Clinical Depression - Causes Types and Treatment by Dr Smita Pandey
Bhat
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
http://child-psychologist.blogspot.com
