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Persistent Depressive Disorder
Classification and external resources
ICD-10 F341
ICD-9 300.4
MedlinePlus 000918
MeSH D019263


Persistent depressive disorder, previously known as Dysthymia (/dɪsˈθmiə/ Template:Respell, from Ancient Greek δυσθυμία, "melancholy") and 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.[1][2] The concept was coined by Dr. Robert Spitzer as a replacement for the term "depressive personality" in the late 1970s.[3]

According to the DSM's definition of Persistent Depressive Disorder, it is a serious state of chronic depression, which persists for at least 2 years (1 year for children and adolescents); it is less acute and severe than major depressive disorder.[4] As Persistent Depressive Disorder 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.

Persistent Depressive Disorder often co-occurs with other mental disorders. A "double depression" is the occurrence of episodes of major depression in addition to Persistent Depressive Disorder. Switching between periods of dysthymic moods and periods hypomanic moods, is indicative of cyclothymia, which is a mild variant of bipolar disorder.

Classical use of the termEdit

The term dysthymia originally referred to a sub-clinical psychotic condition, and the Greek roots of the term dysthymia (dys- (bad) and thymia) suggest the interpretation: "abnormal or disordered feelings". Classical dysthymia refers to "feeling" something as a reality which is not a reality (for example "feeling" that one knows what others think) - or to "understanding" an underlying social dynamic which is not real. This definition of dysthymia used to cover a broad band of disorders, many of which may very likely result in anti-social behaviors. In ancient times, it was believed that the thymus "gland" was the heart of all emotions, and if one were to be depressed, said person had a "dysfunctional thymus" or "Dysthymia". Dysthymia was not considered a specific disorder, but this name was given to any type of depression in general.

Dysthymia in historyEdit

Dysthymia dates back at least as far as ancient Greek and Roman civilization as recorded in the works of Sophocles and Virgil. Many societal occurrences of dysthymia occur within groups of individuals leading stressful lives. Clinical descriptions of dysthymia date from 1881, when Jean de Caseet-Maneut, a leading physician at that time, investigated the phenomemon in Paris. Records also appear sporadically in medical and psychological journals.

Signs and symptomsEdit

Persistent Depressive Disorder 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 Persistent Depressive Disorder may result in people withdrawing from stress and avoiding opportunities for failure. In more severe cases of Persistent Depressive Disorder, people may even withdraw from daily activities.[5] They will usually find little pleasure in usual activities and pastimes. Diagnosis of Persistent Depressive Disorder 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, Persistent Depressive Disorder often occurs at the same time as other psychological disorders, which adds a level of complexity in determining the presence of Persistent Depressive Disorder, particularly because there is often an overlap in the symptoms of disorders.[6] There is a high incidence of comorbid illness in those with Persistent Depressive Disorder. Suicidal behavior is also a particular problem with persons with Persistent Depressive Disorder. It is vital to look for signs of major depression, panic disorder, generalised anxiety disorder, alcohol and substance misuse and personality disorder.[7]

CausesEdit

There are no known biological causes that apply consistently and pervasively to all cases of Persistent Depressive Disorder, which may be a result of the diverse nature of the disorder.[6] However, there are some indications that there is some genetic predisposition to Persistent Depressive Disorder: "The rate of depression in the families of people with Persistent Depressive Disorder is as high as fifty percent for the early-onset form of the disorder".[4] Other factors linked with Persistent Depressive Disorder include: stress, social isolation, and lack of social support.[6]

Co-occurring conditionsEdit

"At least three-quarters of patients with Persistent Depressive Disorder also have a chronic physical illness or another psychiatric disorder such as one of the anxiety disorders, cyclothymia, drug addiction, or alcoholism".[4] 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%).[6] People with Persistent Depressive Disorder have a higher-than-average chance of developing major depression.[8] In a 10 year follow up study, it was found that 95% of Persistent Depressive Disorder patients had an episode of a major depression.[9] When an intense episode of depression occurs on top of Persistent Depressive Disorder the state is called "double depression."[8]

Double depressionEdit

Double depression occurs when a person experiences a major depressive episode on top of the already-existing condition of Persistent Depressive Disorder. 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 Persistent Depressive Disorder may accept these worsening symptoms as inevitable, it can delay treatment. When and if such people seek out treatment, the treatment may not be very effective in the case that only the symptoms of the major depression are addressed, but not the dysthymic symptoms.[10] 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.[8] 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.[10]

It has been suggested that the best way to prevent double-depression is by treating the Persistent Depressive Disorder. 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 something of an additive effect on treating dysthymic symptoms and preventing them from worsening.[10]

PathophysiologyEdit

There is evidence indicating that there may be neurological indicators of early onset of Persistent Depressive Disorder. There are several brain structures (corpus callosum and frontal lobe) that are different between women with Persistent Depressive Disorder and those without Persistent Depressive Disorder. This may indicate that there is a developmental difference between these two groups.[11]

Another study, which used fMRI techniques to assess the differences between individuals with Persistent Depressive Disorder 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 Persistent Depressive Disorder 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).[12]

A study comparing healthy individuals to people with Persistent Depressive Disorder 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 Persistent Depressive Disorder 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 Persistent Depressive Disorder. This provides neurological evidence toward the lack of emotion that individuals with Persistent Depressive Disorder have compared to healthy people.[13]

There is some evidence of a genetic basis for all types of depressions, including Persistent Depressive Disorder. 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 Persistent Depressive Disorder is in part caused by heredity.[14]

A new model has recently surfaced in the literature regarding the HPA axis (structures in the brain that get activated in response to stress)[15] and its involvement with Persistent Depressive Disorder (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.[16] Since this model is highly provisional, further research is still needed.

Neurophysiological functioningEdit

There is a common belief that low levels of the neurotransmitter serotonin play a central role in the development and course of affective disorders, Persistent Depressive Disorder included.[17] 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.[18] 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.[18] Though this may be the case, it does not prove that serotonin, or any other sort of chemical imbalance is a cause of Persistent Depressive Disorder.[18] Further research is needed in this area, as no conclusive results have been found in the neurophysiological functioning of Persistent Depressive Disorder.[18]

DiagnosisEdit

The Diagnostic and Statistical Manual of Mental Disorders (DSM), published by the American Psychiatric Association, characterizes dysthymic disorder.[19] 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 Persistent Depressive Disorder 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:[20][21]

  1. 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.
  2. When depressed, the patient has two or more of:
    1. decreased or increased appetite
    2. decreased or increased sleep (insomnia or hypersomnia)
    3. Fatigue or low energy
    4. Reduced self-esteem
    5. Decreased concentration or problems making decisions
    6. Feels hopeless or pessimistic
  3. During this two-year period, the above symptoms are never absent longer than two consecutive months.
  4. During the first two years of this syndrome, the patient has not had a major depressive episode.
  5. The patient has not had any manic, hypomanic, or mixed episodes.
  6. The patient has never fulfilled criteria for cyclothymic disorder.
  7. The depression does not exist only as part of a chronic psychosis (such as schizophrenia or delusional disorder).
  8. The symptoms are often not directly caused by a medical illness or by substances, including drug abuse, or other medications.
  9. The symptoms may cause significant problems or distress in social, work, academic, or other major areas of life functioning.[19]

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.[6] For younger adults with Persistent Depressive Disorder, 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 Persistent Depressive Disorder the psychological symptoms are associated with medical conditions and/or stressful life events and losses.[22]

Persistent Depressive Disorder can be contrasted with major depressive disorder by assessing the acute nature of the symptoms. Persistent Depressive Disorder is far more chronic (long lasting) than major depressive disorder, in which symptoms may be present for as little as 2 weeks. Also Persistent Depressive Disorder often presents itself at an earlier age than Major Depressive Disorder.[23]

PreventionEdit

Though there is no clear-cut way to prevent Persistent Depressive Disorder from occurring, some suggestions have been made. Since Persistent Depressive Disorder 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.[24]

TreatmentsEdit

Often, people with Persistent Depressive Disorder 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.[25] 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.[26] 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 Persistent Depressive Disorder is first diagnosed.[25] 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.

TherapyEdit

Psychotherapy is often effective in treating Persistent Depressive Disorder. 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.[25] Other forms of talk-therapy (e.g. psychodynamic psychotherapy, interpersonal psychotherapy) have also been said to be effective in treating the disorder.[27] It may be helpful for people diagnosed with Persistent Depressive Disorder to develop better coping skills, search for the root cause of symptoms, and work on changing faulty beliefs (e.g., I am worthless).[25]

In addition to individual psychotherapy, both group psychotherapy and self-help, or support groups, can be an effective line of treatment for Persistent Depressive Disorder as well.[25] 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.[25]

Medications Edit

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.[25] Studies have found that the mean response to antidepressant medications for people with Persistent Depressive Disorder is 55%, compared with a 31% response rate to a placebo.[27] The most commonly prescribed antidepressants/SSRIs for Persistent Depressive Disorder 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.[25] 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.[25] 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.[25]

In a meta-analytic study from 2005, it was found that SSRIs and TCAs are equally effective in treating Persistent Depressive Disorder. They also found that MAOIs have a slight advantage over the use of other medication in treating this disorder.[28] Though, the author of this study cautions that MAOIs should not necessarily be the first line of defense in the treatment of Persistent Depressive Disorder, as they are often less tolerable than their counterparts, such as SSRIs.[28]

Combination of therapy and medicationEdit

A combination of antidepressant medication and psychotherapy has consistently been shown to be the most effective line of treatment for people diagnosed with Persistent Depressive Disorder.[25] 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 Persistent Depressive Disorder. Looking at various studies involving treatment for Persistent Depressive Disorder, 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.[25]

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.[29]

Treatment ResistanceEdit

Because of Persistent Depressive Disorder's chronic nature, it may be treated as treatment resistant depression.[27] In such a case, augmentation is often recommended. Such treatment augmentations can include electroconvulsive therapy but new technologies such as transcranial magnetic stimulation are being studied as a safer alternative. In additon the and use of non-standard medications such as lithium pharmacology, thyroid hormone augmentation, buspirone, bupropion, stimulants, and mirtazapine maybe recommended. Additionally, if the person also suffers from seasonal affective disorder, light therapy can be useful in helping augment therapeutic effects.[27]

EpidemiologyEdit

Globally Persistent Depressive Disorder occurs in about 105 million people a year (1.5% of the population).[30] It is slightly more common in women (1.8%) than in men (1.3%).[30] The lifetime prevalence rate of Persistent Depressive Disorder 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.[6]

The 5th edition of the Diagnostic and Statistical Manual of Mental Disorders was released in 2013 and includes a number of changes. One of those changes was this disorder. Dysthymia is gone, replaced with something called “persistent depressive disorder.” The new condition includes both chronic major depressive disorder and the previous dysthymic disorder. Why this change? “An inability to find scientifically meaningful differences between these two conditions led to their combination with specifiers included to identify different pathways to the diagnosis and to provide continuity with DSM-IV.”

See alsoEdit

References Edit

  1. (2011) Psychology, 2nd, 564, Worth Publishers.
  2. Dysthymic Disorder. BehaveNet. URL accessed on 2013-06-23.
  3. includeonly>Brody, Jane. "Help awaits those who live with sadness", p. 54.
  4. 4.0 4.1 4.2 (February 2005). Depressive Disorder.htm Persistent Depressive Disorder.
  5. Niculescu, A.B. and Akiskal, H.S. (2001). Proposed Endophenotypes of Persistent Depressive Disorder: Evolutionary, Clinical, and Pharmacogenomic Considerations. Molecular Psychiatry 6 (4): 363–366.
  6. 6.0 6.1 6.2 6.3 6.4 6.5 Sansone, R. A. MD and Sansone, L. A. MD (2009). Dysthymic Disorder: Forlorn and Overlooked?. Psychiatry 6 (5): 46–50.
  7. Baldwin, Rudge S. and Thomas S. (1995). Persistent Depressive Disorder: Options in Pharmacotherapy. Practical Therpeutics 4 (6): 422 to 430.
  8. 8.0 8.1 8.2 Double Depression: Hopelessness Key Component Of Mood Disorder.
  9. (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.
  10. 10.0 10.1 10.2 Double Depression: Definition, Symptoms, Treatment, and More. Webmd.com (2012-01-07). Retrieved on 2012-07-01.
  11. 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 Persistent Depressive Disorder and Depressive Personality Disorder. Biological Psychiatry 52 (12): 1134–1143.
  12. Ravindran, A. V., Smith, A. Cameron, C., Bhatal, R., Cameron, I., Georgescu, T. M., Hogan, M. J. (2009). Toward a Functional Neuroanatomy of Persistent Depressive Disorder: A Functional Magnetic Resonance Imaging Study. Journal of Affective Disorders 119: 9–15.
  13. 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 Persistent Depressive Disorder: Behavioral and Neurophysiological Indicators. Biological Psychiatry 77 (2): 197–204.
  14. 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.
  15. Schacter, Gilbert, Wegner (2011). Psychology, 2nd, 631, Worth.
  16. J Griffiths, A V Ravindran, Z Merali and H Anisman (2000). Persistent Depressive Disorder: a review of pharmacological and behavioral factors. Molecular Psychiatry 5 (3).
  17. Nash, R. A. (1996). The Serotonin Connection. The Journal of Orthomolecular Medicine 11.
  18. 18.0 18.1 18.2 18.3 (2005). Serotonin and depression: A disconnect between the advertisements and the scientific literature. PLoS medicine 2 (12): e392.
  19. 19.0 19.1 (June 2000) American Psychiatric Association Diagnostic and Statistical Manual of Mental Disorders DSM-IV-TR, 4th, American Psychiatric Publishing.
  20. (2007) Adult Psychopathology and Diagnosis, 5th, John Wiley.
  21. 300.4, ICD9, Accessed 2009 May 2
  22. Bellino, S., Patria, L., Ziero, S., Rocca, G., Bogetto, F. (2001). Clinical Features of Persistent Depressive Disorder and Age: a Clinical Investigation. Psychiatry Review 103 (2–3): 219–228.
  23. Goodman, S. H., Schwab-Stone, M., Lahey, B. B., Shaffer, D. and Jensen, P. S. (2000). Major Depression and Persistent Depressive Disorder 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.
  24. Depressive Disorder/DS01111/DSECTION=prevention Persistent Depressive Disorder (dysthymic disorder): Prevention. MayoClinic.com (2010-08-26). Retrieved on 2012-07-01.
  25. 25.00 25.01 25.02 25.03 25.04 25.05 25.06 25.07 25.08 25.09 25.10 25.11 John M. Grohol (2008), Depressive Disorder-treatment/ Persistent Depressive Disorder Treatment. psychcentral.com
  26. Common Signs and Symptoms of Depression. alternativedepressiontherapy.com
  27. 27.0 27.1 27.2 27.3 Medscape: Medscape Access. Emedicine.medscape.com. Retrieved on 2012-07-01.
  28. 28.0 28.1 (2005). Orphan comparisons and indirect meta-analysis: A case study on antidepressant efficacy in Persistent Depressive Disorder comparing tricyclic antidepressants, selective serotonin reuptake inhibitors, and monoamine oxidase inhibitors by using general linear models. Journal of Clinical Psychopharmacology 25 (2): 127–31.
  29. (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.
  30. 30.0 30.1 Vos, T (2012 Dec 15). 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.

Further readingEdit

  • Group, W. P. A. D. W. (1995). Dysthymia in clinical practice. British Journal of Psychiatry, 166(2), 174-183.
  • Klein, D. N., & Riso, L. P. (1991). The utility of the dysthymia construct. PsycCRITIQUES, 36(10), 851-852.
  • Kocsis, J. H., & Frances, A. J. (1987). A critical discussion of DSM-III dysthymic disorder. American Journal of Psychiatry, 144(12), 1534-1542.
  • Koponen, H., Lepola, U., & Leinonen, E. (1995). Dysthymia: A review. Nordic Journal of Psychiatry, 49(2), 129-132.

External linksEdit


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