Sunday, June 27, 2010

Dr Smita Pandey Bhat - Psychologist Gurgaon Delhi


Clinical Depression - Causes Types and Treatment

Clinical depression (also called major depressive disorder, or unipolar depression when compared to bipolar disorder) is a state of intense sadness, melancholia or despair that has advanced to the point of being disruptive to an individual's social functioning and/or activities of daily living.

A person suffering from depression may feel tired, sad, irritable, lazy, unmotivated, and apathetic. Clinical depression is generally acknowledged to be more serious than normal depressed feelings. It often leads to constant negative thinking and sometimes substance abuse. Extreme depression can culminate in its sufferers attempting or committing suicide.
Without careful assessment, delirium can easily be confused with depression and a number of other psychiatric disorders because many of the signs and symptoms are conditions present in depression, as well as other mental illnesses including dementia and psychosis.

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.(Schildkraut,1965) Since these suggestions, many other causes for clinical depression have been proposed.(Castren,2005)

Prevalence:
Clinical depression affects about 7% - 18%(Bland,1997) of the population on at least one occasion in their lives, before the age of 40.About twice as many females as males report or receive treatment for clinical depression, due to stress and adversity, 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(Murray and Lopez,1997).



Types of depression:
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 clinical 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"; periods of depression may occur as discrete events or recur over the lifespan. Episodes of major or clinical depression may be further divided into mild, major or severe. Where 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 on one 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, 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.
• Depression with Psychotic Features - Some people with Major Depressive or Manic episode 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 categories of depression
Dysthymia is a long-term, mild depression that lasts for a minimum of two years. There must be persistent depressed mood continuously for at least two years. By definition the symptoms are not as severe as with Major Depression, although those with Dysthymia are vulnerable to co-occurring episodes of Major Depression. This disorder often begins in adolescence and crosses the lifespan. People who are diagnosed with major depressive episodes and dysthymic disorder are diagnosed with double depression. Dysthymic disorder develops first and then one or more major depressive episodes happen later.
Bipolar I Disorder is an episodic illness in which moods may cycle between mania and depression. In the United States, Bipolar Disorder was previously called Manic Depression. This term is no longer favored by the medical community, however, even though depression plays a much stronger (in terms of disability and potential for suicide) role in the disorder. "Manic Depression" is still often used in the non-medical community. Bipolar II Disorder is an episodic illness that is defined primarily by depression but evidences episodes of hypomania.
Postpartum Depression or Post-Natal Depression is clinical depression that occurs within two years of childbirth. Owing to physical, mental and emotional exhaustion combined with sleep-deprivation, motherhood can "set women up", so to speak, for clinical depression.(Kathy,2005)
Premenstrual dysphoria is a pattern of recurrent depressive symptoms tied to the menstrual cycle. The premenstrual decline in brain serotonin function is strongly correlated with the concomitant worsening of self-rated cardinal mood symptoms.(Eriksson et al , 2006) Of considerable clinical importance, the recent understanding of premenstrual dysphoria as depression points directly to effective treatment with Selective serotonin reuptake inhibitor (SSRI) antidepressants. Previously, disrupting ovarian cyclicity had been the only recognized treatment. A recent review of studies of a number of SSRIs has revealed that they can effectively ameliorate symptoms of premenstrual dysphoria and may actually work best when taken only during the part of the menstrual cycle when dysphoric symptoms are evident.
Recurrent brief depressive disorder (or recurrent brief depression) is in the ICD-10 classification. It is described as meeting the criteria for a mild, moderate or severe depressive episode; the depressive episodes have occurred about once per month over the last year; individual episodes last less than two weeks (typically less than 2-3 days), and they do not occur solely in relation to the menstrual cycle. Some people are at risk of self-harm, as well as the disruption to everyday life, particularly work

The role of anxiety in depression
Anxiety: 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(van Praag,2005). 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.
Causes of clinical depression:
Physiological causes
Genetic predisposition
The tendency to develop depression may be inherited: according to the National Institute of Mental Health there is some evidence that depression may run in families, though this familial trend probably includes both biological and environmental factors.
Brain chemicals called neurotransmitters allow electrical signals to move from the axon of one nerve cell to the neuron of another. A shortage of neurotransmitters impairs brain communication.
Neurological:
Many modern antidepressant drugs change levels of certain neurotransmitters, namely serotonin and norepinephrine (noradrenaline). However, the relationship between serotonin, SSRIs, and depression usually 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. Evidence has shown the involvement of neurogenesis in depression, though the role is not exactly known.(Castren,2005). Recent research has suggested that there may be a link between depression and neurogenesis of the hippocampus. 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 dysthemic mood. That is why treatment usually results in an increase of serotonin levels in the brain which would in turn stimulate neurogenesis and therefore increase the total mass of the Hippocampus and restores mood and memory, therefore assisting in the fight against the mood disorder.
In about one-third of individuals diagnosed with attention-deficit hyperactivity disorder (ADHD), a developmental neurological disorder, depression is recognized as comorbid Dysthymia,(Hallowell,Edward and Ratey,2005) 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
Medical conditions
Certain illnesses, including cardiovascular disease(Maney and Maney,2004) hepatitis, mononucleosis, hypothyroidism, 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.
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(Felicity,2004) This link has been at least partly validated by studies using dietary supplements in schools and by a double-blind test in a prison. An excess of omega-6 fatty acids in the diet was shown to cause depression in rats.Depression can also be caused by a magnesium deficiency or lower magnesium levels.
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.

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. About two new mothers out of a thousand experience the more serious depressive disorder Postnatal Psychosis which includes hallucinations and/or delusions.
Socio- psychological causes
Psychological factors
Low self-esteem and self-defeating or distorted thinking are connected with depression. 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). 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.
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 symptom.
Life experiences
Job loss, poverty, financial difficulties, gambling addiction, 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.
Evolution: Potential adaptive advantages of clinical depression:
Evolutionary analyses examine the ways in which depression as a response to certain environmental stimuli may act as an adaptive advantage and increase genetic fitness, either of the individual or the society as a whole.
The psychic pain hypothesis
Psychic pain, such as depression, is analogous to physical pain. The function of physical pain is to inform the organism that it is suffering damage, to motivate it to withdraw from the source of damage, and to learn to avoid such damage-causing circumstances in the future. Analogously, depression informs the sufferer that current circumstances, such as the loss of a mate, are imposing a threat to biological fitness, it motivates the sufferer to cease activities that led to the costly situation, if possible, and it causes him or her to learn to avoid similar circumstances in the future. Proponents of this view tend to focus on low mood, and regard clinical depression as a dysfunctional extreme of low mood..
Rank theory
Rank theory: If an individual is involved in a lengthy fight for dominance in a social group and is clearly losing, depression causes the individual to back down and accept the submissive role. In doing so, the individual is protected from unnecessary harm. In this way, depression helps maintain a social hierarchy. This theory is a special case of a more general theory derived from the psychic pain hypothesis: that the cognitive response that produces modern-day depression evolved as a mechanism that allows people to assess whether they are in pursuit of an unreachable goal, and if they are, to motivate them to desist.
Honest signaling theory
When social partners have conflicts of interest, 'cheap' signals of need, such as crying, might not be believed. Biologists and economists have proposed that signals with inherent costs can credibly signal information when there are conflicts of interest. The symptoms of major depression, such as loss of interest in virtually all activities and suicidality, are inherently costly, but, as costly signaling theory requires, the costs differ for individuals in different states. For individuals who are not genuinely in need, the fitness cost of major depression is very high because it threatens the flow of fitness benefits. For individuals who are in genuine need, however, the fitness cost of major depression is low because the individual is not generating many fitness benefits. Thus, only an individual in genuine need can afford to suffer major depression. Major depression therefore serves as an honest, or credible, signal of need
Social navigation or niche change theory
The social navigation, bargaining, or niche change hypothesis (Schildkraut,1965) suggests that depression, operationally defined as a combination of prolonged anhedonia and psychomotor retardation or agitation, provides a focused sober perspective on socially imposed constraints hindering a person’s pursuit of major fitness enhancing projects. Simultaneously, publicly displayed symptoms, which reduce the depressive's ability to conduct basic life activities, serve as a social signal of need; the signal's costliness for the depressive certifies its honesty. Finally, for social partners who find it uneconomical to respond helpfully to an honest signal of need, the same depressive symptoms also have the potential to extort relevant concessions and compromises. Depression’s extortionary power comes from the fact that it retards the flow of just those goods and services such partners have come to expect from the depressive under status quo socioeconomic arrangements.
Thus depression may be a social adaptation especially useful in motivating a variety of social partners, all at once, to help the depressive initiate major fitness-enhancing changes in their socioeconomic life. There are extraordinarily diverse circumstances under which this may become necessary in human social life, ranging from loss of rank or a key social ally which makes the current social niche uneconomic to having a set of creative new ideas about how to make a livelihood which begs for a new niche. The social navigation hypothesis emphasizes that an individual can become tightly ensnared in an overly restrictive matrix of social exchange contracts, and that this situation sometimes necessitates a radical contractual upheaval that is beyond conventional methods of negotiation. Regarding the treatment of depression, this hypothesis calls into question any assumptions by the clinician that the typical cause of depression is related to maladaptive perverted thinking processes or other purely endogenous sources. The social navigation hypothesis calls instead for a penetrating analysis of the depressive’s talents and dreams, identification of relevant social constraints (especially those with a relatively diffuse non-point source within the social network of the depressive), and practical social problem-solving therapy designed to relax those constraints enough to allow the depressive to move forward with their life under an improved set of social contracts(Watson and Andrews ,2002).
Bargaining theory
This theory is similar to the honest signaling, niche change, and social navigation theory. It basically adds one additional element to honest signaling theory. The fitness of social partners is generally correlated. When a wife suffers depression and reduces her investment in offspring, for example, the husband's fitness is also put at risk. Thus, not only do the symptoms of major depression serve as costly and therefore honest signals of need, they also compel social partners to respond to that need in order to prevent their own fitness from being reduced..
Diagnosis
It is hard for people who have not experienced clinical depression, either personally or by regular exposure to people suffering it, to understand its emotional impact and severity, interpreting it instead as being similar to "having the blues" or "feeling down." As the list of symptoms below indicates, clinical depression is a serious, potentially lethal systemic disorder characterized by the psychiatric profession as interlocking physical, affective, and cognitive symptoms that have consequences for function and survival well beyond sad or painful feelings.
DSM-IV-TR criteria
According to the DSM-IV-TR criteria for diagnosing a major depressive disorder (cautionary statement) one of the following two elements must be present for a period of at least two weeks:
• Depressed mood, or
• Anhedonia
It is sufficient to have either of these symptoms in conjunction with five of a list of other symptoms over a two-week period. These include:
• Feelings of overwhelming sadness and/or fear, or the seeming inability to feel emotion (emptiness).
• A decrease in the amount of interest or pleasure in all, or almost all, daily activities.
• Changing appetite and marked weight gain or loss.
• Disturbed sleep patterns, such as insomnia, loss of REM sleep, or excessive sleep (hypersomnia).
• Psychomotor agitation or retardation nearly every day.
• Fatigue, mental or physical, also loss of energy.
• Intense feelings of guilt, nervousness, helplessness, hopelessness, worthlessness, isolation/loneliness and/or anxiety.
• Trouble concentrating, keeping focus or making decisions or a generalized slowing and obtunding of cognition, including memory.
• Recurrent thoughts of death (not just fear of dying), desire to just "lie down and die" or "stop breathing", recurrent suicidal ideation without a specific plan, or a suicide attempt or a specific plan for committing suicide.
• Feeling and/or fear of being abandoned by those close to one.
Other symptoms
Other symptoms often reported but not usually taken into account in diagnosis include:
• Self-loathing.
• A decrease in self-esteem.
• Inattention to personal hygiene.
• Sensitivity to noise.
• Physical aches and pains, and the belief these may be signs of serious illness.
• Fear of 'going mad'.
• Change in perception of time.
• Periods of sobbing.
• Possible behavioral changes, such as aggression and/or irritability.
An additional indicator could be the excessive use of drugs or alcohol. Depressed adolescents are at particular risk of further destructive behaviours, such as eating disorders and self-harm.
A recent study in Journal of Nervous and Mental Disease showed that alternative symptoms of depression including diminished drive, hopelessness and helplessness, lack of reactivity, anger, psychic and somatic anxiety can be as effective as current DSM-IV criteria in diagnosis. According to this study, diminished drive has a higher diagnostic criteria than all others except for depressed mood with sensitivity of 88.2 of specificity of 69.9(Mc Glinchey et al., 2006)
Depression in children is not as obvious as it is in adults. Children may show symptoms such as:
• Loss of appetite.
• Irritability.
• Sleep problems, such as recurrent nightmares.
• Learning or memory problems where none existed before.
• Significant behavioral changes; such as withdrawal, social isolation, and aggression.
Treatment
Treatment of depression varies broadly among individuals. The level, type, and methods of intervention vary dramatically. There are two primary modes of treatment that are typically used in conjunction; medication and psychotherapy. A significant number of recent studies have indicated that changes in lifestyle such as regular exercise and dietary supplements have beneficial effects.(Castren,2005)
In most cases, one particular medication or combination of medications can provide significant change, although, in some cases, the condition does not respond well. Treatment-resistant depression warrants a full assessment, which may lead to the introduction of psychotherapy, a focus on lifestyle change, an increase of medication, or a change in medication.
In emergencies, hospitalization is an intervention employed to keep at-risk individuals safe until they cease to be a danger to themselves or others. An alternative treatment program is partial hospitalization, 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 often in the case of children and adolescents, academics.
Medication
Medication that relieves the symptoms of depression has been available for several decades. Typical first-line therapy for depression is the use of a selective serotonin reuptake inhibitor, such as citalopram (Celexa), fluoxetine (Prozac), paroxetine (Paxil), and sertraline (Zoloft). Under some circumstances, medication and psychotherapy may be more effective than either treatment separately(Thase,1999). Selective serotonin reuptake inhibitors (SSRIs)
Selective serotonin reuptake inhibitors (SSRIs) are a family of antidepressants considered to be the current standard of drug treatment. It is thought that one cause of depression is an inadequate amount of serotonin, a chemical used in the brain to transmit signals between neurons. SSRIs are said to work by preventing the reuptake of serotonin by the presynaptic nerve, thus maintaining higher levels of 5-HT in the synapse. Recently, however, work by two researchers has called into question the link between serotonin deficiency and symptoms of depression, noting that the efficacy of SSRIs as treatment does not in itself prove the link.(Lacasse and Leo,2005). Recent research indicates that these drugs may interact with transcription factors known as "clock genes", which may be important for the addictive properties of drugs of abuse and possibly in obesity.(Yuferov et al., 2005)
Recent randomized controlled trials in Archives of General Psychiatry showed that up to one-third of effects of SSRI Treatment can be seen in first week. Early effects also shown to have secondary effect of reducing absolute reduction in HDRS score by 50 percent. Even more recent studies, published by the Archives of General Psychiatry note that 25% of so-called clinical depression does not meet a disease criteria and should be considered to be ordinary sadness and adjustment to the difficulties in life.
This family of drugs includes fluoxetine (Prozac), paroxetine (Paxil), escitalopram (Lexapro), citalopram (Celexa), and sertraline (Zoloft). These antidepressants typically have fewer adverse side effects than the tricyclics or the MAOIs, although such effects as drowsiness, dry mouth, nervousness, anxiety, insomnia, decreased appetite, and decreased ability to function sexually may occur. Some side effects may decrease as a person adjusts to the drug, but other side effects may be persistent. Though safer than first generation antidepressants, SSRI's may not work as often, suggesting the role of norepinephrine. However, it should be noted that all psycho-active medications extend the reaction time, thus increasing the likelihood of falls and road crashes.
Serotonin-norepinephrine reuptake inhibitors (SNRIs)
Serotonin-norepinephrine reuptake inhibitors (SNRIs) such as venlafaxine (Effexor) and duloxetine (Cymbalta) are a newer form of antidepressant that works on both norepinephrine and 5-HT. They typically have similar side effects to the SSRIs, although there may be a withdrawal syndrome on discontinuation that may necessitate dosage tapering.
Noradrenergic and specific serotonergic antidepressants (NASSAs)
Noradrenergic and specific serotonergic antidepressants (NASSAs) form a newer class of antidepressants which purportedly work to increase norepinephrine (noradrenaline) and serotonin neurotransmission by blocking presynaptic alpha-2 adrenergic receptors while at the same time minimizing serotonin related side-effects by blocking certain serotonin receptors. The only example of this class in clinical use is mirtazapine (Avanza, Zispin, Remeron).
Norepinephrine (noradrenaline) reuptake inhibitors (NRIs)
Norepinephrine (noradrenaline) reuptake inhibitors (NRIs) such as reboxetine (Edronax) act via norepinephrine (also known as noradrenaline). NRIs are thought to have a positive effect on concentration and motivation in particular, though they have been known to increase aggression.
Norepinephrine-dopamine reuptake inhibitors
Norepinephrine-dopamine reuptake inhibitors such as bupropion (Wellbutrin, Zyban) inhibit the neuronal reuptake of dopamine and norepinephrine (noradrenaline).
Tricyclic antidepressants (TCAs)
Tricyclic antidepressants are the oldest and include such medications as amitriptyline and desipramine. Tricyclics block the reuptake of certain neurotransmitters such as norepinephrine (noradrenaline) and serotonin. They are used less commonly now due to the development of more selective and safer drugs. Several side effects include increased heart rate, drowsiness, dry mouth, constipation, urinary retention, blurred vision, dizziness, confusion, and sexual dysfunction. Toxicity occurs at approximately ten times normal dosages. However, tricyclic antidepressants are still used because of their high potency, especially in severe cases of clinical depression.
Monoamine oxidase inhibitor (MAOIs)
Monoamine oxidase inhibitors (MAOIs) such as phenelzine (Nardil) may be used if other antidepressant medications are ineffective. Because there are potentially fatal interactions between this class of medication and certain foods (particularly those containing Tyramine), as well as certain drugs, classic MAOIs are rarely prescribed anymore. MAOIs work by blocking the enzyme monoamine oxidase which breaks down the neurotransmitters dopamine, serotonin, and norepinephrine (noradrenaline). MAOIs can be as effective as tricyclic antidepressants, although they can have a higher incidence of dangerous side effects (as a result of inhibition of cytochrome P450 in the liver). A new generation of MAOIs has been introduced; moclobemide (Manerix), known as a reversible inhibitor of monoamine oxidase A (RIMA), acts in a more short-lived and selective manner and does not require a special diet. Additionally, Emsam is a classic MAOI (selegiline) delivered through a transdermal patch, so as to avoid interactions in the digestive tract that otherwise occur when delivered orally.
Augmentor drugs
Some antidepressants have been found to work more effectively in some patients when used in combination with another drug. Such "augmentor" drugs include tryptophan (Tryptan) and buspirone (Buspar).
Tranquillizers and sedatives, typically the benzodiazepines, may be prescribed to ease anxiety and promote sleep. Because of their high potential for fostering dependence, these medications are intended only for short-term or occasional use. Medications often are used not for their primary function but to exploit what are normally side effects. Quetiapine fumarate (Seroquel) is designed primarily to treat schizophrenia and bipolar disorder, but a frequently reported side-effect is somnolence. Therefore, this drug can be used in place of an antianxiety agent such as clonazepam (Klonopin, Rivotril).
Antipsychotics such as risperidone (Risperdal), olanzapine (Zyprexa), and Quetiapine (Seroquel) are prescribed as mood stabilizers and are also effective in treating anxiety. Their use as mood stabilizers is a recent phenomenon and is controversial with some patients. Antipsychotics (typical or atypical) may also be prescribed in an attempt to augment an antidepressant, to make antidepressant blood concentration higher, or to relieve psychotic or paranoid symptoms often accompanying clinical depression. However, they may have serious side effects, particularly at high dosages, which may include blurred vision, muscle spasms, restlessness, tardive dyskinesia, and weight gain.
Antidepressants by their nature behave similarly to psychostimulants. Antianxiety medications by their nature are depressants. Close medical supervision is critical to proper treatment if a patient presents with both illnesses because the medications tend to work against each other.
Psycho-stimulants are sometimes added to an antidepressant regimen if the patient suffers from anhedonia, hypersomnia and/or excessive eating as well as low motivation. These symptoms which are common in atypical depression can be quickly resolved with the addition of low to moderate dosages of amphetamine or methylphenidate (brand names Adderall and Ritalin, respectively)as these chemicals enhance motivation and social behavior, as well as suppress appetite and sleep. These chemicals are also known to restore sex drive. Extreme caution must be used however with certain populations. Stimulants are known to trigger manic episodes in people suffering from bipolar disorder. They are also easily abused as they are effective substitutes for Methamphetamine when used recreationally. Close supervision of those with substance abuse disorders is urged. Emotionally labile patients should avoid stimulants, as they exacerbate mood shifting.
Lithium remains the standard treatment for bipolar disorder and is often used in conjunction with other medications, depending on whether mania or depression is being treated. Lithium's potential side effects include thirst, tremors, light-headedness, and nausea or diarrhea. Some of the anticonvulsants, such as carbamazepine (Tegretol), sodium valproate (Epilim), and lamotrigine (Lamictal), are also used as mood stabilizers, particularly in bipolar disorder.
Medication failure
Approximately 30% of patients have remission of depression with medications(Trivedi et al, 2006) For patients with inadequate response, either adding sustained-release bupropion(initially 200 mg per day then increase by 100 mg up to total of 400 mg per day) or buspirone (up to 60 mg per day) for augmentation as a second drug can cause remission in approximately 30% of patients, while switching medications can achieve remission in about 25% of patients.
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 haven't already responded well to an SSRI because of their similar function: SSRIs allow the brain to use its serotonin more effectively, while 5-HTP induces production of more serotonin.
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.(Roberto et al,.2002) 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.)
Dehydroepiandrosterone (DHEA), available as a supplement in the U.S., has been shown to be effective in small trials.
Magnesium supplementation has gathered some attention as a possible treatment for depression.Some case reports demonstrate rapid recovery from major depression using magnesium treatment. "The possibility that magnesium deficiency is the cause of most major depression and related mental health problems including IQ loss and addiction is enormously important to public health and is recommended for immediate further study"
St John's Wort Except under medical supervision, St. John's Wort should not be used with SSRIs or MAOIs due to the risk of serotonin syndrome
Ginkgo Biloba Effective natural antidepressant 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 a mood enhancement supplement against stress. Also popular for treating depression, insomnia, moodiness, fatigue, poor memory, lack of focus, mental tension and endurance.
Zinc has had an antidepressant effect in an experiment.
Biotin: a deficiency has caused a severe depression. The patient's symptoms improved after the deficiency was corrected.
Vitamin B-12: Symptoms of a vitamin B-12 deficiency can include depression and other psychiatric disorders.
Cannabis, users who use once a week or less have been shown to have fewer symptoms of depression than non-users in one study.
Psychotherapy
In psychotherapy, or counseling, one receives assistance in understanding and resolving habits or problems that may be contributing to or the cause of the depression. This may be done individually or with a group and is conducted by mental health professionals such as psychiatrists, psychologists, clinical social workers, or psychiatric nurses.
Effective psychotherapy may result in different habitual thinking and action which leads to a lower relapse rate than antidepressant drugs alone. Medication, however, may yield quicker results and be strongly indicated in a crisis. Medication and psychotherapy are generally complementary, and both may be used at the same time.
Psychotherapy
There are many counseling approaches, but all are aimed at improving one's personal and interpersonal functioning. Cognitive behavioral therapy has been demonstrated in carefully controlled studies to be among the foremost of the recent wave of methods which achieve more rapid and lasting results than traditional "talk therapy" analysis. Cognitive therapy, often combined with behavioral therapy, focuses on how people think about themselves and their relationships. It helps depressed people learn to replace negative depressive thoughts with realistic ones, as well as develop more effective coping behaviors and skills. 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. Interpersonal psychotherapy focuses on the social and interpersonal triggers that cause their depression. 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. Behavioral therapy is based on the assumption that behaviors are learned. This type of therapy attempts to teach people more healthful types of behaviors. 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.
Transcranial magnetic stimulation
Repetitive transcranial magnetic stimulation (rTMS) is under study as a possible treatment for depression. Initially designed as a tool for physiological studies of the brain, this technique shows promise as a means of alleviating depression. In this therapy, a powerful magnetic field is used to stimulate the left prefrontal cortex, an area of the brain that typically shows abnormal activity in depressed people.
Recent work in Poland suggested that weak, variable magnetic fields may offer relief from depression in those who have not responded to medication. However, some of the existing work has been questioned, with claims that the effect is not as significant once environmental conditions are controlled.
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.
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 electroshock. Advocacy groups and scientific critics, such as Dr Peter Breggin, 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
Bright light (both sunlight and artificial light) is shown to be effective in seasonal affective disorder, and sometimes may be effective in other types of depression, especially atypical depression or depression with "seasonal phenotype" (overeating, oversleeping, weight gain, apathy).
Exercise
It is widely believed that physical activity and exercise help depressed patients and promote quicker and better relief from depression. They are also thought to help antidepressants and psychotherapy work better and faster. It can be difficult to find the motivation to exercise if the depression is severe, but sufferers should be encouraged to take part in some form of regularly scheduled physical activity. A workout need not be strenuous; many find walking, for example, to be of great help. Exercise produces higher levels of chemicals in the brain, notably dopamine, serotonin, and norepinephrine. In general this leads to improvements in mood, which is effective in countering depression.
Meditation
Meditation is increasingly seen as a useful treatment for some cases of depression. 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. 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.
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 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.
Adverse reactions
Aspartame was associated with a significant difference in number and severity of symptoms for patients with a history of depression in an experiment. However, the main findings of this 1993 study have not been replicated since, and its methodology has been criticized on the basis that unrelated symptoms were aggregated artificially, thereby boosting the statistical difference between the aspartame and the placebo conditions.
Recurrence
Recurrence is more likely if treatment has not resulted in full remission of symptoms.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.
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.

Dr Smita Pandey Bhat
Clinical Psychologist
Gurgaon, Delhi - NCR, INDIA

Email : dr.smitapandey@gmail.com
Url : http://child-psychologist.blogspot.com



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