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Clinical depression



Depression
Classification & external resources
ICD-10 F32., F33.
ICD-9 296
OMIM 608516
DiseasesDB 3589
MedlinePlus 003213
eMedicine med/532 

  Clinical depression (also called major-depressive disorder or unipolar depression) is a common psychiatric disorder, characterized by a persistent lowering of mood, loss of interest in usual activities and diminished ability to experience pleasure.

While the term "depression" is commonly used to describe a temporary decreased mood when one "feels blue", clinical depression is a serious illness that involves the body, mood, and thoughts that cannot simply be willed or wished away. It is often a disabling disease that affects a person's work, family and school life, sleeping and eating habits, general health and ability to enjoy life.[1] The course of clinical depression varies widely: depression can be a once in a life-time event or have multiple recurrences, it can appear either gradually or suddenly, and either last for few months or be a life-long disorder. Having depression is a major risk factor for suicide; in addition, people with depression suffer from higher mortality from other causes.[2]

Clinical depression is usually treated by psychotherapy, antidepressants, or a combination of the two. Clinical depression may be a stand alone issue having differing features in patients, or as part of a larger medical issue, such as in patients with bipolar disorder or chronic pain.

Additional recommended knowledge

Contents

Signs and symptoms

Clinical depression can present with a variety of symptoms, however almost all patients display a marked change in mood, a deep feeling of sadness, and a noticeable loss of interest or pleasure in favorite activities. Other symptoms include:

  • Persistent sad, anxious, or "empty" mood
  • Loss of appetite and/or weight loss, or conversely overeating and weight gain
  • Insomnia, early-morning awakening, or oversleeping
  • Restlessness or irritability
  • Feelings of worthlessness, inappropriate guilt, helplessness
  • Feelings of hopelessness, pessimism
  • Difficulty thinking, concentrating, remembering, or making decisions
  • Thoughts of death or suicide or attempts at suicide
  • Loss of interest or pleasure in hobbies and activities that were once enjoyed, including sex
  • Decreased energy, fatigue, feeling "slowed down" or sluggish
  • Persistent physical symptoms that do not respond to treatment, such as headaches, digestive disorders, and chronic pain

Not all patients will present every symptom, and the severity of symptoms will vary widely among individuals. Symptoms must, however, persist for at least two weeks before being considered a potential sign of depression, with the exception of suicidal thoughts or attempts.[3][1]

Diagnosis of clinical depression in children is more difficult than in adults and is often left undiagnosed, and thus untreated, because the symptoms in children are often written off as normal childhood moodiness. Diagnosis is also made difficult because children are more likely than adults to show different symptoms depending on the situation.[4]

While some children still function reasonably well, most who are suffering depression will suffer from a noticeable change in their social activities and life, a loss of interest in school and poor academic performance, and possibly drastic changes in appearance. They may also begin abusing drugs and/or alcohol, particularly past the age of 12. Although much rarer than in adults, children with major depression may attempt suicide or have suicidal thoughts even before the age of twelve.[4]

Diagnosis

Before a diagnosis of depression is made, a physician should perform a complete medical exam to rule out any possible physical cause for the suspected depression. If no such cause is found, a psychological evaluation should be done by the physician or by referral to a psychiatrist or psychologist.[1] The evaluation will include a complete history of symptoms, a discussion of alcohol and drug use, and whether the patient has had or is having suicidal thoughts or thinking about death. The evaluation will also include a family medical history to see if other family members suffer from any form of depression or similar mood disorder.[1]

There are several criteria lists and diagnostic tools that can also aid in the diagnosis of depression. Most are based on the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), which is a book published by the American Psychiatric Association that defines the criteria used to diagnose various mental disorders, including depression.

The Beck Depression Inventory, originally created by Dr. Aaron T. Beck in 1961, is a 21-question patient completed survey that covers items related to the basic symptoms of depression, such as hopelessness and irritability, cognitions such as guilt or feelings of being punished, as well as physical symptoms such as fatigue, weight loss, and lack of interest in sex.[5] The Beck Inventory is one of the most widely used diagnostic tools for self-diagnosis of depression, although its primary purpose is not the diagnosis of depression, but determining the severity and presence of symptoms.[6]

There are also two Patient Health Questionaires available that are also self-administered questionnaires. The PHQ-2 has only two questions that asks about the frequency of depressed mood and a loss of interest in doing things, with a positive to either question indicating the need for further testing.[7] The PHQ-9 is a slightly more detailed nine question survey covering some of the major symptoms of depression and the frequency a person has experienced them. It is based directly on the diagnostic criteria listed in the DSM-IV and often used as a follow up to a positive PHQ-2 test.[8]

Epidemiology

Clinical depression affects about 7–18% of the population on at least one occasion in their lives, before the age of 40. In some countries, such as Australia, one in four women and one in six men will suffer from depression. In Canada, major depression affects approximately 1.35 million people[citation needed], and in the USA approximately 14 million adults per year[9].

People who have had one episode of depression may be more than normally likely to have more episodes in the future, so the first time a young person becomes depressed is important both as a personal and public health concern.[citation needed]

About twice as many females as males report or receive treatment for clinical depression, though this imbalance is shrinking over the course of recent history; this difference seems to completely disappear after the age of 50–55. Clinical depression is currently the leading cause of disability in North America as well as other countries, and is expected to become the second leading cause of disability worldwide (after heart disease) by the year 2020, according to the World Health Organization.[10]

Recent studies suggest that the diagnostic criteria for depression are far too broad, resulting in diagnosis of clinical depression in people who are not truly clinically depressed and who have shown normal responses to negative events.[11]

Types

The diagnostic category major depressive disorder appears in the Diagnostic and Statistical Manual of Mental Disorders of the American Psychiatric Association. The term is generally not used in countries which instead use the ICD-10 system, but the diagnosis of depressive episode is very similar to an episode of major depression. Clinical depression also usually refers to acute or chronic depression severe enough to need treatment. Minor depression is a less-used term for a subclinical depression that does not meet criteria for major depression but where there are at least two symptoms present for two weeks.

Major depression

Major depression or, more properly, major depressive disorder (MDD), is characterized by a severely depressed mood that persists for at least two weeks. Major depressive disorder is specified as either "a single episode" or "recurrent", depending on whether periods of depression occur as discrete events or recur within an individual's lifespan. Episodes of major or clinical depression may be further divided into mild, major or severe. If the patient has already had an episode of mania or markedly elevated mood, a diagnosis of bipolar disorder (also called bipolar affective disorder) is usually made instead of MDD; depression without periods of elation or mania is therefore sometimes referred to as unipolar depression because the mood remains at one emotional state ("pole"). The diagnosis also usually excludes cases where the symptoms are a normal result of bereavement. Diagnosticians recognize several possible subtypes of major depressive disorder. ICD-10 does not specify a melancholic subtype, but does distinguish by presence or absence of psychosis.

  • Depression with melancholic features – melancholia is characterized by a loss of pleasure (anhedonia) in most or all activities, a failure of reactivity to pleasurable stimuli, a quality of depressed mood more pronounced than that of grief or loss, a worsening of symptoms in the morning hours, early morning waking, psychomotor retardation, anorexia (excessive weight loss, not to be confused with Anorexia Nervosa), or excessive guilt.
  • Depression with atypical features – atypical depression is characterized by mood reactivity (paradoxical anhedonia) and positivity, significant weight gain or increased appetite ("comfort eating"),[12] excessive sleep or somnolence (hypersomnia), leaden paralysis, or significant social impairment as a consequence of hypersensitivity to perceived interpersonal rejection. Contrary to its name, atypical depression is the most common form of depression.[13]
  • Depression with Psychotic Features – Some people with major depressive or manic episodes may experience psychotic features. They may be presented with hallucinations or delusions that are either mood-congruent (content coincident with depressive themes) or non-mood-congruent (content not coincident with depressive themes). It is clinically more common to encounter a delusional system as an adjunct to depression than to encounter hallucinations, whether visual or auditory.

Other disorders featuring depressed mood

  • Dysthymia is a chronic, mild depression in which a person suffers from a depressive mood almost daily over a span of at least two years without episodes of major depression. The symptoms are not as severe as those for major depression, although people with dysthymia are vulnerable to co-occurring episodes of major depression (sometimes referred to as "double depression").[citation needed]
  • Bipolar disorder is an episodic illness characterized by alternating states of mania, hypomania and depression. In the United States, bipolar disorder was previously called "manic depression", however this term is no longer favored by the medical community.
  • Postnatal depression or postpartum depression is a form of clinical depression that occurs after childbirth. Postnatal depression primarily occurs in women, less commonly in men, with similar symptoms and treatment methods as clinical depression, however postnatal depression generally lasts only a few weeks with proper diagnosis and treatment.
  • Recurrent brief depression (RBD) is distinguished from clinical depression primarily by differences in duration. Patients with RBD have depressive episodes about once per month, with individual episodes lasting less than two weeks and typically less than 2–3 days. Diagnosis of RBD requires that the episodes occur over the span of at least one year and, in female patients, independently of the menstrual cycle. People with clinical depression can develop RBD, and visa versa, with both illnesses having similar risks.[14]

Overlapping psychological features

Anxiety

The different types of depression and anxiety are classified separately by the DSM-IV-TR, with the exception of hypomania, which is included in the bipolar disorder category. Despite the different categories, depression and anxiety can indeed be co-occurring (occurring together), independently (without mood congruence), or comorbid (occurring together, with overlapping symptoms, and with mood congruence). In an effort to bridge the gap between the DSM-IV-TR categories and what clinicians actually encounter, experts such as Herman Van Praag of Maastricht University have proposed ideas such as anxiety/aggression-driven depression.[15] This idea refers to an anxiety/depression spectrum for these two disorders, which differs from the mainstream perspective of discrete diagnostic categories.

Although there is no specific diagnostic category for the comorbidity of depression and anxiety in the DSM or ICD, the National Comorbidity Survey (US) reports that 58 percent of those with major depression also suffer from lifetime anxiety. Supporting this finding, two widely accepted clinical colloquialisms include

  • Agitated depression - a state of depression that presents as anxiety and includes akathisia (heightened restlessness), suicide, insomnia (not early morning wakefulness), nonclinical (meaning "doesn't meet the standard for formal diagnosis") and nonspecific panic, and a general sense of dread.
  • Akathitic depression - a state of depression that presents as anxiety or suicidality and includes akathisia but does not include symptoms of panic. Some consider it a form of mixed state.

It is also clear that even mild anxiety symptoms can have a major impact on the course of a depressive illness, and the commingling of any anxiety symptoms with the primary depression is important to consider. A pilot study by Ellen Frank et al., at the University of Pittsburgh, found that depressed or bipolar patients with lifetime panic symptoms experienced significant delays in their remission.[citation needed] These patients also had higher levels of residual impairment, or the ability to get back into the swing of things. On a similar note, Robert Sapolsky of Stanford University and others also argue that the relationship between stress, anxiety, and depression could be measured and demonstrated biologically.[16] To that point, a[17] study by Heim and Nemeroff et al., of Emory University, found that depressed and anxious women with a history of childhood abuse recorded higher heart rates and the stress hormone ACTH when subjected to stressful situations.

Hypomania

Hypomania, as the name suggests, is a state of mind or behavior that is "below" (hypo) mania. In other words, a person in a hypomanic state often displays behavior that has all the hallmarks of a full-blown mania (e.g., marked elevation of mood that is characterized by euphoria, overactivity, disinhibition, impulsivity, a decreased need for sleep, hypersexuality), but these symptoms, though disruptive and seemingly out of character, are not so pronounced as to be considered a diagnosably manic episode. In a psychiatric context, it is important to identify the possible presence and characteristics of manic and hypomanic episodes, since these may lead to a diagnosis of bipolar disorder, which is medically treated differently from depression.

Another important point is that hypomania is a diagnostic category that includes both anxiety and depression. It often presents as a state of anxiety that occurs in the context of a clinical depression. Patients in a hypomanic state often describe a sense of extreme generalized or specific anxiety, recurring panic attacks, night terrors, guilt, and agency (as it pertains to codependence and counterdependence). All of this happens while they are in a state of retarded or somnolent depression. This is the type of depression in which a person is lethargic and unable to move through life. The terms retarded and somnolent are shorthand for states of depression that include lethargy, hypersomnia, a lack of motivation, a collapse of ADLs (activities of daily living), and social withdrawal. This is similar to the shorthand used to describe an "agitated" or "akathitic" depression.

In considering the hypomania-depression connection, a distinction should be made between anxiety, panic, and stress. Anxiety is a physiological state that is caused by the sympathetic nervous system. Anxiety does not need an outside influence to occur. Panic is related to the "fight or flight" mechanism. It is a reaction, induced by an outside stimulus, and is a product of the sympathetic nervous system and the cerebral cortex. More plainly, panic is an anxiety state that we are thinking about. Finally, stress is a psychosocial reaction, influenced by how a person filters nonthreatening external events. This filtering is based on one's own ideas, assumptions, and expectations.

Causes

Current theories regarding the risk factors and causes of clinical depression can be broadly classified into two categories, Physiological and Sociopsychological:

Physiological

Genetic predisposition

The tendency to develop depression may be inherited: according to the National Institute of Mental Health[18] there is some evidence that depression may run in families. Most experts believe that both biological and psychological factors play a role.

 

Neurological

Many modern antidepressant drugs change levels of certain neurotransmitters, namely serotonin and norepinephrine (noradrenaline). However, the relationship between serotonin, SSRIs, and depression is typically greatly oversimplified when presented to the public, though this may be due to the lack of scientific knowledge regarding the mechanisms of action.[19] Evidence has shown the involvement of neurogenesis in depression, though the role is not exactly known.[20] Recent research has suggested that there may be a link between depression and neurogenesis of the hippocampus.[21] This horseshoe-shaped structure is a center for both mood and memory. Loss of neurons in the hippocampus is found in depression and correlates with impaired memory and dysthymic mood. The most widely accepted explanation for this is that the drugs increase serotonin levels in the brain which in turn stimulate neurogenesis and therefore increase the total mass of the hippocampus and would in theory restore mood and memory, therefore assisting in the fight against the mood disorder. However, whether environmental confounds could contribute to this remains a subject of controversy.[citation needed]

In about one-third of individuals diagnosed with attention-deficit hyperactivity disorder (ADHD), a disorder widely believed to be neurological and developmental, depression is recognized as comorbid.[22] Dysthymia, a form of chronic, low-level depression, is particularly common in adults with undiagnosed ADHD who have encountered years of frustrating ADHD-related problems with education, employment, and interpersonal relationships.[23]

New evidence shows that individuals with clinical depression exhibit markedly higher levels of monoamine oxidase A (MAO-A) in the brain compared to people without depression.[24] MAO-A is an enzyme which reacts with and decreases the concentration of monoamines such as serotonin, norephinephrine and dopamine. Lower concentrations of monoamines is a well known cause of depression.[25]

Medical conditions

Certain illnesses, including cardiovascular disease,[26] hepatitis, mononucleosis, hypothyroidism, fructose malabsorption,[27] sleep apnea, and organic brain damage caused by degenerative conditions such as Parkinson disease, Multiple Sclerosis or by traumatic blunt force injury may contribute to depression, as may certain prescription drugs such as hormonal contraception methods and steroids. Depression also occurs in patients with chronic pain, such as chronic back pain, much more frequently than in the general population.

Dietary

The increase in depression in industrialised societies has been linked to diet, particularly to reduced levels of omega-3 fatty acids in intensively farmed food and processed foods.[citation needed]

Sleep quality

Poor sleep quality co-occurs with major depression. Major depression leads to alterations in the function of the hypothalamus and pituitary causing excessive release of cortisol which can lead to poor sleep quality. Individuals suffering from Major Depression have been found to have an abnormal sleep architecture, often entering REM sleep sooner than usual, along with highly emotionally-charged dreaming. Antidepressant drugs, which often function as REM sleep suppressants, may serve to dampen abnormal REM activity and thus allow for a more restorative sleep to occur.

Seasonal affective disorder

Seasonal affective disorder (SAD) is a type of depressive disorder that occurs in the winter when daylight hours are short. It is believed that the body's production of melatonin, which is produced at higher levels in the dark, plays a major part in the onset of SAD and that many sufferers respond well to bright light therapy, also known as phototherapy.[citation needed]

Postpartum depression

Postpartum depression refers to the intense, sustained, and sometimes disabling depression experienced by women after giving birth. Postpartum depression, which has incidence rate of 10-15%, typically sets in within three months of labor and can last for as long as three months.[28] About two new mothers out of a thousand experience the more serious depressive disorder Postnatal Psychosis which includes hallucinations and/or delusions.

Sociopsychological

Psychological factors

Low self-esteem and self-defeating or distorted thinking are connected with depression. However, it has been proposed that it is the result of depression and not necessarily the cause of it. This is still debated in the scientific community. Although it is not clear which is the cause and which is the effect, it is known that depressed persons who are able to make corrections in their thinking patterns can show improved mood and self-esteem (Cognitive Behavioral Therapy).[citation needed] Psychological factors related to depression include the complex development of one's personality and how one has learned to cope with external environmental factors such as stress.[citation needed]

Early experiences

Events such as the death of a parent, issues with biological development, school related problems, abandonment or rejection, neglect, chronic illness, and physical, psychological, or sexual abuse can also increase the likelihood of depression later in life. Post-traumatic stress disorder (PTSD) includes depression as one of its major symptoms.[citation needed]

Life experiences

Job loss, poverty, financial difficulties, gambling addiction, eating disorders, long periods of unemployment, the loss of a spouse or other family member, rape, divorce or the end of a committed relationship, involuntary celibacy, inability to have proper sex or premature ejaculation or other traumatic events may trigger depression. Long-term stress at home, work, or school can also be involved.

Treatment and services

The treatment of depression is highly individualized to the patient, based on the patient's unique combination of biological, psychological and social health factors and the severity of their condition.[29] The three most conventional treatments for depression include medication, psychotherapy, and Electroconvulsive therapy, however new treatments and less conventional options are also available, including self help, life style changes, and vagus nerve stimulation.[29]

If there is an imminent threat of suicide or the patient is a danger to others, hospitalization is employed as an intervention method to keep at-risk individuals safe until they cease to be a danger to themselves or others. At-risk individuals may also be placed in a partial hospitalization therapy, in which the patient sleeps at home but spends most of the day in a psychiatric hospital setting. This intensive treatment usually involves group therapy, individual therapy, medication management, and is used often in the case of children and adolescents.

Drug therapy

Sufferers of moderate and severe depression may benefit from the use of antidepressant drugs. Selective serotonin reuptake inhibitors, such as citalopram (Celexa), fluoxetine (Prozac), paroxetine (Paxil), and sertraline (Zoloft), are the primary medications considered for patients, having fewer side effects than the older monoamine oxidase inhibitors (MAOIs). MAOIs may be the best medication for a small number of patients, however those patients will have to avoid a variety of foods and decongestant medications to reduce the chances of a hypertensive crisis.[1] Bupropion (Wellbutrin, Zyban), an atypical antidepressant that acts as a norepinephrine and dopamine reuptake inhibitor, is also considered to be effective in the treatment of depression,[30] without sexual dysfunction or sexual side effects[31] and without weight gain. Bupropion has also been shown to be more effective than SSRIs at improving symptoms such as hypersomnia and fatigue in depressed patients.[32]

A patient's doctor may have to change the antidepressant taken, adjust the dosages of medications, or try different combinations of antidepressants before finding the most effective option for the patient; response rates to the first agent administered may be as low as 50%.[33] It may take anywhere from 3 to 8 weeks after the start of medication before its therapeutic effects can be fully discovered. Patients are generally advised not to stop taking an antidepressant suddenly and to continue its use for at least four months to prevent the chance of recurrence. For patients that have chronic depression, medication may need to be continued for the remainder of their life.[1]

Psychotherapy

There are a number of psychotherapies for depression. These psychotherapies may be provided individually or in a group format. Psychotherapy can be delivered by a variety of mental health professionals, including psychiatrists, psychologists, clinical social workers, or psychiatric nurses.

The most studied form of psychotherapy for depression is cognitive therapy (also called Cognitive behavioral therapy). Several clinical trials have shown that CBT is as effective as anti-depressant medications, even among more severely depressed patients. While the precise mechanisms of change in CBT remain an active area of research, CBT is thought to work by teaching patients to learn a set of cognitive and behavioral skills, which they can employ on their own.

A number of other psychotherapies for depression exist. There is evidence that behavioral therapy (called behavioral activation in the treatment of depression) and interpersonal therapy are effective treatments for depression. Interpersonal psychotherapy focuses on the social and interpersonal triggers that cause their depression. Behavioral therapy is based on the assumption that behaviors are learned. This type of therapy attempts to teach people more healthful types of behaviors. Therapy can be used to help a person develop or improve interpersonal skills in order to allow him or her to communicate more effectively and reduce stress. Narrative therapy gives attention to each person's "dominant story" by means of therapeutic conversations, which also may involve exploring unhelpful ideas and how they came to prominence. Possible social and cultural influences may be explored if the client deems it helpful. Supportive therapy encourages people to discuss their problems and provides them with emotional support. The focus is on sharing information, ideas, and strategies for coping with daily life. Family therapy helps people live together more harmoniously and undo patterns of destructive behavior.

Earlier research initially suggested that psychotherapy, specifically cognitive-behavioral therapy, was not as effective as medication in the treatment of depression, however recent research suggests that CBT can perform as well as anti-depressant medication in the treatment of moderate to severe depression treated on an outpatient basis.[citation needed] With more complex and chronic forms of depression the most effective treatment is often a combination of medication and psychotherapy.[34]

Electroconvulsive therapy

Electroconvulsive therapy (ECT), also known as electroshock or electroshock treatment, uses short bursts of a controlled current of electricity (typically fixed at 0.9 ampere) into the brain to induce a brief, artificial seizure while the patient is under general anesthesia.

In contrast to direct electroshock of years ago, most countries now allow ECT to be administered only under anaesthesia. In a typical regimen of treatment, a patient receives three treatments per week over three or four weeks. Repeat sessions may be needed. Short-term memory loss, disorientation, and headache are very common side effects. Detailed neuropsychological testing in clinical studies has not been able to prove permanent effects on memory. ECT offers the benefit of a very fast response; however, this response has been shown not to last unless maintenance electroshock or maintenance medication is used. Whereas antidepressants usually take around a month to take effect, the results of ECT have been shown to be much faster. For this reason, it is the treatment of choice in emergencies (e.g., in catatonic depression in which the patient has ceased oral intake of fluid or nutrients).

There remains much controversy over ECT. Advocacy groups and scientific critics, such as Dr Peter Breggin,[35] call for restrictions on its use or complete abolishment. Like all forms of psychiatric treatment, electroshock can be given without a patient's consent, but this is subject to legal conditions dependent on the jurisdiction. In Oregon patient consent is necessary by statute.

Other methods of treatment

Light therapy

Light therapy involves exposing a person to bright light, usually from a fluorescent bulb, for a regular interval daily, usually in the morning. The evaluation of light therapy has provided unique challenges in the area of experimental design to researchers attempting to evaluate its effectiveness, especially in comparison to antidepressant medications. Like other forms of treatment for depression, the mechanisms of action of light therapy are poorly understood. There is evidence that light therapy, similarly to both some antidepressant medications and total sleep deprivation, has an antidepressant effect through affecting serotonin transport.[36]

Bright light (both sunlight and artificial light) has been shown to be effective in seasonal affective disorder.[37] It has also been shown to be effective in non-seasonal depression as well.[38] A randomized controlled trial published in 2005 found light therapy to be about as effective as most antidepressants[39]. Light therapy has the advantage of producing faster results (typically within one week) than treatment by most antidepressants (many of which take several weeks for any noticeable effects).[40] A preliminary study found that light therapy is comparable to antidepressants for postpartum depression, and called for further studies.[41] It also avoids some of the side effects of such medication. However, like SSRI's, it also leaves patients vulnerable to mood sensitivity to rapid tryptophan depletion.[42]

Acupuncture

In studies, acupuncture appears to be helpful in reducing depression; one study by the National Institute of Health found a 43% decrease in depression by those receiving acupuncture specifically targeting depression.[43] Other studies have found acupuncture as effective as medication; however, the placebo effect was not able to be ruled out.[44]

Exercise

Studies have indicated that changes in lifestyle, such as regular exercise, when used in conjunction with medication with non-suicidal patients can have beneficial effects in the prevention of depression returning. Patients that completed 30 minutes of brisk exercise at least 3 times a week were found to have a significantly lower incidence of relapse.[45]

Hypnotherapy

In recent years, cognitive hypnotherapy, in conjunction with behavior therapy has been cited as an alternative method of treating clinical depression.[46] Some studies have shown that hypnotherapy can help to reduce symptoms and to aid in teaching coping skills and strategies to help reduce the chance for recurrence.[47]

Meditation

Meditation is increasingly seen as a useful treatment for some cases of depression.[48] The current professional opinion on meditation is that it represents at least a complementary method of treating depression, a view that has been endorsed by the Mayo Clinic.[49] Since the late 1990s, much research has been carried out to determine how meditation affects the brain (see the main article on meditation). Although the effects on the mind are complex, they are often quite positive, encouraging a calm, reflective, and rational state of mind that can be of great help against depression.[citation needed]

Deep brain stimulation

Though still experimental, a new form of treatment called deep brain stimulation offers some hope in the relief of treatment resistant clinical depression. Published in the journal Neuron (2005), Helen Mayberg described the implanting of electrodes in a region of the brain known as Area 25.[50] The electrodes act in an inhibitory fashion, on an otherwise overactive region of the brain. Further research is required before it becomes available as a method of treatment, but it offers hope for those suffering from treatment resistant depression.

Archaic methods

Insulin shock therapy is an old and largely abandoned treatment of severe depressions, psychoses, catatonic states, and other mental disorders. It consists of induction of hypoglycemic coma by intravenous infusion of insulin.

Atropinic shock therapy, also known as atropinic coma therapy, is an old and rarely used method. It consists of induction of atropinic coma by rapid intravenous infusion of atropine.

Atropinic shock treatment is considered safe, but it entails prolonged coma (4–5 hours), with careful monitoring and preparation, and it has many unpleasant side effects, such as blurred vision.

Self-medication

Self-medication is the use of drugs or alcohol to treat a perceived or real malady, usually of a psychological nature. Typically the use of non-prescription chemicals are taken with the intent of the user to alter a mood state for a temporary amount of time. In one study, cannabis users who use once a week or less were shown to have fewer symptoms of depression.[51]

Herbal and dietary supplements

5-HTP supplements are claimed to provide more raw material to the body's natural serotonin production process. There is a reasonable indication that 5-HTP may not be effective for those who have not already responded well to an SSRI because of their similar function: SSRIs prolong serotonin concentrations in the synapse, while 5-HTP induces production of more serotonin.[52]

S-adenosyl methionine (SAM-e) is a derivative of the amino acid methionine that is found throughout the human body, where it acts as a methyl donor and participates in other biochemical reactions. It is available as a prescription antidepressant in Europe and an over-the-counter dietary supplement in the United States. Clinical trials have shown SAM-e to be as effective as standard antidepressant medication, with fewer side effects; however, some studies have reported an increased incidence of mania resulting from SAM-e use compared to other antidepressants.[53][54] Its mode of action is unknown.

Omega-3 fatty acids (found naturally in oily fish, flax seeds, hemp seeds, walnuts, and canola oil) have also been found to be effective when used as a dietary supplement (although only fish-based omega-3 fatty acids have shown antidepressant efficacy.[55]) In addition to the total amount of omega 3 oils in the body, the level of omega 6 fatty acids have also been found to be implicated. An excess of omega 6 appears to be associated with depression.[56]

Dehydroepiandrosterone (DHEA), available as a supplement in the U.S., has been shown to be effective in small trials.[57]

Magnesium supplementation has gathered some attention as a possible treatment for depression.[58] Some case reports demonstrate rapid recovery from major depression using magnesium treatment.[59]

St John's Wort Except under medical supervision, St. John's Wort should not be used with SSRIs or MAOIs because of the risk of serotonin syndrome.[60]

Ginkgo Biloba Effective natural antidepressant[61] said to stabilise cell membranes, inhibiting lipid breakdown and aiding cell use of oxygen and glucose - so subsequently a mental and vascular stimulant that improves neurotransmitter production. Also popular for treating mental concentration (such as for Alzheimer's and stroke patients).

Siberian Ginseng [Eleutherococcus senticosus] Although not a true panax ginseng it is claimed by some to be a mood enhancement supplement against stress. The claims are that it is effective for treating depression, insomnia, moodiness, fatigue, poor memory, lack of focus, mental tension and endurance. There is little or no scientific evidence to support these claims.

Zinc has had an antidepressant effect in an experiment.[62]

Biotin: a deficiency has caused a severe depression. The patient's symptoms improved after the deficiency was corrected.

B vitamins: Symptoms of a deficiency in vitamins such as vitamin B6, B12 and others can include depression and other psychiatric disorders.[63]

Chromium: Evidence has emerged that supplementing with high doses of chromium (ie: in doses of several hundred to 100 mg) exerts antidepressant effects[64]. It has been found to enhance the availability of serotonin and norepinephrine. Chromium in the form of chromium picolinate has generated some controversy as it has been shown to increase damage to DNA in the ovary cells of hamsters, possible increasing the risk of cancer.[65]

Rhodiola Rosea: Rhodiola is a herb growing in cold climates that has just recently been introduced to the west. It has been shown to help alleviate depression and fatigue. It is believed to elevate extracellular levels of monoamines and beta-endorphins.[66]

Transcranial magnetic and cranial electrotherapy stimulation

There are as-yet unproven claims that using magnets or electrical currents can, in some yet to be explained way, reduce depression. In Repetitive transcranial magnetic stimulation (rTMS) a magnetic field is applied to the left prefrontal cortex.

Cranial electrotherapy stimulation devices (CES devices) use electrodes placed on or just behind the ear to generate an very small electrical current. In normal healthy males this microcurrent has been shown to affect alpha wave and beta wave brain activity, which according to the authors,"suggest beneficial changes in mental state".[67] Unlike transcranial magnetic stimulation and vagus nerve stimulation, CES devices are small, relatively inexpensive, and are designed for home use. Unlike vagus nerve stimulation, no surgery is required.

According to a 2002 review, there have been no controlled trials of SES for clinical depression as a primary diagnosis.[68] Several double-blind studies of mixed groups of psychiatric patients have been conducted in the 1970s. The results were inconclusive and largely negative in one of these trials.[69] In another trial, no difference between the placebo and treatment groups were found on any of the five measures employed.[70] A third trial reported overall inconclusive results; however, four out of six clinically depressed patients dropped out of the study because of the massive worsening of depressive symptoms, with two of them becoming actively suicidal.[71] One of the authors of the third study cautioned that CES “should not be used as a treatment of choice” for the patients with the primary diagnosis of depression, “and should be used with caution if this diagnosis is suspected.”[72] Many preliminary, small-scale studies have been conducted which show the effectiveness of CES therapy[73][74][75][76]; however, to date there exists no consensus or even prospective clinical trials to support its use.

All of the CES devices currently on the market have been granted marketing authorization by the FDA based on the legacy waver, that is because a sufficiently similar device had been marketed before 1976, when the new regulations requiring controlled testing were introduced.[77] Such approval is sometimes misunderstood as evidence of efficacy, it should only be taken as lack of evidence of harm. The FDA considers them to be the class III devices—"devices for which insufficient information exists to assure that general controls and special controls provide reasonable assurance of safety and effectiveness"[78]

Vagus nerve stimulation

Vagus nerve stimulation therapy is a treatment used since 1997 to control seizures in epileptic patients and has recently been approved for treating resistant cases of treatment-resistant depression (TRD). The VNS Therapy device is implanted in a patient's chest with wires that connect it to the vagus nerve, which it stimulates to reach a region of the brain associated with moods. The device delivers controlled electrical currents to the vagus nerve at regular intervals.

Prognosis

Recurrence is more likely if treatment has not resulted in full remission of symptoms.4 In fact, current guidelines for antidepressant use recommend 4 to 6 months of continuing treatment after symptom resolution to prevent relapse.

Combined evidence from many randomized controlled trials indicates that continuing antidepressant medications after recovery substantially reduces (halves) the chances of relapse. This preventive effect probably lasts for at least the first 36 months of use.[79]

Anecdotal evidence suggests that chronic disease is accompanied by recurrence after prolonged treatment with antidepressants (tachyphylaxis). Psychiatric texts suggest that physicians respond to recurrence by increasing dosage, complementing the medication with a different class, or changing the medication class entirely. The reason for recurrence in these cases is as poorly understood as the change in brain physiology induced by the medications themselves. Possible reasons may include aging of the brain or worsening of the condition. Most SSRI psychiatric medications were developed for short-term use (a year or less) but are widely prescribed for indefinite periods.[80]

History

The modern idea of depression appears similar to the much older concept of melancholia. The name melancholia derives from "black bile", one of the "four humours" postulated by Galen.

Clinical depression was originally considered to be a chemical imbalance in transmitters in the brain, a theory based on observations made in the 1950s of the effects of reserpine and isoniazid in altering monoamine neurotransmitter levels and affecting depressive symptoms.[81] Since these suggestions, many other causes for clinical depression have been proposed.[20]

Potential evolutionary advantages of clinical depression

Main article: Evolutionary advantages of clinical depression

Some medical professionals and anthropologists have formed several theories as to how depression may have evolutionary advantages. Depression, as a response to environmental stimuli, may be an an adaptive advantage that can increase genetic fitness.

See also

Books by psychologists and psychiatrists

  • Beck, A. T., Rush, A. J., Shaw, B. F., Emery, G. (1987). Cognitive therapy of depression. New York: Guilford.
  • Burns, David D. (1999). Feeling Good : The New Mood Therapy. Avon.
  • Griffin, J., Tyrrell, I. (2004) How to lift Depression – Fast. HG Publishing. ISBN 1-899398-41-4
  • Jacobson, Edith: "Depression; Comparative Studies of Normal, Neurotic, and Psychotic Conditions", International Universities Press, 1976, ISBN 0-8236-1195-7
  • Klein, D. F., & Wender, P. H. (1993). Understanding depression: A complete guide to its diagnosis and treatment. New York: Oxford University Press.
  • Kramer, Peter D. (2005). Against Depression. New York: Viking Adult.
  • Plesman, J. (1986). Getting off the Hook, Sydney Australia. A self-help book available on the internet.
  • Rowe, Dorothy (2003). Depression: The way out of your prison. London: Brunner-Routledge.
  • Sarbadhikari, S. N. (ed.) (2005) Depression and Dementia: Progress in Brain Research, Clinical Applications and Future Trends. Hauppauge, Nova Science Publishers. ISBN 1-59454-114-0.
  • Weissman, M. M., Markowitz, J. C., & Klerman, G. L. (2000). Comprehensive guide to interpersonal psychotherapy. New York: Basic Books.
  • Bieling, Peter J. & Anthony, Martin M. (2003) Ending The Depression Cycle. New Harbinger Publications. ISBN 1572243333

Historical account

  • Healy, David. (1999). The Antidepressant Era, Paperback Edition, Harvard University Press. ISBN 0-674-03958-0

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This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Clinical_depression". A list of authors is available in Wikipedia.
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