Tag: PDD: Persistent Depressive Disorder

What is Double Depression?

Published on by Andrew Marshall1 Comment

Introduction

Double depression refers to the co-existence of major depressive disorder (MDD) and persistent depressive disorder (PDD), the latter previously referred to as dysthymia. Research has shown that double depression tends to be more severe than either MDD or PDD alone and that individuals with double depression experience relapse more often than those with either MDD or PDD alone. However, there is some research that indicates few differences exist between double depression, MDD, and PDD; as a result, those researchers conclude that double depression is not a distinct disorder.

The literature that details the pharmaceutical treatment of double depression is sparse. Although there are studies that demonstrate that certain medications, such as selective serotonin reuptake inhibitors (SSRIs), are effective methods of treatment, those studies lack placebo controls; therefore, the studies’ conclusions are questionable.

Research has found that, as is the case with other depressive disorders, pharmaceutical and therapeutic treatments combined are more effective than the use of either form of treatment alone. Individuals with double depression tend to experience more functional impairment than those with either MDD or PDD alone. As a result, researchers emphasize the need for unique treatments for double depression to be developed and implemented.

Presentation

Individuals with double depression meet the DSM-5 classification criteria for both MDD and PDD. Goldney and Fisher (2004) determined that, in a sample of 3,010 individuals from southern portions of Australia calculated a prevalence rate of double depression of 2.2%. Jonas et al. (2003) reported a prevalence rate of double depression in the United States of 3.4%—based upon an assessment of 7,667 Americans. The prevalence rate of double depression can be compared to rates of PDD at 6.2%, major depressive episode (MDE) at 8.6%, and major depressive episode with severity (MDE-s) at 7.7%. Keller and Shapiro (1982) found that 26% of patients within a sample of 101 met the criteria for both MDD and PDD; however, the aforementioned sample is much smaller—and much more inclined to inaccuracies—than the samples (3,010 and 7,667) described above. Thus, double depression is less common than other forms of depression, but it is still a form of depression that warrants medical attention in the form of behavioral therapies; pharmaceutical treatments; or, both (Miller, Norman, and Keitner, 1999).

The characteristics of those with double depression tend to be more severe in nature than those associated with those who have either MDD or PDD. Levitt, Joffe, and MacDonald (1991) found that those with double depression experience fluctuations in mood at an earlier point in life, a more substantial number of depressive episodes, as well as co-morbid disorders of anxieties more often than their MDD-alone counterparts. Goldney and Fisher (2004) reported that individuals with double depression seek medical attention more often than those with either MDD or PDD alone. Leader and Klein (1996) found that individuals with double depression experience a more substantial level of social impairment, which includes factors such as leisure pursuits and relationship characteristics, than those with either MDD or PDD. Dixon and Thyer (1998) concluded that individuals with double depression experiences recoveries on a more frequent basis than their counterparts who have MDD alone (88% to 69%); however, individuals with double depression experience the most substantial rates of relapse of all of those who suffer from chronic depression. In addition, remission from MDD tends to happen faster than remission from PDD (Dixon & Thyer, 1998).

Miller, Norman, and Dow (1986) reported that individuals with double depression endure a more severe path of illness, but experience few differences with respect to social impairment compared to their MDD-alone counterparts. In addition, McCullough et al. (2000) found that, with the exception that patients with double depression tended to experience of more severe illness, few differences were apparent. Therefore, the conclusions drawn in previous research that are associated with the nature of the clinical presentation of double depression are mixed. Multiple scientists emphasize the need for additional research to determine adequate treatments for those with double depression, as depression is a disease that places a considerable burden upon communities and societies; furthermore, those researchers predict depression will be, in an economic sense, the second-most burdensome disease on societies come 2020.

Treatment

Research on pharmaceutical treatment of double depression in particular is sparse. Certain medications, such as fluoxetine, were found in numerous studies to be effective at reducing symptom severity; however, these studies involved open-label trials, double-blind randomised trials that lack placebo conditions, and small sample sizes. Thus, placebo-controlled trials are needed in order to determine adequate and unique treatments for double depression. In addition, the considerable burden depression places upon communities and societies (Goldney & Fisher, 2004) emphasizes the need for additional research into the treatment of chronic depression.

Hellerstein et al. (1994) theorised that antidepressant medications could be used to ameliorate both MDD and PDD; a pharmaceutical trial found that fluoxetine facilitated remission in 57.1% of patients after five months of treatment. In addition, Miller, Norman, and Keitner (1999) conducted an intervention in which one cohort received pharmaceutical treatment while another cohort received both pharmaceutical and therapeutic treatment. Their results indicated that those who received the combined intervention were more functional—in a social sense—as well as relieved of their depression than those who received the pharmaceutical intervention alone (Miller, Norman, & Keitner, 1999). However, the researchers found that the effect disappeared at both the 6 and 12-month follow-up assessments.

Vasile et al. (2012) conducted a pharmaceutical trial with 16 patients with double depression (who had comorbid alcohol dependence) who were treated and monitored for six months. Results showed that three antidepressants – venlafaxine, duloxetine, and milnacipran – were associated with substantial improvement; venlafaxine was the most effective of the three antidepressants.

Koran, Aboujaoude, and Gamel (2007) conducted a pharmaceutical trial with 24 adults who received duloxetine over the course of a 12-week period. Results showed that duloxetine was successful in the treatment of both PDD as well as double depression. However, the researchers’ trial was an open-label trial; as a result, the researchers called for a double-blind and placebo-controlled trial to be conducted in order to further validate the benefits the medication seems to provide.

In addition, Waslick et al. (1999) used duloxetine to treat 19 children and adolescents with either PDD or double depression; after eight weeks of pharmaceutical treatment, 11 of the patients failed to meet the classification criteria for one of the two disorders, which led to the conclusion that duloxetine was a medication that appeared to provide relief from PDD and double depression in children and adolescents. However, the aforementioned trial (in addition to Koran et al.’s (2007) trial) was an open-label trial, which the authors noted as a limitation.

Hirschfield et al. (1998) conducted a 12-week randomised controlled trial (RCT) that involved the administration of sertraline or imipramine, after which 324 of 623 patients either qualified for remission or experienced a substantive improvement in clinical presentation. In a double-blind, fixed-dose trial that involved the use of either the monoamine oxidase inhibitor (MAOI) moclobemide or the SSRI fluoxetine, Duarte, Mikkelsen, and DeliniStula (1996) were able to facilitate a minimum of a 50% score reduction on the Hamilton Depression Rating Scale (HDRS). 71% of cases that involved moclobemide – versus 38% of cases that involved fluoxetine – were determined to achieve the aforementioned desired outcome. As a result, the researchers concluded that both antidepressants were similar in their abilities to treat double depression in an effective fashion. However, the lack of a placebo control undermines the extent to which the results can be applied.

Marin, Kocsis, Frances, and Parides (1994) conducted an eight-week open trial that entailed the administration of desipramine to 42 individuals with double depression and 33 individuals with PDD. The researchers found that 70% of the PDD patients experienced a substantial improvement in clinical presentation; the proportion associated with the double depression-cohort was said to be similar. However, the lack of blindness as well as a placebo control notes a considerable limitation of the aforementioned research.

Goldney and Bain (2006) found that those who have double depression receive some form of treatment on a more substantial basis than their MDD-alone and PDD-alone counterparts. To elaborate, the authors measured that, in Australia, 41.4% of those evaluated with double depression received treatment three or more times over the course of the previous month, whereas 34.5% of those with MDD alone; 23.2% of those with PDD alone; and 10.3% of those who were not depressed received treatment three or more times over the course of the previous month (Goldney & Bain, 2006). In addition, the researchers concluded that those with double depression acquire a more substantial number of treatment visits per month (a mean of 4.3) when compared to their MDD-alone counterparts (a mean of 3.0); their PDD-alone counterparts (a mean of 2.6); and their non-depressed counterparts (a mean of 1.5).

Prognosis

Although double depression is less prevalent than either MDD or PDD, it is still a form of depression that warrants medical attention in the form of behavioural therapies; pharmaceutical treatments; or, both. Miller, Norman, and Keitner (1999) found that the use of both behavioural and pharmaceutical treatments was more effective on a short-term basis in the reduction of depression than the use of pharmaceutical treatments alone.

Klein, Shankman, and Rose (2008) determined that poor maternal-child relationship, histories of sexual abuse, co-morbid disorders of anxieties, and lower educational attainment predicted an increased HAM-D score after a decade; the researchers also determined that those same factors predicted, after a decade, increased functional impairment. In addition, the results showed that the life course of depression did not differ to a substantial extent between individuals with MDD-alone and double depression.

Hirschfield et al. (1998) conducted a 12-week RCT that involved the administration of sertraline or imipramine, in which the most notable predictors of treatment response were educational attainment and relationship status; in addition, the authors noted the apparent influence of intrinsic personal traits. However, Hirschfield et al. noted the limitation of a lack of a placebo control.

Klein, Taylor, Harding, and Dickstein (1988) reported that, via their assessment of clinical, familial, and socio-environmental characteristics of those with chronic depression, at a six-month follow-up, individuals with double depression experienced decreased rates of remission, increased manifestations of clinical depressive phenomena, increased functional impairment, and increased likelihood of the development and onset of a hypomanic episode than their MDD-alone counterparts; as a result, the authors underscore the importance of the creation of a distinct classification of double depression due to its unique episodic path.

Controversies

Previous research on the clinical presentation of double depression tends to be mixed. Numerous studies indicate that the course of double depression tends to be more severe in nature. In addition, numerous studies demonstrate that individuals with double depression seek medical attention to a more substantial extent than those with either MDD or PDD. However, Miller, Norman, and Dow (1986) determined that individuals with MDD or PDD versus individuals with double depression experienced similar levels of social impairment. In addition, McCullough and colleagues found that there were few additional differences overall between the characteristics of those with double depression versus those with either MDD or PDD.

Research on the course of double depression is also mixed. Klein, Taylor, Harding, and Dickstein (1988) found that remission in individuals with double depression is less probable than it is in individuals with either MDD or PDD; the researchers also noted that those with double depression are more prone to the development and onset of a hypomanic episode than those with either MDD or PDD. In addition, Klein, Shankman, and Rose (2008) and Hirschfield et al. (1998) both concluded that educational status predicted treatment outcome. However, Levitt, Joffe, and MacDonald (1991) demonstrated that the courses of the respective depressive disorders did not differ to a substantial extent. While Klein, Shankman, and Rose (2008) advocate for the creation of a distinct classification of double depression in the future edition(s) of the DSM, Levitt and colleagues (as well as McCullough and colleagues) seem to indicate that, due to the numerous similarities as well as limited differences between double depression and either MDD or PDD, the creation of such a classification would be inappropriate and incorrect. Remick, Sadovnick, Lam, Zis, and Yee (1996) determine that the heritable bases of MDD, PDD, and double depression are similar and that, as a result, the three disorders are unable to be differentiated.

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What is Dysthymia?

Published on by Andrew Marshall19 Comments

Introduction

Dysthymia, also known as persistent depressive disorder (PDD), is a mental and behavioural disorder, specifically a disorder primarily of mood, consisting of the same cognitive and physical problems as depression, but with longer-lasting symptoms.

The concept was coined by Robert Spitzer as a replacement for the term “depressive personality” in the late 1970s.

In the Diagnostic and Statistical Manual of Mental Disorders (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 than major depressive disorder, but not necessarily less severe.

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. In the DSM-5, dysthymia is replaced by persistent depressive disorder. 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.

Epidemiology

Globally dysthymia occurs in about 105 million people a year (1.5% of the population). It is 38% more common in women (1.8% of women) than in men (1.3% of men). 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.

Signs and Symptoms

Dysthymia characteristics include an extended period of depressed mood combined with at least two other symptoms which may include insomnia or hypersomnia, fatigue or low energy, eating changes (more or less), low self-esteem, or feelings of hopelessness. Poor concentration or difficulty making decisions are treated as another possible symptom. Irritability is one of the more common symptoms in children and adolescents.

Mild degrees of dysthymia may result in people withdrawing from stress and avoiding opportunities for failure. In more severe cases of dysthymia, people may 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 behaviour is also a particular problem with those with dysthymia. It is vital to look for signs of major depression, panic disorder, generalised anxiety disorder, alcohol and substance use disorders, and personality disorder.

Causes

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.

Co-Occurring Conditions

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.

“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 use disorders (up to 50%). People with dysthymia have a higher-than-average chance of developing major depression. A 10-year follow-up study 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

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.

Pathophysiology

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 in women with dysthymia than in 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 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.

Diagnosis

The Diagnostic and Statistical Manual of Mental Disorders IV (DSM-IV), published by the American Psychiatric Association, characterises 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:

  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. Feelings of hopelessness or pessimism
  3. During this two-year period, the above symptoms are never absent longer than two consecutive months.
  4. During the duration of the two-year period, the patient may have had a perpetual 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 substance use or other medications.
  9. 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 hospitalisations, 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.

Prevention

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.

Treatment

Persistent depressive disorder can be treated with psychotherapy and pharmacotherapy. The overall rate and degree of treatment success is somewhat lower than for non-chronic depression, and a combination of psychotherapy and pharmacotherapy shows best results.

Therapy

Psychotherapy can be effective in treating dysthymia. In a meta-analytic study from 2010, psychotherapy had a small but significant effect when compared to control groups. However, psychotherapy is significantly less effective than pharmacotherapy in direct comparisons.

There are many different types of therapy, and some are more effective than others.

  • The empirically most studied type of treatment is cognitive-behavioural therapy.
    • This type of therapy is very effective for non-chronic depression, and it appears to be also effective for chronic depression.
  • Cognitive behavioural analysis system of psychotherapy (CBASP) has been designed specifically to treat PDD.
    • Empirical results on this form of therapy are inconclusive: While one study showed remarkably high treatment success rates, a later, even larger study showed no significant benefit of adding CBASP to treatment with antidepressants.
  • Schema therapy and psychodynamic psychotherapy have been used for PDD, though good empirical results are lacking.
  • Interpersonal psychotherapy has also been said to be effective in treating the disorder, though it only shows marginal benefit when added to treatment with antidepressants.

Medications

In a 2010 meta-analysis, the benefit of pharmacotherapy was limited to selective serotonin reuptake inhibitors (SSRIs) rather than tricyclic antidepressants (TCA).

According to a 2014 meta-analysis, antidepressants are at least as effective for persistent depressive disorder as for major depressive disorder. The first line of pharmacotherapy is usually SSRIs due to their purported 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 defence in the treatment of dysthymia, as they are often less tolerable than their counterparts, such as SSRIs.

Tentative evidence supports the use of amisulpride to treat dysthymia but with increased side effects.

Combination Treatment

When pharmacotherapy alone is compared with combined treatment with pharmacotherapy plus psychotherapy, there is a strong trend in favour of combined treatment. 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 behavioural therapy and pharmacotherapy, whereas only 48% of people responded positively to just CBT or medication alone.

A 2019 Cochrane review of 10 studies involving 840 participants could not conclude with certainty that continued pharmacotherapy with antidepressants (those used in the studies) was effective in preventing relapse or recurrence of persistent depressive disorder. The body of evidence was too small for any greater certainty although the study acknowledges that continued psychotherapy may be beneficial when compared to no treatment.

Resistance

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.