Escitalopram

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Escitalopram

This article is about the left handed version of the medication. For its racemic form, see citalopram.

 

Escitalopram

Clinical data
Trade names	Cipralex, Lexapro, others
AHFS/Drugs.com	Monograph
MedlinePlus	a603005
License data	US FDA: Lexapro
Pregnancy category	AU: C US: C (Risk not ruled out)
Routes of administration	By mouth
Drug class	Selective serotonin reuptake inhibitor
ATC code	N06AB10 (WHO)
Legal status
Legal status	AU: S4 (Prescription only) CA: ℞-only UK: POM (Prescription only) US: ℞-only In general: ℞ (Prescription only)
Pharmacokinetic data
Bioavailability	80%
Protein binding	~56%
Metabolism	Liver, specifically the enzymes CYP3A4 and CYP2C19
Elimination half-life	27–32 hours
Identifiers
CAS Number	128196-01-0
PubChem CID	146570
DrugBank	DB01175
ChemSpider	129277
UNII	4O4S742ANY
ChEBI	CHEBI:36791
ChEMBL	ChEMBL1508
CompTox Dashboard (EPA)	DTXSID8048440
ECHA InfoCard	100.244.188
Chemical and physical data
Formula	C20H21FN2O
Molar mass	324.392 g/mol (414.43 as oxalate) g·mol−1
3D model (JSmol)	Interactive image

Escitalopram, sold under the brand names Cipralex and Lexapro among others, is an antidepressant of the selective serotonin reuptake inhibitor (SSRI) class. Escitalopram is mainly used to treat major depressive disorder or generalized anxiety disorder. It is taken by mouth.

Common side effects include trouble sleeping, nausea, sexual problems, and feeling tired. More serious side effects may include suicide in people under the age of 25. It is unclear if use during pregnancy or breastfeeding is safe. Escitalopram is the (S)-stereoisomer of the earlier medication citalopram, hence the name escitalopram.

Escitalopram was approved for medical use in the United States in 2002. In the United States the wholesale cost is about $2.04 per month as of 2017. In the United Kingdom, as of 2018, non-proprietary escitalopram is around 1 / 20th as costly as the proprietary version. Escitalopram is sometimes replaced by twice the dose of citalopram. In 2016 it was the 26th most prescribed medication in the United States with more than 25 million prescriptions.

 

 

Medical uses

Escitalopram has FDA approval for the treatment of major depressive disorder in adolescents and adults, and generalized anxiety disorder in adults. In European countries and Australia, it is approved for depression (MDD) and anxiety disorders, these include: general anxiety disorder (GAD), social anxiety disorder (SAD), obsessive-compulsive disorder (OCD), and panic disorder with or without agoraphobia.

Depression

Escitalopram was approved by regulatory authorities for the treatment of major depressive disorder on the basis of four placebo controlled, double-blind trials, three of which demonstrated a statistical superiority over placebo.

Controversy existed regarding the effectiveness of escitalopram compared with its predecessor, citalopram. The importance of this issue followed from the greater cost of escitalopram relative to the generic mixture of isomers of citalopram, prior to the expiration of the escitalopram patent in 2012, which led to charges of evergreening. Accordingly, this issue has been examined in at least 10 different systematic reviews and meta analyses. As of 2012, reviews had concluded (with caveats in some cases) that escitalopram is modestly superior to citalopram in efficacy and tolerability.

A 2011 review concluded that second-generation antidepressants appear equally effective, although they may differ in onset and side effects. Treatment guidelines issued by the National Institute of Health and Clinical Excellence and by the American Psychiatric Association generally reflect this viewpoint.

In 2018, a systematic review and network meta-analysis comparing the efficacy and acceptability of 21 antidepressant drugs showed escitalopram to be one of the most effective.

Anxiety disorder

Escitalopram appears to be effective in treating general anxiety disorder, with relapse on escitalopram at 20% rather than placebo at 50%.

Escitalopram appears effective in treating social anxiety disorder.

Other

Escitalopram, as well as other SSRIs, is effective in reducing the symptoms of premenstrual syndrome, whether taken in the luteal phase only or continuously. There are no good data available for escitalopram as treatment for seasonal affective disorder as of 2011. SSRIs do not appear to be useful for preventing tension headaches or migraines.

Side effects

Escitalopram, like other SSRIs, has been shown to affect sexual functions causing side effects such as decreased libido, delayed ejaculation, and anorgasmia.

An analysis conducted by the FDA found a statistically insignificant 1.5 to 2.4-fold (depending on the statistical technique used) increase of suicidality among the adults treated with escitalopram for psychiatric indications. The authors of a related study note the general problem with statistical approaches: due to the rarity of suicidal events in clinical trials, it is hard to draw firm conclusions with a sample smaller than two million patients.

Escitalopram is not associated with weight gain. For example, 0.6 kg mean weight change after 6 months of treatment with escitalopram for depression was insignificant and similar to that with placebo (0.2 kg).

Citalopram and escitalopram are associated with dose-dependent QT interval prolongation and should not be used in those with congenital long QT syndrome or known pre-existing QT interval prolongation, or in combination with other medicines that prolong the QT interval. ECG measurements should be considered for patients with cardiac disease, and electrolyte disturbances should be corrected before starting treatment. In December 2011, the UK implemented new restrictions on the maximum daily doses at 20 mg for adults and 10 mg for those older than 65 years or with liver impairment. There are concerns of higher rates of QT prolongation and torsades de pointes compared with other SSRIs. The U.S. Food and Drug Administration and Health Canada did not similarly order restrictions on escitalopram dosage, only on its predecessor citalopram.

Discontinuation symptoms

Escitalopram discontinuation, particularly abruptly, may cause certain withdrawal symptoms such as "electric shock" sensations (also known as "brain shivers" or "brain zaps"), dizziness, acute depressions and irritability, as well as heightened senses of akathisia.

Sexual dysfunction

Some people experience persistent sexual side effects after they stop taking SSRIs. This is known as post-SSRI sexual dysfunction (PSSD). Common symptoms include genital anesthesia, erectile dysfunction, anhedonia, decreased libido, premature ejaculation, vaginal lubrication issues, and nipple insensitivity in women. Rates are unknown, and there is no established treatment.

Pregnancy

Antidepressant exposure (including escitalopram) is associated with shorter duration of pregnancy (by three days), increased risk of preterm delivery (by 55%), lower birth weight (by 75 g), and lower Apgar scores (by <0 .4="" a="" abortion.="" advantages="" an="" antidepressant="" associated="" association="" baby.="" during="" effects="" exposure="" heart="" in="" increased="" is="" may="" negative="" not="" of="" on="" outweigh="" p="" points="" possible="" pregnancy="" problems="" risk="" spontaneous="" ssri="" tentative="" the="" their="" there="" thus="" use="" with="">

Overdose

Excessive doses of escitalopram usually cause relatively minor untoward effects, such as agitation and tachycardia. However, dyskinesia, hypertonia, and clonus may occur in some cases. Therapeutic blood levels of escitalopram are usually in the range of 20–80 μg/L but may reach 80–200 μg/L in the elderly, patients with hepatic dysfunction, those who are poor CYP2C19 metabolizers or following acute overdose. Monitoring of the drug in plasma or serum is generally accomplished using chromatographic methods. Chiral techniques are available to distinguish escitalopram from its racemate, citalopram. Escitalopram seems to be less dangerous than citalopram in overdose and comparable to other SSRIs.

Pharmacology

Mechanism of action

Escitalopram increases intrasynaptic levels of the neurotransmitter serotonin by blocking the reuptake of the neurotransmitter into the presynaptic neuron. Of the SSRIs currently available, escitalopram has the highest selectivity for the serotonin transporter (SERT) compared to the norepinephrine transporter (NET), making the side-effect profile relatively mild in comparison to less-selective SSRIs.

Escitalopram is a substrate of P-glycoprotein and hence P-glycoprotein inhibitors such as verapamil and quinidine may improve its blood brain barrier penetrability. In a preclinical study in rats combining escitalopram with a P-glycoprotein inhibitor, its antidepressant-like effects were enhanced.

Interactions

Escitalopram, similarly to other SSRIs, inhibits CYP2D6 and hence may increase plasma levels of a number of CYP2D6 substrates such as aripiprazole, risperidone, tramadol, codeine, etc. As escitalopram is only a weak inhibitor of CYP2D6, analgesia from tramadol may not be affected. Escitalopram should be taken with caution when using St. John's wort. Exposure to escitalopram is increased moderately, by about 50%, when it is taken with omeprazole. The authors of this study suggested that this increase is unlikely to be of clinical concern. Caution should be used when taking cough medicine containing dextromethorphan (DXM) as serotonin syndrome has been reported.

Bupropion has been found to significantly increase citalopram plasma concentration and systemic exposure; as of April 2018 the interaction with escitalopram had not been studied, but some monographs warned of the potential interaction.

Escitalopram can also prolong the QT interval and hence it is not recommended in patients that are concurrently on other medications that also have the ability to prolong the QT interval. These drugs include antiarrhythmics, antipsychotics, tricyclic antidepressants, some antihistamines (astemizole, mizolastine) and some antiretrovirals (ritonavir, saquinavir, lopinavir). Being a SSRI, escitalopram should not be given concurrently with MAOIs or other serotonergic medications.

History

Cipralex brand escitalopram 10mg package and tablet sheet

Escitalopram was developed in close cooperation between Lundbeck and Forest Laboratories. Its development was initiated in the summer of 1997, and the resulting new drug application was submitted to the U.S. FDA in March 2001. The short time (3.5 years) it took to develop escitalopram can be attributed to the previous extensive experience of Lundbeck and Forest with citalopram, which has similar pharmacology.

The FDA issued the approval of escitalopram for major depression in August 2002 and for generalized anxiety disorder in December 2003. On May 23, 2006, the FDA approved a generic version of escitalopram by Teva. On July 14 of that year, however, the U.S. District Court of Delaware decided in favor of Lundbeck regarding the patent infringement dispute and ruled the patent on escitalopram valid.

In 2006, Forest Laboratories was granted an 828-day (2 years and 3 months) extension on its US patent for escitalopram. This pushed the patent expiration date from December 7, 2009 to September 14, 2011. Together with the 6-month pediatric exclusivity, the final expiration date was March 14, 2012. 

Society and culture

Allegations of illegal marketing

In 2004, two separate civil suits alleging illegal marketing of citalopram and escitalopram for use by children and teenagers by Forest were initiated by two whistleblowers, one by a practicing physician named Joseph Piacentile, and the other by a Forest salesman named Christopher Gobble. In February 2009, these two suits received support from the US Attorney for Massachusetts and were combined into one. Eleven states and the District of Columbia have also filed notices of intention to intervene as plaintiffs in the action. The suits allege that Forest illegally engaged in off-label promoting of Lexapro for use in children, that the company hid the results of a study showing lack of effectiveness in children, and that the company paid kickbacks to physicians to induce them to prescribe Lexapro to children. It was also alleged that the company conducted so-called "seeding studies" that were, in reality, marketing efforts to promote the drug's use by doctors. Forest responded to these allegations that it "is committed to adhering to the highest ethical and legal standards, and off-label promotion and improper payments to medical providers have consistently been against Forest policy." In 2010 Forest Pharmaceuticals Inc., agreed to pay more than $313 million to settle the charges over Lexapro and two other drugs, Levothroid and Celexa.

Brand names

Escitalopram is sold under many brand names worldwide such as Cipralex and Lexapro.

Cyclothymia

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Cyclothymia

 

Cyclothymia
Other names	Cyclothymic disorder
Graphical representation of cyclothymia compared with bipolar disorder and major depression
Specialty	Psychiatry, clinical psychology
Symptoms	Periods of depression and elevated mood
Complications	Suicide, self-harm
Causes	Unknown
Risk factors	Family history
Differential diagnosis	Bipolar disorder, borderline personality disorder, substance misuse disorder
Treatment	Psychotherapy, medications
Frequency	0.4-1% at some point in life

Cyclothymia, also known as cyclothymic disorder, is a mental disorder that involves numerous periods of symptoms of depression and periods of symptoms of hypomania. These symptoms, however, are not sufficient to be a major depressive episode or a hypomanic episode. Symptoms must last for more than one year in children and two years in adults.

The cause is unknown. Risk factors include a family history of bipolar disorder. Cyclothymia differs from bipolar in that major depression, mania, or hypomania have never occurred.

Treatment is generally with counselling and mood stabilizers such as lithium. It is estimated that 0.4-1% of people have cyclothymia at some point in their life. Onset is typically in late childhood to early adulthood. Males and females are affected equally often.

Symptoms

People with cyclothymia experience both depressive phases and hypomanic phases (which are less severe than a full hypomanic episode). The depressive and manic symptoms in cyclothymia last for variable amounts of time due to the unstable and reactive nature of the disorder. The depressive phases are similar to major depressive disorder and are characterized by dulled thoughts and sensations and the lack of motivation for intellectual or social activities. Most people with cyclothymia are generally fatigued and tend to sleep frequently and for long periods of time. However, other people experience insomnia.

Other symptoms of cyclothymic depression include indifference toward people or activities that used to be extremely important. Cyclothymic depression also leads to difficulty making decisions. In addition, people with this condition tend to be critical and complain easily. Suicidal thoughts are common, even in mild forms of cyclothymia. In the depressive state, people with cyclothymia also experience physical complaints including frequent headaches, tightness in the head and chest, an empty sensation in the head, weakness, weight loss, and hair loss.

The distinguishing factor between typical depression and cyclothymic depression is that in cyclothymic depression, there are instances of hypomania. People with cyclothymia can switch from the depressive state to the hypomanic state without warning to them or others. The duration and frequency of phases is unpredictable.

In the hypomanic state, people's thoughts become faster and they become more sociable and talkative. They may engage in spending sprees, spontaneous actions, have heightened self-esteem, and greater vanity. In contrast to a regular manic state that would be associated with bipolar I, symptoms in the hypomanic phase generally occur in a less severe form.

Comorbidities

Cyclothymia commonly occurs in conjunction with other disorders. Between 20-50 percent of people with depression, anxiety, and related disorders also have cyclothymia. When people with cyclothymia seek mental health resources it tends to be for symptoms of their comorbid condition rather than for their symptoms of cyclothymia. In children and adolescents, the most common comorbidities with cyclothymia are anxiety disorders, impulse control issues, eating disorders, and ADHD. In adults, cyclothymia also tends to be comorbid with impulse control issues. Sensation-seeking behaviors occur in hypomanic states. These often include gambling and compulsive sexuality in men, or compulsive buying and binge eating in women.

In addition to sensation-related disorders, cyclothymia has also been associated with atypical depression. In one study, a connection was found between interpersonal sensitivity, mood reactivity (i.e., responding to actual or potential positive events with brighter mood), and cyclothymic mood swings, all of which are symptoms of atypical depression. Cyclothymia also tends to occur in conjunction with separation anxiety, where a person has anxiety as a result of separation from a caregiver, friend, or loved one. Other issues that tend to co-occur with cyclothymia include social anxiety, fear of rejection and a tendency toward hostility to those connected with past pain and rejection. People with cyclothymia tend to seek intense interpersonal relationships when in a hypomanic state and isolation when in a depressed state. This generally leads to short, tumultuous relationships.

Causes

The cause is unknown. Risk factors include a family history of bipolar disorder.

First-degree relatives of people with cyclothymia have major depressive disorder, bipolar I disorder, and bipolar II disorder more often than the general population. Substance-related disorders also may be at a higher risk within the family. First-degree relatives of a bipolar I individuals may have a higher risk of cyclothymic disorder than the general population.

Diagnosis

Cyclothymia is classified in DSM-5 as a subtype of bipolar disorder. The criteria are:

1. Periods of elevated mood and depressive symptoms for at least half the time during the last two years for adults and one year for children and teenagers.
2. Periods of stable moods last only two months at most.
3. Symptoms create significant problems in one or more areas of life.
4. Symptoms do not meet the criteria for bipolar disorder, major depression, or another mental disorder.
5. Symptoms are not caused by substance use or a medical condition.

The DSM-5 criteria for cyclothymia are restrictive according to some researchers. This affects the diagnosis of cyclothymia because fewer people get diagnosed than potentially could. This means that a person who has some symptoms of the disorder might not be able to get treatment because they do not meet all of the necessary criteria described in DSM-5. Furthermore, it also leads to more attention being placed on depression and other bipolar-spectrum disorders because if a person does not meet all the criteria for cyclothymia they are often given a depression or bipolar spectrum diagnosis. Improper diagnosis may lead some people with cyclothymia to be treated for a comorbid disorder rather than having their cyclothymic tendencies addressed.

Cyclothymia is often not recognized by the affected individual or medical professionals due to its ostensibly mild symptoms. In addition, it is difficult to identify and classify. Due to disagreement and misconceptions among health and mental health professionals, cyclothymia is often diagnosed as "bipolar not otherwise specified". Cyclothymia is also often confused with borderline personality disorder due to their similar symptoms, especially in older adolescents and young adults.

Most people with the disorder present in a depressive state, not realizing that their hypomanic states are abnormal. Mild manic episodes tend to be interpreted as part of the person's personality or simply a heightened mood. In addition, the disorder often manifests during childhood or adolescence, making it even more difficult for the person to distinguish between symptoms of the disorder and their personality. For example, people may think that they just suffer from mood swings and not realize that these are a result of a psychiatric condition.

Management

Cognitive behavioral therapy (CBT) is considered potentially effective for people diagnosed with cyclothymia.

Medication can be used in addition to behavioral approaches. However, mood stabilizers should be used before antidepressants, and if antidepressants are used they should be used with caution. Antidepressants are a concern due to the possibility of inducing hypomanic switches or rapid cycling.

History

In 1883, Karl Ludwig Kahlbaum identified a disorder characterized by recurring mood cycles. The disorder contained both melancholic and manic episodes that occurred in a milder form than in bipolar disorder. This condition was coined "cyclothymia" by Kahlbaum and his student Ewald Hecker. Kahlbaum developed his theory of cyclothymia through his work with people presenting with these symptoms at the Kahlbaum Sanitarium in Goerlitz, Silesia (Germany). He was recognized as a leading hypnotherapist and psychotherapist of his day. He was a progressive in the field of mental health, believing that mental illness should not carry a stigma and that people dealing with mental health issues should be treated humanely. Kalhbaum was the first to recognize that people with cyclothymia often do not seek help for the disorder due to its mild symptoms.

Cyclothymia has been conceptualized in a variety of ways, including as a subtype of bipolar disorder, a temperament, a personality trait, and a personality disorder. There is also an argument that cyclothymia should be considered a neurodevelopmental disorder. The two defining features of the disorder, according to DSM-5, are the presence of depressive episodes and hypomania. Cyclothymia is also classified as a subtype of bipolar disorder in DSM-5, but some researchers disagree with this classification and argue that it should be primarily defined as an exaggeration of mood and emotional instability. In the past, cyclothymia has been conceptualized to include other characteristics in addition to the flux between depression and hypomania, such as mood reactivity, impulsivity, and anxiety.

Epidemiology

Cyclothymia, known today as cyclothymic disorder, tends to be underdiagnosed due to its low intensity. The exact rates for cyclothymia have not been widely studied. Some studies estimate that between 5 and 8% are affected at some point in their life whereas other studies suggest a rate ranging from 0.4 to 2.5%.

Males appear to be affected equally often, though women are more likely to receive treatment. Cyclothymia is diagnosed in around fifty percent of people with depression who are evaluated in psychiatric outpatient settings.

Etymology

Cyclothymia is derived from the Greek word κυκλοθυμία (from κῦκλος kyklos, "circle" and θυμός thymos, "mood, emotion"). Therefore, it means "to cycle or circle between moods or emotions".

Research

Whether subtypes of bipolar disorder, such as cyclothymia, truly represent separate disorders or are part of a unique bipolar spectrum is debated in research. Cyclothymia is typically not described in research studies or diagnosed in clinical settings, making it less recognizable and less understood by professionals. This absence of cyclothymia in research and clinical settings suggests that cyclothymia is either being diagnosed as another mood disorder or as a non-affective psychiatric disorder or not coming to scientific or clinical attention due to a lack of diagnostic clarity or because the nature of cyclothymia is still highly contested. Additionally, the current diagnostic criterion for cyclothymia emphasizes that symptoms are persistent, which suggests that they are enduring traits rather than a psychological state, thus, it has been argued that it should be diagnosed as a personality disorder. Since the symptoms tend to overlap with personality disorders, the validity and distinction between these two diagnostic categories has been debated.

Lastly, the tendency of cyclothymia to be comorbid with other mental disorders makes diagnosis difficult. These issues prevent consensus on the definition of cyclothymia and its relationship with other mental disorders among researchers and clinicians. This lack of consensus on an operational definition and symptom presentation is especially pronounced with children and adolescents because the diagnostic criteria have not been adequately adapted to take into account their developmental level.

Society and culture

Actor Stephen Fry has spoken about his experience with cyclothymia, which was depicted in the documentary Stephen Fry: The Secret Life of the Manic Depressive. 

Singer Charlene Soraia had cyclothymia and wrote a song about her experiences with the disorder.

Dysthymia

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Dysthymia

 

Dysthymia
Other names	Persistent depressive disorder, dysthymic disorder, chronic depression,
Pronunciation	/dɪsˈθaɪmiə/ dis-THY-mee-ə
Specialty	Psychiatry, clinical psychology
Symptoms	Low mood, low self-esteem, loss of interest in normally enjoyable activities, low energy, pain without a clear cause
Complications	Self harm, suicide
Usual onset	Normally early adulthood
Causes	Genetic, environmental, and psychological factors
Risk factors	Family history, major life changes, certain medications, chronic health problems, substance abuse
Treatment	Counseling, antidepressant medication, electroconvulsive therapy
Frequency	104 million (2015)

Dysthymia, also known as persistent depressive disorder (PDD), is a mood disorder consisting of the same cognitive and physical problems as 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.

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 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. 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.

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. 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.

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 abuse (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 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. 

Diagnosis

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:

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 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.

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.

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.

Treatments

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.

Therapy

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.

Medications

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 defense 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

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.

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.

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.

Mood (psychology -- updated)

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Mood_(psychology)

In psychology, a mood is an affective state. In contrast to emotions or feelings, moods are less specific, less intense and less likely to be provoked or instantiated by a particular stimulus or event. Moods are typically described as having either a positive or negative valence. In other words, people usually talk about being in a good mood or a bad mood.

Mood also differs from temperament or personality traits which are even longer-lasting. Nevertheless, personality traits such as optimism and neuroticism predispose certain types of moods. Long term disturbances of mood such as clinical depression and bipolar disorder are considered mood disorders. Mood is an internal, subjective state but it often can be inferred from posture and other behaviors. "We can be sent into a mood by an unexpected event, from the happiness of seeing an old friend to the anger of discovering betrayal by a partner. We may also just fall into a mood."

Research also shows that a person's mood can influence how they process advertising. Mood has been found to interact with gender to affect consumer processing of information.

Etymology

Etymologically, the word mood derives from the Old English mōd which denoted military courage, but could also refer to a person's humor, temper, or disposition at a particular time. The cognate Gothic mōds translates both θυμός "mood, spiritedness" and ὀργή "anger". 

Types of mood

Positive mood

 

Positive mood can be caused by many different aspects of life as well as have certain effects on people as a whole. Good mood is usually considered a state without an identified cause; people cannot pinpoint exactly why they are in a good mood. People seem to experience a positive mood when they have a clean slate, have had a good night sleep, and feel no sense of stress in their life. 

There have been many studies done on the effect of positive emotion on the cognitive mind and there is speculation that positive mood can affect our minds in good or bad ways. Generally, positive mood has been found to enhance creative problem solving and flexible yet careful thinking. Some studies have stated that positive moods let people think creatively, freely, and be more imaginative. Positive mood can also help individuals in situations in which heavy thinking and brainstorming is involved. In one experiment, individuals who were induced with a positive mood enhanced performance on the Remote Associates Task (RAT), a cognitive task that requires creative problem solving. Moreover, the study also suggests that being in a positive mood broadens or expands the breadth of attentional selection such that information that may be useful to the task at hand becomes more accessible for use. Consequently, greater accessibility of relevant information facilitates successful problem solving. Positive mood also facilitates resistance to temptations, especially with regards to unhealthy food choices.

Positive mood has also been proven to show negative effects on cognition as well. According to the article "Positive mood is associated with implicit use of distraction", "There is also evidence that individuals in positive moods show disrupted performance, at least when distracting information is present". The article states that other things in their peripheral views can easily distract people who are in good moods; an example of this would be if you were trying to study in the library (considering you are in a positive mood) you see people constantly walking around or making small noises. The study is basically stating that it would be harder for positive moods to focus on the task at hand. In particular, happy people may be more sensitive to the hedonic consequences of message processing than sad people. Thus, positive moods are predicted to lead to decreased processing only when thinking about the message is mood threatening. In comparison, if message processing allows a person to maintain or enhance a pleasant state then positive moods need not lead to lower levels of message scrutiny than negative moods. It is assumed that initial information regarding the source either confirms or disconfirms mood-congruent expectations. Specifically, a positive mood may lead to more positive expectations concerning source trustworthiness or likability than a negative mood. As a consequence, people in a positive mood should be more surprised when they encounter an untrustworthy or dislikable source rather than a trustworthy or likable source.

Negative mood

Like positive moods, negative moods have important implications for human mental and physical wellbeing. Moods are basic psychological states that can occur as a reaction to an event or can surface for no apparent external cause. Since there is no intentional object that causes the negative mood, it has no specific start and stop date. It can last for hours, days, weeks, or longer. Negative moods can manipulate how individuals interpret and translate the world around them, and can also direct their behavior. 

Negative moods can affect an individual's judgment and perception of objects and events. In a study done by Niedenthal and Setterland (1994), research showed that individuals are tuned to perceive things that are congruent with their current mood. Negative moods, mostly low-intense, can control how humans perceive emotion-congruent objects and events. For example, Niedenthal and Setterland used music to induce positive and negative moods. Sad music was used as a stimulus to induce negative moods, and participants labeled other things as negative. This proves that people's current moods tend to affect their judgments and perceptions. These negative moods may lead to problems in social relationships. For example, one maladaptive negative mood regulation is an overactive strategy in which individuals over dramatize their negative feelings in order to provoke support and feedback from others and to guarantee their availability. A second type of maladaptive negative mood regulation is a disabling strategy in which individuals suppress their negative feelings and distance themselves from others in order to avoid frustrations and anxiety caused by others' unavailability.

Negative moods have been connected with depression, anxiety, aggression, poor self-esteem, physiological stress and decrease in sexual arousal. In some individuals, there is evidence that depressed or anxious mood may increase sexual interest or arousal. In general, men were more likely than women to report increased sexual drive during negative mood states. Negative moods are labeled as nonconstructive because it can affect a person's ability to process information; making them focus solely on the sender of a message, while people in positive moods will pay more attention to both the sender and the context of a message. This can lead to problems in social relationships with others.

Negative moods, such as anxiety, often lead individuals to misinterpret physical symptoms. According to Jerry Suls, a professor at the University of Iowa, people who are depressed and anxious tend to be in rumination. However, although an individual's affective states can influence the somatic changes, these individuals are not hypochondriacs.

Although negative moods are generally characterized as bad, not all negative moods are necessarily damaging. The Negative State Relief Model states that human beings have an innate drive to reduce negative moods. People can reduce their negative moods by engaging in any mood-elevating behavior (called Mood repair strategies), such as helping behavior, as it is paired with positive value such as smiles and thank you. Thus negative mood increases helpfulness because helping others can reduce one's own bad feelings.

Factors which affect mood

Lack of sleep

Sleep has a complex, and as yet not fully elucidated, relationship with mood. Most commonly if a person is sleep deprived he/she will become more irritable, angry, more prone to stress, and less energized throughout the day. "Studies have shown that even partial sleep deprivation has a significant effect on mood. University of Pennsylvania researchers found that subjects who were limited to only 4.5 hours of sleep a night for one week reported feeling more stressed, angry, sad, and mentally exhausted. When the subjects resumed normal sleep, they reported a dramatic improvement in mood." Generally, evening oriented people, as compared to morning ones, show decreased energy and pleasantness and heightened tension.

However, in a subset of cases sleep deprivation can, paradoxically, lead to increased energy and alertness and enhanced mood. This effect is most marked in persons with an eveningeness type (so called night-owls) and people suffering from depression. For this reason it has sometimes been used as a treatment for major depressive disorder.

Nutrition

Traditional dietary patterns characterized by vegetables, fruit, meat, fish, and whole grains, as opposed to a western pattern diet characterized by processed foods, refined grains, sugary products, and beer were associated with lower odds for major depression or dysthymia (mood disorder) and for anxiety disorders in women. Red meat is found to be protective against mood and anxiety disorders. Fruits and vegetables are associated with positive mood, independent of demographic or lifestyle factors. Research indicates that alcohol and energy drinks are associated with mood changes.

Facial expression

Research studies have indicated that voluntary facial expressions, such as smiling, can produce effects on the body that are similar to those that result from the actual emotion, such as happiness. Paul Ekman and his colleagues have studied facial expressions of emotions and have linked specific emotions to the movement of specific facial muscles. Each basic emotion is associated with a distinctive facial expression. Sensory feedback from the expression contributes to the emotional feeling. Example: Smiling if you want to feel happy. Facial expressions have a large effect on self-reported anger and happiness which then affects your mood. Ekman has found that these expressions of emotion are universal and recognizable across widely divergent cultures.

Mood disorders

Depression, chronic stress, bipolar disorder, etc. are considered mood disorders. It has been suggested that such disorders result from chemical imbalances in the brain's neurotransmitters, however some research challenges this hypothesis.

Social mood

The idea of social mood as a "collectively shared state of mind" (Nofsinger 2005; Olson 2006) is attributed to Robert Prechter and his socionomics. The notion is used primarily in the field of economics (investments).

In sociology, philosophy, and psychology, crowd behavior is the formation of a common mood directed toward an object of attention.