwab-Stone, M., Lahey, B. B., Shaffer, D. and Jensen, P. S. (2000). "Major Depression and Dysthymia in Children and Adolescents: Discriminant Validity and Differential Consequences in a Community Sample". Journal of American Academy of Child and Adolescent Psychiatry. 39 (6): 761–771. doi:10.1097/00004583-200006000-00015.
- Dysthymia (dysthymic disorder): Prevention. MayoClinic.com (2010-08-26). Retrieved on 2012-07-01.
- John M. Grohol (2008), Dysthymia Treatment. psychcentral.com
- Common Signs and Symptoms of Depression. alternativedepressiontherapy.com
- Dysthymic Disorder~treatment at eMedicine
- Ballesteros, J (2005). "Orphan comparisons and indirect meta-analysis: A case study on antidepressant efficacy in dysthymia comparing tricyclic antidepressants, selective serotonin reuptake inhibitors, and monoamine oxidase inhibitors by using general linear models". Journal of Clinical Psychopharmacology. 25 (2): 127–31. doi:10.1097/01.jcp.0000155826.05327.c1. PMID 15738743.
- Cuijpers, P; Van Straten, A; Van Oppen, P; Andersson, G (2008). "Are psychological and pharmacologic interventions equally effective in the treatment of adult depressive disorders? A meta-analysis of comparative studies". The Journal of Clinical Psychiatry. 69 (11): 1675–85; quiz 1839–41. doi:10.4088/JCP.v69n1102. PMID 18945396.
- Vos, T (Dec 15, 2012). "Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010.". Lancet. 380 (9859): 2163–96. doi:10.1016/S0140-6736(12)61729-2. PMID 23245607.